Supranuclear Palsy, Progressive
Multiple System Atrophy
Cerebral Palsy
Bulbar Palsy, Progressive
Guadeloupe
tau Proteins
Parkinson Disease
Tauopathies
Neurodegenerative Diseases
Neurofibrillary Tangles
Ophthalmoplegia
Parkinsonian Disorders
Bell Palsy
Hypokinesia
Basal Ganglia
Neurofibrils
Tegmentum Mesencephali
Handwriting
Atrophy
Muscle Hypertonia
Lisuride
Pick Disease of the Brain
Dementia
Ocular Motility Disorders
Basal Ganglia Diseases
Movement Disorders
Brain
Benzilates
Guam
Lewy Body Disease
Speech Disorders
Parkinson Disease, Postencephalitic
Neck Muscles
Olivopontocerebellar Atrophies
Frontotemporal Dementia
Nerve Degeneration
Gait Disorders, Neurologic
Intralaminar Thalamic Nuclei
Frontal Lobe
Frontotemporal Lobar Degeneration
Magnetic Resonance Imaging
Parkinson Disease, Secondary
Neuropsychological Tests
Facial Muscles
Cognition Disorders
Levodopa
Alzheimer Disease
Muscle Rigidity
Mesencephalon
Facial Paralysis
Brain Diseases
Reflex, Abnormal
Pons
Disease Progression
Putamen
Diffusion Tensor Imaging
Blinking
Neurologic Examination
Lewy Bodies
Case-Control Studies
Substantia Nigra
Dopamine Agents
Cerebral Cortex
Hallucinations
Neuroimaging
Saccades
Abducens Nerve Diseases
Association of an extended haplotype in the tau gene with progressive supranuclear palsy. (1/251)
We describe two extended haplotypes that cover the human tau gene. In a total of approximately 200 unrelated caucasian individuals there is complete disequilibrium between polymorphisms which span the gene (which covers approximately 100 kb of DNA). This suggests that the establishment of the two haplotypes was an ancient event and either that recombination is suppressed in this region, or that recombinant genes are selected against. Furthermore, we show that the more common haplotype (H1) is significantly over-represented in patients with progressive supranuclear palsy (PSP), extending earlier reports of an association between an intronic dinucleotide polymorphism and PSP. (+info)EMG responses to free fall in elderly subjects and akinetic rigid patients. (2/251)
OBJECTIVES: The EMG startle response to free fall was studied in young and old normal subjects, patients with absent vestibular function, and patients with akinetic-rigid syndromes. The aim was to detect any derangement in this early phase of the "landing response" in patient groups with a tendency to fall. In normal subjects the characteristics of a voluntary muscle contraction (tibialis anterior) was also compared when evoked by a non-startling sound and by the free fall startle. METHODS: Subjects lay supine on a couch which was unexpectedly released into free fall. Latencies of multiple surface EMG recordings to the onset of free fall, detected by a head mounted linear accelerometer, were measured. RESULTS AND CONCLUSIONS: (1) EMG responses in younger normal subjects occurred at: sternomastoid 54 ms, abdominals 69 ms, quadriceps 78 ms, deltoid 80 ms, and tibialis anterior 85 ms. This pattern of muscle activation, which is not a simple rostrocaudal progression, may be temporally/spatially organised in the startle brainstem centres. (2) Voluntary tibialis EMG activation was earlier and stronger in response to a startling stimulus (fall) than in response to a non-startling stimulus (sound). This suggests that the startle response can be regarded as a reticular mechanism enhancing motor responsiveness. (3) Elderly subjects showed similar activation sequences but delayed by about 20 ms. This delay is more than can be accounted for by slowing of central and peripheral motor conduction, therefore suggesting age dependent delay in central processing. (4) Avestibular patients had normal latencies indicating that the free fall startle can be elicited by non-vestibular inputs. (5) Latencies in patients with idiopathic Parkinson's disease were normal whereas responses were earlier in patients with multiple system atrophy (MSA) and delayed or absent in patients with Steele-Richardson-Olszewski (SRO) syndrome. The findings in this patient group suggest: (1) lack of dopaminergic influence on the timing of the startle response, (2) concurrent cerebellar involvement in MSA may cause startle disinhibition, and (3) extensive reticular damage in SRO severely interferes with the response to free fall. (+info)Whipple's disease mimicking progressive supranuclear palsy: the diagnostic value of eye movement recording. (3/251)
Treatable causes of parkinsonian syndromes are rare; Whipple's disease is one of them. A patient is described who presented with a parkinsonian syndrome and abnormal vertical gaze. Measurement of eye movements showed marked slowing of upward saccades, moderate slowing of downward saccades, a full range of voluntary vertical eye movements, curved trajectories of oblique saccades, and absence of square wave jerks. These features, atypical of progressive supranuclear palsy, suggested the diagnosis of Whipple's disease, which was subsequently confirmed by polymerase chain reaction analysis of intestinal biopsy material. Precise measurement of the dynamic properties of saccadic eye movements in parkinsonian patients may provide a means of identifying treatable disorders. (+info)The tau gene A0 polymorphism in progressive supranuclear palsy and related neurodegenerative diseases. (4/251)
Progressive supranuclear palsy is characterised pathologically by the deposition of neurofibrillary tangles consisting of tau protein. Patients with the disease have been reported to have a more frequent occurrence of one allele of an intronic polymorphism of the tau gene. Other diseases which may involve tau deposition include frontotemporal dementia and corticobasal degeneration. This polymorphism has been studied in a series of subjects with progressive supranuclear palsy, corticobasal degeneration, frontotemporal dementia, idiopathic Parkinson's disease, and normal controls to (1) confirm this association in a large series and (2) to investigate a possible role for this association in other disorders which involve tau deposition. The results confirm the finding of an overrepresentation of the A0 allele and the A0/A0 genotype in patients with progressive supranuclear palsy, in the largest series reported to date. The A0 allele was found in 91% of patients with progressive supranuclear palsy as opposed to 73% of controls (p<0.001) and the A0/A0 genotype was seen in 84% of patients as compared with 53% of controls (p<0.01). There was no significant difference between patients with Parkinson's disease, frontotemporal dementia, or corticobasal degeneration, and controls. The A0 allele may have a direct effect on tau isoform expression in progressive supranuclear palsy or it may be in linkage disequilibrium with an adjacent determinant of tau gene expression. The explanation for this difference between a predisposition factor to progressive supranuclear palsy and the other conditions may lie in the molecular pathology of these diseases. (+info)Clinical genetics of familial progressive supranuclear palsy. (5/251)
Recent studies have shown that progressive supranuclear palsy (PSP) could be inherited, but the pattern of inheritance and the spectrum of the clinical findings in relatives are unknown. We here report 12 pedigrees, confirmed by pathology in four probands, with familial PSP. Pathological diagnosis was confirmed according to recently reported internationally agreed criteria. The spectrum of the clinical phenotypes in these families was variable including 34 typical cases of PSP (12 probands plus 22 secondary cases), three patients with postural tremor, three with dementia, one with parkinsonism, two with tremor, dystonia, gaze palsy and tics, and one with gait disturbance. The presence of affected members in at least two generations in eight of the families and the absence of consanguinity suggests autosomal dominant transmission with incomplete penetrance. We conclude that hereditary PSP is more frequent than previously thought and that the scarcity of familial cases may be related to a lack of recognition of the variable phenotypic expression of the disease. (+info)The genetics of disorders with synuclein pathology and parkinsonism. (6/251)
Despite being considered the archetypal non-genetic neurological disorder, genetic analysis of Parkinson's disease has shown that there are at least three genetic loci. Furthermore, these analyses have suggested that the phenotype of the pathogenic loci is wider than simple Parkinson's disease and may include Lewy body dementia and some forms of essential tremor. Identification of alpha-synuclein as the first of the loci involved in Parkinson's disease and the identification of this protein in pathological deposits in other disorders has led to the suggestion that it may share pathogenic mechanisms with multiple system atrophy, Alzheimer's disease and prion disease and that these mechanisms are related to a synuclein pathway to cell death. Finally, genetic analysis of the synuclein diseases and the tau diseases may indicate that this synuclein pathway is an alternative to the tau pathway to cell death. (+info)Progressive supranuclear palsy (Steele-Richardson-Olszewski disease). (7/251)
Progressive supranuclear palsy is a neurodegenerative disease which affects the brainstem and basal ganglia. Patients present with disturbance of balance, a disorder of downward gaze and L-DOPA-unresponsive parkinsonism and usually develop progressive dysphagia and dysarthria leading to death from the complications of immobility and aspiration. Treatment remains largely supportive but, potentially, treatments based on cholinergic therapy may be useful. As in Alzheimer's disease, the neuronal degeneration is associated with the deposition of hyperphosphorylated tau protein as neurofibrillary tangles but there are important distinctions between the two diseases. Evidence from familial fronto-temporal dementia with parkinsonism linked to chromosome 17 suggests that tau protein deposition is a primary pathogenic event in some neurodegenerative diseases. The understanding of the mechanism of tau deposition in progressive supranuclear palsy is likely to be of importance in unravelling its aetiology. (+info)A role for the substantia nigra pars reticulata in the gaze palsy of progressive supranuclear palsy. (8/251)
We examined the topography and degree of cell loss within basal ganglia structures commonly involved in progressive supranuclear palsy in order to identify any relationship between degeneration in these nuclei and gaze palsy. Serial section analyses and unbiased quantitative techniques were applied to brain tissue from six cases with progressive supranuclear palsy (four with gaze palsy and two without) and six controls with no neurological or neuropathological abnormalities. The total number of nucleolated neurons within the substantia nigra pars compacta (SNc) and reticulata (SNr), the subthalamic nucleus, and the internal and external segments of the globus pallidus was determined for all subjects and the data expressed as percentages of control values to compare degeneration across these basal ganglia structures. The density of neurofibrillary tangles was also evaluated within these structures. Despite significant subcortical neurofibrillary tangle formation in all cases, there was considerable variability in the degree of neuronal cell loss in all basal ganglia regions, except the SNc which was consistently affected. There was no correlation between the ranked density of neurofibrillary tangles and the degree of neuronal cell loss in any basal ganglia region. Comparisons between cases with and without gaze palsy revealed a 40% greater decrease in the number of SNr neurons in cases with gaze palsy (75 +/- 8% loss) compared with those without (35 +/- 14% loss). This was the largest difference between these cases. As the SNr projects to the superior colliculus, degeneration of this basal ganglia structure may disrupt eye movements in progressive supranuclear palsy. (+info)Progressive Supranuclear Palsy (PSP) is a rare neurological disorder characterized by the progressive degeneration of brain cells that regulate movement, thoughts, behavior, and eye movements. The term "supranuclear" refers to the location of the damage in the brain, specifically above the level of the "nuclei" which are clusters of nerve cells that control voluntary movements.
The most common early symptom of PSP is a loss of balance and difficulty coordinating eye movements, particularly vertical gaze. Other symptoms may include stiffness or rigidity of muscles, slowness of movement, difficulty swallowing, changes in speech and writing, and cognitive decline leading to dementia.
PSP typically affects people over the age of 60, and its progression can vary from person to person. Currently, there is no cure for PSP, and treatment is focused on managing symptoms and maintaining quality of life.
Multiple System Atrophy (MSA) is a rare, progressive neurodegenerative disorder that affects multiple systems in the body. It is characterized by a combination of symptoms including Parkinsonism (such as stiffness, slowness of movement, and tremors), cerebellar ataxia (lack of muscle coordination), autonomic dysfunction (problems with the autonomic nervous system which controls involuntary actions like heart rate, blood pressure, sweating, and digestion), and pyramidal signs (abnormalities in the corticospinal tracts that control voluntary movements).
The disorder is caused by the degeneration of nerve cells in various parts of the brain and spinal cord, leading to a loss of function in these areas. The exact cause of MSA is unknown, but it is thought to involve a combination of genetic and environmental factors. There is currently no cure for MSA, and treatment is focused on managing symptoms and improving quality of life.
Cerebral palsy (CP) is a group of disorders that affect a person's ability to move and maintain balance and posture. According to the Mayo Clinic, CP is caused by abnormal brain development or damage to the developing brain that affects a child's ability to control movement.
The symptoms of cerebral palsy can vary in severity and may include:
* Spasticity (stiff or tight muscles)
* Rigidity (resistance to passive movement)
* Poor coordination and balance
* Weakness or paralysis
* Tremors or involuntary movements
* Abnormal gait or difficulty walking
* Difficulty with fine motor skills, such as writing or using utensils
* Speech and language difficulties
* Vision, hearing, or swallowing problems
It's important to note that cerebral palsy is not a progressive condition, meaning that it does not worsen over time. However, the symptoms may change over time, and some individuals with CP may experience additional medical conditions as they age.
Cerebral palsy is usually caused by brain damage that occurs before or during birth, but it can also be caused by brain injuries that occur in the first few years of life. Some possible causes of cerebral palsy include:
* Infections during pregnancy
* Lack of oxygen to the brain during delivery
* Traumatic head injury during birth
* Brain bleeding or stroke in the newborn period
* Genetic disorders
* Maternal illness or infection during pregnancy
There is no cure for cerebral palsy, but early intervention and treatment can help improve outcomes and quality of life. Treatment may include physical therapy, occupational therapy, speech therapy, medications to manage symptoms, surgery, and assistive devices such as braces or wheelchairs.
Progressive bulbar palsy (PBP) is a form of motor neuron disease (MND), also known as Amyotrophic Lateral Sclerosis (ALS). It is characterized by the progressive degeneration of the motor neurons in the brainstem, which control vital functions such as swallowing, speaking, chewing, and breathing.
In PBP, these symptoms gradually worsen over time, often resulting in severe disability and ultimately death due to respiratory failure. The progression of the disease can vary from person to person, but it typically advances more slowly than other forms of ALS. There is currently no cure for PBP or any other form of MND, and treatment is focused on managing symptoms and maintaining quality of life.
I'm sorry for any confusion, but "Guadeloupe" is not a medical term. It is actually an overseas region and department of France, located in the Caribbean Sea. Guadeloupe is an archipelago consisting of several islands, with a total land area of approximately 1,700 square kilometers (656 square miles) and a population of around 400,000 people.
If you have any questions related to medical terminology or health-related topics, I would be happy to try and help answer them for you.
Tau proteins are a type of microtubule-associated protein (MAP) found primarily in neurons of the central nervous system. They play a crucial role in maintaining the stability and structure of microtubules, which are essential components of the cell's cytoskeleton. Tau proteins bind to and stabilize microtubules, helping to regulate their assembly and disassembly.
In Alzheimer's disease and other neurodegenerative disorders known as tauopathies, tau proteins can become abnormally hyperphosphorylated, leading to the formation of insoluble aggregates called neurofibrillary tangles (NFTs) within neurons. These aggregates disrupt the normal function of microtubules and contribute to the degeneration and death of nerve cells, ultimately leading to cognitive decline and other symptoms associated with these disorders.
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.
Tauopathies are a group of neurodegenerative disorders that are characterized by the abnormal accumulation and aggregation of the microtubule-associated protein Tau in neurons and glial cells. These misfolded Tau proteins form insoluble inclusions, such as neurofibrillary tangles (NFTs) and neuropil threads, which are associated with the degeneration and loss of neurons in specific regions of the brain.
Tauopathies include several well-known diseases, such as Alzheimer's disease (AD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and frontotemporal dementia with Parkinsonism-17 (FTDP-17). The exact cause of Tauopathies remains unclear, but genetic mutations, environmental factors, or a combination of both may contribute to the development and progression of these disorders.
The accumulation of abnormal Tau aggregates is believed to play a central role in the neurodegenerative process, leading to cognitive decline, motor impairment, and other neurological symptoms associated with Tauopathies. The diagnosis of Tauopathies typically involves clinical evaluation, imaging studies, and sometimes postmortem examination of brain tissue. Currently, there are no effective disease-modifying treatments for Tauopathies, but ongoing research is focused on developing therapies that target Tau aggregation and clearance to slow down or halt the progression of these debilitating disorders.
Neurodegenerative diseases are a group of disorders characterized by progressive and persistent loss of neuronal structure and function, often leading to cognitive decline, functional impairment, and ultimately death. These conditions are associated with the accumulation of abnormal protein aggregates, mitochondrial dysfunction, oxidative stress, chronic inflammation, and genetic mutations in the brain. Examples of neurodegenerative diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, Amyotrophic Lateral Sclerosis (ALS), and Spinal Muscular Atrophy (SMA). The underlying causes and mechanisms of these diseases are not fully understood, and there is currently no cure for most neurodegenerative disorders. Treatment typically focuses on managing symptoms and slowing disease progression.
Neurofibrillary tangles are a pathological hallmark of several neurodegenerative disorders, most notably Alzheimer's disease. They are intracellular inclusions composed of abnormally phosphorylated and aggregated tau protein, which forms paired helical filaments. These tangles accumulate within the neurons, leading to their dysfunction and eventual death. The presence and density of neurofibrillary tangles are strongly associated with cognitive decline and disease progression in Alzheimer's disease and other related dementias.
Ophthalmoplegia is a medical term that refers to the paralysis or weakness of the eye muscles, which can result in double vision (diplopia) or difficulty moving the eyes. It can be caused by various conditions, including nerve damage, muscle disorders, or neurological diseases such as myasthenia gravis or multiple sclerosis. Ophthalmoplegia can affect one or more eye muscles and can be partial or complete. Depending on the underlying cause, ophthalmoplegia may be treatable with medications, surgery, or other interventions.
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.
Bell palsy is a peripheral facial nerve palsy, which means that it is a weakness or paralysis of the facial nerves (cranial nerve VII) that causes sudden asymmetric weakness on one side of the face. The symptoms can vary from mild to severe and may include:
* Sudden weakness or paralysis on one side of the face
* Drooping of the mouth, causing difficulty with smiling, eating, drinking, or speaking
* Inability to close one eye
* Dryness of the eye and mouth
* Changes in taste sensation
* Discomfort around the jaw and behind the ear
* Headache
* Increased sensitivity to sound
The exact cause of Bell palsy is not known, but it is believed to be related to inflammation or swelling of the facial nerve. It may also be associated with viral infections such as herpes simplex virus or HIV. In most cases, Bell palsy resolves on its own within a few weeks to months, although some people may experience residual symptoms such as facial weakness or asymmetry. Treatment typically involves corticosteroids and antiviral medications, which can help reduce inflammation and speed up recovery.
Hypokinesia is a term used in medicine to describe decreased or reduced mobility and amplitude of movements. It can be seen in various medical conditions, most notably in Parkinson's disease. In this condition, hypokinesia manifests as bradykinesia (slowness of movement), akinesia (absence of movement), or both. Hypokinesia can also affect facial expressions, leading to a mask-like appearance. Other causes of hypokinesia include certain medications, stroke, and other neurological disorders.
The basal ganglia are a group of interconnected nuclei, or clusters of neurons, located in the base of the brain. They play a crucial role in regulating motor function, cognition, and emotion. The main components of the basal ganglia include the striatum (made up of the caudate nucleus, putamen, and ventral striatum), globus pallidus (divided into external and internal segments), subthalamic nucleus, and substantia nigra (with its pars compacta and pars reticulata).
The basal ganglia receive input from various regions of the cerebral cortex and other brain areas. They process this information and send output back to the thalamus and cortex, helping to modulate and coordinate movement. The basal ganglia also contribute to higher cognitive functions such as learning, decision-making, and habit formation. Dysfunction in the basal ganglia can lead to neurological disorders like Parkinson's disease, Huntington's disease, and dystonia.
Neurofibrils are thin, thread-like structures found within the cytoplasm of nerve cells (neurons). They are primarily composed of various proteins and are involved in maintaining the structure and function of neurons. Neurofibrils include two types: neurofilaments and microtubule-associated protein tau (TAU) proteins.
Neurofilaments are intermediate filaments that provide structural support to neurons, while TAU proteins are involved in microtubule assembly, stability, and intracellular transport. Abnormal accumulation and aggregation of these proteins can lead to neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS).
The tegmentum mesencephali, also known as the mesencephalic tegmentum, is a region in the midbrain (mesencephalon) of the brainstem. It contains several important structures including the periaqueductal gray matter, the nucleus raphe, the reticular formation, and various cranial nerve nuclei. The tegmentum mesencephali plays a crucial role in various functions such as pain modulation, sleep-wake regulation, eye movement control, and cardiovascular regulation.
I'm sorry for any confusion, but "handwriting" is not a term that has a specific medical definition. Handwriting refers to the personal style or manner in which a person writes by hand. It can vary from person to person and can be influenced by factors such as an individual's fine motor skills, cultural background, and personal preferences.
However, in a broader context, there are certain medical conditions that can affect handwriting, such as neurological disorders (like stroke, Parkinson's disease, or cerebral palsy) or orthopedic issues (like arthritis or fractures). In these cases, healthcare professionals might assess a person's handwriting as part of the diagnostic process or to monitor the progression or treatment response of a condition. But again, handwriting itself is not a medical term with a specific definition.
Atrophy is a medical term that refers to the decrease in size and wasting of an organ or tissue due to the disappearance of cells, shrinkage of cells, or decreased number of cells. This process can be caused by various factors such as disuse, aging, degeneration, injury, or disease.
For example, if a muscle is immobilized for an extended period, it may undergo atrophy due to lack of use. Similarly, certain medical conditions like diabetes, cancer, and heart failure can lead to the wasting away of various tissues and organs in the body.
Atrophy can also occur as a result of natural aging processes, leading to decreased muscle mass and strength in older adults. In general, atrophy is characterized by a decrease in the volume or weight of an organ or tissue, which can have significant impacts on its function and overall health.
Muscle hypertonia is a term used to describe an increased tone or tension in the muscles, which can be caused by various medical conditions. This state leads to a reduced ability to stretch the muscle fully, and it may interfere with normal movement. The two main types of muscle hypertonia are spasticity and rigidity.
1. Spasticity: It is a velocity-dependent increase in muscle tone, which means that the resistance to passive movement increases as the speed of the movement increases. This type of hypertonia is often associated with upper motor neuron lesions, such as those caused by stroke, spinal cord injury, or multiple sclerosis.
2. Rigidity: It is a constant and non-velocity dependent increase in muscle tone, meaning that the resistance to passive movement remains consistent regardless of the speed. This type of hypertonia can be seen in conditions like Parkinson's disease.
It is essential to diagnose and manage muscle hypertonia effectively to prevent complications such as contractures, pain, and decreased functional abilities. Treatment options may include physical therapy, medications (like antispasticity agents), orthoses, or surgical interventions in severe cases.
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.
Pick's disease, also known as Frontotemporal dementia (FTD), is a rare form of degenerative brain disorder that affects the frontal and temporal lobes of the brain. It is characterized by progressive shrinkage (atrophy) of these regions, resulting in a decline in cognitive abilities, behavioral changes, and language difficulties.
The medical definition of Pick's disease includes the following key features:
1. Progressive deterioration of cognitive functions, including memory, judgment, and problem-solving skills.
2. Changes in personality, emotional blunting, and loss of social inhibitions.
3. Language difficulties, such as difficulty with word finding, grammar, and comprehension.
4. Presence of abnormal protein deposits called Pick bodies or Pick cells in the affected brain regions.
5. Exclusion of other causes of dementia, such as Alzheimer's disease, vascular dementia, or Lewy body dementia.
Pick's disease typically affects people between the ages of 40 and 60, and it tends to progress more rapidly than other forms of dementia. Currently, there is no cure for Pick's disease, and treatment focuses on managing symptoms and improving quality of life.
Dementia is a broad term that describes a decline in cognitive functioning, including memory, language, problem-solving, and judgment, severe enough to interfere with daily life. It is not a specific disease but rather a group of symptoms that may be caused by various underlying diseases or conditions. Alzheimer's disease is the most common cause of dementia, accounting for 60-80% of cases. Other causes include vascular dementia, Lewy body dementia, frontotemporal dementia, and Huntington's disease.
The symptoms of dementia can vary widely depending on the cause and the specific areas of the brain that are affected. However, common early signs of dementia may include:
* Memory loss that affects daily life
* Difficulty with familiar tasks
* Problems with language or communication
* Difficulty with visual and spatial abilities
* Misplacing things and unable to retrace steps
* Decreased or poor judgment
* Withdrawal from work or social activities
* Changes in mood or behavior
Dementia is a progressive condition, meaning that symptoms will gradually worsen over time. While there is currently no cure for dementia, early diagnosis and treatment can help slow the progression of the disease and improve quality of life for those affected.
Ocular motility disorders refer to a group of conditions that affect the movement of the eyes. These disorders can result from nerve damage, muscle dysfunction, or brain injuries. They can cause abnormal eye alignment, limited range of motion, and difficulty coordinating eye movements. Common symptoms include double vision, blurry vision, strabismus (crossed eyes), nystagmus (involuntary eye movement), and difficulty tracking moving objects. Ocular motility disorders can be congenital or acquired and may require medical intervention to correct or manage the condition.
Basal ganglia diseases are a group of neurological disorders that affect the function of the basal ganglia, which are clusters of nerve cells located deep within the brain. The basal ganglia play a crucial role in controlling movement and coordination. When they are damaged or degenerate, it can result in various motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and difficulty with balance and walking.
Some examples of basal ganglia diseases include:
1. Parkinson's disease - a progressive disorder that affects movement due to the death of dopamine-producing cells in the basal ganglia.
2. Huntington's disease - an inherited neurodegenerative disorder that causes uncontrolled movements, emotional problems, and cognitive decline.
3. Dystonia - a movement disorder characterized by sustained or intermittent muscle contractions that cause twisting and repetitive movements or abnormal postures.
4. Wilson's disease - a rare genetic disorder that causes excessive copper accumulation in the liver and brain, leading to neurological and psychiatric symptoms.
5. Progressive supranuclear palsy (PSP) - a rare brain disorder that affects movement, gait, and balance, as well as speech and swallowing.
6. Corticobasal degeneration (CBD) - a rare neurological disorder characterized by progressive loss of nerve cells in the cerebral cortex and basal ganglia, leading to stiffness, rigidity, and difficulty with movement and coordination.
Treatment for basal ganglia diseases varies depending on the specific diagnosis and symptoms but may include medication, surgery, physical therapy, or a combination of these approaches.
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.
The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:
1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.
The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.
I could not find a medical definition for "Benzilates" as it is not a recognized term in medicine or pharmacology. It seems that you may have made a typographical error, and the correct term you are looking for might be "benzoylates." Benzoylates refer to salts or esters of benzoic acid, which have various uses including as preservatives and pharmaceutical ingredients.
If you meant something else by "Benzilates," please provide more context so I can give a more accurate response.
I'm sorry for any confusion, but "Guam" is not a medical term. It is a territorial island in the Pacific Ocean and is an organized, unincorporated territory of the United States. Guam is known for its unique Chamorro culture, beautiful beaches, and historical sites. If you have any questions about medical terms or topics, I'd be happy to help with those instead!
Lewy body disease, also known as dementia with Lewy bodies, is a type of progressive degenerative dementia that affects thinking, behavior, and movement. It's named after Dr. Friedrich Lewy, the scientist who discovered the abnormal protein deposits, called Lewy bodies, that are characteristic of this disease.
Lewy bodies are made up of a protein called alpha-synuclein and are found in the brain cells of individuals with Lewy body disease. These abnormal protein deposits are also found in people with Parkinson's disease, but they are more widespread in Lewy body disease, affecting multiple areas of the brain.
The symptoms of Lewy body disease can vary from person to person, but they often include:
* Cognitive decline, such as memory loss, confusion, and difficulty with problem-solving
* Visual hallucinations and delusions
* Parkinsonian symptoms, such as stiffness, tremors, and difficulty walking or moving
* Fluctuations in alertness and attention
* REM sleep behavior disorder, where a person acts out their dreams during sleep
Lewy body disease is a progressive condition, which means that the symptoms get worse over time. Currently, there is no cure for Lewy body disease, but medications can help manage some of the symptoms.
Speech disorders refer to a group of conditions in which a person has difficulty producing or articulating sounds, words, or sentences in a way that is understandable to others. These disorders can be caused by various factors such as developmental delays, neurological conditions, hearing loss, structural abnormalities, or emotional issues.
Speech disorders may include difficulties with:
* Articulation: the ability to produce sounds correctly and clearly.
* Phonology: the sound system of language, including the rules that govern how sounds are combined and used in words.
* Fluency: the smoothness and flow of speech, including issues such as stuttering or cluttering.
* Voice: the quality, pitch, and volume of the spoken voice.
* Resonance: the way sound is produced and carried through the vocal tract, which can affect the clarity and quality of speech.
Speech disorders can impact a person's ability to communicate effectively, leading to difficulties in social situations, academic performance, and even employment opportunities. Speech-language pathologists are trained to evaluate and treat speech disorders using various evidence-based techniques and interventions.
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.
Neck muscles, also known as cervical muscles, are a group of muscles that provide movement, support, and stability to the neck region. They are responsible for various functions such as flexion, extension, rotation, and lateral bending of the head and neck. The main neck muscles include:
1. Sternocleidomastoid: This muscle is located on either side of the neck and is responsible for rotating and flexing the head. It also helps in tilting the head to the same side.
2. Trapezius: This large, flat muscle covers the back of the neck, shoulders, and upper back. It is involved in movements like shrugging the shoulders, rotating and extending the head, and stabilizing the scapula (shoulder blade).
3. Scalenes: These three pairs of muscles are located on the side of the neck and assist in flexing, rotating, and laterally bending the neck. They also help with breathing by elevating the first two ribs during inspiration.
4. Suboccipitals: These four small muscles are located at the base of the skull and are responsible for fine movements of the head, such as tilting and rotating.
5. Longus Colli and Longus Capitis: These muscles are deep neck flexors that help with flexing the head and neck forward.
6. Splenius Capitis and Splenius Cervicis: These muscles are located at the back of the neck and assist in extending, rotating, and laterally bending the head and neck.
7. Levator Scapulae: This muscle is located at the side and back of the neck, connecting the cervical vertebrae to the scapula. It helps with rotation, extension, and elevation of the head and scapula.
Olivopontocerebellar atrophies (OPCA) are a group of rare, progressive neurodegenerative disorders that primarily affect the cerebellum, olive (inferior olivary nucleus), and pons in the brainstem. The condition is characterized by degeneration and atrophy of these specific areas, leading to various neurological symptoms.
The term "olivopontocerebellar atrophies" encompasses several subtypes, including:
1. Hereditary spastic paraplegia with cerebellar ataxia (SPG/ATA) - Autosomal dominant or recessive inheritance pattern.
2. Hereditary dentatorubral-pallidoluysian atrophy (DRPLA) - Autosomal dominant inheritance pattern.
3. Idiopathic OPCA - No known genetic cause, possibly related to environmental factors or spontaneous mutations.
Symptoms of olivopontocerebellar atrophies may include:
* Progressive cerebellar ataxia (gait and limb incoordination)
* Dysarthria (slurred speech)
* Oculomotor abnormalities (nystagmus, gaze palsy)
* Spasticity (stiffness and rigidity of muscles)
* Dysphagia (difficulty swallowing)
* Tremors or dystonia (involuntary muscle contractions)
Diagnosis typically involves a combination of clinical examination, neuroimaging studies (MRI), genetic testing, and exclusion of other possible causes. Currently, there is no cure for olivopontocerebellar atrophies, but supportive care can help manage symptoms and improve quality of life.
Frontotemporal dementia (FTD) is a group of disorders caused by progressive degeneration of the frontal and temporal lobes of the brain. These areas of the brain are associated with personality, behavior, and language.
There are three main types of FTD:
1. Behavioral variant FTD (bvFTD): This type is characterized by changes in personality, behavior, and judgment. Individuals may become socially inappropriate, emotionally indifferent, or impulsive. They may lose interest in things they used to enjoy and have difficulty with tasks that require planning and organization.
2. Primary progressive aphasia (PPA): This type affects language abilities. There are two main subtypes of PPA: semantic dementia and progressive nonfluent aphasia. Semantic dementia is characterized by difficulty understanding words and objects, while progressive nonfluent aphasia is characterized by problems with speech production and articulation.
3. Motor neuron disease (MND) associated FTD: Some individuals with FTD may also develop motor neuron disease, which affects the nerves that control muscle movement. This can lead to weakness, stiffness, and wasting of muscles, as well as difficulty swallowing and speaking.
FTD is a degenerative disorder, meaning that symptoms get worse over time. There is no cure for FTD, but there are treatments available to help manage symptoms and improve quality of life. The exact cause of FTD is not known, but it is believed to be related to abnormalities in certain proteins in the brain. In some cases, FTD may run in families and be caused by genetic mutations.
Nerve degeneration, also known as neurodegeneration, is the progressive loss of structure and function of neurons, which can lead to cognitive decline, motor impairment, and various other symptoms. This process occurs due to a variety of factors, including genetics, environmental influences, and aging. It is a key feature in several neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. The degeneration can affect any part of the nervous system, leading to different symptoms depending on the location and extent of the damage.
A gait disorder is a disturbance in the ability to walk that can't be attributed to physical disabilities such as weakness or paralysis. Neurologic gait disorders are those specifically caused by underlying neurological conditions. These disorders can result from damage to the brain, spinal cord, or peripheral nerves that disrupts communication between the muscles and the brain.
Neurologic gait disorders can present in various ways, including:
1. **Spastic Gait:** This is a stiff, foot-dragging walk caused by increased muscle tone (hypertonia) and stiffness (spasticity). It's often seen in conditions like cerebral palsy or multiple sclerosis.
2. **Ataxic Gait:** This is a broad-based, unsteady, and irregular walk caused by damage to the cerebellum, which affects balance and coordination. Conditions such as cerebellar atrophy or stroke can cause this type of gait disorder.
3. **Parkinsonian Gait:** This is a shuffling walk with small steps, flexed knees, and difficulty turning. It's often seen in Parkinson's disease.
4. **Neuropathic Gait:** This is a high-stepping walk caused by foot drop (difficulty lifting the front part of the foot), which results from damage to the peripheral nerves. Conditions such as diabetic neuropathy or Guillain-Barre syndrome can cause this type of gait disorder.
5. **Choreic Gait:** This is an irregular, dance-like walk caused by involuntary movements (chorea) seen in conditions like Huntington's disease.
6. **Mixed Gait:** Sometimes, a person may exhibit elements of more than one type of gait disorder.
The specific type of gait disorder can provide important clues about the underlying neurological condition and help guide diagnosis and treatment.
The Intralaminar Thalamic Nuclei are a group of nuclei located within the thalamus, a part of the brain that serves as a relay station for sensory and motor signals. These nuclei are situated between the laminae (layers) of the thalamus and are characterized by their intricate internal organization. They play a crucial role in various functions, including attention, consciousness, and sleep-wake regulation. The Intralaminar Thalamic Nuclei have extensive connections with the cerebral cortex and other subcortical structures, making them an essential component of the brain's neural circuitry.
The frontal lobe is the largest lobes of the human brain, located at the front part of each cerebral hemisphere and situated in front of the parietal and temporal lobes. It plays a crucial role in higher cognitive functions such as decision making, problem solving, planning, parts of social behavior, emotional expressions, physical reactions, and motor function. The frontal lobe is also responsible for what's known as "executive functions," which include the ability to focus attention, understand rules, switch focus, plan actions, and inhibit inappropriate behaviors. It is divided into five areas, each with its own specific functions: the primary motor cortex, premotor cortex, Broca's area, prefrontal cortex, and orbitofrontal cortex. Damage to the frontal lobe can result in a wide range of impairments, depending on the location and extent of the injury.
Frontotemporal lobar degeneration (FTLD) is a group of disorders characterized by the progressive degeneration of the frontal and temporal lobes of the brain. These areas of the brain are involved in decision-making, behavior, emotion, and language. FTLD can be divided into several subtypes based on the specific clinical features and the underlying protein abnormalities.
The three main subtypes of FTLD are:
1. Behavioral variant frontotemporal dementia (bvFTD): This subtype is characterized by changes in personality, behavior, and judgment. People with bvFTD may lose their social inhibitions, become impulsive, or develop compulsive behaviors. They may also have difficulty with emotional processing and empathy.
2. Primary progressive aphasia (PPA): This subtype is characterized by the gradual deterioration of language skills. People with PPA may have difficulty speaking, understanding spoken or written language, or both. There are three subtypes of PPA: nonfluent/agrammatic variant, semantic variant, and logopenic variant.
3. Motor neuron disease (MND) with FTLD: This subtype is characterized by the degeneration of motor neurons, which are the nerve cells responsible for controlling voluntary muscle movements. People with MND with FTLD may develop symptoms of amyotrophic lateral sclerosis (ALS), such as muscle weakness, stiffness, and twitching, as well as cognitive and behavioral changes associated with FTLD.
The underlying protein abnormalities in FTLD include:
1. Tau protein: In some forms of FTLD, the tau protein accumulates and forms clumps called tangles inside nerve cells. This is also seen in Alzheimer's disease.
2. TDP-43 protein: In other forms of FTLD, the TDP-43 protein accumulates and forms clumps inside nerve cells.
3. Fused in sarcoma (FUS) protein: In a small number of cases, the FUS protein accumulates and forms clumps inside nerve cells.
FTLD is typically a progressive disorder, meaning that symptoms worsen over time. There is currently no cure for FTLD, but there are treatments available to help manage symptoms and improve quality of life.
Medical Definition:
Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.
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.
Neuropsychological tests are a type of psychological assessment that measures cognitive functions, such as attention, memory, language, problem-solving, and perception. These tests are used to help diagnose and understand the cognitive impact of neurological conditions, including dementia, traumatic brain injury, stroke, Parkinson's disease, and other disorders that affect the brain.
The tests are typically administered by a trained neuropsychologist and can take several hours to complete. They may involve paper-and-pencil tasks, computerized tasks, or interactive activities. The results of the tests are compared to normative data to help identify any areas of cognitive weakness or strength.
Neuropsychological testing can provide valuable information for treatment planning, rehabilitation, and assessing response to treatment. It can also be used in research to better understand the neural basis of cognition and the impact of neurological conditions on cognitive function.
Facial muscles, also known as facial nerves or cranial nerve VII, are a group of muscles responsible for various expressions and movements of the face. These muscles include:
1. Orbicularis oculi: muscle that closes the eyelid and raises the upper eyelid
2. Corrugator supercilii: muscle that pulls the eyebrows down and inward, forming wrinkles on the forehead
3. Frontalis: muscle that raises the eyebrows and forms horizontal wrinkles on the forehead
4. Procerus: muscle that pulls the medial ends of the eyebrows downward, forming vertical wrinkles between the eyebrows
5. Nasalis: muscle that compresses or dilates the nostrils
6. Depressor septi: muscle that pulls down the tip of the nose
7. Levator labii superioris alaeque nasi: muscle that raises the upper lip and flares the nostrils
8. Levator labii superioris: muscle that raises the upper lip
9. Zygomaticus major: muscle that raises the corner of the mouth, producing a smile
10. Zygomaticus minor: muscle that raises the nasolabial fold and corner of the mouth
11. Risorius: muscle that pulls the angle of the mouth laterally, producing a smile
12. Depressor anguli oris: muscle that pulls down the angle of the mouth
13. Mentalis: muscle that raises the lower lip and forms wrinkles on the chin
14. Buccinator: muscle that retracts the cheek and helps with chewing
15. Platysma: muscle that depresses the corner of the mouth and wrinkles the skin of the neck.
These muscles are innervated by the facial nerve, which arises from the brainstem and exits the skull through the stylomastoid foramen. Damage to the facial nerve can result in facial paralysis or weakness on one or both sides of the face.
Cognitive disorders are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. These disorders can be caused by various factors such as brain injury, degenerative diseases, infection, substance abuse, or developmental disabilities. Examples of cognitive disorders include dementia, amnesia, delirium, and intellectual disability. It's important to note that the specific definition and diagnostic criteria for cognitive disorders may vary depending on the medical source or classification system being used.
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.
Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. It's the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.
The early signs of the disease include forgetting recent events or conversations. As the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to carry out everyday tasks.
Currently, there's no cure for Alzheimer's disease. However, treatments can temporarily slow the worsening of dementia symptoms and improve quality of life.
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.
The mesencephalon, also known as the midbrain, is the middle portion of the brainstem that connects the hindbrain (rhombencephalon) and the forebrain (prosencephalon). It plays a crucial role in several important functions including motor control, vision, hearing, and the regulation of consciousness and sleep-wake cycles. The mesencephalon contains several important structures such as the cerebral aqueduct, tectum, tegmentum, cerebral peduncles, and several cranial nerve nuclei (III and IV).
Facial paralysis is a loss of facial movement due to damage or dysfunction of the facial nerve (cranial nerve VII). This nerve controls the muscles involved in facial expressions, such as smiling, frowning, and closing the eyes. Damage to one side of the facial nerve can cause weakness or paralysis on that side of the face.
Facial paralysis can result from various conditions, including:
1. Bell's palsy - an idiopathic (unknown cause) inflammation of the facial nerve
2. Trauma - skull fractures, facial injuries, or surgical trauma to the facial nerve
3. Infections - Lyme disease, herpes zoster (shingles), HIV/AIDS, or bacterial infections like meningitis
4. Tumors - benign or malignant growths that compress or invade the facial nerve
5. Stroke - damage to the brainstem where the facial nerve originates
6. Congenital conditions - some people are born with facial paralysis due to genetic factors or birth trauma
Symptoms of facial paralysis may include:
* Inability to move one or more parts of the face, such as the eyebrows, eyelids, mouth, or cheeks
* Drooping of the affected side of the face
* Difficulty closing the eye on the affected side
* Changes in saliva and tear production
* Altered sense of taste
* Pain around the ear or jaw
* Speech difficulties due to weakened facial muscles
Treatment for facial paralysis depends on the underlying cause. In some cases, such as Bell's palsy, spontaneous recovery may occur within a few weeks to months. However, physical therapy, medications, and surgical interventions might be necessary in other situations to improve function and minimize complications.
Brain diseases, also known as neurological disorders, refer to a wide range of conditions that affect the brain and nervous system. These diseases can be caused by various factors such as genetics, infections, injuries, degeneration, or structural abnormalities. They can affect different parts of the brain, leading to a variety of symptoms and complications.
Some examples of brain diseases include:
1. Alzheimer's disease - a progressive degenerative disorder that affects memory and cognitive function.
2. Parkinson's disease - a movement disorder characterized by tremors, stiffness, and difficulty with coordination and balance.
3. Multiple sclerosis - a chronic autoimmune disease that affects the nervous system and can cause a range of symptoms such as vision loss, muscle weakness, and cognitive impairment.
4. Epilepsy - a neurological disorder characterized by recurrent seizures.
5. Brain tumors - abnormal growths in the brain that can be benign or malignant.
6. Stroke - a sudden interruption of blood flow to the brain, which can cause paralysis, speech difficulties, and other neurological symptoms.
7. Meningitis - an infection of the membranes surrounding the brain and spinal cord.
8. Encephalitis - an inflammation of the brain that can be caused by viruses, bacteria, or autoimmune disorders.
9. Huntington's disease - a genetic disorder that affects muscle coordination, cognitive function, and mental health.
10. Migraine - a neurological condition characterized by severe headaches, often accompanied by nausea, vomiting, and sensitivity to light and sound.
Brain diseases can range from mild to severe and may be treatable or incurable. They can affect people of all ages and backgrounds, and early diagnosis and treatment are essential for improving outcomes and quality of life.
An abnormal reflex in a medical context refers to an involuntary and exaggerated response or lack of response to a stimulus that is not expected in the normal physiological range. These responses can be indicative of underlying neurological disorders or damage to the nervous system. Examples include hyperreflexia (overactive reflexes) and hyporeflexia (underactive reflexes). The assessment of reflexes is an important part of a physical examination, as it can provide valuable information about the functioning of the nervous system.
The pons is a part of the brainstem that lies between the medulla oblongata and the midbrain. Its name comes from the Latin word "ponte" which means "bridge," as it serves to connect these two regions of the brainstem. The pons contains several important structures, including nerve fibers that carry signals between the cerebellum (the part of the brain responsible for coordinating muscle movements) and the rest of the nervous system. It also contains nuclei (clusters of neurons) that help regulate various functions such as respiration, sleep, and facial movements.
Disease progression is the worsening or advancement of a medical condition over time. It refers to the natural course of a disease, including its development, the severity of symptoms and complications, and the impact on the patient's overall health and quality of life. Understanding disease progression is important for developing appropriate treatment plans, monitoring response to therapy, and predicting outcomes.
The rate of disease progression can vary widely depending on the type of medical condition, individual patient factors, and the effectiveness of treatment. Some diseases may progress rapidly over a short period of time, while others may progress more slowly over many years. In some cases, disease progression may be slowed or even halted with appropriate medical interventions, while in other cases, the progression may be inevitable and irreversible.
In clinical practice, healthcare providers closely monitor disease progression through regular assessments, imaging studies, and laboratory tests. This information is used to guide treatment decisions and adjust care plans as needed to optimize patient outcomes and improve quality of life.
The putamen is a round, egg-shaped structure that is a part of the basal ganglia, located in the forebrain. It is situated laterally to the globus pallidus and medially to the internal capsule. The putamen plays a crucial role in regulating movement and is involved in various functions such as learning, motivation, and habit formation.
It receives input from the cerebral cortex via the corticostriatal pathway and sends output to the globus pallidus and substantia nigra pars reticulata, which are also part of the basal ganglia circuitry. The putamen is heavily innervated by dopaminergic neurons from the substantia nigra pars compacta, and degeneration of these neurons in Parkinson's disease leads to a significant reduction in dopamine levels in the putamen, resulting in motor dysfunction.
Diffusion Tensor Imaging (DTI) is a type of magnetic resonance imaging (MRI) technique that allows for the measurement and visualization of water diffusion in biological tissues, particularly in the brain. DTI provides information about the microstructural organization and integrity of nerve fibers within the brain by measuring the directionality of water diffusion in the brain's white matter tracts.
In DTI, a tensor is used to describe the three-dimensional diffusion properties of water molecules in each voxel (three-dimensional pixel) of an MRI image. The tensor provides information about the magnitude and direction of water diffusion, which can be used to calculate various diffusion metrics such as fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD). These metrics provide insights into the structural properties of nerve fibers, including their orientation, density, and integrity.
DTI has numerous clinical applications, such as in the diagnosis and monitoring of neurological disorders like multiple sclerosis, traumatic brain injury, and neurodegenerative diseases. It can also be used for presurgical planning to identify critical white matter tracts that need to be preserved during surgery.
Cholinergic fibers are nerve cell extensions (neurons) that release the neurotransmitter acetylcholine at their synapses, which are the junctions where they transmit signals to other neurons or effector cells such as muscles and glands. These fibers are a part of the cholinergic system, which plays crucial roles in various physiological processes including learning and memory, attention, arousal, sleep, and muscle contraction.
Cholinergic fibers can be found in both the central nervous system (CNS) and the peripheral nervous system (PNS). In the CNS, cholinergic neurons are primarily located in the basal forebrain and brainstem, and their projections innervate various regions of the cerebral cortex, hippocampus, thalamus, and other brain areas. In the PNS, cholinergic fibers are responsible for activating skeletal muscles through neuromuscular junctions, as well as regulating functions in smooth muscles, cardiac muscles, and glands via the autonomic nervous system.
Dysfunction of the cholinergic system has been implicated in several neurological disorders, such as Alzheimer's disease, Parkinson's disease, and myasthenia gravis.
An autopsy, also known as a post-mortem examination or obduction, is a medical procedure in which a qualified professional (usually a pathologist) examines a deceased person's body to determine the cause and manner of death. This process may involve various investigative techniques, such as incisions to study internal organs, tissue sampling, microscopic examination, toxicology testing, and other laboratory analyses. The primary purpose of an autopsy is to gather objective evidence about the medical conditions and factors contributing to the individual's demise, which can be essential for legal, insurance, or public health purposes. Additionally, autopsies can provide valuable insights into disease processes and aid in advancing medical knowledge.
Blinking is the rapid and repetitive closing and reopening of the eyelids. It is a normal physiological process that helps to keep the eyes moist, protected and comfortable by spreading tears over the surface of the eye and removing any foreign particles or irritants that may have accumulated on the eyelid or the conjunctiva (the mucous membrane that covers the front of the eye and lines the inside of the eyelids).
Blinking is controlled by the facial nerve (cranial nerve VII), which sends signals to the muscles that control the movement of the eyelids. On average, people blink about 15-20 times per minute, but this rate can vary depending on factors such as mood, level of attention, and visual tasks. For example, people tend to blink less frequently when they are concentrating on a visual task or looking at a screen, which can lead to dry eye symptoms.
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.
Lewy bodies are abnormal aggregates of alpha-synuclein protein that develop in nerve cells (neurons) in the brain. They are named after Frederick Lewy, a German-American neurologist who discovered them while working with Dr. Alois Alzheimer. The presence of Lewy bodies is a hallmark feature of Lewy body dementia, which includes both Parkinson's disease dementia and dementia with Lewy bodies.
Lewy bodies can lead to the dysfunction and death of neurons in areas of the brain that control movement, cognition, and behavior. This can result in a range of symptoms, including motor impairments, cognitive decline, visual hallucinations, and mood changes. The exact role of Lewy bodies in the development and progression of these disorders is not fully understood, but they are believed to contribute to the neurodegenerative process that underlies these conditions.
A case-control study is an observational research design used to identify risk factors or causes of a disease or health outcome. In this type of study, individuals with the disease or condition (cases) are compared with similar individuals who do not have the disease or condition (controls). The exposure history or other characteristics of interest are then compared between the two groups to determine if there is an association between the exposure and the disease.
Case-control studies are often used when it is not feasible or ethical to conduct a randomized controlled trial, as they can provide valuable insights into potential causes of diseases or health outcomes in a relatively short period of time and at a lower cost than other study designs. However, because case-control studies rely on retrospective data collection, they are subject to biases such as recall bias and selection bias, which can affect the validity of the results. Therefore, it is important to carefully design and conduct case-control studies to minimize these potential sources of bias.
Eye movements, also known as ocular motility, refer to the voluntary or involuntary motion of the eyes that allows for visual exploration of our environment. There are several types of eye movements, including:
1. Saccades: rapid, ballistic movements that quickly shift the gaze from one point to another.
2. Pursuits: smooth, slow movements that allow the eyes to follow a moving object.
3. Vergences: coordinated movements of both eyes in opposite directions, usually in response to a three-dimensional stimulus.
4. Vestibulo-ocular reflex (VOR): automatic eye movements that help stabilize the gaze during head movement.
5. Optokinetic nystagmus (OKN): rhythmic eye movements that occur in response to large moving visual patterns, such as when looking out of a moving vehicle.
Abnormalities in eye movements can indicate neurological or ophthalmological disorders and are often assessed during clinical examinations.
Gait is a medical term used to describe the pattern of movement of the limbs during walking or running. It includes the manner or style of walking, including factors such as rhythm, speed, and step length. A person's gait can provide important clues about their physical health and neurological function, and abnormalities in gait may indicate the presence of underlying medical conditions, such as neuromuscular disorders, orthopedic problems, or injuries.
A typical human gait cycle involves two main phases: the stance phase, during which the foot is in contact with the ground, and the swing phase, during which the foot is lifted and moved forward in preparation for the next step. The gait cycle can be further broken down into several sub-phases, including heel strike, foot flat, midstance, heel off, and toe off.
Gait analysis is a specialized field of study that involves observing and measuring a person's gait pattern using various techniques, such as video recordings, force plates, and motion capture systems. This information can be used to diagnose and treat gait abnormalities, improve mobility and function, and prevent injuries.
The Substantia Nigra is a region in the midbrain that plays a crucial role in movement control and reward processing. It is composed of two parts: the pars compacta and the pars reticulata. The pars compacta contains dopamine-producing neurons, whose loss or degeneration is associated with Parkinson's disease, leading to motor symptoms such as tremors, rigidity, and bradykinesia.
In summary, Substantia Nigra is a brain structure that contains dopamine-producing cells and is involved in movement control and reward processing. Its dysfunction or degeneration can lead to neurological disorders like Parkinson's disease.
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.
A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.
For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.
It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.
The cerebral cortex is the outermost layer of the brain, characterized by its intricate folded structure and wrinkled appearance. It is a region of great importance as it plays a key role in higher cognitive functions such as perception, consciousness, thought, memory, language, and attention. The cerebral cortex is divided into two hemispheres, each containing four lobes: the frontal, parietal, temporal, and occipital lobes. These areas are responsible for different functions, with some regions specializing in sensory processing while others are involved in motor control or associative functions. The cerebral cortex is composed of gray matter, which contains neuronal cell bodies, and is covered by a layer of white matter that consists mainly of myelinated nerve fibers.
A hallucination is a perception in the absence of external stimuli. They are sensory experiences that feel real, but are generated from inside the mind rather than by external reality. Hallucinations can occur in any of the senses, causing individuals to hear sounds, see visions, or smell odors that aren't actually present. They can range from relatively simple experiences, such as seeing flashes of light, to complex experiences like seeing and interacting with people or objects that aren't there. Hallucinations are often associated with certain medical conditions, mental health disorders, or the use of certain substances.
Neuroimaging is a medical term that refers to the use of various techniques to either directly or indirectly image the structure, function, or pharmacology of the nervous system. It includes techniques such as computed tomography (CT), magnetic resonance imaging (MRI), functional MRI (fMRI), positron emission tomography (PET), single-photon emission computed tomography (SPECT), and diffusion tensor imaging (DTI). These techniques are used to diagnose and monitor various neurological and psychiatric conditions, as well as to understand the underlying mechanisms of brain function in health and disease.
A saccade is a quick, rapid, and ballistic conjugate eye movement that shifts the point of fixation from one target to another. It helps in rapidly repositioning the fovea (the central part of the retina with the highest visual acuity) to focus on different targets of interest in the visual scene. Saccades are essential for efficient scanning and exploration of our environment, allowing us to direct our high-resolution vision towards various points of interest. They typically take only about 20-200 milliseconds to complete and can reach peak velocities of up to 500 degrees per second or more, depending on the amplitude of the movement. Saccades are a critical component of normal visual function and are often studied in fields such as ophthalmology, neurology, and neuroscience.
The abducens nerve, also known as the sixth cranial nerve, is responsible for controlling the lateral rectus muscle of the eye, which enables the eye to move outward. Abducens nerve diseases refer to conditions that affect this nerve and can result in various symptoms, primarily affecting eye movement.
Here are some medical definitions related to abducens nerve diseases:
1. Abducens Nerve Palsy: A condition characterized by weakness or paralysis of the abducens nerve, causing difficulty in moving the affected eye outward. This results in double vision (diplopia), especially when gazing towards the side of the weakened nerve. Abducens nerve palsy can be congenital, acquired, or caused by various factors such as trauma, tumors, aneurysms, infections, or diseases like diabetes and multiple sclerosis.
2. Sixth Nerve Palsy: Another term for abducens nerve palsy, referring to the weakness or paralysis of the sixth cranial nerve.
3. Internuclear Ophthalmoplegia (INO): A neurological condition affecting eye movement, often caused by a lesion in the medial longitudinal fasciculus (MLF), a bundle of nerve fibers that connects the abducens nucleus with the oculomotor nucleus. INO results in impaired adduction (inward movement) of the eye on the side of the lesion and nystagmus (involuntary eye movements) of the abducting eye on the opposite side when attempting to look towards the side of the lesion.
4. One-and-a-Half Syndrome: A rare neurological condition characterized by a combination of INO and internuclear ophthalmoplegia with horizontal gaze palsy on the same side, caused by damage to both the abducens nerve and the paramedian pontine reticular formation (PPRF). This results in limited or no ability to move the eyes towards the side of the lesion and impaired adduction of the eye on the opposite side.
5. Brainstem Encephalitis: Inflammation of the brainstem, which can affect the abducens nerve and other cranial nerves, leading to various neurological symptoms such as diplopia (double vision), ataxia (loss of balance and coordination), and facial weakness. Brainstem encephalitis can be caused by infectious agents, autoimmune disorders, or paraneoplastic syndromes.
6. Multiple Sclerosis (MS): An autoimmune disorder characterized by inflammation and demyelination of the central nervous system, including the brainstem and optic nerves. MS can cause various neurological symptoms, such as diplopia, nystagmus, and INO, due to damage to the abducens nerve and other cranial nerves.
7. Wernicke's Encephalopathy: A neurological disorder caused by thiamine (vitamin B1) deficiency, often seen in alcoholics or individuals with malnutrition. Wernicke's encephalopathy can affect the brainstem and cause various symptoms such as diplopia, ataxia, confusion, and oculomotor abnormalities.
8. Pontine Glioma: A rare type of brain tumor that arises from the glial cells in the pons (a part of the brainstem). Pontine gliomas can cause various neurological symptoms such as diplopia, facial weakness, and difficulty swallowing due to their location in the brainstem.
9. Brainstem Cavernous Malformation: A benign vascular lesion that arises from the small blood vessels in the brainstem. Brainstem cavernous malformations can cause various neurological symptoms such as diplopia, ataxia, and facial weakness due to their location in the brainstem.
10. Pituitary Adenoma: A benign tumor that arises from the pituitary gland, located at the base of the brain. Large pituitary adenomas can compress the optic nerves and cause various visual symptoms such as diplopia, visual field defects, and decreased vision.
11. Craniopharyngioma: A benign tumor that arises from the remnants of the Rathke's pouch, a structure that gives rise to the anterior pituitary gland. Craniopharyngiomas can cause various neurological and endocrine symptoms such as diplopia, visual field defects, headaches, and hormonal imbalances due to their location near the optic nerves and pituitary gland.
12. Meningioma: A benign tumor that arises from the meninges, the protective covering of the brain and spinal cord. Meningiomas can cause various neurological symptoms such as diplopia, headaches, and seizures depending on their location in the brain or spinal cord.
13. Chordoma: A rare type of malignant tumor that arises from the remnants of the notochord, a structure that gives rise to the spine during embryonic development. Chordomas can cause various neurological and endocrine symptoms such as diplopia, visual field defects, headaches, and hormonal imbalances due to their location near the brainstem and spinal cord.
14. Metastatic Brain Tumors: Malignant tumors that spread from other parts of the body to the brain. Metastatic brain tumors can cause various neurological symptoms such as diplopia, headaches, seizures, and cognitive impairment depending on their location in the brain.
15. Other Rare Brain Tumors: There are many other rare types of brain tumors that can cause diplopia or other neurological symptoms, including gliomas, ependymomas, pineal region tumors, and others. These tumors require specialized diagnosis and treatment by neuro-oncologists and neurosurgeons with expertise in these rare conditions.
In summary, diplopia can be caused by various brain tumors, including pituitary adenomas, meningiomas, chordomas, metastatic brain tumors, and other rare types of tumors. It is important to seek medical attention promptly if you experience diplopia or other neurological symptoms, as early diagnosis and treatment can improve outcomes and quality of life.
Progressive supranuclear palsy
Deaths in January 2017
Dementia
Claude McKinney
Procerus sign
Parkinson-plus syndrome
Charles Guthrie, Baron Guthrie of Craigiebank
Frontotemporal lobar degeneration
Apraxia of lid opening
Lytico-bodig disease
Deaths in March 2008
Tauopathy
Clive Goodyear
Corticobasal degeneration
Deaths in January 2015
Conjugate gaze palsy
Tau protein
Deaths in July 2007
Deaths in July 2018
Neurofibrillary tangle
Dementia with Lewy bodies
Di-deuterated linoleic acid ethyl ester
Deaths in June 2021
Frontotemporal dementia
Leonard Krieger
Krembil Research Institute
Retrotope
Deaths in August 2012
Deaths in April 2009
Veena Sahasrabuddhe
Jeff Golub
Progressive supranuclear palsy - Wikipedia
Progressive Supranuclear Palsy: Practice Essentials, Background, Pathophysiology
Progressive supranuclear palsy | Alzheimer Society of Canada
MDS SIC Blog: Immunotherapy in Progressive Supranuclear Palsy
Progressive Supranuclear Palsy Archives - Planet Ayurveda
Validity and reliability of the preliminary NINDS neuropathologic criteria for progressive supranuclear palsy and related...
Total Protein - Progressive Supranuclear Palsy: Brain: Cerebellum | P1236039PSP | Biochain
Progressive supranuclear palsy news and latest updates
gDNA - Progressive Supranuclear Palsy: Brain: Cerebellum, from a single donor | D1236039PSP | Biochain
Caregiver burden in family members caring for persons with progressive supranuclear palsy and corticobasal syndrome -...
Sequence analysis of tau in familial and sporadic progressive supranuclear palsy | Journal of Neurology, Neurosurgery &...
US FDA grants orphan drug status for Mithridion's MCD-386CR to treat progressive supranuclear palsy
18</sup>F]-Fdg Pet Identified Superior Colliculi Hypometabolism in Progressive Supranuclear Palsy | OMICS...
Diagnosis of progressive supra nuclear palsy | Progressive supra nuclear palsy | Respiratory | Conditions we treat | Adults | ...
Clinical correlations of microstructural changes in progressive supranuclear palsy<...
136 Care of patients with progressive supranuclear palsy in the hospice setting: an audit | BMJ Supportive & Palliative Care
18 F-AV1451 PET imaging and multimodal MRI changes in progressive supranuclear palsy
Frontal corpus callosum alterations in progressive supranuclear palsy but not in Parkinson's disease
Progressive Supranuclear Palsy (PSP) - Neurologic Disorders - MSD Manual Professional Edition
EEG in Dementia and Encephalopathy: Overview, Dementia, Vascular Dementia
Progressive Supranuclear Palsy | SeniorNavigator
News • Supranuclear Palsy, Progressive
Supranuclear Palsy, Progressive | Profiles RNS
Bayesian Disease Progression Modeling and Clinical Trial Design for Progressive Supranuclear Palsy - Richardson's Syndrome -...
Progressive supranuclear palsy: diagnosis and management | Practical Neurology
Symptoms of Progressive Supranuclear Palsy
Glossary of Terms | Parkinson's Disease
Glossary of Terms | Parkinson's Disease
Parkinsonism5
- A 56 year old woman presented with parkinsonism associated with apathy, cognitive impairment, vertical supranuclear gaze palsy, walking difficulties, postural instability with falls and dysarthria . (omicsonline.org)
- An atypical variant of progressive supranuclear palsy (PSP), a rare late-onset neurodegenerative disease, by prominent early parkinsonism (tremor, limb bradykinesia, axial and limb rigidity) rather than falls and cognitive change. (nih.gov)
- Follow this link to review classifications for Progressive supranuclear palsy-parkinsonism syndrome in Orphanet. (nih.gov)
- Dejerine and Thomas first used the term olivopontocerebellar atrophy (OPCA) in 1900 when they described 2 patients with a degenerative disorder leading to progressive cerebellar dysfunction and parkinsonism. (medscape.com)
- Some members may present primarily with amyotrophy, and others may present with primary supranuclear gaze palsy, parkinsonism, schizophrenialike thought disorder, or progressive aphasia and/or apraxia. (medscape.com)
Parkinson's5
- Progressive supranuclear palsy (PSP) is a life-limiting progressive neurological disease which can be mistaken for Parkinson's disease early in its course. (bmj.com)
- We agree with Andrew Lees on the value of the applause sign (i.e. ask a PSP patient to clap 3 times, and they typically perseverative by clapping more than 3 times) and a lack of decrement on hypokinesia tests (e.g. sequential finger tapping or in micrographic writing, without a progressive reduction in amplitude) to differentiate Progressive Supranuclear Palsy from Parkinson's disease. (bmj.com)
- Progressive supra-nuclear palsy (PSP) is a debilitating and rapidly progressing form of atypical Parkinson's disease. (mdsabstracts.org)
- Discriminating progressive supranuclear palsy from Parkinson's disease using wearable technology and machine learning. (ox.ac.uk)
- BACKGROUND: Progressive supranuclear palsy (PSP), a neurodegenerative conditions may be difficult to discriminate clinically from idiopathic Parkinson's disease (PD). (ox.ac.uk)
Corticobasal degeneration3
- They include multiple system atrophy (MSA), progressive supranuclear palsy (PSP ), corticobasal degeneration (CBD) and Dementia with Lewy bodies (DLB). (parkinson.ca)
- To address these issues, we examined the morphology and differential distribution of pathologic lesions in three disorders: progressive supranuclear palsy, Pick's disease, and corticobasal degeneration. (elsevierpure.com)
- The Society for Progressive Supranuclear Palsy, is a 501(c)3 organization dedicated to increasing awareness of progressive supranuclear palsy and corticobasal degeneration, advancing research toward a cure, educating health professionals, and providing support, education and hope for persons with PSP and CBD and their families. (rareshare.org)
Ophthalmoplegia4
- Supranuclear ophthalmoplegia is a condition that affects the movement of the eyes. (medlineplus.gov)
- People with supranuclear ophthalmoplegia are unable to move their eyes at will in all directions, especially looking upward. (medlineplus.gov)
- Tests will be done to check for diseases linked with supranuclear ophthalmoplegia. (medlineplus.gov)
- Treatment depends on the cause and symptoms of the supranuclear ophthalmoplegia. (medlineplus.gov)
Gaze3
- Progressive supranuclear palsy (PSP) is a neurodegenerative disease (see the image below) whose characteristics include supranuclear, initially vertical, gaze dysfunction accompanied by extrapyramidal symptoms and cognitive dysfunction. (medscape.com)
- Although progressive supranuclear palsy is defined by its akinetic rigidity, vertical supranuclear gaze palsy and falls, cognitive impairments are an important determinant of patients' and carers' quality of life. (cardiff.ac.uk)
- Possible PSP requires the presence of a gradually progressive disorder with onset at age 40 or later, either vertical supranuclear gaze palsy or both slowing of vertical saccades and prominent postural instability with falls in the first year of onset, as well as no evidence of other diseases that could explain these features. (neurology.org)
Dementia4
- Progressive supranuclear palsy is a rare, degenerative central nervous system disorder that progressively impairs voluntary eye movements and causes bradykinesia, muscular rigidity with progressive axial dystonia, pseudobulbar palsy, and dementia. (msdmanuals.com)
- Alzheimer disease (AD) is the most common progressive degenerative form of dementia, strongly associated with advancing age. (medscape.com)
- Pick disease (named after Arnold Pick) is a progressive dementia defined by clinical and pathologic criteria. (medscape.com)
- Two types of primary progressive aphasia are identified: (1) semantic dementia, in which meaning systems are lost from language, and (2) nonfluent primary progressive aphasia. (medscape.com)
Clinical6
- Mithridion, Inc. a privately-owned clinical stage drug development company focusing on serious Central Nervous System (CNS) disorders, announces that the US Food and Drug Administration (FDA) has awarded orphan drug designation for MCD-386CR, its lead drug candidate, for the treatment of Progressive Supranuclear Palsy (PSP). (pharmabiz.com)
- The clinical definition of multiple system atrophy (MSA) is a progressive, idiopathic, degenerative process beginning in adulthood. (medscape.com)
- We recruited 23 patients with progressive supranuclear palsy (using clinical diagnostic criteria, nine with subsequent pathological confirmation) and 22 age- and education-matched controls. (cardiff.ac.uk)
- To improve the specificity and sensitivity of the clinical diagnosis of progressive supranuclear palsy (PSP, Steele-Richardson-Olszewski syndrome), the National Institute of Neurological Disorders and Stroke (NINDS) and the Society for PSP, Inc. (SPSP) sponsored an international workshop to develop an accurate and universally accepted set of criteria for this disorder. (neurology.org)
- Objective: To describe clinical features and identify prognostic predictors in progressive supranuclear palsy (PSP). (ncl.ac.uk)
- Ling H. Clinical approach to progressive supranuclear palsy. (medlineplus.gov)
Amyotrophic-lateral-s1
- Primary lateral sclerosis Amyotrophic lateral sclerosis and other motor neuron diseases are characterized by steady, relentless, progressive degeneration of corticospinal tracts, anterior horn cells, bulbar motor nuclei. (msdmanuals.com)
Late-onset neurodegenerative disease1
- Progressive supranuclear palsy (PSP) is a late-onset neurodegenerative disease involving the gradual deterioration and death of specific volumes of the brain. (wikipedia.org)
Steele-Richards1
- Progressive supranuclear palsy (PSP), also called Steele-Richardson-Olszewski syndrome, is one of the most common atypical parkinsonian syndromes. (neurology.org)
Diagnosis3
- Progressive Supranuclear Palsy (PSP) is a rare primary tauopathy, e.g. a disorder caused by the deposit of abnormal tau protein in the brain (tau is a protein that stabilises neuron cells in the nervous system), neurodegenerative disease that usually affects people in their 50s, 60s and 70s, and is generally fatal within 5-7 years of diagnosis. (vivli.org)
- A diagnosis of Progressive Supranuclear Palsy is not to be given lightly, as for any other disease. (bmj.com)
- Methods: Record-based diagnosis according to National Institute of Neurological Disorders and Stroke-Society for Progressive Supranuclear Palsy criteria was performed in 187 cases of PSP. (ncl.ac.uk)
Multiple system1
- Multiple System Atrophy (MSA) is a progressive brain disorder caused by loss of nerve cells in specific areas of the brain. (parkinson.ca)
Symptoms2
- Symptoms of progressive supranuclear palsy usually begin in late middle age. (msdmanuals.com)
- Symptoms for Progressive Supranuclear Palsy has not been added yet. (rareshare.org)
Dystonia1
- Dystonia is a common symptom of cerebral palsy and several neurodegenerative conditions. (clevelandclinic.org)
Brain5
- Ayurvedic Treatment of Progressive Supranuclear Palsy Introduction Herbal Remedies About Progressive Supranuclear PalsyProgressive supranuclear palsy is a disorder of the brain, which has a serious impact on the balance of the body, eye movements, gait and walking. (planetayurveda.com)
- There is no cure for progressive supranuclear palsy (PSP), a brain disorder marked by walking and balance difficulties. (medicalxpress.com)
- PSP is a progressive brain disease in which neurons degenerate in regions of the brain vital for eye movements, balance, walking, speech, and cognition. (pharmabiz.com)
- This article is an overview of a rare brain disorder called Progressive Supranuclear Palsy (PSP). (seniornavigator.org)
- Progressive Supranuclear Palsy is a rare degenerative disorder involving the gradual deterioration and death of selected areas of the brain. (rareshare.org)
Cerebral1
- 2020) found that 44.4% of Swedish children with cerebral palsy used a form of AAC either exclusively or to supplement their speech. (asha.org)
Alzheimer's2
- It consists of residues K 254 -F 378 of 3R tau, while other taupathies (including Alzheimer's disease, progressive supranuclear palsy, and corticobasal ganglionic degeneration) either have 4Rtau or a combination of 3R and 4Rtau. (medscape.com)
- Initial letter and semantic category fluency in Alzheimer's disease, Huntington's disease, and progressive supranuclear palsy. (bvsalud.org)
Neurological disease1
- This book illustrates the neurological disease progressive supranuclear palsy (PSP) told through the eyes of a child whose grandmother is inflicted with this disease. (psp.org)
Syndrome3
- Using Downgaze Palsy Progression Rate to Model Survival in Progressive Supranuclear Palsy-Richardson Syndrome. (uchicago.edu)
- Introduction: In the present study, midbrain atrophy and the pons-to-midbrain area ratio (P/M ratio) were investigated as diagnostic markers for presymptomatic progressive supranuclear palsy-Richardson's syndrome (Pre-PSP-RS). (elsevierpure.com)
- Primary progressive aphasia is a focal atrophy syndrome that may be associated with Pick disease, Alzheimer disease, or other pathology. (medscape.com)
Dysfunction2
- Additionally, the H2 haplotype, combined with vascular dysfunction, seems to be a factor of vascular progressive supranuclear palsy. (wikipedia.org)
- Accumulation of abnormal protein leads to progressive neuronal dysfunction and loss. (medscape.com)
Parkinsonian1
- Assessment of these square-wave jerks and diminished vertical saccades is especially useful for diagnosing progressive supranuclear palsy, because these movements set PSP patients apart from other parkinsonian patients. (wikipedia.org)
Cognitive1
- Cortical synapse loss, the probable substrate of cognitive impairment in Alzheimer disease (AD), has not previously been evaluated in progressive supranuclear palsy (PSP). (bvsalud.org)
Multimodal1
- We conclude that patients with progressive supranuclear palsy have a multimodal deficit in social cognition. (cardiff.ac.uk)
Atrophy2
- Sagittal T1-weighted image shows atrophy of midbrain, preservation of pontine volume, and atrophy of the tectum, suggestive of progressive supranuclear palsy (Steele-Olszewski-Richardson disease). (medscape.com)
- This deficit is due, in part, to progressive atrophy in a network of frontal cortical regions linked to the integration of socially relevant stimuli and interpretation of their social meaning. (cardiff.ac.uk)
Upgaze1
- Patients tend to have difficulty looking down (a downgaze palsy) followed by the addition of an upgaze palsy. (wikipedia.org)
Neuropathologic1
- We investigated the validity and reliability of diagnoses made by eight neuropathologists who used the preliminary NINDS neuropathologic diagnostic criteria for progressive supranuclear palsy (PSP) and related disorders. (nih.gov)
Subtypes1
- New evidence supports the observation that, over time, different subtypes of progressive supranuclear palsy (PSP) converge to a common phenotype. (neurodiem.tw)
Disorders1
- Disorders of supranuclear control of ocular motility. (medlineplus.gov)
Axial1
- Enfermedad degenerativa del sistema nervioso central caracterizada por dificultades en el equilibrio, TRASTORNOS DE LA MOTILIDAD OCULAR (oftalmoplejia supranuclear), DISARTRIA, dificultades de la deglución y DISTONÍA axial. (bvsalud.org)
Descriptor1
- Supranuclear Palsy, Progressive" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uchicago.edu)
Examination1
- Progressive supranucelar palsy (SPS) is diagnosed following a neurological examination by a medical consultant. (manchesterneurophysio.co.uk)
Disease3
- Progressive supranuclear palsy (PSP) is a progressive neurodegenerative disease that lacks any disease modifying therapy. (movementdisorders.org)
- Disease course and treatment patterns in progressive supranuclear palsy: A real-world study. (uchicago.edu)
- Progressive supranuclear palsy (PSP) is a rare, rapidly progressive, neurodegenerative disease characterized by falls and ocular movement disturbances. (unict.it)
Cortical1
- Cortical synapse loss in progressive supranuclear palsy. (bvsalud.org)
Abstract2
- Abstract: Objectives: Progressive supranuclear palsy (PSP) is characterized by deposition of straight filament tau aggregates in the grey matter (GM) of deep nuclei and cerebellum. (cam.ac.uk)
- Exercise and physical activity for people with Progressive Supranuclear Palsy [abstract]. (mdsabstracts.org)
Patients6
- Hypometabolism in the fronto-mesial cortex and in the anterior cingulate cortex were reported in patients with progressive supranuclear palsy (PSP). (omicsonline.org)
- We report here that 18 F-FDG PET could demonstrate brainstem changes in patients with progressive supranuclear palsy (PSP). (omicsonline.org)
- In patients with progressive supranuclear palsy (PSP), previous reports have shown a severe white matter (WM) damage involving supra and infratentorial regions including cerebellum. (maastrichtuniversity.nl)
- But, patients with Progressive Supranuclear Palsy have suffered disproportionately from delays and diagnostic hesitation, often long past any reasonable doubt. (bmj.com)
- This impairment of social cognition is important to consider for those managing and caring for patients with progressive supranuclear palsy. (cardiff.ac.uk)
- We describe the results of a study of the spinal cord of 5 patients with progressive supranuclear palsy (PSP). (uni-luebeck.de)
Primary progres1
- 60-80%) and semantic variant of primary progressive aphasia (svPPA). (medscape.com)