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.
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.
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)
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.
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)
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.
One of the centrally acting MUSCARINIC ANTAGONISTS used for treatment of PARKINSONIAN DISORDERS and drug-induced extrapyramidal movement disorders and as an antispasmodic.
Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.
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.
A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.
Benzophenones are synthetic organic compounds characterized as aromatic ketones, often used in chemical synthesis for various applications including sunscreen formulations due to their UV-absorbing properties.
A semisynthetic ergotamine alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion.
Drugs that bind to and activate dopamine receptors.
An ergot derivative that acts as an agonist at dopamine D2 receptors (DOPAMINE AGONISTS). It may also act as an antagonist at dopamine D1 receptors, and as an agonist at some serotonin receptors (SEROTONIN RECEPTOR AGONISTS).
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.
Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS; MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)
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.
One of the AROMATIC-L-AMINO-ACID DECARBOXYLASES, this enzyme is responsible for the conversion of DOPA to DOPAMINE. It is of clinical importance in the treatment of Parkinson's disease.
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)
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.
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.
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)
A series of structurally-related alkaloids that contain the ergoline backbone structure.
Continuous involuntary sustained muscle contraction which is often a manifestation of BASAL GANGLIA DISEASES. When an affected muscle is passively stretched, the degree of resistance remains constant regardless of the rate at which the muscle is stretched. This feature helps to distinguish rigidity from MUSCLE SPASTICITY. (From Adams et al., Principles of Neurology, 6th ed, p73)
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.
Performance of complex motor acts.
Enzyme that catalyzes the movement of a methyl group from S-adenosylmethionone to a catechol or a catecholamine.
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 syndrome characterized by a silent and inert state without voluntary motor activity despite preserved sensorimotor pathways and vigilance. Bilateral FRONTAL LOBE dysfunction involving the anterior cingulate gyrus and related brain injuries are associated with this condition. This may result in impaired abilities to communicate and initiate motor activities. (From Adams et al., Principles of Neurology, 6th ed, p348; Fortschr Neurol Psychiatr 1995 Feb;63(2):59-67)
Cell-surface proteins that bind dopamine with high affinity and trigger intracellular changes influencing the behavior of cells.
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.
Hydrazines are organic compounds containing the functional group R-NH-NH2, where R represents an organic group, and are used in pharmaceuticals, agrochemicals, and rocket fuels, but can be highly toxic and carcinogenic with potential for environmental damage.
Compounds with a benzene ring fused to a thiazole ring.
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.
A plant genus of the family FABACEAE that is the source of mucuna gum.
Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.
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.
A chemically heterogeneous group of drugs that have in common the ability to block oxidative deamination of naturally occurring monoamines. (From Gilman, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p414)
Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.
An inhibitor of the last step of noradrenaline biosynthesis.
Marked impairments in the development of motor coordination such that the impairment interferes with activities of daily living. (From DSM-V)
Clinical signs and symptoms caused by nervous system injury or dysfunction.
An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.
Tetrahydroisoquinolinol alkaloids in both dextro and levo forms, originally found in SALSOLA plants.
Therapy with two or more separate preparations given for a combined effect.
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.

Viral gene delivery selectively restores feeding and prevents lethality of dopamine-deficient mice. (1/1391)

Dopamine-deficient mice (DA-/- ), lacking tyrosine hydroxylase (TH) in dopaminergic neurons, become hypoactive and aphagic and die by 4 weeks of age. They are rescued by daily treatment with L-3,4-dihydroxyphenylalanine (L-DOPA); each dose restores dopamine (DA) and feeding for less than 24 hr. Recombinant adeno-associated viruses expressing human TH or GTP cyclohydrolase 1 (GTPCH1) were injected into the striatum of DA-/- mice. Bilateral coinjection of both viruses restored feeding behavior for several months. However, locomotor activity and coordination were partially improved. A virus expressing only TH was less effective, and one expressing GTPCH1 alone was ineffective. TH immunoreactivity and DA were detected in the ventral striatum and adjacent posterior regions of rescued mice, suggesting that these regions mediate a critical DA-dependent aspect of feeding behavior.  (+info)

Dopamine correlates of neurological and psychological status in untreated Parkinsonism. (2/1391)

Thirty-seven untreated Parkinsonism patients showed significant positive correlations among decreased excretion of free dopamine, MMPI scores indicative of schizophrenic-like looseness of thinking, and the severity of all Parkinsonism signs except tremor. The data could indicate that abnormalities of dopamine metabolism may underlie both the motor and mental abnormalities of Parkinsonism.  (+info)

Aromatic L-amino acid decarboxylase: conformational change in the flexible region around Arg334 is required during the transaldimination process. (3/1391)

Aromatic L-amino acid decarboxylase (AADC) catalytic mechanism has been proposed to proceed through two consecutive intermediates (i.e., Michaelis complex and the external aldimine). Limited proteolysis of AADC that preferentially digested at the C-terminal side of Arg334 was slightly retarded in the presence of dihydroxyphenyl acetate that formed a stable Michaelis complex. On the contrary, AADC was scarcely digested in the presence of L-dopa methyl ester that formed a stable external aldimine. Similar protection by the substrate analogs was observed in the chemical modification experiment. From these results, we concluded that the region around Arg334 must be exposed and flexible in the unliganded state, and forming the Michaelis complex generated a subtle conformational change, then underwent marked conformational change during the subsequent transaldimination process prerequisite to forming the external aldimine. For further analyses, we constructed a mutant gene encoding in tandem the two peptides of AADC cleaved at the Asn327-Met328 bond inside the putative flexible region. The gene product, fragmentary AADC, was still active with L-dopa as substrate, but its k(cat) value was decreased 57-fold, and the Km value was increased 9-fold compared with those of the wild-type AADC. The absorption spectra of the fragmentary AADC in the presence of L-dopa methyl ester showed shift in the equilibrium of the transaldimination from the external aldimine to the Michaelis complex. Tryptic digestion of the fragmentary AADC removed seven amino acid residues, Met328-Arg334, and resulted in complete inactivation. Susceptibility of the fragmentary enzyme to trypsin was not changed by L-dopa methyl ester revealing the loss of appropriate conformational change in the flexible region induced by substrate binding. From these results we propose that the conformational change in the flexible region is required during the transaldimination process.  (+info)

Both the antioxidant and D3 agonist actions of pramipexole mediate its neuroprotective actions in mesencephalic cultures. (4/1391)

Pramipexole (PPX) is a full intrinsic activity, direct-acting dopamine (DA) agonist possessing 7-fold higher affinity for D3 than for D2 receptors. It also is a potent antioxidant. PPX was previously shown to be neuroprotective because it dose dependently attenuated the DA neuron loss produced by levodopa in mesencephalic cultures. Several different drugs with properties similar to PPX were studied here to better understand the mechanism or mechanisms responsible for this neuroprotective effect. The D3-preferring agonist 7-hydroxy-diphenylaminotetralin (7-OH-DPAT) and the D3 antagonist U99194, respectively, increased and decreased the neuroprotective effects of PPX in a dose-dependent fashion. Addition of the selective D2 agonist U95666 or the D2/D3 antagonists domperidone or raclopride did not affect PPX's neuroprotective effect. Interestingly, 7-OH-DPAT by itself did not attenuate the DA neuron loss produced by levodopa. However, when 7-OH-DPAT was combined with a low dose of the antioxidants U101033E or alpha-tocopherol, the toxic effects of levodopa were attenuated. Similar results were observed when the D3-preferring agonist PD128, 907 was studied. In addition, media conditioned by exposure of mesencephalic cultures incubated with all D3-preferring agonists studied was shown to enhance the growth of DA neurons in freshly harvested recipient cultures implicating a D3-mediated trophic activity in the neuroprotective effect. These data suggest that PPX's neuroprotective actions in the levodopa toxicity model are a consequence of its combined actions as a D3 receptor agonist and an antioxidant.  (+info)

Vesicular monoamine transporter-2 and aromatic L-amino acid decarboxylase enhance dopamine delivery after L-3, 4-dihydroxyphenylalanine administration in Parkinsonian rats. (5/1391)

Medical therapy in Parkinson's disease (PD) is limited by the short-duration response and development of dyskinesia that result from chronic L-3,4-dihydroxyphenylalanine (L-DOPA) therapy. These problems occur partly because the loss of dopamine storage sites leads to erratic dopamine delivery. Vesicular monoamine transporter-2 (VMAT-2) plays a critical role in dopamine storage by packaging dopamine into synaptic vesicles and regulating sustained release of dopamine. To restore the capacity to produce and store dopamine in parkinsonian rats, primary skin fibroblast cells (PF) were genetically modified with aromatic L-amino acid decarboxylase (AADC) and VMAT-2 genes. After incubation with L-DOPA in culture, the doubly transduced fibroblast cells (PFVMAA) produced and stored dopamine at a much higher level than the cells with either gene alone. PFVMAA cells in culture released dopamine gradually in a constitutive manner. Genetically modified fibroblast cells were grafted in parkinsonian rat striata, and L-DOPA was systemically administered. Higher dopamine levels were sustained for a longer duration in rats grafted with PFVMAA cells than in those grafted with either control cells or cells with AADC alone. These findings underscore the importance of dopamine storage capacity in determining the efficacy of L-DOPA therapy and illustrate a novel method of gene therapy combined with precursor administration to overcome the major obstacles of PD treatment.  (+info)

Studies on the role of dopamine in the degeneration of 5-HT nerve endings in the brain of Dark Agouti rats following 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') administration. (6/1391)

1. We investigated whether dopamine plays a role in the neurodegeneration of 5-hydroxytryptamine (5-HT) nerve endings occurring in Dark Agouti rat brain after 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') administration. 2. Haloperidol (2 mg kg(-1) i.p.) injected 5 min prior and 55 min post MDMA (15 mg kg(-1) i.p.) abolished the acute MDMA-induced hyperthermia and attenuated the neurotoxic loss of 5-HT 7 days later. When the rectal temperature of MDMA + haloperidol treated rats was kept elevated, this protective effect was marginal. 3. MDMA (15 mg kg(-1)) increased the dopamine concentration in the dialysate from a striatal microdialysis probe by 800%. L-DOPA (25 mg kg(-1) i.p., plus benserazide, 6.25 mg kg(-1) i.p.) injected 2 h after MDMA (15 mg kg(-1)) enhanced the increase in dopamine in the dialysate, but subsequent neurodegeneration was unaltered. L-DOPA (25 mg kg(-1)) injected before a sub-toxic dose of MDMA (5 mg kg(-1)) failed to induce neurodegeneration. 4. The MDMA-induced increase in free radical formation in the hippocampus (indicated by increased 2,3- and 2,5-dihydroxybenzoic acid in a microdialysis probe perfused with salicylic acid) was unaltered by L-DOPA. 5. The neuroprotective drug clomethiazole (50 mg kg(-1) i.p.) did not influence the MDMA-induced increase in extracellular dopamine. 6. These data suggest that previous observations on the protective effect of haloperidol and potentiating effect of L-DOPA on MDMA-induced neurodegeneration may have resulted from effects on MDMA-induced hyperthermia. 7. The increased extracellular dopamine concentration following MDMA may result from effects of MDMA on dopamine re-uptake, monoamine oxidase and 5-HT release rather than an 'amphetamine-like' action on dopamine release, thus explaining why the drug does not induce degeneration of dopamine nerve endings.  (+info)

Efficacy, safety, and tolerance of the non-ergoline dopamine agonist pramipexole in the treatment of advanced Parkinson's disease: a double blind, placebo controlled, randomised, multicentre study. (7/1391)

OBJECTIVES: Pramipexole, a non-ergot dopamine D2/D3 receptor agonist, was investigated as an add on drug in advanced parkinsonian patients with motor fluctuations to assess efficacy, safety, and tolerance. METHODS: Seventy eight patients of either sex with advanced Parkinson's disease and treatment complications such as motor fluctuations were enrolled into a double blind, placebo controlled, randomised, multicentre study (phase II) and assigned to add on treatment with pramipexole (n=34) versus placebo (n=44) to a previously stabilised antiparkinsonian medication (7 week dose titration interval, 4 week maintenance period). The primary end point of efficacy was the change from baseline in the total score of the unified Parkinson's disease rating scale (UPDRS) in the on "period" (2 hours after intake of study medication). Safety and tolerability were assessed on the basis of adverse events, vital signs, laboratory measurements, and ECG recordings. RESULTS: There was a significant improvement of the pramipexole group in UPDRS total scores, subscores part II, III (activities of daily living and motor examination), and IV (complications of therapy). Mean UPDRS total score decreased by 37.3% under pramipexole compared with 12.2% under placebo (p<0.001). Patients under pramipexole reported an overall reduction in "off" periods of 12%--resulting in 1.7 more hours "on" time a day--compared with an increase in "off" periods of 2% under placebo. There were no unexpected safety results. The adverse event profile disclosed a high tolerability. The most important adverse events under pramipexole were fatigue, dyskinesia, and vivid dreams. CONCLUSION: Pramipexole administration is an efficacious and well tolerated add on therapy in patients with advanced Parkinson's disease with an improvement in activities of daily living, motor function, and treatment associated complications.  (+info)

Impairment of EEG desynchronisation before and during movement and its relation to bradykinesia in Parkinson's disease. (8/1391)

OBJECTIVE: It has been suggested that the basal ganglia act to release cortical elements from idling (alpha) rhythms so that they may become coherent in the gamma range, thereby binding together those distributed activities necessary for the effective selection and execution of a motor act. This hypothesis was tested in 10 patients with idiopathic Parkinson's disease. METHODS: Surface EEG was recorded during self paced squeezing of the hand and elbow flexion performed separately, simultaneously, or sequentially. Recordings were made after overnight withdrawal of medication and, again, 1 hour after levodopa. The medication related improvement in EEG desynchronisation (in the 7.5-12.5 Hz band) over the 1 second before movement and during movement were separately correlated with the improvement in movement time for each electrode site. Correlation coefficients (r) > 0.632 were considered significant (p<0.05). RESULTS: Improvement in premovement desynchronisation correlated with reduction in bradykinesia over the contralateral sensorimotor cortex and supplementary motor area in flexion and squeeze, respectively. However, when both movements were combined either simultaneously or sequentially, this correlation shifted anteriorly, to areas overlying prefrontal cortex. Improvement in EEG desynchronisation during movement only correlated with reduction in bradykinesia in two tasks. Correlation was seen over the supplementary motor area during flexion, and central prefrontal and ipsilateral premotor areas during simultaneous flex and squeeze. CONCLUSIONS: The results are consistent with the idea that the basal ganglia liberate frontal cortex from idling rhythms, and that this effect is focused and specific in so far as it changes with the demands of the task. In particular, the effective selection and execution of more complex tasks is associated with changes over the prefrontal cortex.  (+info)

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.

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.

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.

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.

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.

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.

Trihexyphenidyl is an anticholinergic medication, which is primarily used to treat symptoms of Parkinson's disease, such as rigidity, tremors, muscle spasms, and poor muscle control. It works by blocking the action of acetylcholine, a neurotransmitter in the brain that is involved in the regulation of motor function. By blocking its action, trihexyphenidyl helps to reduce the symptoms of Parkinson's disease.

In addition to its use in Parkinson's disease, trihexyphenidyl may also be used to treat other conditions, such as drug-induced extrapyramidal symptoms (EPS), which are movement disorders that can occur as a side effect of certain medications, including antipsychotic drugs.

It is important to note that trihexyphenidyl can have significant side effects, particularly at higher doses, including dry mouth, blurred vision, dizziness, drowsiness, and difficulty urinating. It may also cause confusion, disorientation, and memory problems, especially in older adults or people with cognitive impairments. As with any medication, trihexyphenidyl should be used under the close supervision of a healthcare provider, who can monitor its effectiveness and potential side effects.

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.

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.

Selegiline is a selective, irreversible MAO-B inhibitor, which is primarily used in the clinical management of Parkinson's disease. It works by blocking the action of monoamine oxidase B (MAO-B), an enzyme responsible for breaking down dopamine, a neurotransmitter involved in movement regulation. By inhibiting MAO-B, selegiline increases the availability of dopamine in the brain, thereby helping to alleviate symptoms of Parkinson's disease such as stiffness, tremors, and spasms.

Selegiline is also available under the brand name Eldepryl, Zelapar, and Emsam. In addition to its use in Parkinson's disease, selegiline has been explored for its potential benefits in treating depression, dementia, and other neurological disorders. However, its use in these conditions is still considered off-label and requires careful consideration of the potential risks and benefits.

It is important to note that MAO inhibitors like selegiline can have serious interactions with certain foods and medications, particularly those containing tyramine, which can lead to a dangerous increase in blood pressure (hypertensive crisis). Therefore, it is crucial to follow strict dietary restrictions and medication guidelines when taking selegiline or any other MAO inhibitor.

Benzophenones are a class of chemical compounds that consist of a diphenylmethane structure with a carbonyl group attached to the central carbon atom. They are known for their ability to absorb ultraviolet (UV) light and are often used as UV absorbers or photoinitiators in various applications, such as plastics, coatings, and personal care products.

In the medical field, benzophenones may be used in topical medications as sunscreen agents or in pharmaceutical formulations as photostabilizers to prevent drug degradation caused by UV light exposure. However, some benzophenones have been found to have potential endocrine-disrupting properties and may pose health concerns at high levels of exposure. Therefore, their use is regulated in certain applications, and alternative sunscreen agents are being explored.

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 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.

Lisuride is a type of medication called a dopamine agonist, which works by stimulating dopamine receptors in the brain. It is primarily used to treat Parkinson's disease and related disorders, as it can help to alleviate symptoms such as stiffness, tremors, spasms, and poor muscle control.

Lisuride may also be used off-label for other conditions, such as certain types of headaches or cluster headaches. It is available in the form of tablets and is typically taken several times a day, with dosages adjusted based on individual patient needs and responses to treatment.

As with any medication, lisuride can have side effects, including nausea, dizziness, drowsiness, hallucinations, and orthostatic hypotension (low blood pressure upon standing). It is important for patients taking this medication to follow their healthcare provider's instructions carefully and report any unusual symptoms or concerns.

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.

Postencephalitic Parkinson's disease (PEPD) is a secondary form of Parkinsonism that occurs as a result of viral encephalitis, most commonly following the 1918-1920 influenza pandemic. It is a rare condition today due to advancements in healthcare and vaccinations.

The infection causes inflammation in the brain, leading to damage in various areas, particularly the substantia nigra pars compacta, where dopamine-producing neurons are located. This results in decreased levels of dopamine, a neurotransmitter essential for smooth and controlled muscle movements.

The symptoms of PEPD can be similar to those seen in primary Parkinson's disease (PD), such as bradykinesia (slowness of movement), rigidity, resting tremors, and postural instability. However, there are some distinct differences between the two conditions:

1. Age at onset: PEPD tends to affect younger individuals, often in their 20s or 30s, while primary PD usually manifests in people over 50.
2. Symptom progression: The progression of symptoms in PEPD is typically more rapid and severe than in primary PD.
3. Non-motor symptoms: PEPD often presents with a wider range of non-motor symptoms, including sleep disturbances, mood changes, autonomic dysfunction, and oculogyric crises (involuntary upward deviation of the eyes).
4. Response to treatment: PEPD may not respond as well to levodopa therapy compared to primary PD, and patients often experience more severe side effects such as dyskinesias (abnormal involuntary movements) and motor fluctuations.

It is essential to differentiate between postencephalitic Parkinson's disease and primary Parkinson's disease, as the treatment approaches and prognosis may differ significantly.

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.

Dopa decarboxylase (DDC) is an enzyme that plays a crucial role in the synthesis of dopamine and serotonin, two important neurotransmitters in the human body. This enzyme is responsible for converting levodopa (L-DOPA), an amino acid precursor, into dopamine, a critical neurotransmitter involved in movement regulation, motivation, reward, and mood.

The gene that encodes dopa decarboxylase is DDC, located on chromosome 7p12.2-p12.1. The enzyme is widely expressed throughout the body, including the brain, kidneys, liver, and gut. In addition to its role in neurotransmitter synthesis, dopa decarboxylase also contributes to the metabolism of certain drugs, such as levodopa and carbidopa, which are used in the treatment of Parkinson's disease.

Deficiencies or mutations in the DDC gene can lead to various neurological disorders, including aromatic L-amino acid decarboxylase deficiency (AADCD), a rare autosomal recessive disorder characterized by decreased levels of dopamine and serotonin. Symptoms of AADCD may include developmental delay, movement disorders, seizures, autonomic dysfunction, and oculogyric crises.

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.

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.

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.

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.

Ergolines are a group of ergot alkaloids that have been widely used in the development of various pharmaceutical drugs. These compounds are known for their ability to bind to and stimulate specific receptors in the brain, particularly dopamine receptors. As a result, they have been explored for their potential therapeutic benefits in the treatment of various neurological and psychiatric conditions, such as Parkinson's disease, migraine, and depression.

However, ergolines can also have significant side effects, including hallucinations, nausea, and changes in blood pressure. In addition, some ergot alkaloids have been associated with a rare but serious condition called ergotism, which is characterized by symptoms such as muscle spasms, vomiting, and gangrene. Therefore, the use of ergolines must be carefully monitored and managed to ensure their safety and effectiveness.

Some specific examples of drugs that contain ergolines include:

* Dihydroergotamine (DHE): used for the treatment of migraine headaches
* Pergolide: used for the treatment of Parkinson's disease
* Cabergoline: used for the treatment of Parkinson's disease and certain types of hormonal disorders

It is important to note that while ergolines have shown promise in some therapeutic areas, they are not without their risks. As with any medication, it is essential to consult with a healthcare provider before using any drug containing ergolines to ensure that it is safe and appropriate for an individual's specific needs.

Muscle rigidity is a term used to describe an increased resistance to passive movement or muscle tone that is present at rest, which cannot be overcome by the person. It is a common finding in various neurological conditions such as Parkinson's disease, stiff-person syndrome, and tetanus. In these conditions, muscle rigidity can result from hyperexcitability of the stretch reflex arc or abnormalities in the basal ganglia circuitry.

Muscle rigidity should be distinguished from spasticity, which is a velocity-dependent increase in muscle tone that occurs during voluntary movement or passive stretching. Spasticity is often seen in upper motor neuron lesions such as stroke or spinal cord injury.

It's important to note that the assessment of muscle rigidity requires a careful physical examination and may need to be evaluated in conjunction with other signs and symptoms to determine an underlying cause.

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.

Motor skills are defined as the abilities required to plan, control and execute physical movements. They involve a complex interplay between the brain, nerves, muscles, and the environment. Motor skills can be broadly categorized into two types: fine motor skills, which involve small, precise movements (such as writing or picking up small objects), and gross motor skills, which involve larger movements using the arms, legs, and torso (such as crawling, walking, or running).

Motor skills development is an essential aspect of child growth and development, and it continues to evolve throughout adulthood. Difficulties with motor skills can impact a person's ability to perform daily activities and can be associated with various neurological and musculoskeletal conditions.

Catechol-O-methyltransferase (COMT) is an enzyme that plays a role in the metabolism of catecholamines, which are neurotransmitters and hormones such as dopamine, norepinephrine, and epinephrine. COMT mediates the transfer of a methyl group from S-adenosylmethionine (SAM) to a catechol functional group in these molecules, resulting in the formation of methylated products that are subsequently excreted.

The methylation of catecholamines by COMT regulates their concentration and activity in the body, and genetic variations in the COMT gene can affect enzyme function and contribute to individual differences in the metabolism of these neurotransmitters. This has been implicated in various neurological and psychiatric conditions, including Parkinson's disease, schizophrenia, and attention deficit hyperactivity disorder (ADHD).

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.

Akinetic mutism is a neurological condition characterized by a severe decrease in initiating and sustaining voluntary movements and speech, along with a decreased level of responsiveness to the environment. It is often caused by damage to the frontal lobe of the brain, particularly to the anterior cingulate cortex and its connections to other parts of the brain.

People with akinetic mutism may appear awake and have their eyes open, but they are generally unresponsive to external stimuli and do not initiate voluntary movements or speech on their own. They may occasionally respond to direct questions or commands, but their responses are often limited and delayed. The condition can be caused by various factors, including brain injury, stroke, tumors, infections, or degenerative diseases such as Parkinson's disease.

Akinetic mutism is distinct from a vegetative state, which is characterized by the absence of both awareness and sleep-wake cycles. In contrast, people with akinetic mutism may retain some degree of awareness and have sleep-wake cycles, although their level of responsiveness is significantly reduced.

Dopamine receptors are a type of G protein-coupled receptor that bind to and respond to the neurotransmitter dopamine. There are five subtypes of dopamine receptors (D1-D5), which are classified into two families based on their structure and function: D1-like (D1 and D5) and D2-like (D2, D3, and D4).

Dopamine receptors play a crucial role in various physiological processes, including movement, motivation, reward, cognition, emotion, and neuroendocrine regulation. They are widely distributed throughout the central nervous system, with high concentrations found in the basal ganglia, limbic system, and cortex.

Dysfunction of dopamine receptors has been implicated in several neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, attention deficit hyperactivity disorder (ADHD), drug addiction, and depression. Therefore, drugs targeting dopamine receptors have been developed for the treatment of these conditions.

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.

Hydrazines are not a medical term, but rather a class of organic compounds containing the functional group N-NH2. They are used in various industrial and chemical applications, including the production of polymers, pharmaceuticals, and agrochemicals. However, some hydrazines have been studied for their potential therapeutic uses, such as in the treatment of cancer and cardiovascular diseases. Exposure to high levels of hydrazines can be toxic and may cause damage to the liver, kidneys, and central nervous system. Therefore, medical professionals should be aware of the potential health hazards associated with hydrazine exposure.

Benzothiazoles are a class of heterocyclic organic compounds that contain a benzene fused to a thiazole ring. They have the chemical formula C7H5NS. Benzothiazoles and their derivatives have a wide range of applications in various industries, including pharmaceuticals, agrochemicals, dyes, and materials science.

In the medical field, benzothiazoles have been studied for their potential therapeutic properties. Some benzothiazole derivatives have shown promising results as anti-inflammatory, antimicrobial, antiviral, and anticancer agents. However, more research is needed to fully understand the medical potential of these compounds and to develop safe and effective drugs based on them.

It's important to note that while benzothiazoles themselves have some biological activity, most of the medical applications come from their derivatives, which are modified versions of the basic benzothiazole structure. These modifications can significantly alter the properties of the compound, leading to new therapeutic possibilities.

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.

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.

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.

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.

Monoamine oxidase inhibitors (MAOIs) are a class of drugs that work by blocking the action of monoamine oxidase, an enzyme found in the brain and other organs of the body. This enzyme is responsible for breaking down certain neurotransmitters, such as serotonin, dopamine, and norepinephrine, which are chemicals that transmit signals in the brain.

By inhibiting the action of monoamine oxidase, MAOIs increase the levels of these neurotransmitters in the brain, which can help to alleviate symptoms of depression and other mood disorders. However, MAOIs also affect other chemicals in the body, including tyramine, a substance found in some foods and beverages, as well as certain medications. As a result, MAOIs can have serious side effects and interactions with other substances, making them a less commonly prescribed class of antidepressants than other types of drugs.

MAOIs are typically used as a last resort when other treatments for depression have failed, due to their potential for dangerous interactions and side effects. They require careful monitoring and dosage adjustment by a healthcare provider, and patients must follow strict dietary restrictions while taking them.

A drug combination refers to the use of two or more drugs in combination for the treatment of a single medical condition or disease. The rationale behind using drug combinations is to achieve a therapeutic effect that is superior to that obtained with any single agent alone, through various mechanisms such as:

* Complementary modes of action: When different drugs target different aspects of the disease process, their combined effects may be greater than either drug used alone.
* Synergistic interactions: In some cases, the combination of two or more drugs can result in a greater-than-additive effect, where the total response is greater than the sum of the individual responses to each drug.
* Antagonism of adverse effects: Sometimes, the use of one drug can mitigate the side effects of another, allowing for higher doses or longer durations of therapy.

Examples of drug combinations include:

* Highly active antiretroviral therapy (HAART) for HIV infection, which typically involves a combination of three or more antiretroviral drugs to suppress viral replication and prevent the development of drug resistance.
* Chemotherapy regimens for cancer treatment, where combinations of cytotoxic agents are used to target different stages of the cell cycle and increase the likelihood of tumor cell death.
* Fixed-dose combination products, such as those used in the treatment of hypertension or type 2 diabetes, which combine two or more active ingredients into a single formulation for ease of administration and improved adherence to therapy.

However, it's important to note that drug combinations can also increase the risk of adverse effects, drug-drug interactions, and medication errors. Therefore, careful consideration should be given to the selection of appropriate drugs, dosing regimens, and monitoring parameters when using drug combinations in clinical practice.

Motor skills disorders are conditions that affect a person's ability to perform coordinated movements. These movements can be simple, such as buttoning a shirt, or complex, such as playing a musical instrument. Motor skills disorders can make it difficult for a person to perform everyday activities and can impact their quality of life.

There are two main types of motor skills: fine motor skills and gross motor skills. Fine motor skills involve the small movements of the hands, fingers, and wrists, such as writing or using utensils. Gross motor skills involve larger movements of the arms, legs, and torso, such as crawling, walking, or running.

Motor skills disorders can affect either fine or gross motor skills, or both. Some common types of motor skills disorders include:

* Developmental coordination disorder (DCD): a condition that affects a child's ability to perform coordinated movements and is often diagnosed in early childhood. Children with DCD may have difficulty with tasks such as tying their shoes, buttoning their clothes, or using scissors.
* Cerebral palsy: a group of disorders that affect movement and muscle tone, caused by damage to the brain before, during, or after birth. Cerebral palsy can cause stiff or floppy muscles, uncontrolled movements, and difficulty with balance and coordination.
* Dyspraxia: a condition that affects a person's ability to plan and perform coordinated movements. People with dyspraxia may have difficulty with tasks such as writing, buttoning their clothes, or playing sports.
* Ataxia: a group of disorders that affect coordination and balance, caused by damage to the cerebellum (the part of the brain that controls movement). Ataxia can cause unsteady gait, poor coordination, and difficulty with fine motor tasks.

Motor skills disorders can be caused by a variety of factors, including genetics, injury, illness, or developmental delays. Treatment for motor skills disorders may include physical therapy, occupational therapy, speech therapy, and medication. In some cases, surgery may also be necessary to treat the underlying cause of the disorder.

Neurologic manifestations refer to the signs and symptoms that occur due to a disturbance or disease of the nervous system, which includes the brain, spinal cord, nerves, and muscles. These manifestations can vary widely depending on the specific location and nature of the underlying problem. They may include motor (movement-related) symptoms such as weakness, paralysis, tremors, or difficulty with coordination; sensory symptoms such as numbness, tingling, or pain; cognitive or behavioral changes; seizures; and autonomic symptoms such as changes in blood pressure, heart rate, or sweating. Neurologic manifestations can be caused by a wide range of conditions, including infections, injuries, degenerative diseases, strokes, tumors, and autoimmune disorders.

Methyldopa is a centrally acting antihypertensive drug, which means it works in the brain to lower blood pressure. It is a synthetic derivative of the amino acid L-DOPA and acts as a false neurotransmitter, mimicking the action of norepinephrine in the brain. This results in decreased sympathetic outflow from the central nervous system, leading to vasodilation and reduced blood pressure. Methyldopa is used primarily for the treatment of hypertension (high blood pressure) and is available in oral formulations.

Salsoline alkaloids are a type of natural toxin found in some plants, particularly in the family Solanaceae, which includes nightshades. These alkaloids consist of several compounds, including salsoline, salsolidine, and isosalsolidine. They can be found in various plants such as *Salsola tuberculatiformis*, *Salsola kali*, and *Rhizothera americana*. Salsoline alkaloids have been reported to have a range of pharmacological effects, including vasoconstrictive, diuretic, and stimulant properties. However, they can also be toxic in high concentrations, causing symptoms such as nausea, vomiting, and seizures.

Combination drug therapy is a treatment approach that involves the use of multiple medications with different mechanisms of action to achieve better therapeutic outcomes. This approach is often used in the management of complex medical conditions such as cancer, HIV/AIDS, and cardiovascular diseases. The goal of combination drug therapy is to improve efficacy, reduce the risk of drug resistance, decrease the likelihood of adverse effects, and enhance the overall quality of life for patients.

In combining drugs, healthcare providers aim to target various pathways involved in the disease process, which may help to:

1. Increase the effectiveness of treatment by attacking the disease from multiple angles.
2. Decrease the dosage of individual medications, reducing the risk and severity of side effects.
3. Slow down or prevent the development of drug resistance, a common problem in chronic diseases like HIV/AIDS and cancer.
4. Improve patient compliance by simplifying dosing schedules and reducing pill burden.

Examples of combination drug therapy include:

1. Antiretroviral therapy (ART) for HIV treatment, which typically involves three or more drugs from different classes to suppress viral replication and prevent the development of drug resistance.
2. Chemotherapy regimens for cancer treatment, where multiple cytotoxic agents are used to target various stages of the cell cycle and reduce the likelihood of tumor cells developing resistance.
3. Cardiovascular disease management, which may involve combining medications such as angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, diuretics, and statins to control blood pressure, heart rate, fluid balance, and cholesterol levels.
4. Treatment of tuberculosis, which often involves a combination of several antibiotics to target different aspects of the bacterial life cycle and prevent the development of drug-resistant strains.

When prescribing combination drug therapy, healthcare providers must carefully consider factors such as potential drug interactions, dosing schedules, adverse effects, and contraindications to ensure safe and effective treatment. Regular monitoring of patients is essential to assess treatment response, manage side effects, and adjust the treatment plan as needed.

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.

... (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease ... van Hilten J; Ramaker C; Stowe R; Nj Ives (2007). "Bromocriptine/levodopa combined versus levodopa alone for early Parkinson's ... Levodopa-induced dyskinesia has long been thought to arise through pathological alterations in pre-synaptic and post-synaptic ... Based on the relationship with levodopa dosing, dyskinesia most commonly occurs at the time of peak l-DOPA plasma ...
... , also known as levodopa and l-3,4-dihydroxyphenylalanine, is an amino acid that is made and used as part of the normal ... "Levodopa Use During Pregnancy". Drugs.com. 12 July 2019. Retrieved 27 September 2020. Cohen PA, Avula B, Katragunta K, Khan I ( ... l-DOPA can be manufactured and in its pure form is sold as a psychoactive drug with the INN levodopa; trade names include ... Because levodopa bypasses the enzyme tyrosine hydroxylase, the rate-limiting step in dopamine synthesis, it is much more ...
l-DOPA (Levodopa; Sinemet, Parcopa, Atamet, Stalevo, Madopar, Prolopa, etc.) l-DOPS (Droxidopa) Methyldopa (Aldomet, Apo- ... d-DOPA (d-3,4-dihydroxyphenylalanine; dextrodopa) is similar to l-DOPA (levodopa), but with opposite chirality. Levo- and ...
Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been on levodopa (L‑DOPA) for ... full free text) Halje P, Tamtè M, Richter U, Mohammed M, Cenci MA, Petersson P (November 2012). "Levodopa-induced dyskinesia is ... Peak-dose dyskinesia - the most common form of levodopa-induced dyskinesia; it correlates with the plateau L‑DOPA plasma level ... Fabbrini G, Brotchie JM, Grandas F, Nomoto M, Goetz CG (April 2007). "Levodopa-induced dyskinesias". Movement Disorders. 22 (10 ...
It also methylates levodopa. COMT inhibitors are indicated for the treatment of Parkinson's disease in combination with ... COMT inhibitors significantly decrease off time in people with Parkinson's disease also taking carbidopa/levodopa. entacapone ( ... The therapeutic benefit of using a COMT inhibitor is based on its ability to prevent the methylation of levodopa to 3-O- ... "Entacapone improves motor fluctuations in levodopa-treated Parkinson's disease patients. Parkinson Study Group". Annals of ...
Levodopa is also effective. However, pergolide and cabergoline are less recommended due to their association with increased ... "Levodopa for the treatment of restless legs syndrome". Cochrane Database of Systematic Reviews. 2011 (5): CD005504. doi:10.1002 ...
Parkinson's disease, e.g. levodopa. Atropine decreases the absorption of levodopa. Preventing travel sickness, relieve stomach ...
In 1969, Yahr and Parkinson's Foundation colleagues published results of the first double-blind trial of levodopa. The ... Yahr's double-blind clinical trial of carbidopa/levodopa (Sinemet®), which remains the gold standard therapy for Parkinson's ... Yahr, Melvin D. (March 1971). "Levodopa and parkinsonism: Clinical impressions". Clinical Pharmacology & Therapeutics. 12 (2): ... "Treatment of Parkinsonism With Levodopa". Archives of Neurology. 21 (4): 343-354. doi:10.1001/archneur.1969.00480160015001. ...
Lu, C. S.; Huang, C.C; Chu, N.S.; Calne, D.B. (1994). "Levodopa failure in chronic manganism". Neurology. 44 (9): 1600-1602. ...
... valproic acid may have efficacy in controlling the symptoms of levodopa-induced DDS that arise from the use of levodopa for the ... Yahr MD, Duvoisin RC, Schear MJ, Barrett RE, Hoehn MM (October 1969). "Treatment of parkinsonism with levodopa". Arch. Neurol. ... The most common treatment is dopamine replacement therapy, which consists in the administration of levodopa (L-Dopa) or ...
Parkinson's disease is commonly treated with medicines such as levodopa to improve muscle control, balance and walking, but ... Lee, Chong S. (May 2001). "Levodopa-induced dyskinesia: Mechanisms and management". BCMJ. 43 (4): 206-209. Berger, Pierre- ...
"Levodopa and Carbidopa: MedlinePlus Drug Information". medlineplus.gov. Retrieved 2021-05-02. "Physical Therapy for Parkinson's ... Williams DR, Hadeed A, al-Din AS, Wreikat AL, Lees AJ (October 2005). "Kufor Rakeb disease: autosomal recessive, levodopa- ... similar to treatment of typical Parkinson's disease and is mainly composed of a combination of two medications called levodopa ...
"Fava Beans, Levodopa, and Parkinson's Disease". Archived from the original on 22 July 2018. Retrieved 17 March 2013. Russ ...
83-. ISBN 978-0-12-396492-2. Fox SH, Brotchie JM (8 October 2014). Levodopa-Induced Dyskinesia in Parkinson's Disease. Springer ... Dipraglurant-IR for Parkinson's disease levodopa-induced dyskinesia - Addex Therapeutics Dipraglurant-ER for dystonia - Addex ... of the mGlu5 receptor which is under development by Addex Therapeutics for the treatment of Parkinson's disease levodopa- ...
Clinical studies have shown that the use of levodopa can lead to visual hallucinations and delusions. In most patients, ... With prolonged use of levodopa, the delusions occupy almost all of a patient's attention. In experimental studies, when the ... Stewart JT (January 2008). "Frégoli syndrome associated with levodopa treatment". Mov. Disord. 23 (2): 308-9. doi:10.1002/mds. ... concentration of levodopa decreases, the number of reported delusions decreases as well. It has been concluded that delusions ...
It is the methyl ester of levodopa. It is used in tablet form as an effervescent prodrug with 250 times the water solubility of ... tablet levodopa. Etilevodopa Hickey P, Stacy M (2011). "Available and emerging treatments for Parkinson's disease: a review". ...
It is the ethyl ester of levodopa. It was never marketed. Melevodopa Djaldetti R, Giladi N, Hassin-Baer S, Shabtai H, Melamed E ... November-December 2003). "Pharmacokinetics of etilevodopa compared to levodopa in patients with Parkinson's disease: an open- ...
Pulikkalpura H, Kurup R, Mathew PJ, Baby S (June 2015). "Levodopa in Mucuna pruriens and its degradation". Scientific Reports. ... Cohen, Pieter A.; Avula, Bharathi; Katragunta, Kumar; Khan, Ikhlas (1 October 2022). "Levodopa Content of Mucuna pruriens ...
"SCA2 may present as levodopa-responsive parkinsonism". Movement Disorders. 18 (4): 425-9. doi:10.1002/mds.10375. PMID 12671950 ...
Madopar/Prolopa (levodopa/benserazide), for Parkinson's disease. Mircera (methoxy polyethylene glycol-epoetin beta), for ...
A phase 2 clinical study showed that ketamine can safely and effectively reduce levodopa-induced dyskinesia in patients with ... Maia M (29 March 2022). "Ketamine Eases Parkinson's Patients' Levodopa-induced Dyskinesia". Archived from the original on 11 ...
Difluoromethyldopa D-DOPA (dextrodopa) L-DOPA (levodopa; trade names Sinemet, Pharmacopa, Atamet, Stalevo, Madopar, Prolopa, ...
The current mainstay of manganism treatment is levodopa and chelation with EDTA. Both have limited and at best transient ... Replenishing the deficit of dopamine with levodopa has been shown to initially improve extrapyramidal symptoms, but the ... Neurologic and laboratory studies during treatment with levodopa". JAMA. 217 (10): 1354-8. doi:10.1001/jama.217.10.1354. PMID ... response to drugs such as levodopa, and affected portion of the basal ganglia. Symptoms are also similar to Lou Gehrig's ...
Pradeep Bhide and Deirdre McCarthy where she completed a dissertation titled "Elucidating the Molecular Etiology of Levodopa ... Jones, Lataisia C. (Cherie') (2017). "Elucidating the Molecular Etiology of Levodopa Responsive Dystonia". {{cite journal}}: ...
Clarke CE, Speller JM (2000). "Lisuride for levodopa-induced complications in Parkinson's disease". The Cochrane Database of ... Clarke CE, Speller JM (2000). "Lisuride versus bromocriptine for levodopa-induced complications in Parkinson's disease". The ... Evidence is insufficient to support lisuride in the treatment of advanced Parkinson's disease as an alternative to levodopa or ... delaying the need for levodopa until lisuride becomes insufficient for controlling the parkinsonian symptoms.[additional ...
His later contributions include the complications of levodopa; the motor control physiology of dystonia, myoclonus, and ...
No interactions were noted with levodopa or selegiline. The drug should not be combined with other ergot derivatives. Dopamine ... together with levodopa and a decarboxylase inhibitor such as carbidopa, in progressive-phase Parkinson's disease; In some ... In a combination study with 2,000 patients also treated with levodopa, the incidence and severity of side effects was ... results of the first year of treatment in a double-blind comparison of cabergoline and levodopa. The PKDS009 Collaborative ...
Patients on DHEC demonstrate a better score than if they were on levodopa on the Webster scale, a standardized rating scale of ... There is also no interference with levodopa metabolism. Although DHEC may come with some acute side-effects described further ... Recent evidence also supports that dopamine receptor agonists, instead of levodopa may slow or prevent the progression of ... Parkinson Study Group (April 2002). "Dopamine transporter brain imaging to assess the effects of pramipexole vs levodopa on ...
Paik, Julia (2020). "Levodopa Inhalation Powder: A Review in Parkinson's Disease". Drugs. 80 (8): 821-828. doi:10.1007/s40265- ... The ongoing researches include the use of inhaled nicotine for smoking cessation, the use of inhaled levodopa for the treatment ...
The disorder responds well to treatment with levodopa. The disease typically starts in one limb, typically one leg. Progressive ... In those with dopamine-responsive dystonia, symptoms typically dramatically improve with low-dose administration of levodopa, ...
Levodopa-induced dyskinesia (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinsons disease ... van Hilten J; Ramaker C; Stowe R; Nj Ives (2007). "Bromocriptine/levodopa combined versus levodopa alone for early Parkinsons ... Levodopa-induced dyskinesia has long been thought to arise through pathological alterations in pre-synaptic and post-synaptic ... Based on the relationship with levodopa dosing, dyskinesia most commonly occurs at the time of peak l-DOPA plasma ...
Levodopa and Carbidopa: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Continue to take levodopa and carbidopa even if you feel well. Do not stop taking levodopa and carbidopa without talking to ... Before taking levodopa and carbidopa,. *tell your doctor and pharmacist if you are allergic to levodopa and carbidopa any other ... You will probably be told to wait at least 12 hours after your last dose of levodopa to take your first dose of levodopa and ...
Other names: L-Tyrosine, 3-hydroxy-; Alanine, 3-(3,4-dihydroxyphenyl)-, L-; β-(3,4-Dihydroxyphenyl)-L-alanine; β-(3,4-Dihydroxyphenyl)alanine; (-)-(3,4-Dihydroxyphenyl)alanine; (-)-Dopa; Dihydroxy-L-phenylalanine; Dopalina; Dopar; DOPA; Eldopal; Helfo-Dopa; Insulamina; L-(-)-Dopa; L-(o-Dihydroxyphenyl)alanine; L-DOPA; Larodopa; Levopa; Pardopa; 3-(3,4-Dihydroxyphenyl)-L-Alanine; 3-Hydroxy-L-tyrosine; 3,4-Dihydroxy-L-phenylalanine; 3,4-Dihydroxyphenylalanine; Alanine, 3-(3,4-dihydroxyphenyl)-, (-)-; Bendopa; Brocadopa; Cidandopa; Deadopa; Dopaidan; Dopal-Fher; Dopasol; DA; Eldopar; L-β-(3,4-Dihydroxyphenyl)alanine; L-(3,4-Dihydroxyphenyl)-α-alanine; L-(3,4-Dihydroxyphenyl)alanine; L-o-Hydroxytyrosine; Levedopa; Maipedopa; Prodopa; Ro 4-6316; Syndopa; 3,4-Dihydroxyphenyl-L-alanine; Dopaflex; Dopal; Doparkine; Doparl; Dopaston; Dopastral; Doprin; Eldopatec; Eurodopa; Ledopa; Parda; Veldopa; Weldopa; Dopaston SE; L-3-(3,4-Dihydroxyphenyl)alanine ...
Compare Levodopa head-to-head with other drugs for uses, ratings, cost, side effects and interactions. ... Levodopa inhalation is an inhaled levodopa preparation that may be used to decrease symptoms of slowness, stiffness, or ... Levodopa has an average rating of 8.0 out of 10 from a total of 1 ratings on Drugs.com. 100% of reviewers reported a positive ... Levodopa Alternatives Compared. View side-by-side comparisons of medication uses, ratings, cost, side effects and interactions. ...
Les distributions Mindblow Inc. is recalling Mindblow brand Energy drinks from the marketplace because of non-permitted ingredients, including Munuca Pruriens Extract (98% L-Dopa) that may pose a serious health risk.. L-Dopa, also known as levodopa…. Continue Reading Energy drinks recalled in Canada over L-Dopa in product ...
... The widely used and well-tolerated drug commonly used to ... The article is "Levodopa Positively Affects Neovascular Age-Related Macular Degeneration," by Anna G. Figueroa, BS, Brennan M. ... This trial demonstrated for the first time that levodopa is safe, well-tolerated and delayed anti-VEGF injection therapy while ... The investigators noted that levodopa may be unlikely as a standalone treatment in patients with newly diagnosed nAMD since 11 ...
When carbidopa and levodopa tablets are to be given to patients who are being treated with levodopa, levodopa must be ... Carbidopa and levodopa tablets are available in a 1:4 ratio of carbidopa to levodopa (25 mg/100 mg) as well as 1:10 ratio (25 ... Since levodopa competes with certain amino acids for transport across the gut wall, the absorption of levodopa may be impaired ... When carbidopa and levodopa are administered together, the half-life of levodopa is increased to about 1.5 hours. At steady ...
... making more levodopa available for delivery to the brain. Levodopa: Levodopa is the metabolic precursor of dopamine, does cross ... Rytary is an extended-release formulation of carbidopa and levodopa. Carbidopa: When levodopa is administered orally, it is ... Carbidopa inhibits the decarboxylation of peripheral levodopa, making more levodopa available for delivery to the brain. ... The recommended starting dosage in levodopa-naïve patients is 23.75 mg / 95 mg taken orally three times a day for the first ...
When carbidopa and levodopa tablets are to be given to patients who are being treated with levodopa, levodopa must be ... Carbidopa and levodopa tablets are available in a 1:4 ratio of carbidopa to levodopa (carbidopa and levodopa tablets 25 mg/100 ... When more levodopa is required, carbidopa and levodopa 25 mg/250 mg should be substituted for carbidopa and levodopa 25 mg/100 ... The incidence of levodopa-induced nausea and vomiting is less with carbidopa and levodopa than with levodopa. In many patients ...
Levodopa and Entacapone) may treat, side effects, dosage, drug interactions, warnings, patient labeling, reviews, and related ... Levodopa. The pharmacokinetic properties of levodopa following the administration of single-dose Stalevo (carbidopa, levodopa ... all of whom received concomitant levodopa plus dopa decarboxylase inhibitor (either carbidopa/levodopa or benserazide/levodopa ... Levodopa And Carbidopa. There are no studies on the pharmacokinetics of levodopa and carbidopa in patients with hepatic ...
Assessment report Levodopa/Carbidopa/Entacapone. Assessment report for levodopa from Levodopa/Carbidopa/Entacapone Orion, 18 ... Toxicity. Levodopa has high acute toxicity.. Risk. The use of levodopa (sales data Sweden 2021) has been considered to result ... Levodopa is readily biodegradable which justifies the phrase Levodopa is degraded in the environment. ... Fass environmental information for levodopa from Sinemet (carbidopa, levodopa) from Organon Sweden (downloaded 2023-02-06). The ...
levodopa from Neuroscience News features breaking science news from research labs, scientists and colleges around the world. ... A new gel that contains levodopa can adhere to nasal tissue. The gel releases levodopa directly into the blood and brain. ... Levodopa, a drug commonly prescribed for the treatment of Parkinsons disease that increases dopamine in the brain was found to ... A new study reveals how bacteria in the gut is able to metabolize levodopa into dopamine in Parkinsons patients.. Read More ...
... often with levodopa or dopamine agonists, to restore the dopaminergic deficit associated with parkinsonian symptoms. Either ... However, control of PD symptoms is superior with levodopa. Moreover, dopamine agonists are less well tolerated overall and are ... Optimizing long-term therapy for Parkinson disease: levodopa, dopamine agonists, and treatment-associated dyskinesia Clin ... The treatment of Parkinson disease (PD) involves pharmacological treatment, often with levodopa or dopamine agonists, to ...
Levodopa Is a Double-Edged Sword for Balance and Gait in People With Parkinsons Disease Mov Disord. 2015 Sep;30(10):1361-70. ... Background: The effects of levodopa on balance and gait function in people with Parkinsons disease (PD) is controversial. This ...
Catechol-O-methyltransferase inhibitors for levodopa-induced complications in Parkinsons disease. Download Prime PubMed App to ... Ropinirole for levodopa-induced complications in Parkinsons disease.. *Ropinirole for levodopa-induced complications in ... Antiparkinson AgentsBenzophenonesCatechol O-Methyltransferase InhibitorsCatecholsEnzyme InhibitorsHumansLevodopaNitriles ... The principle aim of COMT inhibitor therapy is to increase the duration of effect of each levodopa dose and thus reduce the ...
Finding a more consistent method of delivering levodopa could help to minimize these periods, and is therefore one of the ... Civitas, however, is studying an inhaled formulation of levodopa for its potential to produce more rapid and continual relief ... MJFF Awardee Studying Inhaled Formulation of Levodopa Featured in the Boston Globe ... MJFF Awardee Studying Inhaled Formulation of Levodopa Featured in the Boston Globe ...
Levodopa (L-DOPA) remains the gold-standard drug available for treating PD. Curcumin has many pharmacological activities, ... Pereira, R.L.; Pain, C.S.; Barth, A.B.; Raffin, R.P.; Guterres, S.S.; Schapoval, E.E.S. Levodopa microparticles for pulmonary ... Levodopa (L-DOPA) remains the gold-standard drug available for treating PD. Curcumin has many pharmacological activities, ... Biodegradable Nanoparticles Loaded with Levodopa and Curcumin for Treatment of Parkinsons Disease by Bassam Felipe Mogharbel ...
Levodopa-induced dyskinesia is one of most vexing problems facing physicians. This paper reviews recent developments on this ... The appearance of levodopa-induced dyskinesia is closely related to plasma levels of levodopa. Most levodopa-induced dyskinesia ... A D2 agonist may be added to the regimen to spare the dose of levodopa. The dose of levodopa can be further reduced by adding a ... Management of established levodopa-induced dyskinesia. Reducing specific doses or the total daily dose of levodopa will reduce ...
Levodopa Market Size, Shares, Trends, Outlook and Forecast to 2028. Market Analysis By Application, Drug Type, and Distribution ... Levodopa Market Restraint. Shortage of drug supply in the market due to delay in manufacturing and supply of levodopa is ... Levodopa Market - Regional Analysis. On the basis of region, the global levodopa market is segmented into North America, Latin ... LEVODOPA MARKET ANALYSIS Levodopa Market by Application (Parkinsons disease and Dopamine Responsive Dystonia), by Drug Type ( ...
Branded and Generic drug prices for CARBIDOPA-LEVODOPA-ENTA ... Drug Price Trends for CARBIDOPA-LEVODOPA-ENTA. ⮩ Send this page ... CARBIDOPA-LEVODOPA-ENTACAPONE 37.5-150-200 MG TAB. 00781-5654-01. 0.56952. EACH. 2023-10-18. ... CARBIDOPA-LEVODOPA-ENTACAPONE 37.5-150-200 MG TAB. 47335-0005-88. 0.56952. EACH. 2023-10-18. ... CARBIDOPA-LEVODOPA-ENTACAPONE 37.5-150-200 MG TAB. 16571-0693-01. 0.56952. EACH. 2023-10-18. ...
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Rats, Animals, Levodopa/therapeutic use, Dopamine Agonists/pharmacology, Antiparkinson Agents/therapeutic use, Rats, Sprague- ... BACKGROUND: Current models of levodopa (L-dopa)-induced dyskinesia (LID) are obtained by treating dopamine-depleted animals ... BACKGROUND: Current models of levodopa (L-dopa)-induced dyskinesia (LID) are obtained by treating dopamine-depleted animals ... article{075112a5-4de4-458a-a45f-fc18a6df65a5, abstract = {{,p,BACKGROUND: Current models of levodopa (L-dopa)-induced ...
A levodopa test performed before surgery in all patients, disclosed the two classic types of levodopa induced dyskinesias in ... levodopa induced dyskinesias. Deep brain stimulation (DBS) has become a widely accepted method for the treatment of Parkinsons ... 1994) Levodopa-induced dyskinesias in Parkinsons disease phenomenology and pathophysiology. Mov Dis 9:2-12. ... Improvement of levodopa induced dyskinesias by thalamic deep brain stimulation is related to slight variation in electrode ...
Background Levodopa use is key to treatment in PD. Its use is associated with the development of LID. Adenosine regulates ... PATH51 Investigating adenosine A2A receptor availability in Parkinsons disease patients with and without levodopa induced ... PATH51 Investigating adenosine A2A receptor availability in Parkinsons disease patients with and without levodopa induced ... patients with and without levodopa induced dyskinesias (LID). ...
Levodopa induced an improvement in the parkinsonian limb akinesia that lasted for 48 h after withdrawal. A shortening in the ... Concomitant short- and long-duration response to levodopa in the 6-OHDA-lesioned rat: a behavioural and molecular study. Jan 1 ... Levodopa reversed the lesion-induced increase in the expression of cytochrome oxidase mRNA in the subthalamic nucleus and ... Animals were treated for 22 days with levodopa or saline. Forelimb akinesia was evaluated prior and following a test dose of ...
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However, dopamine agonists or levodopa were reintroduced in all 14 patients 16 ± 14 weeks after surgery (levodopa-equivalent ... The residual motor score, which was unresponsive to levodopa, was not improved by STN stimulation since, as stated by the ... 4, 5] probably as a result of the dramatic reduction in levodopa treatment. [4] In support of the latter hypothesis, we ... In their study, parkinsonian motor disability was ameliorated by only 45%. [1] This response to levodopa is lower than that ...
A long-term comparison between the combined regimen bromocriptine/levodopa and levodopa monotherapy--first interim report ... Mizuno, Y. 1982: A study on long-term levodopa therapy in Parkinson's disease Nihon Naika Gakkai Zasshi. Journal of the ... Marsden, C.D.; Parkes, J.D. 1977: Success and problems of long-term levodopa therapy in Parkinson's disease Lancet 1(8007 ... Marsden, C.D.; Parkes, J.D. 1977: Success and problems of long-term levodopa therapy in Parkinson's disease Lancet 1(8007 ...

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