Abnormal involuntary movements which primarily affect the extremities, trunk, or jaw that occur as a manifestation of an underlying disease process. Conditions which feature recurrent or persistent episodes of dyskinesia as a primary manifestation of disease may be referred to as dyskinesia syndromes (see MOVEMENT DISORDERS). Dyskinesias are also a relatively common manifestation of BASAL GANGLIA DISEASES.
Abnormal movements, including HYPERKINESIS; HYPOKINESIA; TREMOR; and DYSTONIA, associated with the use of certain medications or drugs. Muscles of the face, trunk, neck, and extremities are most commonly affected. Tardive dyskinesia refers to abnormal hyperkinetic movements of the muscles of the face, tongue, and neck associated with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS). (Adams et al., Principles of Neurology, 6th ed, p1199)
The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.
Agents used in the treatment of Parkinson's disease. The most commonly used drugs act on the dopaminergic system in the striatum and basal ganglia or are centrally acting muscarinic antagonists.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
The representation of the phylogenetically oldest part of the corpus striatum called the paleostriatum. It forms the smaller, more medial part of the lentiform nucleus.
Syndromes which feature DYSKINESIAS as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions.
Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as CHOREATIC DISORDERS. Chorea is also a frequent manifestation of BASAL GANGLIA DISEASES.
A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.
Drugs used in the treatment of movement disorders. Most of these act centrally on dopaminergic or cholinergic systems. Among the most important clinically are those used for the treatment of Parkinson disease (ANTIPARKINSON AGENTS) and those for the tardive dyskinesias.
A dopamine D2 agonist. It is used in the treatment of parkinson disease, particularly for alleviation of tremor. It has also been used for circulatory disorders and in other applications as a D2 agonist.
Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.
Transference of brain tissue, either from a fetus or from a born individual, between individuals of the same species or between individuals of different species.
A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.
A beta-hydroxylated derivative of phenylalanine. The D-form of dihydroxyphenylalanine has less physiologic activity than the L-form and is commonly used experimentally to determine whether the pharmacological effects of LEVODOPA are stereospecific.
Lens-shaped structure on the inner aspect of the INTERNAL CAPSULE. The SUBTHALAMIC NUCLEUS and pathways traversing this region are concerned with the integration of somatic motor function.
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
An inhibitor of DOPA DECARBOXYLASE that does not enter the central nervous system. It is often given with LEVODOPA in the treatment of parkinsonism to prevent the conversion of levodopa to dopamine in the periphery, thereby increasing the amount that reaches the central nervous system and reducing the required dose. It has no antiparkinson actions when given alone.
Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.
A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.
Transference of fetal tissue between individuals of the same species or between individuals of different species.
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
A plant genus of the family FABACEAE that is the source of mucuna gum.
An inhibitor of DOPA DECARBOXYLASE, preventing conversion of LEVODOPA to dopamine. It is used in PARKINSON DISEASE to reduce peripheral adverse effects of LEVODOPA. It has no antiparkinson actions by itself.
An antiviral that is used in the prophylactic or symptomatic treatment of influenza A. It is also used as an antiparkinsonian agent, to treat extrapyramidal reactions, and for postherpetic neuralgia. The mechanisms of its effects in movement disorders are not well understood but probably reflect an increase in synthesis and release of dopamine, with perhaps some inhibition of dopamine uptake.
Drugs that bind to and activate dopamine receptors.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
Therapy for MOVEMENT DISORDERS, especially PARKINSON DISEASE, that applies electricity via stereotactic implantation of ELECTRODES in specific areas of the BRAIN such as the THALAMUS. The electrodes are attached to a neurostimulator placed subcutaneously.
Several groups of nuclei in the thalamus that serve as the major relay centers for sensory impulses in the brain.
An attitude or posture due to the co-contraction of agonists and antagonist muscles in one region of the body. It most often affects the large axial muscles of the trunk and limb girdles. Conditions which feature persistent or recurrent episodes of dystonia as a primary manifestation of disease are referred to as DYSTONIC DISORDERS. (Adams et al., Principles of Neurology, 6th ed, p77)
Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of CEREBELLAR DISEASES, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of PARKINSON DISEASE.
A traditional grouping of drugs said to have a soothing or calming effect on mood, thought, or behavior. Included here are the ANTI-ANXIETY AGENTS (minor tranquilizers), ANTIMANIC AGENTS, and the ANTIPSYCHOTIC AGENTS (major tranquilizers). These drugs act by different mechanisms and are used for different therapeutic purposes.
The adaptation of therapeutic approaches such as pharmacological (DRUG CHRONOTHERAPY), surgical, radiological, or physical to the known variations in biological RHYTHMICITY, such as CIRCADIAN RHYTHMS. The treatment is aimed at supporting normal rhythms, or modifying the timing of therapy to achieve maximal efficacy and minimal adverse effect.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
An antiepileptic agent related to the barbiturates; it is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite. Adverse effects are reported to be more frequent than with PHENOBARBITAL. (From Martindale, The Extra Pharmacopoeia, 30th ed, p309)
Application of electric current in treatment without the generation of perceptible heat. It includes electric stimulation of nerves or muscles, passage of current into the body, or use of interrupted current of low intensity to raise the threshold of the skin to pain.
A genus of the family CEBIDAE consisting of four species: S. boliviensis, S. orstedii (red-backed squirrel monkey), S. sciureus (common squirrel monkey), and S. ustus. They inhabit tropical rain forests in Central and South America. S. sciureus is used extensively in research studies.
Muscles of facial expression or mimetic muscles that include the numerous muscles supplied by the facial nerve that are attached to and move the skin of the face. (From Stedman, 25th ed)
Acquired and inherited conditions that feature DYSTONIA as a primary manifestation of disease. These disorders are generally divided into generalized dystonias (e.g., dystonia musculorum deformans) and focal dystonias (e.g., writer's cramp). They are also classified by patterns of inheritance and by age of onset.
The largest and most lateral of the BASAL GANGLIA lying between the lateral medullary lamina of the GLOBUS PALLIDUS and the EXTERNAL CAPSULE. It is part of the neostriatum and forms part of the LENTIFORM NUCLEUS along with the GLOBUS PALLIDUS.
The black substance in the ventral midbrain or the nucleus of cells containing the black substance. These cells produce DOPAMINE, an important neurotransmitter in regulation of the sensorimotor system and mood. The dark colored MELANIN is a by-product of dopamine synthesis.
A semisynthetic ergotamine alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion.
Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of dopaminergic neurons. They remove DOPAMINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS and are the target of DOPAMINE UPTAKE INHIBITORS.
A species of the genus MACACA which typically lives near the coast in tidal creeks and mangrove swamps primarily on the islands of the Malay peninsula.
The observable response an animal makes to any situation.
Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.
A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279)
The art, technique, or business of producing motion pictures for entertainment, propaganda, or instruction.
A selective D1 dopamine receptor agonist used primarily as a research tool.
Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D2-class receptor genes contain INTRONS, and the receptors inhibit ADENYLYL CYCLASES.
Surgery performed on the nervous system or its parts.
Techniques used mostly during brain surgery which use a system of three-dimensional coordinates to locate the site to be operated on.
A subtype of dopamine D2 receptors that are highly expressed in the LIMBIC SYSTEM of the brain.
Drugs that bind to and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.
The phylogenetically newer part of the CORPUS STRIATUM consisting of the CAUDATE NUCLEUS and PUTAMEN. It is often called simply the striatum.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D1-class receptor genes lack INTRONS, and the receptors stimulate ADENYLYL CYCLASES.
Relatively invariant mode of behavior elicited or determined by a particular situation; may be verbal, postural, or expressive.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Surgically placed electric conductors through which ELECTRIC STIMULATION is delivered to or electrical activity is recorded from a specific point inside the body.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The middle of the three primitive cerebral vesicles of the embryonic brain. Without further subdivision, midbrain develops into a short, constricted portion connecting the PONS and the DIENCEPHALON. Midbrain contains two major parts, the dorsal TECTUM MESENCEPHALI and the ventral TEGMENTUM MESENCEPHALI, housing components of auditory, visual, and other sensorimoter systems.
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.
Behavioral manifestations of cerebral dominance in which there is preferential use and superior functioning of either the left or the right side, as in the preferred use of the right hand or right foot.
Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in SCHIZOPHRENIA; senile dementia; transient psychosis following surgery; or MYOCARDIAL INFARCTION; etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus.
The period during a surgical operation.
Dominance of one cerebral hemisphere over the other in cerebral functions.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS.
A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.
The making of a radiograph of an object or tissue by recording on a photographic plate the radiation emitted by radioactive material within the object. (Dorland, 27th ed)
Electric conductors through which electric currents enter or leave a medium, whether it be an electrolytic solution, solid, molten mass, gas, or vacuum.
A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.
Electrodes with an extremely small tip, used in a voltage clamp or other apparatus to stimulate or record bioelectric potentials of single cells intracellularly or extracellularly. (Dorland, 28th ed)
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.

Cluster headache-like disorder in childhood. (1/193)

This paper reviews the diagnostic features of cluster headache-like disorder and describes its presentation in childhood. Case note summaries of patients with this condition are presented in the context of a brief summary of the literature. Four patients (two girls; aged 12 to 15 years) with cluster headache-like disorder were seen over a period of four years in the paediatric neurology department of Birmingham Children's Hospital. Their histories and clinical courses are described. All had a history of "thrashing around" or bizarre behaviour during attacks, which had distracted attention from the headache and seemed to contribute to delay in diagnosis. It appears that cluster headache-like disorder does occur in childhood but is not common and can be mistaken for other conditions. A history of thrashing around accompanied by headache is very suggestive. Recognition of the symptoms in the general paediatric clinic would allow rapid diagnosis.  (+info)

Motor disorder in Huntington's disease begins as a dysfunction in error feedback control. (2/193)

A steady progression of motor dysfunction takes place in Huntington's disease (HD). The origin of this disturbance with relation to the motor control process is not understood. Here we studied reaching movements in asymptomatic HD gene-carriers (AGCs) and subjects with manifest HD. We found that movement jerkiness, which characterizes the smoothness and efficiency of motion, was a sensitive indicator of presymptomatic HD progression. A large fraction of AGCs displayed elevated jerk even when more than seven years remained until predicted disease onset. Movement termination was disturbed much more than initiation and was highly variable from trial to trial. Analysis of this variability revealed that the sensitivity of end-movement jerk to subtle, self-generated early-movement errors was greater in HD subjects than in controls. Additionally, we found that HD corrective responses to externally-generated force pulses were greatly disturbed, indicating that HD subjects display aberrant responses to both external and self-generated errors. Because feedback corrections are driven by error and are delayed such that they predominantly affect movement termination, these findings suggest that a dysfunction in error correction characterizes the motor control deficit in early HD. This dysfunction may be observed years before clinical disease onset and grows worse as the disease progresses.  (+info)

Long-term follow-up of unilateral pallidotomy in advanced Parkinson's disease. (3/193)

BACKGROUND: Although the short-term benefits of posteroventral pallidotomy for patients with advanced Parkinson's disease have been well documented, little is known about the long-term outcome of the procedure. METHODS: We conducted a long-term follow-up study of a cohort of 40 patients who had undergone unilateral posteroventral medial pallidotomy between 1993 and 1996. Twenty patients were not evaluated because they had undergone a second surgical procedure (11 patients) or had died (2) or because they had dementia or another debilitating illness (4), lived too far away (1), or had been lost to follow-up (2). We conducted serial postoperative assessments of parkinsonism in the remaining 20 patients while they were taking medications ("on" period) and after overnight withdrawal of the drugs ("off" period). The mean follow-up time was 52 months (range, 41 to 64). RESULTS: The combined off-period score for activities of daily living and motor function on the Unified Parkinson's Disease Rating Scale was 18.0 percent better at the last evaluation than at base line (95 percent confidence interval, 4.9 to 31.0 percent; P=0.01). Significant improvements were also evident in the off-period scores for contralateral tremor (65.4 percent improvement, P=0.007), rigidity (43.2 percent, P=0.03), and bradykinesia (18.2 percent, P=0.04) and in the on-period score for contralateral dyskinesia (70.6 percent, P<0.001). Changes in medication did not contribute to the sustained improvement. The 20 patients who could not be included in the long-term analysis had similar base-line characteristics but a worse response to surgery at six months. CONCLUSIONS: In the group of patients with advanced Parkinson's disease who could be enrolled in our long-term follow-up study of unilateral posteroventral medial pallidotomy (20 patients from the original cohort of 40), significant early improvements in off-period contralateral signs of parkinsonism were sustained for up to five and a half years. There was a sustained significant improvement in on-period contralateral dyskinesia but not in other on-period signs of parkinsonism.  (+info)

Functional anatomy of movement disorders. (4/193)

Models of basal ganglia function are described which encapsulate the principal pathophysiological mechanisms underlying parkinsonian akinesia on the one hand and abnormal involuntary movement disorders (dyskinesias) on the other. In Parkinson's disease, degeneration of the nigrostriatal dopamine system leads to overactivity of the 'indirect' striatopallidal projection to the lateral (external) segment of the globus pallidus. This causes inhibition of lateral pallidal neurons, which in turn project to the subthalamic nucleus. Disinhibition of the subthalamic nucleus leads to abnormal subthalamic overactivity and, as a consequence, overactivity of medial (internal) pallidal output neurons. Dyskinesias, such as are observed in Huntington's disease, levodopa-induced dyskinesia and ballism, share mechanistic features in common and are associated with decreased neuronal activity in both the subthalamic nucleus and the medial globus pallidus.  (+info)

Long term outcome of unilateral pallidotomy: follow up of 15 patients for 3 years. (5/193)

OBJECTIVES: With the advent of new antiparkinsonian drug therapy and promising results from subthalamic and pallidal stimulation, this study evaluated the long term efficacy of unilateral pallidotomy, a technique which has gained popularity over the past decade for the management of advanced Parkinson's disease. METHODS: The 15 patients reported here are part of the original cohort of 24 patients who underwent posteroventral pallidotomy for motor fluctuations and disabling dyskinesias 3 years ago as part of a prospective study. Evaluation scales included the unified Parkinson's disease rating scale, the Goetz dyskinesia scale, and the Purdue pegboard test. RESULTS: When compared with the prepallidotomy scores, the reduction in the limb dyskinesias and off state tremor scores persisted on the side contralateral to pallidotomy at the end of 3 years (dyskinesias were reduced by 64% (p<0.01) and tremor by 63% (p<0.05). Other measures tended to deteriorate. The dosage of antiparkinsonian medications did not change significantly from 3 months prepallidotomy to 3 years postpallidotomy. CONCLUSIONS: Although unilateral pallidotomy is useful in controlling the contralateral dyskinesias and tremor 3 years after surgery, all other early benefits disappear and activities of daily living continue to worsen.  (+info)

Firing patterns and correlations of spontaneous discharge of pallidal neurons in the normal and the tremulous 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine vervet model of parkinsonism. (6/193)

To investigate the role of the basal ganglia in parkinsonian tremor, we recorded hand tremor and simultaneous activity of several neurons in the external and internal segments of the globus pallidus (GPe and GPi) in two vervet monkeys, before and after systemic treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and development of parkinsonism with tremor of 5 and 11 Hz. In healthy monkeys, only 11% (20/174) of the GPe cells and 3% (1/29) of the GPi cells displayed significant 3-19 Hz oscillations. After MPTP treatment, 39% (107/271) of the GPe cells and 43% (26/61) of the GPi cells developed significant oscillations. Oscillation frequencies of single cells after MPTP treatment were bimodally distributed around 7 and 13 Hz. For 10% of the oscillatory cells that were recorded during tremor periods, there was a significant tendency for the tremor and neuronal oscillations to appear simultaneously. Cross-correlation analysis revealed a very low level of correlated activity between pallidal neurons in the normal state; 95.6% (477/499) of the pairs were not correlated, and oscillatory cross-correlograms were found in only 1% (5/499) of the pairs. After MPTP treatment, the correlations increased dramatically, and 40% (432/1080) of the cross-correlograms had significant oscillations, centered around 13-14 Hz. Phase shifts of the cross-correlograms of GPe pairs, but not of GPi, were clustered around 0 degrees. The results illustrate that MPTP treatment changes the pattern of activity and synchronization in the GPe and GPi. These changes are related to the symptoms of Parkinson's disease and especially to the parkinsonian tremor.  (+info)

The subthalamic nucleus, hemiballismus and Parkinson's disease: reappraisal of a neurosurgical dogma. (7/193)

The subthalamic nucleus (STN) currently is considered to play a key role in the pathophysiological origin of the parkinsonian state and is therefore the main target for surgical treatment of Parkinson's disease. The authors review the incidence of hemichorea/ballism (HCB) as a complication of thalamotomy, pallidotomy or campotomy procedures before the introduction of levodopa therapy, including the few reported cases accompanied by a neuropathological study. The literature shows that only a small number of parkinsonian patients with HCB had a lesion of the STN. Preliminary data in Parkinson's disease patients submitted to a subthalamotomy with current functional stereotaxy also indicate that HCB is a very rare complication. To explain this observation, we suggest that the parkinsonian state is characterized by an increased threshold for the induction of dyskinesia following STN lesioning. This arises as a consequence of reduced activity in the 'direct' GABA projection to the globus pallidus medialis (GPm) which accompanies dopamine depletion. Lesioning of the STN reduces excitation of the GPm, and theoretically this should induce dyskinesias. However, an STN lesion also, simultaneously, further reduces the hypoactivity in the globus pallidus lateralis (GPl) that is a feature of Parkinson's disease, and hence may compensate for GPm hypoactivity, thus self-stabilizing basal ganglia output activity and reducing the risk of HCB. We conclude that lesioning of the STN in Parkinson's disease is a feasible approach in some circumstances.  (+info)

Involuntary movements after anterior cerebral artery territory infarction. (8/193)

BACKGROUND AND PURPOSE: Patients with anterior cerebral artery territory infarction presenting with involuntary movements have rarely been described in the literature. CASE DESCRIPTIONS: The author reports 9 such patients: 3 with asterixis, 5 with hemiparkinsonism (tremor, rigidity, hypokinesia), and 1 with both. Asterixis developed in the acute stage in patients with minimal arm weakness, whereas parkinsonism was usually observed after the motor dysfunction improved in patients with initially severe limb weakness. Asterixis correlated with small lesions preferentially involving the prefrontal area; parkinsonism is related to relatively large lesions involving the supplementary motor area. CONCLUSIONS: Anterior cerebral artery territory infarction should be included in the differential diagnosis of asterixis and hemiparkinsonism.  (+info)

Dyskinesias are a type of movement disorder characterized by involuntary, erratic, and often repetitive muscle movements. These movements can affect any part of the body and can include twisting, writhing, or jerking motions, as well as slow, writhing contortions. Dyskinesias can be caused by a variety of factors, including certain medications (such as those used to treat Parkinson's disease), brain injury, stroke, infection, or exposure to toxins. They can also be a side effect of some medical treatments, such as radiation therapy or chemotherapy.

Dyskinesias can have a significant impact on a person's daily life, making it difficult for them to perform routine tasks and affecting their overall quality of life. Treatment for dyskinesias depends on the underlying cause and may include medication adjustments, surgery, or physical therapy. In some cases, dyskinesias may be managed with the use of assistive devices or by modifying the person's environment to make it easier for them to move around.

Drug-induced dyskinesia is a movement disorder that is characterized by involuntary muscle movements or abnormal posturing of the body. It is a side effect that can occur from the long-term use or high doses of certain medications, particularly those used to treat Parkinson's disease and psychosis.

The symptoms of drug-induced dyskinesia can vary in severity and may include rapid, involuntary movements of the limbs, face, or tongue; twisting or writhing movements; and abnormal posturing of the arms, legs, or trunk. These symptoms can be distressing and negatively impact a person's quality of life.

The exact mechanism by which certain medications cause dyskinesia is not fully understood, but it is thought to involve changes in the levels of dopamine, a neurotransmitter that plays a key role in regulating movement. In some cases, adjusting the dose or switching to a different medication may help alleviate the symptoms of drug-induced dyskinesia. However, in severe cases, additional treatments such as deep brain stimulation or botulinum toxin injections may be necessary.

Levodopa, also known as L-dopa, is a medication used primarily in the treatment of Parkinson's disease. It is a direct precursor to the neurotransmitter dopamine and works by being converted into dopamine in the brain, helping to restore the balance between dopamine and other neurotransmitters. This helps alleviate symptoms such as stiffness, tremors, spasms, and poor muscle control. Levodopa is often combined with carbidopa (a peripheral decarboxylase inhibitor) to prevent the conversion of levodopa to dopamine outside of the brain, reducing side effects like nausea and vomiting.

Antiparkinson agents are a class of medications used to treat the symptoms of Parkinson's disease and related disorders. These agents work by increasing the levels or activity of dopamine, a neurotransmitter in the brain that is responsible for regulating movement and coordination.

There are several types of antiparkinson agents, including:

1. Levodopa: This is the most effective treatment for Parkinson's disease. It is converted to dopamine in the brain and helps to replace the missing dopamine in people with Parkinson's.
2. Dopamine agonists: These medications mimic the effects of dopamine in the brain and can be used alone or in combination with levodopa. Examples include pramipexole, ropinirole, and rotigotine.
3. Monoamine oxidase B (MAO-B) inhibitors: These medications block the breakdown of dopamine in the brain and can help to increase its levels. Examples include selegiline and rasagiline.
4. Catechol-O-methyltransferase (COMT) inhibitors: These medications block the breakdown of levodopa in the body, allowing it to reach the brain in higher concentrations. Examples include entacapone and tolcapone.
5. Anticholinergic agents: These medications block the action of acetylcholine, another neurotransmitter that can contribute to tremors and muscle stiffness in Parkinson's disease. Examples include trihexyphenidyl and benztropine.

It is important to note that antiparkinson agents can have side effects, and their use should be carefully monitored by a healthcare professional. The choice of medication will depend on the individual patient's symptoms, age, overall health, and other factors.

Parkinson's disease is a progressive neurodegenerative disorder that affects movement. It is characterized by the death of dopamine-producing cells in the brain, specifically in an area called the substantia nigra. The loss of these cells leads to a decrease in dopamine levels, which results in the motor symptoms associated with Parkinson's disease. These symptoms can include tremors at rest, stiffness or rigidity of the limbs and trunk, bradykinesia (slowness of movement), and postural instability (impaired balance and coordination). In addition to these motor symptoms, non-motor symptoms such as cognitive impairment, depression, anxiety, and sleep disturbances are also common in people with Parkinson's disease. The exact cause of Parkinson's disease is unknown, but it is thought to be a combination of genetic and environmental factors. There is currently no cure for Parkinson's disease, but medications and therapies can help manage the symptoms and improve quality of life.

The Globus Pallidus is a structure in the brain that is part of the basal ganglia, a group of nuclei associated with movement control and other functions. It has two main subdivisions: the external (GPe) and internal (GPi) segments. The GPe receives input from the striatum and sends inhibitory projections to the subthalamic nucleus, while the GPi sends inhibitory projections to the thalamus, which in turn projects to the cerebral cortex. These connections allow for the regulation of motor activity, with abnormal functioning of the Globus Pallidus being implicated in various movement disorders such as Parkinson's disease and Huntington's disease.

Movement disorders are a group of neurological conditions that affect the control and coordination of voluntary movements. These disorders can result from damage to or dysfunction of the cerebellum, basal ganglia, or other parts of the brain that regulate movement. Symptoms may include tremors, rigidity, bradykinesia (slowness of movement), akathisia (restlessness and inability to remain still), dystonia (sustained muscle contractions leading to abnormal postures), chorea (rapid, unpredictable movements), tics, and gait disturbances. Examples of movement disorders include Parkinson's disease, Huntington's disease, Tourette syndrome, and dystonic disorders.

Chorea is a medical term that describes an involuntary movement disorder characterized by brief, irregular, and abrupt jerky movements. These movements often occur randomly and can affect any part of the body. Chorea can also cause difficulty with coordination and balance, and can sometimes be accompanied by muscle weakness or rigidity.

The term "chorea" comes from the Greek word "χορεία" (khoréia), which means "dance," reflecting the graceful, dance-like movements that are characteristic of this condition. Chorea can occur as a symptom of various underlying medical conditions, including neurological disorders such as Huntington's disease, Sydenham's chorea, and cerebral palsy, as well as metabolic disorders, infections, and certain medications.

Treatment for chorea depends on the underlying cause of the condition and may include medications to help control the involuntary movements, physical therapy to improve coordination and balance, and lifestyle modifications to reduce the risk of injury from falls or other accidents. In some cases, surgery may be recommended as a last resort for severe or refractory chorea.

Apomorphine is a non-selective dopamine receptor agonist, which means that it activates dopamine receptors in the brain. It has a high affinity for D1 and D2 dopamine receptors and is used medically to treat Parkinson's disease, particularly in cases of severe or intractable motor fluctuations.

Apomorphine can be administered subcutaneously (under the skin) as a solution or as a sublingual (under the tongue) film. It works by stimulating dopamine receptors in the brain, which helps to reduce the symptoms of Parkinson's disease such as stiffness, tremors, and difficulty with movement.

In addition to its use in Parkinson's disease, apomorphine has also been investigated for its potential therapeutic benefits in other neurological disorders, including alcohol use disorder and drug addiction. However, more research is needed to establish its safety and efficacy in these conditions.

Anti-dyskinetic agents are a class of medications that are used to treat or manage dyskinesias, which are involuntary movements or abnormal muscle contractions. These medications work by blocking or reducing the activity of dopamine, a neurotransmitter in the brain that is involved in movement control.

Dyskinetic symptoms can occur as a side effect of long-term use of levodopa therapy in patients with Parkinson's disease. Anti-dyskinetic agents such as amantadine, anticholinergics, and dopamine agonists may be used to manage these symptoms.

Amantadine works by increasing the release of dopamine and blocking its reuptake, which can help reduce dyskinesias. Anticholinergic medications such as trihexyphenidyl and benztropine work by blocking the action of acetylcholine, another neurotransmitter that can contribute to dyskinesias. Dopamine agonists such as pramipexole and ropinirole mimic the effects of dopamine in the brain and can help reduce dyskinesias by reducing the dose of levodopa required for symptom control.

It is important to note that anti-dyskinetic agents may have side effects, and their use should be carefully monitored by a healthcare provider.

Piribedil is an agonist of dopamine receptors, specifically D2, D3, and D4 receptors. It is primarily used in the treatment of Parkinson's disease to help manage symptoms such as rigidity, tremors, and bradykinesia (slowness of movement). Piribedil can also stimulate dopamine receptors in the brain, which can improve cognitive function and mood. Additionally, it has been studied for its potential benefits in treating other neurological disorders, including Alzheimer's disease and stroke.

It is important to note that the use of piribedil should be under the supervision of a healthcare professional, as it can have side effects and interactions with other medications. It is not commonly used in many countries due to the availability of other more established treatments for Parkinson's disease.

Dopamine agents are medications that act on dopamine receptors in the brain. Dopamine is a neurotransmitter, a chemical messenger that transmits signals in the brain and other areas of the body. It plays important roles in many functions, including movement, motivation, emotion, and cognition.

Dopamine agents can be classified into several categories based on their mechanism of action:

1. Dopamine agonists: These medications bind to dopamine receptors and mimic the effects of dopamine. They are used to treat conditions such as Parkinson's disease, restless legs syndrome, and certain types of dopamine-responsive dystonia. Examples include pramipexole, ropinirole, and rotigotine.
2. Dopamine precursors: These medications provide the building blocks for the body to produce dopamine. Levodopa is a commonly used dopamine precursor that is converted to dopamine in the brain. It is often used in combination with carbidopa, which helps to prevent levodopa from being broken down before it reaches the brain.
3. Dopamine antagonists: These medications block the action of dopamine at its receptors. They are used to treat conditions such as schizophrenia and certain types of nausea and vomiting. Examples include haloperidol, risperidone, and metoclopramide.
4. Dopamine reuptake inhibitors: These medications increase the amount of dopamine available in the synapse (the space between two neurons) by preventing its reuptake into the presynaptic neuron. They are used to treat conditions such as attention deficit hyperactivity disorder (ADHD) and depression. Examples include bupropion and nomifensine.
5. Dopamine release inhibitors: These medications prevent the release of dopamine from presynaptic neurons. They are used to treat conditions such as Tourette's syndrome and certain types of chronic pain. Examples include tetrabenazine and deutetrabenazine.

It is important to note that dopamine agents can have significant side effects, including addiction, movement disorders, and psychiatric symptoms. Therefore, they should be used under the close supervision of a healthcare provider.

Brain tissue transplantation is a medical procedure that involves the surgical implantation of healthy brain tissue into a damaged or diseased brain. The goal of this procedure is to replace the non-functioning brain cells with healthy ones, in order to restore lost function or improve neurological symptoms.

The brain tissue used for transplantation can come from various sources, including fetal brain tissue, embryonic stem cells, or autologous cells (the patient's own cells). The most common type of brain tissue transplantation is fetal brain tissue transplantation, where tissue from aborted fetuses is used.

Brain tissue transplantation has been explored as a potential treatment for various neurological conditions, including Parkinson's disease, Huntington's disease, and stroke. However, the procedure remains highly experimental and is not widely available outside of clinical trials. There are also ethical concerns surrounding the use of fetal brain tissue, which has limited its widespread adoption.

It is important to note that while brain tissue transplantation holds promise as a potential treatment for neurological disorders, it is still an area of active research and much more needs to be learned about its safety and efficacy before it becomes a standard treatment option.

Oxidopamine is not a recognized medical term or a medication commonly used in clinical practice. However, it is a chemical compound that is often used in scientific research, particularly in the field of neuroscience.

Oxidopamine is a synthetic catecholamine that can be selectively taken up by dopaminergic neurons and subsequently undergo oxidation, leading to the production of reactive oxygen species. This property makes it a useful tool for studying the effects of oxidative stress on dopaminergic neurons in models of Parkinson's disease and other neurological disorders.

In summary, while not a medical definition per se, oxidopamine is a chemical compound used in research to study the effects of oxidative stress on dopaminergic neurons.

Dihydroxyphenylalanine is not a medical term per se, but it is a chemical compound that is often referred to in the context of biochemistry and neuroscience. It is also known as levodopa or L-DOPA for short.

L-DOPA is a precursor to dopamine, a neurotransmitter that plays a critical role in regulating movement, emotion, and cognition. In the brain, L-DOPA is converted into dopamine through the action of an enzyme called tyrosine hydroxylase.

L-DOPA is used medically to treat Parkinson's disease, a neurological disorder characterized by motor symptoms such as tremors, rigidity, and bradykinesia (slowness of movement). In Parkinson's disease, the dopamine-producing neurons in the brain gradually degenerate, leading to a deficiency of dopamine. By providing L-DOPA as a replacement therapy, doctors can help alleviate some of the symptoms of the disease.

It is important to note that L-DOPA has potential side effects and risks, including nausea, dizziness, and behavioral changes. Long-term use of L-DOPA can also lead to motor complications such as dyskinesias (involuntary movements) and fluctuations in response to the medication. Therefore, it is typically used in combination with other medications and under the close supervision of a healthcare provider.

The subthalamic nucleus (STN) is a small, lens-shaped structure located in the basal ganglia of the brain. It plays a crucial role in motor control and has been identified as a key target for deep brain stimulation surgery in the treatment of Parkinson's disease and other movement disorders.

The STN is involved in the regulation of movement, balance, and posture, and helps to filter and coordinate signals that are sent from the cerebral cortex to the thalamus and then on to the motor neurons in the brainstem and spinal cord. In Parkinson's disease, abnormal activity in the STN can contribute to symptoms such as tremors, rigidity, and difficulty initiating movements.

Deep brain stimulation of the STN involves implanting electrodes into the nucleus and delivering electrical impulses that help to regulate its activity. This can lead to significant improvements in motor function and quality of life for some people with Parkinson's disease.

Parkinsonian disorders are a group of neurological conditions characterized by motor symptoms such as bradykinesia (slowness of movement), rigidity, resting tremor, and postural instability. These symptoms are caused by the degeneration of dopamine-producing neurons in the brain, particularly in the substantia nigra pars compacta.

The most common Parkinsonian disorder is Parkinson's disease (PD), which is a progressive neurodegenerative disorder. However, there are also several other secondary Parkinsonian disorders, including:

1. Drug-induced parkinsonism: This is caused by the use of certain medications, such as antipsychotics and metoclopramide.
2. Vascular parkinsonism: This is caused by small vessel disease in the brain, which can lead to similar symptoms as PD.
3. Dementia with Lewy bodies (DLB): This is a type of dementia that shares some features with PD, such as the presence of alpha-synuclein protein clumps called Lewy bodies.
4. Progressive supranuclear palsy (PSP): This is a rare brain disorder that affects movement, gait, and eye movements.
5. Multiple system atrophy (MSA): This is a progressive neurodegenerative disorder that affects multiple systems in the body, including the autonomic nervous system, motor system, and cerebellum.
6. Corticobasal degeneration (CBD): This is a rare neurological disorder that affects both movement and cognition.

It's important to note that while these disorders share some symptoms with PD, they have different underlying causes and may require different treatments.

Secondary Parkinson's disease, also known as acquired or symptomatic Parkinsonism, is a clinical syndrome characterized by the signs and symptoms of classic Parkinson's disease (tremor at rest, rigidity, bradykinesia, and postural instability) but caused by a known secondary cause. These causes can include various conditions such as brain injuries, infections, drugs or toxins, metabolic disorders, and vascular damage. The underlying pathology of secondary Parkinson's disease is different from that of classic Parkinson's disease, which is primarily due to the degeneration of dopamine-producing neurons in a specific area of the brain called the substantia nigra pars compacta.

Benserazide is a type of medication called an inhibitor of peripheral aromatic amino acid decarboxylase. It is often used in combination with levodopa to treat Parkinson's disease. Benserazide works by preventing the conversion of levodopa to dopamine outside of the brain, which helps to reduce the side effects of levodopa and increase the amount of dopamine that reaches the brain. This can help to improve the symptoms of Parkinson's disease, such as stiffness, tremors, and difficulty with movement.

Benserazide is available in combination with levodopa under the brand name Madopar. It is taken orally, usually in the form of tablets. The specific dosage of benserazide will depend on the individual's needs and should be determined by a healthcare professional.

It is important to note that benserazide can interact with other medications, so it is important to inform your doctor about all the medications you are taking before starting treatment with benserazide. Additionally, benserazide may cause side effects, such as nausea, dizziness, and dry mouth. If you experience any severe or persistent side effects while taking benserazide, you should contact your healthcare provider.

Adrenergic agents are a class of drugs that bind to and activate adrenergic receptors, which are cell surface receptors found in the nervous system and other tissues. These receptors are activated by neurotransmitters such as norepinephrine and epinephrine (also known as adrenaline), which are released by the sympathetic nervous system in response to stress or excitement.

Adrenergic agents can be classified based on their mechanism of action and the specific receptors they bind to. There are two main types of adrenergic receptors: alpha and beta receptors, each with several subtypes. Some adrenergic agents bind to both alpha and beta receptors, while others are selective for one or the other.

Adrenergic agents have a wide range of therapeutic uses, including the treatment of asthma, cardiovascular diseases, glaucoma, and neurological disorders. They can also be used as diagnostic tools to test the function of the sympathetic nervous system. Some examples of adrenergic agents include:

* Alpha-agonists: These drugs bind to alpha receptors and cause vasoconstriction (narrowing of blood vessels), which can be useful in the treatment of hypotension (low blood pressure) or nasal congestion. Examples include phenylephrine and oxymetazoline.
* Alpha-antagonists: These drugs block the action of alpha receptors, leading to vasodilation (widening of blood vessels) and a decrease in blood pressure. Examples include prazosin and doxazosin.
* Beta-agonists: These drugs bind to beta receptors and cause bronchodilation (opening of the airways), increased heart rate, and increased force of heart contractions. They are used in the treatment of asthma, chronic obstructive pulmonary disease (COPD), and other respiratory disorders. Examples include albuterol and salmeterol.
* Beta-antagonists: These drugs block the action of beta receptors, leading to a decrease in heart rate, blood pressure, and bronchodilation. They are used in the treatment of hypertension, angina (chest pain), and heart failure. Examples include metoprolol and atenolol.
* Nonselective alpha- and beta-antagonists: These drugs block both alpha and beta receptors and are used in the treatment of hypertension, angina, and heart failure. Examples include labetalol and carvedilol.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a chemical compound that can cause permanent parkinsonian symptoms. It is not a medication or a treatment, but rather a toxin that can damage the dopamine-producing neurons in the brain, leading to symptoms similar to those seen in Parkinson's disease.

MPTP itself is not harmful, but it is metabolized in the body into a toxic compound called MPP+, which accumulates in and damages dopaminergic neurons. MPTP was discovered in the 1980s when a group of drug users in California developed parkinsonian symptoms after injecting a heroin-like substance contaminated with MPTP.

Since then, MPTP has been used as a research tool to study Parkinson's disease and develop new treatments. However, it is not used clinically and should be handled with caution due to its toxicity.

Fetal tissue transplantation is a medical procedure that involves the surgical implantation of tissue from developing fetuses into patients for therapeutic purposes. The tissue used in these procedures typically comes from elective abortions, and can include tissues such as neural cells, liver cells, pancreatic islets, and heart valves.

The rationale behind fetal tissue transplantation is that the developing fetus has a high capacity for cell growth and regeneration, making its tissues an attractive source of cells for transplantation. Additionally, because fetal tissue is often less mature than adult tissue, it may be less likely to trigger an immune response in the recipient, reducing the risk of rejection.

Fetal tissue transplantation has been explored as a potential treatment for a variety of conditions, including Parkinson's disease, diabetes, and heart disease. However, the use of fetal tissue in medical research and therapy remains controversial due to ethical concerns surrounding the sourcing of the tissue.

Methyl-phenyl-tetrahydropyridine (MPTP) poisoning is a rare neurological disorder that occurs due to the accidental exposure or intentional intake of MPTP, a chemical compound that can cause permanent parkinsonian symptoms. MPTP is metabolized into MPP+, which selectively destroys dopaminergic neurons in the substantia nigra pars compacta region of the brain, leading to Parkinson's disease-like features such as rigidity, bradykinesia, resting tremors, and postural instability. MPTP poisoning can be a model for understanding Parkinson's disease pathophysiology and developing potential treatments.

Mucuna is a genus of tropical leguminous plants, and the term is often used in a medical context to refer to one specific species: Mucuna pruriens. This plant, also known as velvet bean, has been used in traditional medicine for various purposes, including the treatment of Parkinson's disease.

Mucuna pruriens contains high levels of L-dopa, a precursor to dopamine, which is a neurotransmitter that plays an important role in regulating movement and mood. As such, Mucuna has been studied as a potential alternative treatment for Parkinson's disease, which is characterized by low levels of dopamine in the brain.

It's worth noting that while some studies have suggested that Mucuna may be effective in reducing symptoms of Parkinson's disease, more research is needed to fully understand its safety and efficacy. Additionally, Mucuna can contain other compounds that may have negative effects, so it should only be used under the guidance of a healthcare professional.

Carbidopa is a peripheral decarboxylase inhibitor used in the treatment of Parkinson's disease. It works by preventing the conversion of levodopa to dopamine outside of the brain, allowing more levodopa to reach the brain and reduce the symptoms of Parkinson's disease. Carbidopa is often combined with levodopa in medication formulations and is available under various brand names, such as Sinemet.

Here are some key points about carbidopa:

* It is a peripheral decarboxylase inhibitor that prevents the conversion of levodopa to dopamine outside of the brain.
* Carbidopa is often combined with levodopa in medication formulations for the treatment of Parkinson's disease.
* By preventing the conversion of levodopa to dopamine outside of the brain, more levodopa can reach the brain and reduce the symptoms of Parkinson's disease.
* Common side effects of carbidopa include nausea, vomiting, and orthostatic hypotension.
* Carbidopa should be used under the guidance of a healthcare professional and dosed appropriately to minimize side effects and maximize therapeutic benefit.

Amantadine is an antiviral medication that is primarily used to prevent and treat certain types of influenza (flu). It works by stopping the virus from multiplying in your body. In addition to its antiviral properties, amantadine also has central nervous system (CNS) stimulant and dopaminergic effects, which make it useful in the treatment of Parkinson's disease and various movement disorders.

The medical definition of Amantadine is:

A synthetic symmetrical tricyclic amine used as an antiviral agent to treat and prevent influenza A infection and as an anti-parkinsonian drug to control extrapyramidal symptoms caused by neuroleptic agents. The antiviral effect may be due to interference with viral uncoating or replication. The anti-parkinsonian effect may be due to a combination of dopamine agonist and NMDA receptor antagonist properties. (Stedman's Medical Dictionary, 28th edition)

Please note that the use of Amantadine for various medical conditions should always be under the supervision of a healthcare professional, as they will consider potential benefits and risks and provide appropriate guidance.

Dopamine agonists are a class of medications that mimic the action of dopamine, a neurotransmitter in the brain that regulates movement, emotion, motivation, and reinforcement of rewarding behaviors. These medications bind to dopamine receptors in the brain and activate them, leading to an increase in dopaminergic activity.

Dopamine agonists are used primarily to treat Parkinson's disease, a neurological disorder characterized by motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and postural instability. By increasing dopaminergic activity in the brain, dopamine agonists can help alleviate some of these symptoms.

Examples of dopamine agonists include:

1. Pramipexole (Mirapex)
2. Ropinirole (Requip)
3. Rotigotine (Neupro)
4. Apomorphine (Apokyn)

Dopamine agonists may also be used off-label to treat other conditions, such as restless legs syndrome or certain types of dopamine-responsive dystonia. However, these medications can have significant side effects, including nausea, dizziness, orthostatic hypotension, compulsive behaviors (such as gambling, shopping, or sexual addiction), and hallucinations. Therefore, they should be used with caution and under the close supervision of a healthcare provider.

The corpus striatum is a part of the brain that plays a crucial role in movement, learning, and cognition. It consists of two structures called the caudate nucleus and the putamen, which are surrounded by the external and internal segments of the globus pallidus. Together, these structures form the basal ganglia, a group of interconnected neurons that help regulate voluntary movement.

The corpus striatum receives input from various parts of the brain, including the cerebral cortex, thalamus, and other brainstem nuclei. It processes this information and sends output to the globus pallidus and substantia nigra, which then project to the thalamus and back to the cerebral cortex. This feedback loop helps coordinate and fine-tune movements, allowing for smooth and coordinated actions.

Damage to the corpus striatum can result in movement disorders such as Parkinson's disease, Huntington's disease, and dystonia. These conditions are characterized by abnormal involuntary movements, muscle stiffness, and difficulty initiating or controlling voluntary movements.

Deep brain stimulation (DBS) is a surgical procedure that involves the implantation of a medical device called a neurostimulator, which sends electrical impulses to specific targets in the brain. The impulses help to regulate abnormal brain activity, and can be used to treat a variety of neurological conditions, including Parkinson's disease, essential tremor, dystonia, and obsessive-compulsive disorder.

During the procedure, electrodes are implanted into the brain and connected to the neurostimulator, which is typically implanted in the chest. The neurostimulator can be programmed to deliver electrical impulses at varying frequencies, amplitudes, and pulse widths, depending on the specific needs of the patient.

DBS is generally considered a safe and effective treatment option for many patients with neurological conditions, although it does carry some risks, such as infection, bleeding, and hardware complications. It is typically reserved for patients who have not responded well to other forms of treatment, or who experience significant side effects from medication.

Thalamic nuclei refer to specific groupings of neurons within the thalamus, a key relay station in the brain that receives sensory information from various parts of the body and transmits it to the cerebral cortex for processing. The thalamus is divided into several distinct nuclei, each with its own unique functions and connections. These nuclei can be broadly categorized into three groups:

1. Sensory relay nuclei: These nuclei receive sensory information from different modalities such as vision, audition, touch, and taste, and project this information to specific areas of the cerebral cortex for further processing. Examples include the lateral geniculate nucleus (vision), medial geniculate nucleus (audition), and ventral posterior nucleus (touch and taste).
2. Association nuclei: These nuclei are involved in higher-order cognitive functions, such as attention, memory, and executive control. They receive inputs from various cortical areas and project back to those same areas, forming closed loops that facilitate information processing and integration. Examples include the mediodorsal nucleus and pulvinar.
3. Motor relay nuclei: These nuclei are involved in motor control and coordination. They receive inputs from the cerebral cortex and basal ganglia and project to the brainstem and spinal cord, helping to regulate movement and posture. Examples include the ventral anterior and ventral lateral nuclei.

Overall, thalamic nuclei play a crucial role in integrating sensory, motor, and cognitive information, allowing for adaptive behavior and conscious experience.

Dystonia is a neurological movement disorder characterized by involuntary muscle contractions, leading to repetitive or twisting movements. These movements can be painful and may affect one part of the body (focal dystonia) or multiple parts (generalized dystonia). The exact cause of dystonia varies, with some cases being inherited and others resulting from damage to the brain. Treatment options include medications, botulinum toxin injections, and deep brain stimulation surgery.

A tremor is an involuntary, rhythmic muscle contraction and relaxation that causes a shaking movement. It's a type of motion disorder that can affect any part of your body, but it most often occurs in your hands. Tremors can be harmless, but they can also be a symptom of a more serious neurological disorder. The cause of tremors isn't always known, but they can be the result of damage to the brain from a stroke, multiple sclerosis, or trauma. Certain medications, alcohol abuse, and drug withdrawal can also cause tremors. In some cases, tremors may be inherited and run in families.

Tremors can be classified based on their cause, appearance, and the situation in which they occur. The two most common types of tremors are:

* Resting tremors, which occur when your muscles are relaxed, such as when your hands are resting on your lap. Parkinson's disease is a common cause of this type of tremor.
* Action tremors, which occur with purposeful movement, such as when you're trying to hold something or when you're using a utensil. Essential tremor, the most common type of tremor, is an action tremor.

Tremors can also be classified based on their frequency (how often they occur) and amplitude (the size of the movement). High-frequency tremors are faster and smaller in amplitude, while low-frequency tremors are slower and larger in amplitude.

In general, tremors are not a life-threatening condition, but they can be embarrassing or make it difficult to perform daily activities. In some cases, tremors may indicate a more serious underlying condition that requires treatment. If you're concerned about tremors or have any questions about your symptoms, it's important to speak with a healthcare provider for an accurate diagnosis and appropriate treatment.

Tranquilizing agents, also known as major tranquilizers or antipsychotic drugs, are a class of medications used primarily to manage psychosis, including schizophrenia, and other mental health disorders. These agents work by blocking dopamine receptors in the brain, which helps reduce the symptoms of psychosis such as hallucinations, delusions, and disordered thinking.

Tranquilizing agents can be further divided into two categories: first-generation antipsychotics (FGAs) and second-generation antipsychotics (SGAs). FGAs, also known as typical antipsychotics, were developed earlier and have a higher risk of side effects such as extrapyramidal symptoms (EPS), which include involuntary movements, stiffness, and tremors. SGAs, also known as atypical antipsychotics, were developed more recently and have a lower risk of EPS but may have other side effects such as weight gain and metabolic issues.

It's important to note that tranquilizing agents should only be prescribed and monitored by a qualified healthcare professional, as they can have significant risks and benefits.

Chronotherapy is a medical treatment strategy that involves adjusting the timing of medication or other treatments based on the body's internal clock or circadian rhythms. The goal of chronotherapy is to optimize the effectiveness and minimize the side effects of treatments by administering them at specific times when they are most likely to be beneficial and well-tolerated.

For example, certain medications may be more effective when given at night because the body's metabolism slows down during sleep, allowing the drug to remain in the system longer. Similarly, some cancer treatments may be more effective when administered in the morning or evening based on the patient's circadian rhythms.

Chronotherapy can also involve adjusting lifestyle factors such as diet, exercise, and light exposure to help regulate the body's internal clock and improve overall health. This approach has been shown to be effective in treating a variety of conditions, including insomnia, depression, asthma, and cardiovascular disease.

Dopamine is a type of neurotransmitter, which is a chemical messenger that transmits signals in the brain and nervous system. It plays several important roles in the body, including:

* Regulation of movement and coordination
* Modulation of mood and motivation
* Control of the reward and pleasure centers of the brain
* Regulation of muscle tone
* Involvement in memory and attention

Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area. It is released by neurons (nerve cells) and binds to specific receptors on other neurons, where it can either excite or inhibit their activity.

Abnormalities in dopamine signaling have been implicated in several neurological and psychiatric conditions, including Parkinson's disease, schizophrenia, and addiction.

Primidone is an anticonvulsant medication primarily used in the treatment of seizure disorders. It is a barbiturate derivative that has sedative and muscle relaxant properties. Primidone is metabolized in the body into two other anticonvulsants, phenobarbital and phenylethylmalonamide (PEMA). Together, these active metabolites help to reduce the frequency and severity of seizures.

Primidone is used primarily for generalized tonic-clonic seizures and complex partial seizures. It may also be considered for use in absence seizures, although other medications are typically preferred for this type of seizure. The medication works by decreasing abnormal electrical activity in the brain, which helps to prevent or reduce the occurrence of seizures.

Like all anticonvulsant medications, primidone carries a risk of side effects, including dizziness, drowsiness, and unsteady gait. It may also cause rash, nausea, vomiting, and loss of appetite in some individuals. In rare cases, primidone can cause more serious side effects such as blood disorders, liver damage, or suicidal thoughts.

It is important for patients taking primidone to be closely monitored by their healthcare provider to ensure that the medication is working effectively and to monitor for any potential side effects. Dosages of primidone may need to be adjusted over time based on the patient's response to treatment and any adverse reactions that occur.

Electric stimulation therapy, also known as neuromuscular electrical stimulation (NMES) or electromyostimulation, is a therapeutic treatment that uses electrical impulses to stimulate muscles and nerves. The electrical signals are delivered through electrodes placed on the skin near the target muscle group or nerve.

The therapy can be used for various purposes, including:

1. Pain management: Electric stimulation can help reduce pain by stimulating the release of endorphins, which are natural painkillers produced by the body. It can also help block the transmission of pain signals to the brain.
2. Muscle rehabilitation: NMES can be used to prevent muscle atrophy and maintain muscle tone in individuals who are unable to move their muscles due to injury or illness, such as spinal cord injuries or stroke.
3. Improving circulation: Electric stimulation can help improve blood flow and reduce swelling by contracting the muscles and promoting the movement of fluids in the body.
4. Wound healing: NMES can be used to promote wound healing by increasing blood flow, reducing swelling, and improving muscle function around the wound site.
5. Muscle strengthening: Electric stimulation can be used to strengthen muscles by causing them to contract and relax repeatedly, which can help improve muscle strength and endurance.

It is important to note that electric stimulation therapy should only be administered under the guidance of a trained healthcare professional, as improper use can cause harm or discomfort.

"Saimiri" is the genus name for the group of primates known as squirrel monkeys. These small, agile New World monkeys are native to Central and South America and are characterized by their slim bodies, long limbs, and distinctive hairless faces with large eyes. They are omnivorous and known for their active, quick-moving behavior in the trees. There are several species of squirrel monkey, including the Central American squirrel monkey (Saimiri oerstedii) and the much more widespread common squirrel monkey (Saimiri sciureus).

Facial muscles, also known as facial nerves or cranial nerve VII, are a group of muscles responsible for various expressions and movements of the face. These muscles include:

1. Orbicularis oculi: muscle that closes the eyelid and raises the upper eyelid
2. Corrugator supercilii: muscle that pulls the eyebrows down and inward, forming wrinkles on the forehead
3. Frontalis: muscle that raises the eyebrows and forms horizontal wrinkles on the forehead
4. Procerus: muscle that pulls the medial ends of the eyebrows downward, forming vertical wrinkles between the eyebrows
5. Nasalis: muscle that compresses or dilates the nostrils
6. Depressor septi: muscle that pulls down the tip of the nose
7. Levator labii superioris alaeque nasi: muscle that raises the upper lip and flares the nostrils
8. Levator labii superioris: muscle that raises the upper lip
9. Zygomaticus major: muscle that raises the corner of the mouth, producing a smile
10. Zygomaticus minor: muscle that raises the nasolabial fold and corner of the mouth
11. Risorius: muscle that pulls the angle of the mouth laterally, producing a smile
12. Depressor anguli oris: muscle that pulls down the angle of the mouth
13. Mentalis: muscle that raises the lower lip and forms wrinkles on the chin
14. Buccinator: muscle that retracts the cheek and helps with chewing
15. Platysma: muscle that depresses the corner of the mouth and wrinkles the skin of the neck.

These muscles are innervated by the facial nerve, which arises from the brainstem and exits the skull through the stylomastoid foramen. Damage to the facial nerve can result in facial paralysis or weakness on one or both sides of the face.

Dystonic disorders are a group of neurological conditions characterized by sustained or intermittent muscle contractions that result in involuntary, repetitive, and often twisting movements and abnormal postures. These movements can affect any part of the body, including the face, neck, limbs, and trunk. Dystonic disorders can be primary, meaning they are caused by genetic mutations or idiopathic causes, or secondary, resulting from brain injury, infection, or other underlying medical conditions.

The most common form of dystonia is cervical dystonia (spasmodic torticollis), which affects the muscles of the neck and results in abnormal head positioning. Other forms of dystonia include blepharospasm (involuntary eyelid spasms), oromandibular dystonia (affecting the muscles of the jaw, face, and tongue), and generalized dystonia (affecting multiple parts of the body).

Dystonic disorders can significantly impact a person's quality of life, causing pain, discomfort, and social isolation. Treatment options include oral medications, botulinum toxin injections, and deep brain stimulation surgery in severe cases.

The putamen is a round, egg-shaped structure that is a part of the basal ganglia, located in the forebrain. It is situated laterally to the globus pallidus and medially to the internal capsule. The putamen plays a crucial role in regulating movement and is involved in various functions such as learning, motivation, and habit formation.

It receives input from the cerebral cortex via the corticostriatal pathway and sends output to the globus pallidus and substantia nigra pars reticulata, which are also part of the basal ganglia circuitry. The putamen is heavily innervated by dopaminergic neurons from the substantia nigra pars compacta, and degeneration of these neurons in Parkinson's disease leads to a significant reduction in dopamine levels in the putamen, resulting in motor dysfunction.

The Substantia Nigra is a region in the midbrain that plays a crucial role in movement control and reward processing. It is composed of two parts: the pars compacta and the pars reticulata. The pars compacta contains dopamine-producing neurons, whose loss or degeneration is associated with Parkinson's disease, leading to motor symptoms such as tremors, rigidity, and bradykinesia.

In summary, Substantia Nigra is a brain structure that contains dopamine-producing cells and is involved in movement control and reward processing. Its dysfunction or degeneration can lead to neurological disorders like Parkinson's disease.

Bromocriptine is a dopamine receptor agonist drug, which means it works by binding to and activating dopamine receptors in the brain. It has several therapeutic uses, including:

* Treatment of Parkinson's disease: Bromocriptine can be used alone or in combination with levodopa to help manage the symptoms of Parkinson's disease, such as stiffness, tremors, spasms, and poor muscle control.
* Suppression of lactation: Bromocriptine can be used to suppress milk production in women who are not breastfeeding or who have stopped breastfeeding but still have high levels of prolactin, a hormone that stimulates milk production.
* Treatment of pituitary tumors: Bromocriptine can be used to shrink certain types of pituitary tumors, such as prolactinomas, which are tumors that secrete excessive amounts of prolactin.
* Management of acromegaly: Bromocriptine can be used to manage the symptoms of acromegaly, a rare hormonal disorder characterized by abnormal growth and enlargement of body tissues, by reducing the production of growth hormone.

Bromocriptine is available in immediate-release and long-acting formulations, and it is usually taken orally. Common side effects of bromocriptine include nausea, dizziness, lightheadedness, and drowsiness. Serious side effects are rare but can include hallucinations, confusion, and priapism (prolonged erection).

Dopamine plasma membrane transport proteins, also known as dopamine transporters (DAT), are a type of protein found in the cell membrane that play a crucial role in the regulation of dopamine neurotransmission. They are responsible for the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron, thereby terminating the signal transduction of dopamine and regulating the amount of dopamine available for further release.

Dopamine transporters belong to the family of sodium-dependent neurotransmitter transporters and are encoded by the SLC6A3 gene in humans. Abnormalities in dopamine transporter function have been implicated in several neurological and psychiatric disorders, including Parkinson's disease, attention deficit hyperactivity disorder (ADHD), and substance use disorders.

In summary, dopamine plasma membrane transport proteins are essential for the regulation of dopamine neurotransmission by mediating the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron.

"Macaca fascicularis" is the scientific name for the crab-eating macaque, also known as the long-tailed macaque. It's a species of monkey that is native to Southeast Asia. They are called "crab-eating" macaques because they are known to eat crabs and other crustaceans. These monkeys are omnivorous and their diet also includes fruits, seeds, insects, and occasionally smaller vertebrates.

Crab-eating macaques are highly adaptable and can be found in a wide range of habitats, including forests, grasslands, and wetlands. They are also known to live in close proximity to human settlements and are often considered pests due to their tendency to raid crops and steal food from humans.

These monkeys are social animals and live in large groups called troops. They have a complex social structure with a clear hierarchy and dominant males. Crab-eating macaques are also known for their intelligence and problem-solving abilities.

In medical research, crab-eating macaques are often used as animal models due to their close genetic relationship to humans. They are used in studies related to infectious diseases, neuroscience, and reproductive biology, among others.

'Animal behavior' refers to the actions or responses of animals to various stimuli, including their interactions with the environment and other individuals. It is the study of the actions of animals, whether they are instinctual, learned, or a combination of both. Animal behavior includes communication, mating, foraging, predator avoidance, and social organization, among other things. The scientific study of animal behavior is called ethology. This field seeks to understand the evolutionary basis for behaviors as well as their physiological and psychological mechanisms.

A neurological examination is a series of tests used to evaluate the functioning of the nervous system, including both the central nervous system (the brain and spinal cord) and peripheral nervous system (the nerves that extend from the brain and spinal cord to the rest of the body). It is typically performed by a healthcare professional such as a neurologist or a primary care physician with specialized training in neurology.

During a neurological examination, the healthcare provider will assess various aspects of neurological function, including:

1. Mental status: This involves evaluating a person's level of consciousness, orientation, memory, and cognitive abilities.
2. Cranial nerves: There are 12 cranial nerves that control functions such as vision, hearing, smell, taste, and movement of the face and neck. The healthcare provider will test each of these nerves to ensure they are functioning properly.
3. Motor function: This involves assessing muscle strength, tone, coordination, and reflexes. The healthcare provider may ask the person to perform certain movements or tasks to evaluate these functions.
4. Sensory function: The healthcare provider will test a person's ability to feel different types of sensations, such as touch, pain, temperature, vibration, and proprioception (the sense of where your body is in space).
5. Coordination and balance: The healthcare provider may assess a person's ability to perform coordinated movements, such as touching their finger to their nose or walking heel-to-toe.
6. Reflexes: The healthcare provider will test various reflexes throughout the body using a reflex hammer.

The results of a neurological examination can help healthcare providers diagnose and monitor conditions that affect the nervous system, such as stroke, multiple sclerosis, Parkinson's disease, or peripheral neuropathy.

Haloperidol is an antipsychotic medication, which is primarily used to treat schizophrenia and symptoms of psychosis, such as delusions, hallucinations, paranoia, or disordered thought. It may also be used to manage Tourette's disorder, tics, agitation, aggression, and hyperactivity in children with developmental disorders.

Haloperidol works by blocking the action of dopamine, a neurotransmitter in the brain, which helps to regulate mood and behavior. It is available in various forms, including tablets, liquid, and injectable solutions. The medication can cause side effects such as drowsiness, restlessness, muscle stiffness, and uncontrolled movements. In rare cases, it may also lead to more serious neurological side effects.

As with any medication, haloperidol should be taken under the supervision of a healthcare provider, who will consider the individual's medical history, current medications, and other factors before prescribing it.

I'm sorry for any confusion, but "Motion Pictures as Topic" is not a medical term or concept. It is actually a subject heading used in library and information sciences to categorize materials related to the study or analysis of motion pictures as a medium or art form. This could include books, articles, and other resources about film theory, film history, film criticism, and so on.

If you have any questions about medical terminology or concepts, I would be happy to help!

The compound 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine is a type of benzazepine derivative. Benzazepines are a class of heterocyclic compounds containing a benzene fused to a diazepine ring. Specifically, 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine is a derivative with a phenyl group attached to the benzazepine ring and two hydroxyl groups at positions 7 and 8 of the diazepine ring.

This compound does not have a specific medical definition, as it is not a drug or a medication that is used in clinical practice. However, like many other chemical compounds, it may have potential uses in pharmaceutical research and development, including as a lead compound for the design and synthesis of new drugs with therapeutic activity.

It's worth noting that the specific biological activity and medical relevance of this compound would depend on its chemical properties and any interactions it may have with biological systems, which would need to be studied in detail through scientific research.

The basal ganglia are a group of interconnected nuclei, or clusters of neurons, located in the base of the brain. They play a crucial role in regulating motor function, cognition, and emotion. The main components of the basal ganglia include the striatum (made up of the caudate nucleus, putamen, and ventral striatum), globus pallidus (divided into external and internal segments), subthalamic nucleus, and substantia nigra (with its pars compacta and pars reticulata).

The basal ganglia receive input from various regions of the cerebral cortex and other brain areas. They process this information and send output back to the thalamus and cortex, helping to modulate and coordinate movement. The basal ganglia also contribute to higher cognitive functions such as learning, decision-making, and habit formation. Dysfunction in the basal ganglia can lead to neurological disorders like Parkinson's disease, Huntington's disease, and dystonia.

Dopamine D2 receptor is a type of metabotropic G protein-coupled receptor that binds to the neurotransmitter dopamine. It is one of five subtypes of dopamine receptors (D1-D5) and is encoded by the gene DRD2. The activation of D2 receptors leads to a decrease in the activity of adenylyl cyclase, which results in reduced levels of cAMP and modulation of ion channels.

D2 receptors are widely distributed throughout the central nervous system (CNS) and play important roles in various physiological functions, including motor control, reward processing, emotion regulation, and cognition. They are also involved in several neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, drug addiction, and Tourette syndrome.

D2 receptors have two main subtypes: D2 short (D2S) and D2 long (D2L). The D2S subtype is primarily located in the presynaptic terminals and functions as an autoreceptor that regulates dopamine release, while the D2L subtype is mainly found in the postsynaptic neurons and modulates intracellular signaling pathways.

Antipsychotic drugs, which are used to treat schizophrenia and other psychiatric disorders, work by blocking D2 receptors. However, excessive blockade of these receptors can lead to side effects such as extrapyramidal symptoms (EPS), tardive dyskinesia, and hyperprolactinemia. Therefore, the development of drugs that selectively target specific subtypes of dopamine receptors is an active area of research in the field of neuropsychopharmacology.

Neurosurgical procedures are operations that are performed on the brain, spinal cord, and peripheral nerves. These procedures are typically carried out by neurosurgeons, who are medical doctors with specialized training in the diagnosis and treatment of disorders of the nervous system. Neurosurgical procedures can be used to treat a wide range of conditions, including traumatic injuries, tumors, aneurysms, vascular malformations, infections, degenerative diseases, and congenital abnormalities.

Some common types of neurosurgical procedures include:

* Craniotomy: A procedure in which a bone flap is temporarily removed from the skull to gain access to the brain. This type of procedure may be performed to remove a tumor, repair a blood vessel, or relieve pressure on the brain.
* Spinal fusion: A procedure in which two or more vertebrae in the spine are fused together using bone grafts and metal hardware. This is often done to stabilize the spine and alleviate pain caused by degenerative conditions or spinal deformities.
* Microvascular decompression: A procedure in which a blood vessel that is causing pressure on a nerve is repositioned or removed. This type of procedure is often used to treat trigeminal neuralgia, a condition that causes severe facial pain.
* Deep brain stimulation: A procedure in which electrodes are implanted in specific areas of the brain and connected to a battery-operated device called a neurostimulator. The neurostimulator sends electrical impulses to the brain to help alleviate symptoms of movement disorders such as Parkinson's disease or dystonia.
* Stereotactic radiosurgery: A non-invasive procedure that uses focused beams of radiation to treat tumors, vascular malformations, and other abnormalities in the brain or spine. This type of procedure is often used for patients who are not good candidates for traditional surgery due to age, health status, or location of the lesion.

Neurosurgical procedures can be complex and require a high degree of skill and expertise. Patients considering neurosurgical treatment should consult with a qualified neurosurgeon to discuss their options and determine the best course of action for their individual situation.

Stereotaxic techniques are minimally invasive surgical procedures used in neuroscience and neurology that allow for precise targeting and manipulation of structures within the brain. These methods use a stereotactic frame, which is attached to the skull and provides a three-dimensional coordinate system to guide the placement of instruments such as electrodes, cannulas, or radiation sources. The main goal is to reach specific brain areas with high precision and accuracy, minimizing damage to surrounding tissues. Stereotaxic techniques are widely used in research, diagnosis, and treatment of various neurological disorders, including movement disorders, pain management, epilepsy, and psychiatric conditions.

Dopamine D3 receptors are a type of G protein-coupled receptor that bind to the neurotransmitter dopamine. They are classified as part of the D2-like family of dopamine receptors, which also includes the D2 and D4 receptors. The D3 receptor is primarily expressed in the limbic areas of the brain, including the hippocampus and the nucleus accumbens, where it plays a role in regulating motivation, reward, and cognition.

D3 receptors have been found to be involved in several neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, and drug addiction. In Parkinson's disease, the loss of dopamine-producing neurons in the substantia nigra results in a decrease in dopamine levels and an increase in D3 receptor expression. This increase in D3 receptor expression has been linked to the development of motor symptoms such as bradykinesia and rigidity.

In schizophrenia, antipsychotic medications that block D2-like receptors, including D3 receptors, are used to treat positive symptoms such as hallucinations and delusions. However, selective D3 receptor antagonists have also been shown to have potential therapeutic effects in treating negative symptoms of schizophrenia, such as apathy and anhedonia.

In drug addiction, D3 receptors have been found to play a role in the rewarding effects of drugs of abuse, such as cocaine and amphetamines. Selective D3 receptor antagonists have shown promise in reducing drug-seeking behavior and preventing relapse in animal models of addiction.

Overall, dopamine D3 receptors play an important role in several neurological and psychiatric disorders, and further research is needed to fully understand their functions and potential therapeutic uses.

Nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels found in the nervous system of many organisms, including humans. These receptors are activated by the endogenous neurotransmitter acetylcholine and the exogenous compound nicotine.

When a nicotinic agonist binds to the receptor, it triggers a conformational change that leads to the opening of an ion channel, allowing the influx of cations such as calcium, sodium, and potassium. This ion flux can depolarize the postsynaptic membrane and generate or modulate electrical signals in excitable tissues, such as neurons and muscles.

Nicotinic agonists have various therapeutic and recreational uses, but they can also produce harmful effects, depending on the dose, duration of exposure, and individual sensitivity. Some examples of nicotinic agonists include:

1. Nicotine: A highly addictive alkaloid found in tobacco plants, which is the prototypical nicotinic agonist. It is used in smoking cessation therapies, such as nicotine gum and patches, but it can also lead to dependence and various health issues when consumed through smoking or vaping.
2. Varenicline: A medication approved for smoking cessation that acts as a partial agonist of nAChRs. It reduces the rewarding effects of nicotine and alleviates withdrawal symptoms, helping smokers quit.
3. Rivastigmine: A cholinesterase inhibitor used to treat Alzheimer's disease and other forms of dementia. It increases the concentration of acetylcholine in the synaptic cleft, enhancing its activity at nicotinic receptors and improving cognitive function.
4. Succinylcholine: A neuromuscular blocking agent used during surgical procedures to induce paralysis and facilitate intubation. It acts as a depolarizing nicotinic agonist, causing transient muscle fasciculations followed by prolonged relaxation.
5. Curare and related compounds: Plant-derived alkaloids that act as competitive antagonists of nicotinic receptors. They are used in anesthesia to induce paralysis and facilitate mechanical ventilation during surgery.

In summary, nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors, leading to various physiological responses. These compounds have diverse applications in medicine, from smoking cessation therapies to treatments for neurodegenerative disorders and anesthesia. However, they can also pose risks when misused or abused, as seen with nicotine addiction and the potential side effects of certain medications.

The neostriatum is a component of the basal ganglia, a group of subcortical nuclei in the brain that are involved in motor control, procedural learning, and other cognitive functions. It is composed primarily of two types of neurons: medium spiny neurons and aspiny interneurons. The neostriatum receives input from various regions of the cerebral cortex and projects to other parts of the basal ganglia, forming an important part of the cortico-basal ganglia-thalamo-cortical loop.

In medical terminology, the neostriatum is often used interchangeably with the term "striatum," although some sources reserve the term "neostriatum" for the caudate nucleus and putamen specifically, while using "striatum" to refer to the entire structure including the ventral striatum (also known as the nucleus accumbens).

Damage to the neostriatum has been implicated in various neurological conditions, such as Huntington's disease and Parkinson's disease.

Dopamine D1 receptors are a type of G protein-coupled receptor that bind to the neurotransmitter dopamine. They are classified as D1-like receptors, along with D5 receptors, and are activated by dopamine through a stimulatory G protein (Gs).

D1 receptors are widely expressed in the central nervous system, including the striatum, prefrontal cortex, hippocampus, and amygdala. They play important roles in various physiological functions, such as movement control, motivation, reward processing, working memory, and cognition.

Activation of D1 receptors leads to increased levels of intracellular cyclic adenosine monophosphate (cAMP) and activation of protein kinase A (PKA), which in turn modulate the activity of various downstream signaling pathways. Dysregulation of dopamine D1 receptor function has been implicated in several neurological and psychiatric disorders, including Parkinson's disease, schizophrenia, attention deficit hyperactivity disorder (ADHD), and drug addiction.

Stereotyped behavior, in the context of medicine and psychology, refers to repetitive, rigid, and invariant patterns of behavior or movements that are purposeless and often non-functional. These behaviors are not goal-directed or spontaneous and typically do not change in response to environmental changes or social interactions.

Stereotypies can include a wide range of motor behaviors such as hand flapping, rocking, head banging, body spinning, self-biting, or complex sequences of movements. They are often seen in individuals with developmental disabilities, intellectual disabilities, autism spectrum disorder, and some mental health conditions.

Stereotyped behaviors can also be a result of substance abuse, neurological disorders, or brain injuries. In some cases, these behaviors may serve as a self-soothing mechanism or a way to cope with stress, anxiety, or boredom. However, they can also interfere with daily functioning and social interactions, and in severe cases, may cause physical harm to the individual.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Implanted electrodes are medical devices that are surgically placed inside the body to interface directly with nerves, neurons, or other electrically excitable tissue for various therapeutic purposes. These electrodes can be used to stimulate or record electrical activity from specific areas of the body, depending on their design and application.

There are several types of implanted electrodes, including:

1. Deep Brain Stimulation (DBS) electrodes: These are placed deep within the brain to treat movement disorders such as Parkinson's disease, essential tremor, and dystonia. DBS electrodes deliver electrical impulses that modulate abnormal neural activity in targeted brain regions.
2. Spinal Cord Stimulation (SCS) electrodes: These are implanted along the spinal cord to treat chronic pain syndromes. SCS electrodes emit low-level electrical pulses that interfere with pain signals traveling to the brain, providing relief for patients.
3. Cochlear Implant electrodes: These are surgically inserted into the cochlea of the inner ear to restore hearing in individuals with severe to profound hearing loss. The electrodes stimulate the auditory nerve directly, bypassing damaged hair cells within the cochlea.
4. Retinal Implant electrodes: These are implanted in the retina to treat certain forms of blindness caused by degenerative eye diseases like retinitis pigmentosa. The electrodes convert visual information from a camera into electrical signals, which stimulate remaining retinal cells and transmit the information to the brain via the optic nerve.
5. Sacral Nerve Stimulation (SNS) electrodes: These are placed near the sacral nerves in the lower back to treat urinary or fecal incontinence and overactive bladder syndrome. SNS electrodes deliver electrical impulses that regulate the function of the affected muscles and nerves.
6. Vagus Nerve Stimulation (VNS) electrodes: These are wrapped around the vagus nerve in the neck to treat epilepsy and depression. VNS electrodes provide intermittent electrical stimulation to the vagus nerve, which has connections to various regions of the brain involved in these conditions.

Overall, implanted electrodes serve as a crucial component in many neuromodulation therapies, offering an effective treatment option for numerous neurological and sensory disorders.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

The mesencephalon, also known as the midbrain, is the middle portion of the brainstem that connects the hindbrain (rhombencephalon) and the forebrain (prosencephalon). It plays a crucial role in several important functions including motor control, vision, hearing, and the regulation of consciousness and sleep-wake cycles. The mesencephalon contains several important structures such as the cerebral aqueduct, tectum, tegmentum, cerebral peduncles, and several cranial nerve nuclei (III and IV).

Encephalitis is defined as inflammation of the brain parenchyma, which is often caused by viral infections but can also be due to bacterial, fungal, or parasitic infections, autoimmune disorders, or exposure to toxins. The infection or inflammation can cause various symptoms such as headache, fever, confusion, seizures, and altered consciousness, ranging from mild symptoms to severe cases that can lead to brain damage, long-term disabilities, or even death.

The diagnosis of encephalitis typically involves a combination of clinical evaluation, imaging studies (such as MRI or CT scans), and laboratory tests (such as cerebrospinal fluid analysis). Treatment may include antiviral medications, corticosteroids, immunoglobulins, and supportive care to manage symptoms and prevent complications.

Functional laterality, in a medical context, refers to the preferential use or performance of one side of the body over the other for specific functions. This is often demonstrated in hand dominance, where an individual may be right-handed or left-handed, meaning they primarily use their right or left hand for tasks such as writing, eating, or throwing.

However, functional laterality can also apply to other bodily functions and structures, including the eyes (ocular dominance), ears (auditory dominance), or legs. It's important to note that functional laterality is not a strict binary concept; some individuals may exhibit mixed dominance or no strong preference for one side over the other.

In clinical settings, assessing functional laterality can be useful in diagnosing and treating various neurological conditions, such as stroke or traumatic brain injury, where understanding any resulting lateralized impairments can inform rehabilitation strategies.

Antipsychotic agents are a class of medications used to manage and treat psychosis, which includes symptoms such as delusions, hallucinations, paranoia, disordered thought processes, and agitated behavior. These drugs work by blocking the action of dopamine, a neurotransmitter in the brain that is believed to play a role in the development of psychotic symptoms. Antipsychotics can be broadly divided into two categories: first-generation antipsychotics (also known as typical antipsychotics) and second-generation antipsychotics (also known as atypical antipsychotics).

First-generation antipsychotics, such as chlorpromazine, haloperidol, and fluphenazine, were developed in the 1950s and have been widely used for several decades. They are generally effective in reducing positive symptoms of psychosis (such as hallucinations and delusions) but can cause significant side effects, including extrapyramidal symptoms (EPS), such as rigidity, tremors, and involuntary movements, as well as weight gain, sedation, and orthostatic hypotension.

Second-generation antipsychotics, such as clozapine, risperidone, olanzapine, quetiapine, and aripiprazole, were developed more recently and are considered to have a more favorable side effect profile than first-generation antipsychotics. They are generally effective in reducing both positive and negative symptoms of psychosis (such as apathy, anhedonia, and social withdrawal) and cause fewer EPS. However, they can still cause significant weight gain, metabolic disturbances, and sedation.

Antipsychotic agents are used to treat various psychiatric disorders, including schizophrenia, bipolar disorder, major depressive disorder with psychotic features, delusional disorder, and other conditions that involve psychosis or agitation. They can be administered orally, intramuscularly, or via long-acting injectable formulations. The choice of antipsychotic agent depends on the individual patient's needs, preferences, and response to treatment, as well as the potential for side effects. Regular monitoring of patients taking antipsychotics is essential to ensure their safety and effectiveness.

The intraoperative period is the phase of surgical treatment that refers to the time during which the surgery is being performed. It begins when the anesthesia is administered and the patient is prepared for the operation, and it ends when the surgery is completed, the anesthesia is discontinued, and the patient is transferred to the recovery room or intensive care unit (ICU).

During the intraoperative period, the surgical team, including surgeons, anesthesiologists, nurses, and other healthcare professionals, work together to carry out the surgical procedure safely and effectively. The anesthesiologist monitors the patient's vital signs, such as heart rate, blood pressure, oxygen saturation, and body temperature, throughout the surgery to ensure that the patient remains stable and does not experience any complications.

The surgeon performs the operation, using various surgical techniques and instruments to achieve the desired outcome. The surgical team also takes measures to prevent infection, control bleeding, and manage pain during and after the surgery.

Overall, the intraoperative period is a critical phase of surgical treatment that requires close collaboration and communication among members of the healthcare team to ensure the best possible outcomes for the patient.

Cerebral dominance is a concept in neuropsychology that refers to the specialization of one hemisphere of the brain over the other for certain cognitive functions. In most people, the left hemisphere is dominant for language functions such as speaking and understanding spoken or written language, while the right hemisphere is dominant for non-verbal functions such as spatial ability, face recognition, and artistic ability.

Cerebral dominance does not mean that the non-dominant hemisphere is incapable of performing the functions of the dominant hemisphere, but rather that it is less efficient or specialized in those areas. The concept of cerebral dominance has been used to explain individual differences in cognitive abilities and learning styles, as well as the laterality of brain damage and its effects on cognition and behavior.

It's important to note that cerebral dominance is a complex phenomenon that can vary between individuals and can be influenced by various factors such as genetics, environment, and experience. Additionally, recent research has challenged the strict lateralization of functions and suggested that there is more functional overlap and interaction between the two hemispheres than previously thought.

Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.

Serotonin receptor agonists are a class of medications that bind to and activate serotonin receptors in the body, mimicking the effects of the neurotransmitter serotonin. These drugs can have various effects depending on which specific serotonin receptors they act upon. Some serotonin receptor agonists are used to treat conditions such as migraines, cluster headaches, and Parkinson's disease, while others may be used to stimulate appetite or reduce anxiety. It is important to note that some serotonin receptor agonists can have serious side effects, particularly when taken in combination with other medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs) or monoamine oxidase inhibitors (MAOIs). This can lead to a condition called serotonin syndrome, which is characterized by symptoms such as agitation, confusion, rapid heart rate, high blood pressure, and muscle stiffness.

Amphetamine is a central nervous system stimulant drug that works by increasing the levels of certain neurotransmitters (chemical messengers) in the brain, such as dopamine and norepinephrine. It is used medically to treat conditions such as attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity, due to its appetite-suppressing effects.

Amphetamines can be prescribed in various forms, including tablets, capsules, or liquids, and are available under several brand names, such as Adderall, Dexedrine, and Vyvanse. They are also known by their street names, such as speed, uppers, or wake-ups, and can be abused for their euphoric effects and ability to increase alertness, energy, and concentration.

Long-term use of amphetamines can lead to dependence, tolerance, and addiction, as well as serious health consequences, such as cardiovascular problems, mental health disorders, and malnutrition. It is essential to use amphetamines only under the supervision of a healthcare provider and follow their instructions carefully.

Autoradiography is a medical imaging technique used to visualize and localize the distribution of radioactively labeled compounds within tissues or organisms. In this process, the subject is first exposed to a radioactive tracer that binds to specific molecules or structures of interest. The tissue is then placed in close contact with a radiation-sensitive film or detector, such as X-ray film or an imaging plate.

As the radioactive atoms decay, they emit particles (such as beta particles) that interact with the film or detector, causing chemical changes and leaving behind a visible image of the distribution of the labeled compound. The resulting autoradiogram provides information about the location, quantity, and sometimes even the identity of the molecules or structures that have taken up the radioactive tracer.

Autoradiography has been widely used in various fields of biology and medical research, including pharmacology, neuroscience, genetics, and cell biology, to study processes such as protein-DNA interactions, gene expression, drug metabolism, and neuronal connectivity. However, due to the use of radioactive materials and potential hazards associated with them, this technique has been gradually replaced by non-radioactive alternatives like fluorescence in situ hybridization (FISH) or immunofluorescence techniques.

An electrode is a medical device that can conduct electrical currents and is used to transmit or receive electrical signals, often in the context of medical procedures or treatments. In a medical setting, electrodes may be used for a variety of purposes, such as:

1. Recording electrical activity in the body: Electrodes can be attached to the skin or inserted into body tissues to measure electrical signals produced by the heart, brain, muscles, or nerves. This information can be used to diagnose medical conditions, monitor the effectiveness of treatments, or guide medical procedures.
2. Stimulating nerve or muscle activity: Electrodes can be used to deliver electrical impulses to nerves or muscles, which can help to restore function or alleviate symptoms in people with certain medical conditions. For example, electrodes may be used to stimulate the nerves that control bladder function in people with spinal cord injuries, or to stimulate muscles in people with muscle weakness or paralysis.
3. Administering treatments: Electrodes can also be used to deliver therapeutic treatments, such as transcranial magnetic stimulation (TMS) for depression or deep brain stimulation (DBS) for movement disorders like Parkinson's disease. In these procedures, electrodes are implanted in specific areas of the brain and connected to a device that generates electrical impulses, which can help to regulate abnormal brain activity and improve symptoms.

Overall, electrodes play an important role in many medical procedures and treatments, allowing healthcare professionals to diagnose and treat a wide range of conditions that affect the body's electrical systems.

Microdialysis is a minimally invasive technique used in clinical and research settings to continuously monitor the concentration of various chemicals, such as neurotransmitters, drugs, or metabolites, in biological fluids (e.g., extracellular fluid of tissues, blood, or cerebrospinal fluid). This method involves inserting a small, flexible catheter with a semipermeable membrane into the region of interest. A physiological solution is continuously perfused through the catheter, allowing molecules to diffuse across the membrane based on their concentration gradient. The dialysate that exits the catheter is then collected and analyzed for target compounds using various analytical techniques (e.g., high-performance liquid chromatography, mass spectrometry).

In summary, microdialysis is a valuable tool for monitoring real-time changes in chemical concentrations within biological systems, enabling better understanding of physiological processes or pharmacokinetic properties of drugs.

A microelectrode is a small electrode with dimensions ranging from several micrometers to a few tens of micrometers in diameter. They are used in various biomedical applications, such as neurophysiological studies, neuromodulation, and brain-computer interfaces. In these applications, microelectrodes serve to record electrical activity from individual or small groups of neurons or deliver electrical stimuli to specific neural structures with high spatial resolution.

Microelectrodes can be fabricated using various materials, including metals (e.g., tungsten, stainless steel, platinum), metal alloys, carbon fibers, and semiconductor materials like silicon. The design of microelectrodes may vary depending on the specific application, with some common types being sharpened metal wires, glass-insulated metal microwires, and silicon-based probes with multiple recording sites.

The development and use of microelectrodes have significantly contributed to our understanding of neural function in health and disease, enabling researchers and clinicians to investigate the underlying mechanisms of neurological disorders and develop novel therapies for conditions such as Parkinson's disease, epilepsy, and hearing loss.

N-Methyl-D-Aspartate (NMDA) receptors are a type of ionotropic glutamate receptor, which are found in the membranes of excitatory neurons in the central nervous system. They play a crucial role in synaptic plasticity, learning, and memory processes. NMDA receptors are ligand-gated channels that are permeable to calcium ions (Ca2+) and other cations.

NMDA receptors are composed of four subunits, which can be a combination of NR1, NR2A-D, and NR3A-B subunits. The binding of the neurotransmitter glutamate to the NR2 subunit and glycine to the NR1 subunit leads to the opening of the ion channel and the influx of Ca2+ ions.

NMDA receptors have a unique property in that they require both agonist binding and membrane depolarization for full activation, making them sensitive to changes in the electrical activity of the neuron. This property allows NMDA receptors to act as coincidence detectors, playing a critical role in synaptic plasticity and learning.

Abnormal functioning of NMDA receptors has been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and chronic pain. Therefore, NMDA receptors are a common target for drug development in the treatment of these conditions.

Nicotine is defined as a highly addictive psychoactive alkaloid and stimulant found in the nightshade family of plants, primarily in tobacco leaves. It is the primary component responsible for the addiction to cigarettes and other forms of tobacco. Nicotine can also be produced synthetically.

When nicotine enters the body, it activates the release of several neurotransmitters such as dopamine, norepinephrine, and serotonin, leading to feelings of pleasure, stimulation, and relaxation. However, with regular use, tolerance develops, requiring higher doses to achieve the same effects, which can contribute to the development of nicotine dependence.

Nicotine has both short-term and long-term health effects. Short-term effects include increased heart rate and blood pressure, increased alertness and concentration, and arousal. Long-term use can lead to addiction, lung disease, cardiovascular disease, and reproductive problems. It is important to note that nicotine itself is not the primary cause of many tobacco-related diseases, but rather the result of other harmful chemicals found in tobacco smoke.

Peak-dose dyskinesia - the most common form of levodopa-induced dyskinesia; it correlates with the plateau L‑DOPA plasma level ... Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with an antipsychotic drug such as ... Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of ... primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are ...
... paroxysmal nonkinesigenic dyskinesia (PNKD), and paroxysmal exercise-induced dyskinesia (PED). Other neurological diseases have ... Paroxysmal Dyskinesia is not a fatal disease. Life can be extremely difficult with this disease depending on the severity. The ... Paroxysmal dyskinesia is a rare disorder, however the number of individuals it affects remains unclear. There are three ... Hypnogenic paroxysmal dyskinesia is a form of epilepsy affecting the frontal lobe. Single genes have been identified on ...
If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal ... The term "tardive dyskinesia" first came into use in 1964. Tardive dyskinesia is characterized by repetitive, involuntary ... 2011). Ninds tardive dyskinesia information page. Retrieved from website: "Tardive Dyskinesia Information Page: National ... Vijayakumar, D; Jankovic, J (May 2016). "Drug-Induced Dyskinesia, Part 2: Treatment of Tardive Dyskinesia". Drugs. 76 (7): 779- ...
... there is a state of biliary dyskinesia. So, biliary dyskinesia is a dynamically (functional...not fixed mechanical[ ... When the dyskinesia is localized at the biliary outlet into the duodenum just as increased tonus of that outlet sphincter of ... Biliary dyskinesia is a disorder of some component of biliary part of the digestive system in which bile cannot physically move ... In general, biliary dyskinesia is the disturbance in the coordination of peristaltic contraction of the biliary ducts, and/or ...
... (PCD) is a rare, autosomal recessive genetic ciliopathy, that causes defects in the action of cilia ... Coren, M. E; Meeks, M; Morrison, I; Buchdahl, R. M; Bush, A (2002). "Primary ciliary dyskinesia: Age at diagnosis and symptom ... "Primary Ciliary Dyskinesia". Retrieved 2007-11-16. Zariwala, Maimoona A; Knowles, Michael R; Omran, Heymut (2007). "Genetic ... Lucas JS, Davis SD, Omran H, Shoemark A (February 2020). "Primary ciliary dyskinesia in the genomics age". Lancet Respir Med. 8 ...
... (PNKD) is an episodic movement disorder first described by Mount and Reback in 1940 under ... NCBI Bookshelf -- GeneReviews -- Familial Paroxysmal Nonkinesigenic Dyskinesia Archives of Neurology - Familial Paroxysmal ... Mount-Reback syndrome Dyskinesias (Paroxysmal) - Treatment (Articles with short description, Short description is different ...
... (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease ... has been shown to reduce dyskinesia. In 2017, the FDA approved the first treatment for levodopa-induced dyskinesia for ... If dyskinesia becomes too severe or impairs the patient's quality of life, a reduction in l-Dopa might be necessary, however ... Attempts to moderate dyskinesia by the use of other treatments such as bromocriptine (Parlodel), a dopamine agonist, appears to ...
Paroxysmal dyskinesia Paroxysmal nonkinesogenic dyskinesia Poon, Michael. Paroxysmal Dyskinesias. Shrine of Neurology. Nov. ... Diagnosis and Treatment of Paroxysmal Dyskinesias Revisited: Paroxysmal Exercise-induced (Exertion-induced) Dyskinesia Medscape ... PED is in the class of paroxysmal dyskinesia which are a group of rare movement disorders characterized by attacks of ... July 2008). "Paroxysmal exercise-induced dyskinesia and epilepsy is due to mutations in SLC2A1, encoding the glucose ...
Paroxysmal dyskinesia Paroxysmal nonkinesogenic dyskinesia Paroxysmal exercise-induced dystonia Khan, W. U.; Staios, G.; Rana, ... which include paroxysmal nonkinesigenic dyskinesia (PNKD) and paroxysmal exercise-induced dyskinesia (PED). While PKD attacks ... NCBI/UW entry on Familial Paroxysmal Kinesigenic Dyskinesia OMIM entries on Familial Paroxysmal Kinesigenic Dyskinesia ( ... Paroxysmal kinesigenic dyskinesia is diagnosed using a strict set of guidelines. These criteria were studied and confirmed by ...
"Punding and dyskinesias". Movement Disorders. 21 (12): 2214-2217. doi:10.1002/mds.21118. PMID 17013916. S2CID 38887798. Evans, ...
Unusual focal dyskinesias". Handbook of Clinical Neurology. Vol. 100. Elsevier. pp. 617-628. doi:10.1016/B978-0-444-52014- ...
Unusual focal dyskinesias". Handbook of Clinical Neurology. Vol. 100. Elsevier. pp. 617-628. doi:10.1016/B978-0-444-52014- ...
Unusual focal dyskinesias". Handbook of Clinical Neurology. Vol. 100. Elsevier. pp. 617-628. doi:10.1016/B978-0-444-52014- ...
Unusual focal dyskinesias". Handbook of Clinical Neurology. Vol. 100. Elsevier. pp. 617-628. doi:10.1016/B978-0-444-52014- ...
Pakkenberg H, Pedersen B (1985). "Medical treatment of dystonia". Dyskinesia. Psychopharmacology Supplementum. Vol. 2. pp. 111- ...
Casey DE (1985). "Tardive dyskinesia: reversible and irreversible". Dyskinesia. Psychopharmacology Supplementum. Vol. 2. pp. 88 ... However, there are numerous adverse effects of antipsychotics, notably tardive dyskinesia (TD). Atypical antipsychotics are ...
... is used to treat tardive dyskinesia in adults. Tardive dyskinesia is a drug-induced neurological injury ... "Tardive dyskinesia". rarediseases.info.nih.gov. 1 June 2017. Archived from the original on 18 June 2017. Retrieved 21 February ... "tardive-dyskinesia". www.priory.com. Retrieved 2016-11-13. Purves D, et al. (2018). Neuroscience (Sixth ed.). Sinauer ... Valbenazine, sold under the trade name Ingrezza, is a medication used to treat tardive dyskinesia. It acts as a vesicular ...
Tardive dyskinesia may reverse upon discontinuation of the offending agent or it may be irreversible, withdrawal may also make ... "Tardive dyskinesia: MedlinePlus Medical Encyclopedia". Archived from the original on 2017-01-31. Retrieved 2017-01-18.[full ... There is a risk of developing a serious condition called tardive dyskinesia as a side effect of antipsychotics, including ... The risk of developing tardive dyskinesia after chronic typical antipsychotic usage varies on several factors, such as age and ...
"Metoclopramide & Tardive Dyskinesia". Tardive Dyskinesia Center. Archived from the original on March 23, 2013. Retrieved March ... antidepressants Tardive dyskinesia associated with use of metoclopramide and many antipsychotic medications Sometimes, putative ...
Mutations in this gene cause ciliary dyskinesia type 15, a disorder due to defects in cilia motility. Alternative splicing ... "Primary Ciliary Dyskinesia". PMID 20301301. {{cite journal}}: Cite journal requires ,journal= (help) Blanchon S, Legendre M, ... "Delineation of CCDC39/CCDC40 mutation spectrum and associated phenotypes in primary ciliary dyskinesia". Journal of Medical ...
... and other conditions including dyskinesias. Stereotypic movement disorder is often misdiagnosed as tics or Tourette syndrome ( ...
Studies have also been conducted which show that long-term prescription of hydroxyzine can lead to tardive dyskinesia after ... "Hydroxyzine-associated tardive dyskinesia". Annals of Neurology. 11 (4): 435. doi:10.1002/ana.410110423. PMID 7103423. S2CID ... previous interactions with phenothiazine derivatives or pre-existing neuroleptic treatment may have contributed to dyskinesia ... years of use, but effects related to dyskinesia have also anecdotally been reported after periods of 7.5 months, such as ...
DNAI1 Ciliary dyskinesia, primary, 10; 612518; KTU Ciliary dyskinesia, primary, 11; 612649; RSPH4A Ciliary dyskinesia, primary ... TXNDC3 Ciliary dyskinesia, primary, 7, with or without situs inversus; 611884; DNAH11 Ciliary dyskinesia, primary, 9, with or ... LRRC50 Ciliary dyskinesia, primary, 3, with or without situs inversus; 608644; DNAH5 Ciliary dyskinesia, primary, 6; 610852; ... PIGA Paroxysmal nonkinesigenic dyskinesia; 118800; MR1 Partington syndrome; 309510; ARX PCWH syndrome; 609136; SOX10 Peeling ...
The percentage of patients affected by side effects like Tardive dyskinesia is significantly high and estimated to be a 20-50% ... And they profit in it". Waln, Olga; Jankovic, Joseph (12 July 2013). "An Update on Tardive Dyskinesia: From Phenomenology to ... Antipsychotic Psychiatry Anti-psychiatry Martha Rosenberg (November 2019). "Drugmakers discover tardive dyskinesia. ... deficit syndrome Neuroleptic malignant syndrome Oculogyric crisis Parkinsonism Somnolence Tardive dyskinesia Weight gain There ...
"Tardive dyskinesia : biological mechanisms and clinical aspects". Mosnaim, A. D.; Wolf, M. E.; Saavedra, I.; Amaro, A. M.; ... Wolf, M. E.; DeWolfe, A. S.; Ryan, J. J.; Lips, O.; Mosnaim, A. D. (September 1, 1985). "Vulnerability to tardive dyskinesia". ... Mosnaim contributed to document the association of tardive dyskinesia and drug-induced parkinsonism, and in identifying sub- ... Wolf, Marion E.; Ryan, Joseph J.; Mosnaim, Aron D. (August 7, 1983). "Cognitive functions in tardive dyskinesia". Psychological ...
Zullino DF, Eap CB, Voirol P (2001). "Ondansetron for tardive dyskinesia". Am J Psychiatry. 158 (4): 657-8. doi:10.1176/appi. ... open-label trial carried out in 2000 found ondansetron to be useful in treating antipsychotic-induced tardive dyskinesia in ... "Use of the selective serotonin 3 receptor antagonist ondansetron in the treatment of neuroleptic-induced tardive dyskinesia". ...
Zaidi SH, Faruqui RA (January 2008). "Aripiprazole is associated with early onset of Tardive Dyskinesia like presentation in a ... Abbasian C, Power P (March 2009). "A case of aripiprazole and tardive dyskinesia". J Psychopharmacol (Oxford). 23 (2): 214-5. ... Maytal G, Ostacher M, Stern TA (June 2006). "Aripiprazole-related tardive dyskinesia". CNS Spectr. 11 (6): 435-9. doi:10.1017/ ... Tardive dyskinesia (As with all antipsychotic medication, patients using aripiprazole may develop the permanent neurological ...
"What Is Tardive Dyskinesia?". WebMD. Retrieved 2023-03-31. Parry P, Allison S, Bastiampillai T (June 2021). "'Pediatric Bipolar ... Extrapyramidal secondary effects may occur with the use of these medications, including tardive dyskinesia, a difficult-to- ...
... on drug-induced dyskinesias in Parkinson's disease and spontaneous dyskinesias". British Medical Journal. 1 (6118): 954-956. ... Clinical trials demonstrated that it can reduce dyskinesia in patients with Parkinson's disease who are taking dopamine ... Casey DE, Gerlach J (March 1980). "Oxiperomide in tardive dyskinesia". Journal of Neurology, Neurosurgery, and Psychiatry. 43 ( ...
A case report of adrafinil-induced orofacial dyskinesia exists. Reports of this side effect also exist for modafinil. Because ... "Adrafinil-induced orofacial dyskinesia". Mov. Disord. 19 (8): 965-6. doi:10.1002/mds.20154. PMID 15300665. S2CID 31816404. ... "Adrafinil-induced orofacial dyskinesia". Movement Disorders. 19 (8): 965-966. doi:10.1002/mds.20154. PMID 15300665. S2CID ...
Peak-dose dyskinesia - the most common form of levodopa-induced dyskinesia; it correlates with the plateau L‑DOPA plasma level ... Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with an antipsychotic drug such as ... Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of ... primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are ...
Dyskinesias can be a side effect of medications used to treat Parkinsons disease. ... Dyskinesias are involuntary movements that can be seen in individuals with certain neurological conditions such as Parkinsons ... Dyskinesias Dyskinesias are involuntary movements that can be seen in individuals with certain neurological conditions such as ... Dyskinesias can be a side effect of medications used to treat Parkinsons disease. Search. ...
Goal 2: Review the genetic causes of primary ciliary dyskinesia. Goal 3: Provide an evaluation strategy to identify the genetic ... The purpose of this overview is to increase the awareness of clinicians regarding primary ciliary dyskinesia and its genetic ... Goal 4: Inform genetic counseling of family members of an individual with primary ciliary dyskinesia. ... Goal 1: Describe the clinical characteristics of primary ciliary dyskinesia. ...
Tardive means delayed and dyskinesia means abnormal movement. ... Tardive means delayed and dyskinesia means abnormal movement. ... Tardive dyskinesia (TD) is a disorder that involves involuntary movements. ... Tardive dyskinesia (TD) is a disorder that involves involuntary movements. ... TD; Tardive syndrome; Orofacial dyskinesia; Involuntary movement - tardive dyskinesia; Antipsychotic drugs - tardive dyskinesia ...
Background Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in ... Fast Five Quiz: How Much Do You Know About Tardive Dyskinesia? * Fast Five Quiz: Tardive Dyskinesia Causes and Associated ... How is tardive dyskinesia (TD) differentiated from other dyskinesias?. What is the role of the Abnormal Involuntary Movement ... How does the prevalence of tardive dyskinesia (TD) vary by age?. How does the prevalence of tardive dyskinesia (TD) vary by sex ...
... the first medication for the treatment of tardive dyskinesia. ... Fast Five Quiz: How Much Do You Know About Tardive Dyskinesia? ... FDA Okays Once-Daily Tardive Dyskinesia, Huntington Chorea Drug * Moderna Sees Up to $4 Billion in 2023 Sales From Private ... The US Food and Drug Administration (FDA) has approved the first medication for the treatment of tardive dyskinesia (TD), the ... Cite this: FDA Approves First Treatment for Tardive Dyskinesia: Valbenazine (Ingrezza) - Medscape - Apr 11, 2017. ...
... activities might be a risk factor for schizophrenia and/or tardive dyskinesia (TD). In the present study, we investigated the ... Jeste DV, Kelsoe JR . (1997): Schizophrenia, tardive dyskinesia, and D3 receptor gene variant: A new twist on dyskinesias? Mol ... Lohr JB, Caligiuri MP . (1996): A double-blind placebo-controlled study of vitamin E treatment of tardive dyskinesia. J Clin ... Adler LA, Peselow E, Rotrosen J, Duncan E, Lee M, Rosenthal M, Angrist B . (1993): Vitamin E treatment of tardive dyskinesia. ...
It will also help determine whether nicotine and/or nicotinic agonists are of benefit in the treatment of dyskinesias that ... However, its use is associated with the development of abnormal involuntary movements or dyskinesias that may be as ... The results will allow for the development of selective nicotinic drugs against levodopa-induced dyskinesias with optimal ... This research may lead to novel therapeutic strategies to reduce dyskinesias that develop with levodopa treatment in ...
... (PCD) is a disorder found to affect formation of the tiny hairs in the respiratory system called ... Primary Ciliary Dyskinesia. Primary Ciliary Dyskinesia (PCD) is a disorder found to affect formation of the tiny hairs in the ... If primary ciliary dyskinesia is associated with situs inversus (mirrored internal organs), the condition is called Kartagener ...
Clozapine Withdrawal-Emergent Dystonias and Dyskinesias: A Case Series. Shakeel Ahmed, K. N. Roy Chengappa, Venkat Rama Naidu, ... These subjects had severe limb-axial and neck dystonias and dyskinesias 5 to 14 days after clozapine withdrawal. Two subjects ... All had mild orolingual tardive dyskinesia prior to clozapine treatment. All subjects had received clozapine for several months ... This report describes 4 subjects who experienced severe dystonias and dyskinesias upon abrupt clozapine withdrawal. ...
Tardive Dyskinesia is a movement disorder and an uncommon side effect of certain medications. TD affects more than 500,000 ... Tardive Dyskinesia. Tardive dyskinesia (TD) is a condition in which people taking certain mental health medicines experience ... Tardive Dyskinesia Symptoms. Tardive dyskinesia can look or feel different from person to person. TD movements occur in one or ... Tardive Dyskinesia Diagnosis. Your doctor might diagnose you with tardive dyskinesia if you:. *have taken neuroleptic ...
An update on tardive dyskinesia. Intermittent neuroleptic therapy and tardive dyskinesia. Movement disorders in the psychiatric ... Overcoming resistance to talking to patients about tardive dyskinesia. Legal liability for tardive dyskinesia. Training ... Management of Tardive Dyskinesia Collected Articles from Hospital and Community Psychiatry. American Psychiatric Association ... Identifying subtypes of tardive dyskinesia. Recognizing and managing akathisia. A clinical guide for diagnosing and managing ...
Expert-Driven Psychiatry Case: Tardive Dyskinesia. Tardive dyskinesia is a neurological movement disorder that can be difficult ... In this tardive dyskinesia (TD) case report, psychiatrist Craig Chepke, MD introduces his patient, James, a 50-year-old man ... In this tardive dyskinesia (TD) case report, psychiatrist Craig Chepke, MD introduces his patient, James, a 50-year-old man ... Because tardive dyskinesia can be difficult to identify, he recommends these best practices:. - Routinely monitor every patient ...
... Clin ... In the long-term management of PD, treatment-associated dyskinesia often becomes sufficiently troublesome as to compromise the ...
... including tips on how to differentiate tardive dyskinesia from other movement disorders ... Two experts discuss the importance of screening for tardive dyskinesia, ... Listen to 2 thought leaders in the psychiatry field discuss the importance of screening for tardive dyskinesia in patients ...
Biliary Dyskinesia: An Underdiagnosed Condition. Evaluation of Its Implications. Bala Thatigotla, MD MRCS. Bronx Lebanon ... INTRODUCTION: Biliary dyskinesia is a underdiagnosed condition. The lack of suspicion, leads to unnecessary investigations, and ... CONCLUSION(S): Symptoms of cholecystitis without gallstones should lead to suspicion of biliary dyskinesia. CCK-HIDA scan is ... METHODS: A retrospective evaluation of 33 consecutive patients diagnosed with biliary dyskinesia between Jan 2006 and Jan 2010 ...
Primary ciliary dyskinesia. In: Cordier J-F , ed. Orphan Lung Diseases. Eur Respir Monogr 2011; 54: 201-217. ... Pulmonary radioaerosol mucociliary clearance in primary ciliary dyskinesia. Woolf T. Walker, Aneurin Young, Michael Bennett, ... Pulmonary radioaerosol mucociliary clearance in primary ciliary dyskinesia. Woolf T. Walker, Aneurin Young, Michael Bennett, ... Pulmonary radioaerosol mucociliary clearance in primary ciliary dyskinesia. Woolf T. Walker, Aneurin Young, Michael Bennett, ...
Scientific publication of the year 1992 of Neurology on dyskinesia in the Annals of Neurology. Clínica Universidad de Navarra ... Selective D2 receptor stimulation induces dyskinesia in parkinsonian monkeys. May 1, 1992 , Magazine: Annals of Neurology ... These results indicate that drug-induced dyskinesia in a primate model of Parkinsons disease is not solely induced by D1 ... All animals developed choreic dyskinesia after a mean treatment period of 12.8 days (range, 1-29). Administration of the D1 ...
Accuracy of diagnostic testing in primary ciliary dyskinesia. Claire L. Jackson, Laura Behan, Samuel A. Collins, Patricia M. ... Accuracy of diagnostic testing in primary ciliary dyskinesia. Claire L. Jackson, Laura Behan, Samuel A. Collins, Patricia M. ... Accuracy of diagnostic testing in primary ciliary dyskinesia. Claire L. Jackson, Laura Behan, Samuel A. Collins, Patricia M. ... Primary ciliary dyskinesia: a consensus statement on diagnostic and treatment approaches in children. Eur Respir J 2009; 34: ...
Primary Ciliary Dyskinesia Team. The North of England Paediatric PCD Management Service is based at Leeds Childrens Hospital, ...
Primary Ciliary Dyskinesia. Home » About Us » Other Illnesses » Primary Ciliary Dyskinesia. PCD test information can be found ... Primary Ciliary Dyskinesia (PCD) in Old English Sheepdogs. Click to download this article. ... Introduction: Primary ciliary dyskinesia (PCD), previously called immotile cilia syndrome (ICS), is a divers group of inherited ... of sampled ciliated cells and of ciliated cells after ciliogenesis confirmed the diagnosis of primary ciliary dyskinesia. ...
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Primary ciliary dyskinesia syndrome is characterised by chronic sinusitis, bronchiectasis, and, in 50% of cases, dextrocardia. ...
Biliary Dyskinesia: Role of the Sphincter of Oddi, Gallbladder and Cholecystokinin Message Subject (Your Name) has sent you a ... Biliary Dyskinesia: Role of the Sphincter of Oddi, Gallbladder and Cholecystokinin. Shakuntala Krishnamurthy, Gerbail T. ... Biliary Dyskinesia: Role of the Sphincter of Oddi, Gallbladder and Cholecystokinin. Shakuntala Krishnamurthy, Gerbail T. ... Biliary Dyskinesia: Role of the Sphincter of Oddi, Gallbladder and Cholecystokinin. Shakuntala Krishnamurthy and Gerbail T. ...
Thalamotomy for severe antipsychotic induced tardive dyskinesia and dystonia. Journal of Neurology, Neurosurgery & Psychiatry ...
Learn about primary ciliary dyskinesia, a genetic condition that causes abnormal cilia and flagella on cells, and find helpful ... Primary ciliary dyskinesia is an inherited genetic condition that causes abnormal cilia and flagella on cells, which prevents ... DNAI1-related primary ciliary dyskinesia exhibits autosomal recessive inheritance, which means that both parents must be ... Infants with primary ciliary dyskinesia experience breathing problems at birth. Other symptoms include year-round nasal ...
... risk factors for developing tardive dyskinesia do NOT include which of the following? a) Age older than 65. b) Exposure to anti ... Thank you for taking our medical quiz on Tardive Dyskinesia! How did you do? According to an interview with Jonathan Meyer, MD ... b) Spontaneous dyskinesias are indistinguishable from TD and are found more commonly in older and/or edentulous patients.. c) ... d) Tardive dyskinesia assessments can be incorporated into routine protocols that are already in place in many clinical ...
Clinical characteristics, functional respiratory decline and follow-up in adult patients with primary ciliary dyskinesia ... Clinical characteristics, functional respiratory decline and follow-up in adult patients with primary ciliary dyskinesia ... Clinical characteristics, functional respiratory decline and follow-up in adult patients with primary ciliary dyskinesia ...
Are you aware of the differential diagnosis of tardive dyskinesia? Test your knowledge with this quick quiz. ... Tardive dyskinesia (TD) presents as involuntary movements of the tongue, lips, jaw, face, trunk, and extremities that occur in ... Fast Five Quiz: Tardive Dyskinesia Causes and Associated Conditions * Fast Five Quiz: How Much Do You Know About Tardive ... Ask the Expert: Clinical Management of Tardive Dyskinesia 0.25 CME / CE / ABIM MOC Credits ...
  • Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with an antipsychotic drug such as haloperidol (Haldol) or amoxapine (Asendin). (wikipedia.org)
  • Tardive dyskinesia (TD) is a disorder that involves involuntary movements. (medlineplus.gov)
  • Tardive means delayed and dyskinesia means abnormal movement. (medlineplus.gov)
  • Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist medications. (medscape.com)
  • In addition to the prototypic orofacial dyskinesia, tardive syndromes also include a spectrum of hyperkinesias occurring during or after prolonged treatment with dopamine antagonists. (medscape.com)
  • The US Food and Drug Administration (FDA) has approved the first medication for the treatment of tardive dyskinesia (TD), the agency said in a statement. (medscape.com)
  • There has been increasing evidence that deranged superoxide dismutase (SOD) activities might be a risk factor for schizophrenia and/or tardive dyskinesia (TD). (nature.com)
  • Several lines of evidence have indicated that free radicals may play a role in the pathophysiology of tardive dyskinesia (TD). (nature.com)
  • Tardive Dyskinesia (TD) is a movement disorder resulting from prolonged use of certain medications, often with psychiatric implications. (psychiatrist.com)
  • In brief videos, Drs McEvoy and Nierenberg discuss symptoms of tardive dyskinesia, how to observe patients (whether in person or via telemedicine), and how to educate patients and families about TD. (psychiatrist.com)
  • In this report, the authors describe the successful management of tardive dyskinesia with quetiapine in a man with schizoaffective disorder and comorbid diabetes with renal and neurologic complications as well as hypothyroidism and hypertension. (psychiatrist.com)
  • Although clinicians are pressed for time, diligence in assessing for tardive dyskinesia in patients taking antipsychotics is crucial, especially now that treatment is available. (psychiatrist.com)
  • In this CME activity, learn how Dr Joseph McEvoy employs MBC for patients with tardive dyskinesia. (psychiatrist.com)
  • Read an article on how to reduce Tardive dyskinesia (TD) symptoms, including the use of the FDA-approved treatment options (valbenazine and deutetrabenazine). (psychiatrist.com)
  • What steps do you take when patients exhibit tardive dyskinesia? (psychiatrist.com)
  • Two medications are FDA-approved to treat tardive dyskinesia, and new long-term evidence has been reported. (psychiatrist.com)
  • The authors of this consensus statement look at the history of the use of the Abnormal Involuntary Movement Scale in tardive dyskinesia studies and outline the challenges of using AIMS results in clinical practice. (psychiatrist.com)
  • Tardive dyskinesia (TD) is a condition in which people taking certain mental health medicines experience uncontrollable repetitive movements of their face, limbs, or other parts of the body, such as facial tics like lip-smacking, tongue thrusting, and rapid blinking. (dbsalliance.org)
  • The estimates of tardive dyskinesia vary considerably in part related to different patient groups investigated. (dbsalliance.org)
  • The primary risk factors for developing tardive dyskinesia relate to chronicity of illness, duration and dose of antipsychotic medication, and treatment with first-generation antipsychotics (older drugs). (dbsalliance.org)
  • Taking certain medicines, including antipsychotics, to treat conditions such as depression and bipolar disorder, can cause tardive dyskinesia likely due, in part, to changing dopamine receptor sensitivity. (dbsalliance.org)
  • A delay between the time someone starts taking a medication and when tardive dyskinesia develops is common. (dbsalliance.org)
  • To detect tardive dyskinesia in people who are taking neuroleptic drugs, and to track the severity of symptoms over time, doctors might also use a tool called the Abnormal Involuntary Movement Scale (AIMS). (dbsalliance.org)
  • Tardive dyskinesia can look or feel different from person to person. (dbsalliance.org)
  • Because the movements that occur are not controllable, people who experience tardive dyskinesia may feel embarrassed by them or fear being in public. (dbsalliance.org)
  • Many people do not know about tardive dyskinesia, and this can lead to misunderstanding. (dbsalliance.org)
  • It's largely unknown why some people who take certain types of medications develop tardive dyskinesia while others don't. (dbsalliance.org)
  • However, there are risk factors that increase the chance of developing tardive dyskinesia. (dbsalliance.org)
  • Additionally, in 2017, the Food and Drug Administration (FDA) approved two medications that may be able to ease or stop symptoms of tardive dyskinesia. (dbsalliance.org)
  • Living with tardive dyskinesia and other movement disorders affects a person's quality of life. (dbsalliance.org)
  • An update on tardive dyskinesia. (appi.org)
  • Intermittent neuroleptic therapy and tardive dyskinesia. (appi.org)
  • Overcoming resistance to talking to patients about tardive dyskinesia. (appi.org)
  • Legal liability for tardive dyskinesia. (appi.org)
  • Training hospital clinicians to diagnose tardive dyskinesia. (appi.org)
  • Identifying subtypes of tardive dyskinesia. (appi.org)
  • APA statement on tardive dyskinesia. (appi.org)
  • Tardive dyskinesia is a neurological movement disorder that can be difficult to identify and diagnose. (psychiatrist.com)
  • In this tardive dyskinesia (TD) case report, psychiatrist Craig Chepke, MD introduces his patient, James, a 50-year-old man retired from the Army who has been diagnosed with bipolar disorder. (psychiatrist.com)
  • Through this case journey, Dr. Chepke will reveal an effective diagnostic process and best practices for tardive dyskinesia treatment, including the only two FDA-approved therapies, patient care, and optimal outcomes. (psychiatrist.com)
  • He talks through a diagnostic journey, ruling out dystonia, akathisia, and drug-induced Parkinson's to ultimately conclude that the patient's symptoms are most suggestive of tardive dyskinesia (TD). (psychiatrist.com)
  • How Can We Screen for and Identify Tardive Dyskinesia? (clinicaloptions.com)
  • Listen to 2 thought leaders in the psychiatry field discuss the importance of screening for tardive dyskinesia in patients receiving antipsychotics, including clinical pearls for identification in various clinical settings. (clinicaloptions.com)
  • Thank you for taking our medical quiz on Tardive Dyskinesia! (physiciansweekly.com)
  • According to an interview with Jonathan Meyer, MD, Clinical Professor of Psychiatry at UCSD, risk factors for developing tardive dyskinesia do NOT include which of the following? (physiciansweekly.com)
  • In discussing the American Psychiatric Association's new recommendations on the treatment of schizophrenia, released in May 2021, take into account more recent data on antipsychotics, which of the following does Jonathan Meyer, MD, NOT say in regard to screening for tardive dyskinesia in high-risk patients? (physiciansweekly.com)
  • d) Tardive dyskinesia assessments can be incorporated into routine protocols that are already in place in many clinical practices, which are used to monitor other antipsychotic-associated adverse events. (physiciansweekly.com)
  • Which of the following does Chirag Shah, PharmD, RPh, NOT say in regard to why tardive dyskinesia (TD) is often underdiagnosed or misdiagnosed? (physiciansweekly.com)
  • Tardive dyskinesia (TD) presents as involuntary movements of the tongue, lips, jaw, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist or partial agonist medications. (medscape.com)
  • With two medications approved for tardive dyskinesia, how do you choose between them? (thecarlatreport.com)
  • Teva Pharmaceutical Industries Ltd., (NYSE and TASE:TEVA) today announced data for deutetrabenazine tablets for the treatment of tardive dyskinesia (TD) and chorea associated with Huntington disease (HD), and pridopidine for the treatment HD will be presented in 18 poster presentations at the 21st International Congress of Parkinson's Disease and Movement Disorders in Vancouver, BC, Canada from June 4-8. (tevapharm.com)
  • Teva has an extensive CNS franchise in movement disorders and neurodegenerative conditions, and we are pleased to share these important data in tardive dyskinesia and Huntington disease with worldwide experts in movement disorders. (tevapharm.com)
  • Tardive dyskinesia is a condition characterized by involuntary, repetitive movements that affect various parts of the body, such as the face, tongue, and limbs. (stuff.com)
  • The US Food and Drug Administration (FDA) has approved deutetrabenazine ( Austedo , Teva) for the treatment of tardive dyskinesia in adults. (medscape.com)
  • Tardive dyskinesia (TD) is a debilitating and often irreversible movement disorder characterized by repetitive and uncontrollable movements of the tongue, lips, face, trunk, and extremities. (medscape.com)
  • In reporting results of the studies at the American Psychiatric Association 2017 Annual Meeting in June, Karen E. Anderson, MD, of Georgetown University, Washington, DC, told Medscape Medical News , "In both studies, we saw significant reduction in tardive dyskinesia starting as early as 2 weeks on the AIMS scale. (medscape.com)
  • Cite this: FDA OKs Deutetrabenazine (Austedo) for Tardive Dyskinesia - Medscape - Aug 30, 2017. (medscape.com)
  • Tardive dyskinesia / Hans Haag, Eckart Rüther, Hanns Hippius. (who.int)
  • Tardive dyskinesia refers to abnormal hyperkinetic movements of the muscles of the face, tongue, and neck associated with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS). (bvsalud.org)
  • Analogue functional analysis of movements associated with tardive dyskinesia. (bvsalud.org)
  • The acute movement disorders that occur as manifestations of effects of neuroleptics and other dopamine antagonists include akathisia, acute dystonia, and other hyperkinetic dyskinesias. (medscape.com)
  • The most common types of levodopa-induced dyskinesia are chorea and dystonia, which often coexist. (bcmj.org)
  • Early morning dystonia is another type of dyskinesia in PD patients. (bcmj.org)
  • When given in conjunction with L-DOPA, however, MDMA markedly decreased dyskinesia by reducing chorea and to a lesser extent dystonia and decreased locomotor activity to the level observed in normal animals. (erowid.org)
  • Paroxysmal exertion-induced dyskinesia (PED) is a form of paroxysmal dyskinesia (see this term), characterized by painless attacks of dystonia of the extremities triggered by prolonged physical activities. (nih.gov)
  • I now have what appears to be exercise-induced dystonia or dyskinesia-sometimes somewhat graceful and sometimes jerkingly, abrupt, and uncontrolled movements in my upper arm. (davisphinneyfoundation.org)
  • My Parkinson's, dyskinesia, and dystonia are all part of what makes me "me. (davisphinneyfoundation.org)
  • Peak-dose L-DOPA-induced dyskinesia has recently[update] been suggested to be associated with cortical dysregulation of dopamine signaling. (wikipedia.org)
  • Withdrawal dyskinesias may also occur as treatment with dopamine antagonists is decreased or withdrawn. (medscape.com)
  • MDMA similarly alleviated dyskinesia induced by the selective dopamine D2/3 agonist pramipexole. (erowid.org)
  • Adenosine regulates dopamine release so dyskinesias may be related to changes in striatal A2A availability. (bmj.com)
  • The team hypothesizes that following the challenge with L-dopa PD patients with dyskinesia will show a sudden increase in the levels of brain dopamine with appearance or worsening of dyskinesias. (michaeljfox.org)
  • They also hypothesize that buspirone will then reduce the levels of brain dopamine generated from the serotonergic terminals after l-dopa administration and this will be associated with a reduction in dyskinesia intensity. (michaeljfox.org)
  • BACKGROUND: Current models of levodopa (L-dopa)-induced dyskinesia (LID) are obtained by treating dopamine-depleted animals with L-dopa. (lu.se)
  • L-DOPA-induced dyskinesias (LID) are debilitating motor symptoms of dopamine-replacement therapy for Parkinson's disease (PD) that emerge after years of L-DOPA treatment. (biorxiv.org)
  • However, the drug, Levo-Dopamine, causes the appearance of uncontrollable, purposeless and utterly debilitating movements, so called "Levo-DopamineInduced Dyskinesia" (LID), in most patients after several years of treatment. (amsny.org)
  • These results indicate that drug-induced dyskinesia in a primate model of Parkinson's disease is not solely induced by D1 receptor activation. (cun.es)
  • Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of Herpes simplex virus type 1. (wikipedia.org)
  • It is characterized by orofacial dyskinesia, hyporeflexia, seizures, aberrant behavior, atrophy of the caudate nucleus and putamen and acanthocytes in the blood with a normal concentration of lipoproteins. (neurologyindia.com)
  • Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been on levodopa (L‑DOPA) for prolonged periods of time. (wikipedia.org)
  • Dyskinesias are involuntary movements that can be seen in individuals with certain neurological conditions such as Parkinson's disease. (centerwatch.com)
  • Dyskinesias can be a side effect of medications used to treat Parkinson's disease. (centerwatch.com)
  • The central hypothesis underlying this proposal is that drugs targeting CNS nicotinic acetylcholine receptors (nAChRs) may be of therapeutic value for the treatment of levodopa-induced dyskinesias in Parkinson's disease. (michaeljfox.org)
  • This research may lead to novel therapeutic strategies to reduce dyskinesias that develop with levodopa treatment in Parkinson's disease patients. (michaeljfox.org)
  • It will also help determine whether nicotine and/or nicotinic agonists are of benefit in the treatment of dyskinesias that occur with levodopa treatment for Parkinson's disease. (michaeljfox.org)
  • Stimulation of D1 striatal receptors has been proposed as the main mechanism mediating levodopa-induced dyskinesia in Parkinson's disease. (cun.es)
  • Levodopa-induced dyskinesia is one of the most difficult problems facing patients with Parkinson's disease. (bcmj.org)
  • With more treatment options available for Parkinson's disease, physicians need to understand the pathogenetic mechanisms underlying levodopa-induced dyskinesia. (bcmj.org)
  • Objective To investigate adenosine 2A (A2A) receptor availability in Parkinson's disease (PD) patients with and without levodopa induced dyskinesias (LID). (bmj.com)
  • In this project the team will explore a possible mechanism responsible for a common complication of long-term L-dopa treatment in Parkinson's disease (PD), L-dopa induced-involuntary movements or dyskinesias. (michaeljfox.org)
  • The study included 22 patients with protracted and complicated Parkinson's disease and L-dopa-induced dyskinesia. (ki.se)
  • If it is approved by the FDA this month, Adamas's ADS-5102 will become the first medicine for treating levodopa-induced dyskinesia in Parkinson's disease. (evaluate.com)
  • Growing preclinical and clinical evidence highlights neurosteroid pathway imbalances in Parkinson's Disease (PD) and L-DOPA-induced dyskinesias (LIDs). (lu.se)
  • The idea that nicotinic drugs may be useful for the treatment of dyskinesias is based on our studies, which show that nicotine reduces levodopa-induced abnormal involuntary movements in a non-human primate parkinsonian model and in hemi-parkinsonian rats. (michaeljfox.org)
  • Furthermore, many patients with PD develop dyskinesia in one part of the body while another part remains parkinsonian. (bcmj.org)
  • Patients will be also assessed clinically to evaluate their parkinsonian symptoms and the presence and severity of dyskinesia. (michaeljfox.org)
  • Two other types, primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are not movement disorders. (wikipedia.org)
  • The purpose of this overview is to increase the awareness of clinicians regarding primary ciliary dyskinesia and its genetic causes and management. (nih.gov)
  • Describe the clinical characteristics of primary ciliary dyskinesia. (nih.gov)
  • Review the genetic causes of primary ciliary dyskinesia. (nih.gov)
  • Provide an evaluation strategy to identify the genetic cause of primary ciliary dyskinesia in a proband. (nih.gov)
  • Inform genetic counseling of family members of an individual with primary ciliary dyskinesia. (nih.gov)
  • Review management of primary ciliary dyskinesia. (nih.gov)
  • In patients with primary ciliary dyskinesia (PCD), province and identification of pathogen. (cdc.gov)
  • Primary ciliary dyskinesia (PCD), previously called immotile cilia syndrome (ICS), is a divers group of inherited structural and functional abnormalities affecting the cilia of the respiratory tract mucosa and other organs which results mainly in recurrent respiratory tract infections. (oldenglishsheepdogclubofamerica.org)
  • Transmission electron microscopy analysis of sampled ciliated cells and of ciliated cells after ciliogenesis confirmed the diagnosis of primary ciliary dyskinesia. (oldenglishsheepdogclubofamerica.org)
  • Unusual inheritance of primary ciliary dyskinesia (Kartagener's syndrome). (bmj.com)
  • Primary ciliary dyskinesia is an inherited genetic condition that causes abnormal cilia and flagella on cells, which prevents the clearance of mucous from the lungs, sinuses, and middle ears. (jewishgenetics.org)
  • Infants with primary ciliary dyskinesia experience breathing problems at birth. (jewishgenetics.org)
  • DNAI1-related primary ciliary dyskinesia exhibits autosomal recessive inheritance , which means that both parents must be carriers to have a 25% chance to have a child with the condition. (jewishgenetics.org)
  • Thomas W. Ferkol, Jr, MD, a pediatric pulmonologist at UNC Health and chief of pulmonology in the UNC Department of Pediatrics, and researchers at Parion Sciences Inc. recently led a phase 2 study of idrevloride in hypertonic saline in people with primary ciliary dyskinesia (PCD). (medicalxpress.com)
  • Their results, which were published in The Lancet Respiratory Medicine , demonstrate that idrevloride in hypertonic saline is safe and associated with a significant improvement in lung function over a 28-day period in individuals with primary ciliary dyskinesia when compared to hypertonic saline alone. (medicalxpress.com)
  • A total of 123 adults and adolescents with primary ciliary dyskinesia aged 12 years or older were randomly assigned to receive idrevloride in hypertonic saline, hypertonic saline alone, idrevloride alone, or placebo. (medicalxpress.com)
  • The ENaC inhibitor has been well-tolerated in multiple clinical trials in healthy volunteers and patients with other respiratory diseases who accumulate excessively concentrated mucus in their lungs, including primary ciliary dyskinesia. (medicalxpress.com)
  • Felix C Ringshausen et al, Safety and efficacy of the epithelial sodium channel blocker idrevloride in people with primary ciliary dyskinesia (CLEAN-PCD): a multinational, phase 2, randomised, double-blind, placebo-controlled crossover trial, The Lancet Respiratory Medicine (2023). (medicalxpress.com)
  • Give as you Live Online is the free and easy way to raise money for PRIMARY CILIARY DYSKINESIA (PCD) FAMILY SUPPORT GROUP when you shop online with 6,000+ stores. (giveasyoulive.com)
  • Simply sign up for an account and start shopping to make a difference for PRIMARY CILIARY DYSKINESIA (PCD) FAMILY SUPPORT GROUP! (giveasyoulive.com)
  • Phenotype-genotype associations in primary ciliary dyskinesia: where do we stand? (ers-education.org)
  • Is primary ciliary dyskinesia a 'biofilm' disease? (ers-education.org)
  • How insignificant are genetic variants of unknown significance in Primary Ciliary Dyskinesia? (ers-education.org)
  • Can nasal-NO be used to differentiate between primary and secondary ciliary dyskinesia? (ers-education.org)
  • Accuracy of diagnostic testing in primary ciliary dyskinesia: are we there yet? (ers-education.org)
  • Last September the extended-release formulation of amantadine hit the primary endpoint of its second phase III trial, Ease Lid 3, showing a significant reduction on the unified dyskinesia rating scale versus placebo. (evaluate.com)
  • Background Mostly derived from chart reviews, where symptoms are recorded in a nonstandardised manner, clinical data about primary ciliary dyskinesia (PCD) are inconsistent, which leads to missing and unreliable information. (ersjournals.com)
  • Primary ciliary dyskinesia (PCD) is a rare, genetic, multi-organ disease characterised by significant genetic and clinical variability [ 1 , 2 ]. (ersjournals.com)
  • Primary ciliary dyskinesia (PCD) is a rare inherited condition. (asthmaandlung.org.uk)
  • Treatment response to pulmonary exacerbation in primary ciliary dyskinesia. (bvsalud.org)
  • Pulmonary exacerbation (Pex) are common in pediatric primary ciliary dyskinesia (PCD), however changes in forced expiratory volume in 1 s precent predicted (FEV1pp) during Pex are not well described. (bvsalud.org)
  • Which of the following describes oral-buccal-lingual dyskinesia, according to an interview with Joseph McEvoy, MD, Professor Emeritus of Psychiatry and Behavioral Sciences, at Duke University School of Medicine? (physiciansweekly.com)
  • Patients may develop fluctuations in motor symptoms and dyskinesias as well as nonmotor symptoms. (psychiatrist.com)
  • Symptoms of cholecystitis without gallstones should lead to suspicion of biliary dyskinesia. (sages.org)
  • When Do Symptoms of Paroxysmal exertion-induced dyskinesia Begin? (nih.gov)
  • Biliary Dyskinesia: An Underdiagnosed Condition. (sages.org)
  • Biliary dyskinesia is a underdiagnosed condition. (sages.org)
  • A retrospective evaluation of 33 consecutive patients diagnosed with biliary dyskinesia between Jan 2006 and Jan 2010 was done. (sages.org)
  • 33 patients were diagnosed with biliary dyskinesia and all underwent laparoscopic cholecystectomy. (sages.org)
  • 26 CT scans, 45 ultrasounds, 12 upper GI endoscopies and 6 cardiac work ups were done before investigation for biliary dyskinesia was initiated. (sages.org)
  • Post-mortem analyses revealed that pregnenolone significantly prevented the increase of validated striatal markers of dyskinesias, such as phospho-Thr-34 DARPP-32 and phospho-ERK 1/2 , as well as D 1 -D 3 receptor co-immunoprecipitation in a fashion similar to dutasteride. (lu.se)
  • However, Lafuente et al did not find evidence of involvement of a polymorphism with a variable number of tandem repeats (VNTD) in the DAT gene (SLC6A3) in dyskinesias induced by antipsychotics. (medscape.com)
  • Few case reports have been devoted to the impact of orolingual dyskinesia or dysphagia as the dominant clinical picture in patients with ChAc. (neurologyindia.com)
  • During early levodopa treatment, peak dose dyskinesia may be apparent only during the maximum antiparkinsonian effect of levodopa. (bcmj.org)
  • However, its use is associated with the development of abnormal involuntary movements or dyskinesias that may be as debilitating as the disease itself. (michaeljfox.org)
  • The proposed studies represent a new research direction for the treatment of levodopa-induced dyskinesias using nicotine or nicotinic receptor agonists. (michaeljfox.org)
  • In the long-term management of PD, treatment-associated dyskinesia often becomes sufficiently troublesome as to compromise the effective dosing of antiparkinsonian medication. (nih.gov)
  • All animals developed choreic dyskinesia after a mean treatment period of 12.8 days (range, 1-29). (cun.es)
  • PD patients often pose challenging problems given the many treatment options available-levodopa-induced dyskinesia can be one of the most troublesome. (bcmj.org)
  • Levodopa-induced dyskinesia refers to involuntary adventitious movements that usually occur after prolonged treatment with levodopa in PD patients. (bcmj.org)
  • Serotoninergic receptors appear to play an important modulatory role in L-DOPA-induced dyskinesia, and this study may provide a framework for the use of serotoninergic agents in the treatment of L-DOPA-induced dyskinesia. (erowid.org)
  • If the study is successful it will encourage the development of new and more selective drugs aimed to damp serotonergic function for the treatment of L-dopa-induced dyskinesias as the current available drugs including buspirone are not well suited to be used on a long term basis as they have sedative effects. (michaeljfox.org)
  • A treatment study published in the journal Brain shows that a drug that stimulates certain serotonin receptors in the brain counteracts the dyskinesia causing effects of L-dopa. (ki.se)
  • The treatment seems to be tolerated well by most Parkinson's patients and counteracts L-dopa-induced dyskinesia via a new mechanism of action," says Professor Svenningsson. (ki.se)
  • Recently, however, the rights to eltoprazine were acquired by the US biotechnology company Amarantus BioScience Holdings, Inc . The compound is now advancing into a larger scale, longer duration study to evaluate the full treatment effect of eltoprazine in Parkinson's patients with L-dopa-induced dyskinesia. (ki.se)
  • Recently, we reached out to people in our community who have dyskinesia and asked them to share stories, treatment ideas, and words of wisdom for managing it. (davisphinneyfoundation.org)
  • Dyskinesia refers to a category of movement disorders that are characterized by involuntary muscle movements, including movements similar to tics or chorea and diminished voluntary movements. (wikipedia.org)
  • Diphasic dyskinesia - occurs when plasma L-DOPA levels are rising or falling. (wikipedia.org)
  • Less common than peak dose dyskinesia is diphasic dyskinesia. (bcmj.org)
  • Most levodopa-induced dyskinesia occurs when antiparkinsonian effects of levodopa are maximal, hence the term peak dose dyskinesia . (bcmj.org)
  • In these patients dyskinesias may appear soon after a single dose of levodopa before any symptomatic effect takes place. (bcmj.org)
  • [1] The threshold dose of levodopa for dyskinesia decreases with a longer duration of disorder, but not for antiparkinsonian effects. (bcmj.org)
  • Ultimately, patients develop dyskinesia even at the dose at which the patient is in an "off" state. (bcmj.org)
  • It was found that a 5 mg and 7.5 mg dose of eltoprazine both significantly reduced the patients' dyskinesia. (ki.se)
  • There are wide individual variations in the nature, severity, and topographical pattern of levodopa-induced dyskinesia. (bcmj.org)
  • Once levodopa-induced dyskinesia has developed, its severity increases but the topographical pattern tends to remain constant. (bcmj.org)
  • The results will allow for the development of selective nicotinic drugs against levodopa-induced dyskinesias with optimal therapeutic efficacy and a minimum of adverse effects. (michaeljfox.org)
  • Ecstasy [3,4-methylenedioxymethamphetamine (MDMA)] was shown to prolong the action of L-3,4-dihydroxyphenylalanine (L-DOPA) while suppressing dyskinesia in a single patient with Parkinson s disease (PD). (erowid.org)
  • Inform people on antipsychotic drugs of the risk of tardive dyskinesia. (ddhealthinfo.org)
  • The low risk of tardive dyskinesia in clozapine-treated individuals has been well estab-lished. (brainkart.com)
  • When coupled with the fact that second- and third-generation antipsychotic medications have come to be employed in treating a wider range of disorders (e.g., autism spectrum disorders, mood disorders, personality disorders, etc.), it is clear that the population of patients exposed to the risk of tardive dyskinesia has expanded. (clinicalschizophrenia.net)
  • Rabbit syndrome is another type of chronic dyskinesia, while orofacial dyskinesia may be related to persistent replication of Herpes simplex virus type 1. (wikipedia.org)
  • We present the case of a 74-year-old patient with no significant pathological history, who is admitted to the neurology ward for orofacial dyskinesias accompanied by hypoesthesia in the left hemiface, a symptomatology that had started insidiously about two months before and worsened progressively over the past 3 weeks. (hindawi.com)
  • The neurological examination revealed such changes as left hemifacial hypoaesthesia, orofacial dyskinesia, extrapyramidal syndrome, bradykinesia and bilateral hypokinesia without motor deficits or coordination disorders, without speech impediments, left plantar extension, and right plantar flexion. (hindawi.com)
  • However, the vast differential diagnosis of orofacial dyskinesia, which excluded use of neuroleptics, demonstrated that it was imperative to go to the next stage, namely, paraclinical tests. (hindawi.com)
  • In addition to the prototypic orofacial dyskinesia, tardive syndromes also include a spectrum of hyperkinesias occurring during or after prolonged treatment with dopamine antagonists. (medscape.com)
  • A related disorder, spontaneous orofacial dyskinesia of the elderly, is observed primarily in the edentulous. (medscape.com)
  • A case of acute dyskinesia in a 42-year-old man with a history of cocaine use and schizophrenia is described. (nih.gov)
  • Are anticholinergic drugs or withdrawal of anticholinergic drugs effective in the treatment of tardive dyskinesia in people with schizophrenia or other similar mental health problems. (cochrane.org)
  • The review includes two small randomised studies with a total of 30 people with schizophrenia who had also developed antipsychotic-induced tardive dyskinesia. (cochrane.org)
  • To determine whether the use or the withdrawal of anticholinergic drugs (benzhexol, benztropine, biperiden, orphenadrine, procyclidine, scopolamine, or trihexylphenidyl) are clinically effective for the treatment of people with both antipsychotic-induced tardive dyskinesia and schizophrenia or other chronic mental illnesses. (cochrane.org)
  • We included reports identified in the search if they were controlled trials dealing with people with antipsychotic-induced tardive dyskinesia and schizophrenia or other chronic mental illness who had been randomly allocated to (a) anticholinergic medication versus placebo (or no intervention), (b) anticholinergic medication versus any other intervention for the treatment of tardive dyskinesia, or (c) withdrawal of anticholinergic medication versus continuation of anticholinergic medication. (cochrane.org)
  • Tardive dyskinesia (TD) is a neurological syndrome associated with long-term use of antipsychotic (neuroleptic) drugs prescribed to treat psychiatric disorders, particularly schizophrenia, as well as some gastrointestinal or neurological conditions. (ddhealthinfo.org)
  • Tardive dyskinesia is a serious side effect sometimes seen in those being treated with certain medications for schizophrenia and bipolar disorder. (rxwiki.com)
  • A possible relationship between gender and age of onset of schizo-phrenia to severity of dyskinesia has been reported as women with late-onset schizophrenia (LOS) and men with early-onset schizophrenia (EOS) had more severe dyskinesia than men with LOS and women with EOS. (brainkart.com)
  • Two other types, primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are not movement disorders. (wikipedia.org)
  • Biliary Dyskinesia, true or false? (surgicaloasis.com)
  • Most of these patients suffer biliary dyskinesia and unfortunately do not get diagnosed for a long time or undergo medical management with little or no response. (surgicaloasis.com)
  • Biliary dyskinesia is a functional disease of gallbladder which could present with the same signs and symptoms of patients with gall stones. (surgicaloasis.com)
  • The low ejection fraction of gallbladder in patients with typical signs and symptoms of gallbladder disease is consistent with biliary dyskinesia and removal of gallbladder is indicated. (surgicaloasis.com)
  • Therefore, the diagnosis of biliary dyskinesia is a diagnosis of exclusion and prior to any surgical intervention the other potential diagnosis needs to be ruled out. (surgicaloasis.com)
  • Biliary dyskinesia. (healthychildren.org)
  • Usually, children with biliary dyskinesia have no stones in the gallbladder. (healthychildren.org)
  • When Do Symptoms of Primary ciliary dyskinesia Begin? (nih.gov)
  • Your healthcare provider or your child's provider will diagnose primary ciliary dyskinesia (PCD) based on your symptoms , family history , and test results. (nih.gov)
  • Here's what the research says about whether vitamins E and B6, melatonin, ginkgo biloba, and BCAAs can help reduce symptoms of tardive dyskinesia. (healthline.com)
  • Learn the definition of dyskinesia, along with its symptoms and causes. (healthline.com)
  • Anxiety, fatigue, and other stress can temporarily increase the severity of the signs and symptoms of ADCY5 -related dyskinesia, while some affected individuals may experience remission periods of days or weeks without abnormal movements. (nih.gov)
  • It is also uncertain whether the withdrawal of anticholinergic medication improves the symptoms of tardive dyskinesia. (cochrane.org)
  • In addition, symptoms may not be observed until the antipsychotic medication is decreased or withdrawn, since tardive dyskinesia may be masked by the drug that has caused the disorder. (ddhealthinfo.org)
  • Tetrabenazine may provide benefit in managing symptoms of tardive dyskinesia unresponsive to other treatment modalities. (nih.gov)
  • Background Mostly derived from chart reviews, where symptoms are recorded in a nonstandardised manner, clinical data about primary ciliary dyskinesia (PCD) are inconsistent, which leads to missing and unreliable information. (medrxiv.org)
  • The symptoms of tardive dyskinesia can negatively affect daily function, emotional wellness, and quality of life. (e-bipolar.com)
  • How can I or my loved one help improve care for people with tardive dyskinesia? (nih.gov)
  • To fully investigate whether the withdrawal of anticholinergic drugs has any positive effects for people with tardive dyskinesia, we need more high quality research data. (cochrane.org)
  • We explain why this happens and a list of medications commonly linked with tardive dyskinesia. (healthline.com)
  • In general, it is assumed that clozapine does not cause tardive dyskinesia. (psychiatrist.com)
  • There is, however, evidence from animal experiments that anticholinergic drugs could cause tardive dyskinesia. (cochrane.org)
  • However, there is also a suggestion from animal experiments that the chronic administration of anticholinergics could cause tardive dyskinesia. (cochrane.org)
  • Can Vitamins or Supplements Treat Tardive Dyskinesia? (healthline.com)
  • RxWiki News) The US Food and Drug Administration (FDA) has approved the first drug to treat tardive dyskinesia. (rxwiki.com)
  • The abnormal movements that occur in ADCY5 -related dyskinesia typically appear as sudden (paroxysmal) jerks, twitches, tremors, muscle tensing (dystonia), or writhing (choreiform) movements, and can affect the limbs, neck, and face. (nih.gov)
  • The abnormal movements associated with ADCY5 -related dyskinesia usually begin between infancy and late adolescence. (nih.gov)
  • In some people with ADCY5 -related dyskinesia, the disorder is generally stable throughout their lifetime. (nih.gov)
  • Life expectancy is not usually affected by ADCY5 -related dyskinesia, and most people with this condition have normal intelligence. (nih.gov)
  • At least 400 people have been diagnosed with ADCY5 -related dyskinesia, but its prevalence is unknown. (nih.gov)
  • As its name suggests, ADCY5 -related dyskinesia is caused by mutations in the ADCY5 gene. (nih.gov)
  • Some ADCY5 gene mutations that cause ADCY5 -related dyskinesia are thought to increase adenylate cyclase 5 enzyme activity and the level of cAMP within cells. (nih.gov)
  • It has been suggested that motor fluctuations and levodopa-induced dyskinesias in PD could be associated with an upregulation of glutamine receptors like N-methyl-D-aspartate (NMDA) and amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) as a result of the chronic, nonphysiologic stimulation of striatal dopaminergic receptors. (medscape.com)
  • [ 1 , 2 ] Clinical data supporting this observation are reinforced by the fact that amantadine, an NMDA receptor antagonist, has proven useful for the treatment of levodopa-induced dyskinesias in PD patients. (medscape.com)
  • The precise cause of levodopa-induced dyskinesias is unknown. (cun.es)
  • Primary ciliary dyskinesia (PCD) is an inherited disorder which affects the movement of tiny hair-like structures on body cells, known as cilia. (nih.gov)
  • Clinical and genetic aspects of primary ciliary dyskinesia/Kartagener syndrome. (medscape.com)
  • Primary ciliary dyskinesia in Amish communities. (medscape.com)
  • Mutations of DNAH 11 in patients with primary ciliary dyskinesia with normal ciliary ultrastructure. (medscape.com)
  • The role of molecular genetic analysis in the diagnosis of primary ciliary dyskinesia. (medscape.com)
  • Chilvers MA, Rutman A, O'Callaghan C. Ciliary beat pattern is associated with specific ultrastructural defects in primary ciliary dyskinesia. (medscape.com)
  • Quantitative analysis of ciliary beating in primary ciliary dyskinesia: a pilot study. (medscape.com)
  • Loss-of-function mutations in a human gene related to Chlamydomonas reinhardtii dynein IC78 result in primary ciliary dyskinesia. (medscape.com)
  • Axonemal dynein intermediate-chain gene (DNAI1) mutations result in situs inversus and primary ciliary dyskinesia (Kartagener syndrome). (medscape.com)
  • DNAH5 mutations are a common cause of primary ciliary dyskinesia with outer dynein arm defects. (medscape.com)
  • Bush A, Ferkol T. Movement: the emerging genetics of primary ciliary dyskinesia. (medscape.com)
  • Factors influencing age at diagnosis of primary ciliary dyskinesia in European children. (medscape.com)
  • The global prevalence and ethnic heterogeneity of primary ciliary dyskinesia gene variants: a genetic database analysis. (medscape.com)
  • Presentation of primary ciliary dyskinesia in children: 30 years' experience. (medscape.com)
  • Clinical Features and Associated Likelihood of Primary Ciliary Dyskinesia in Children and Adolescents. (medscape.com)
  • In patients with primary ciliary dyskinesia (PCD), province and identification of pathogen. (cdc.gov)
  • Functional and structural lung evaluations are part of the follow-up of patients with primary ciliary dyskinesia (PCD). (nih.gov)
  • Conditions which feature recurrent or persistent episodes of dyskinesia as a primary manifestation of disease may be referred to as dyskinesia syndromes (see MOVEMENT DISORDERS). (embl.de)
  • Although the study did not meet its primary efficacy endpoint, a well-established scale used to assess dyskinesia, the UDysRS, demonstrated anti-dyskinetic effects by mesdopetam,' Nicholas Waters, executive vice president and head of Research & Development, IRLAB, said in a statement. (neurologylive.com)
  • Primary ciliary dyskinesia (PCD) is an inherited (called genetic ) condition. (chestnet.org)
  • Primary ciliary dyskinesia (PCD) is a rare genetic condition that can lead to chronic ear and sinus infections, pulmonary disease, situs inversus , and fertility issues. (chestnet.org)
  • How serious is Primary Ciliary Dyskinesia? (chestnet.org)
  • Mutations in RSPH1 cause primary ciliary dyskinesia with a unique clinical and ciliary phenotype. (bvsalud.org)
  • RATIONALE Primary ciliary dyskinesia (PCD) is a genetically heterogeneous recessive disorder of motile cilia , but the genetic cause is not defined for all patients with PCD. (bvsalud.org)
  • We carried out a retrospective descriptive study to determine prevalence and risk factors for tardive dyskinesia [‎TD]‎ among psychotic patients treated with conventional neuroleptics in 4 centres in Saudi Arabia. (who.int)
  • To determine the prevalence of tardive dyskinesia (TD) identified by clinicians in naturalistic data in a real-world treatment setting. (psychiatrist.com)
  • Treatment of tardive dyskinesia with tetrabenazine may be limited by cost and clinically significant adverse effects such as depression, parkinsonism, and somnolence. (nih.gov)
  • What can severe tardive dyskinesia (TD) of the tongue look like, and how might it differ from moderate TD of the tongue or drug-induced Parkinsonism? (neurocrinemedical.com)
  • Fast Five Quiz: Tardive Dyskinesia Causes and Associated Conditions - Medscape - Jan 19, 2022. (medscape.com)
  • Tardive means delayed and dyskinesia means abnormal movement. (medlineplus.gov)
  • Dyskinesia refers to a category of movement disorders that are characterized by involuntary muscle movements, including movements similar to tics or chorea and diminished voluntary movements. (wikipedia.org)
  • Dyskinesia can be anything from a slight tremor of the hands to an uncontrollable movement of the upper body or lower extremities. (wikipedia.org)
  • Tardive dyskinesia (TD) is a movement disorder that can cause uncontrolled movements in parts of your body. (healthline.com)
  • Tardive dyskinesia is an involuntary movement disorder caused by certain psychiatric medications. (healthline.com)
  • A drug currently approved for tardive dyskinesia (TD) is also effective at treating Huntington's disease (HD)-associated chorea, a movement disorder that affects most patients with HD, new phase 3 trial results show. (medscape.com)
  • Tardive dyskinesia (TD) is a movement disorder characterized by uncontrollable, abnormal, and repetitive movements of the face, torso, and/or other body parts. (nih.gov)
  • In addition to the many topic headings linked to on the main CMDG.org page, there are many other less common / rare conditions that can be associated with differing movement disorders (including a variety of dyskinesias). (cmdg.org)
  • Tardive dyskinesia is an involuntary movement that causes the face, mouth, tongue and jaw to convulse, spasm and grimace. (cochrane.org)
  • Literature was accessed through MEDLINE (1966-September 2010) and The Cochrane Library using the terms tetrabenazine, tardive dyskinesia, and movement disorders. (nih.gov)
  • Tardive dyskinesia (TD) is a persistent and potentially disabling movement disorder associated with antipsychotic use. (springer.com)
  • T ardive dyskinesia (TD) is an involuntary, generally irreversible movement disorder associated with long-term antipsychotic medication treatment. (psychiatrist.com)
  • Tardive dyskinesia is a movement disorder distinguished by a range of involuntary and repetitive muscle movements in the face, neck, arms, and legs. (e-bipolar.com)
  • New As a movement disorder commonly induced by antipsychotic medications, tardive dyskinesia (TD) is important to study in medical school. (themighty.com)
  • New The treatment landscape for tardive dyskinesia (TD), a movement disorder that can develop after the use of antipsychotic medications, is rapidly evolving. (themighty.com)
  • The striatum is widely viewed as the fulcrum of pathophysiology in Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID). (nih.gov)
  • If you've been taking a Parkinson's drug that contains levodopa - for example, co-beneldopa or co-careldopa - for some time, you may develop motor fluctuations, wearing off and dyskinesia. (parkinsons.org.uk)
  • Clozapine treatment was reinitiated, and within 2 weeks the dyskinesia had subsided. (nih.gov)
  • Dyskinesia occurring in the context of cocaine use, and clozapine withdrawal-associated dyskinesia were considered to be the main differential diagnoses. (nih.gov)
  • Withdrawal-emergent respiratory dyskinesia with risperidone treated with clozapine. (nih.gov)
  • It is not possible to recommend these drugs or the withdrawal of these drugs as a treatment for tardive dyskinesia. (cochrane.org)
  • It is estimated that tardive dyskinesia affects at least 500,000 people in the United States. (e-bipolar.com)
  • Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been on levodopa (L‑DOPA) for prolonged periods of time. (wikipedia.org)
  • I understand that talampanel is currently under study for the management of severe dyskinesias in Parkinson's disease (PD). (medscape.com)
  • RESEARCH OBJECTIVES Dyskinesias constitute an important complication of the treatment of Parkinson's disease (PD). (nih.gov)
  • Neuroleptic-induced tardive dyskinesia (TD) is a syndrome con-sisting of abnormal, involuntary movements caused by long-term treatment with antipsychotic medication. (brainkart.com)
  • Others may experience more severe dyskinesia, which can prevent them from carrying out simple tasks. (parkinsons.org.uk)
  • Many cases of tardive dyskinesia are mild and TD does not always progress in severity, though some people develop severe and disabling TD. (ddhealthinfo.org)
  • Ciliary dyskinesia with transposition of ciliary microtubules is a genetic disease. (nih.gov)
  • O n the 30th of December, right before the cursed 2016 is considered past, TARDIVE DYSKINESIA will present their new album, titled " Harmonic Confusion ", live at Kyttaro music venue. (metalpaths.com)
  • Dyskinesias are abnormal movements, usually caused by neurological diseases or by drugs used to treat neurological (e.g., levodopa) or psychiatric diseases (e.g., neuroleptics). (pharmawiki.in)
  • Tardive dyskinesia is a side effect caused by neuroleptic drugs. (healthline.com)
  • Fast Five Quiz: How Much Do You Know About Tardive Dyskinesia? (medscape.com)
  • Currently, there is a lack of data coupled with the risk of significant adverse effects to recommend the routine use of tetrabenazine in the management of tardive dyskinesia. (nih.gov)
  • TD Symptom Tracker is a revolutionary app enabling users to track, record, and monitor the involuntary movements associated with Tardive Dyskinesia. (matellio.com)
  • However, more than half of all patients treated with levodopa or other dopaminergic agonists will subsequently develop dyskinesias after approximately five years. (nih.gov)
  • The double-blind, placebo-controlled study randomly assigned 156 patients with PD experiencing troublesome dyskinesia to either 3 doses of mesdopetam (2.5, 5.0, and 7.5 mg BID) or placebo. (neurologylive.com)
  • In 2019, IRLAB announced an in-depth analysis on data from a concluded phase 2a study of mesdopetam, formerly known as IRL790, in patients with PD-induced dyskinesia. (neurologylive.com)
  • Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist medications. (medscape.com)
  • You might not feel too affected by mild dyskinesia, or might even be unaware of them, even though they might be visible to another person. (parkinsons.org.uk)
  • However even when mild, it is widely held that the appearance of dyskinesias foreshadows the development of other, more disabling motor complications. (nih.gov)
  • Dyskinesia is a symptom of several medical disorders that are distinguished by their underlying cause. (wikipedia.org)