What is Parkinson’s disease?
Parkinson’s disease (PD) was first described in 1817 by Dr. James Parkinson, a British physician, for whom the disease was named. It is a disease that is characterized by four major features:
- Rest tremor of a limb (shaking with the limb at rest)
- Slowness of movement (bradykinesia)
- Rigidity (stiffness, increased resistance to passive movement) of the limbs or trunk
- Poor balance (postural instability)
When at least two of these symptoms are present, and especially if they are more evident on one side than the other, a diagnosis of PD is made, unless there are atypical features that suggest an alternative diagnosis. Patients may first realize something is wrong when they develop a tremor in a limb; movements are slowed and activities take longer to perform; or they experience stiffness and have balance problems. Initially, symptoms are a variable combination of tremor, bradykinesia, rigidity and postural instability. Symptoms typically begin on one side of the body and spread over time to the other side.
Changes occur in facial expression, so that there is a certain facial fixity (blank expression showing little emotion) or a staring appearance (due to reduced frequency of eye blinking). Complaints of a frozen shoulder or foot drag on the affected side are not uncommon. As symptoms come on gradually, older patients may attribute these changes to aging. The tremor is thought to be “shakiness,” bradykinesia is regarded as normal “slowing down,” and stiffness is attributed to arthritis. The stooped posture, common to PD, may be attributed to age or osteoporosis. Both younger and older patients may experience initial symptoms for a year or more before seeking medical evaluation.
Parkinson’s disease affects 1 in 100 people over the age of 60, with the average age of onset being 60 years. It can also affect younger people. Young-onset Parkinson’s disease (onset at age 40 or younger) is estimated to occur in 5 – 10% of patients with PD.
Disease Progression
After Alzheimer’s disease, Parkinson’s disease is the most common neurodegenerative disease.
It is a chronic, progressive disease that results when nerve cells in a part of the midbrain, called the substantia nigra, die or are impaired. These nerve cells produce dopamine, an important chemical messenger that transmits signals from the substantia nigra to another part of the brain called the corpus striatum. These signals allow for coordinated movement. When the dopamine-secreting cells in the substantia nigra die, the other movement control centers in the brain become unregulated. These disturbances in the control centers of the brain cause the symptoms of PD. When 80% of the dopamine-producing cells in the substantia nigra are depleted, symptoms of PD develop.
Initially the symptoms are mild, usually on one side of the body, and may not require medical treatment. Rest tremor is a major characteristic of PD, and the most common presenting symptom, but some patients never develop it. Tremor may be the least disabling symptom, but is often the most embarrassing to the patient. Patients may keep their affected hand in their pocket, behind their back, or hold something to control the tremor, which may be more psychologically distressing than any physical limitation that it imposes.
Over time, initial symptoms become worse. A mild tremor becomes more bothersome and more noticeable. Difficulties may develop with cutting food or handling utensils with the affected limb. Bradykinesia (slowness in movement) becomes a significant problem and the most disabling symptom. Slowness may interfere with daily routines; getting dressed, shaving or showering may take much of the day. Mobility is impaired and difficulty develops in getting into or out of a chair or a car, or turning over in bed. Walking is slower and there is a stooped posture, with the head and shoulders hanging forward. The voice becomes soft and monotonous. A disturbance of balance may lead to falls. Handwriting becomes small (“micrographia”) and illegible. Automatic movements, such as arm swing when walking, are reduced.
Symptoms may originally be restricted to one limb, but will typically spread over time to the other limb on the same side. They eventually progress to the other side of the body. Generally this progression is gradual, but the rate of progression varies in different patients. As symptoms progress, it is important for patients to talk with their physicians so that optimal treatment can be established. The goal of treatment is not to abolish symptoms, but rather to help the patient manage their symptoms, function independently, and make the appropriate adjustments to a chronic illness. The illness will not go away, but management of its symptoms can be successful in reducing disability or other handicap.
Patients are aware of the progressive nature of the illness and this may become a source of much anxiety. It is not uncommon for patients to over-monitor themselves and their symptoms, compare themselves to other Parkinson’s disease patients whom they may meet (length of diagnosis, level of symptoms, etc.), and avoid situations such as support groups, where they may see patients who are worse off than they are. Concern about the progression of the disease and the ability to continue working is frequently voiced.
It is not possible to predict with any confidence the likely course of the disease in an individual patient. The rate of progression and resulting level of disability vary in different patients. Some guide to the likely outcome in individual patients is provided by the course of the illness since diagnosis, but this is no more than suggestive.
When the disorder is such that normal activities of daily living are impaired, at least to some extent, symptomatic treatment is begun.
Is PD Inherited?
There is a family history of Parkinson’s disease in 5-10% of patients. It may affect people of the same generation (e.g., a brother or sister) or in two generations, such as a father and son. Environmental toxins such as manganese, carbon monoxide, and, rarely, certain pesticides cause diseases that resemble PD. However, most people with Parkinson’s disease have not been exposed to these toxins. In less than 1% of cases, PD is clearly familial. Several gene mutations have been shown to cause Parkinson disease in a few families, but these have not been found in most individuals with PD. Studies of identical twins in which one twin was known to have PD showed no increase in the incidence of PD in the other twin compared to the general population of patients over the age of 60 years. However, among identical twins younger than 50, if one member of the twinship has Parkinson’s disease, there is an increased risk of PD in the other twin. This indicates heredity may play a role in young-onset cases. Currently, researchers suspect that the cause of Parkinson’s disease in most individuals reflects a combination of genetic factors and environmental exposures.
What Else Could It Be?
There are many causes of tremor other than Parkinson’s disease, and it generally requires examination by a neurologist to distinguish between them.
Other Parkinsonism Syndromes
The characteristic symptom-complex of Parkinson’s disease (tremor, rigidity, bradykinesia, postural instability) is termed parkinsonism. This is a general term and not all patients with parkinsonism have typical Parkinson’s disease. Early in the disease process it may be difficult to know whether a patient has typical Parkinson’s disease or a syndrome that mimics it. The development of additional symptoms and the subsequent course of the disease generally points to the correct diagnosis.
Recognizing other causes of Parkinsonism
A number of patients with parkinsonism do not have PD. One study of patients with parkinsonism found that 65% had PD, 18% had drug-induced parkinsonism, 7% had vascular parkinsonism (i.e. from blocking-up of the small blood vessels feeding the brain) and 10% had atypical parkinsonism. Atypical parkinsonism should be considered particularly in patients with poor dopaminergic responsiveness, early loss of balance, prominent intellectual changes (dementia), rapid onset or progression, conspicuous postural hypotension, and little or no tremor. The present of neurological findings not associated with classic Parkinson’s disease, such as myoclonic jerking (shock-like sudden muscle contractions), should also suggest other diagnostic possibilities. The autonomic nervous system regulates the “involuntary” internal functions of the body, such as blood pressure, heart rate, and bladder, rectum, and sexual function. It may be affected in certain atypical parkinsonian syndromes.
Medication-induced Parkinsonism
Although tremor and postural instability may be less prominent, this condition may be indistinguishable from Parkinson’s disease. Medications frequently associated with the development of parkinsonism include antipsychotics, metaclopramide, reserpine, tetrabenazine and some calcium-channel blockers (especially cinnarizine and flunarizine). The parkinsonism usually resolves within weeks to months after discontinuing the offending medication.
Progressive Supranuclear Palsy (PSP)
Early onset of imbalance, frequent falls, rigidity of the trunk, and (eventually) eye-movement problems characterize PSP. Symptoms usually begin after age 50 and progress more rapidly than with Parkinson’s disease. The most characteristic eye movement abnormality is a vertical gaze paralysis. Upgaze and downgaze are therefore limited. Patients may present with frequent falls while walking downstairs, because they cannot look down. Dementia develops later in the disease. There is no specific treatment for PSP. Dopaminergic treatment should be tried but often provides little benefit. Supportive measures such as speech therapy, physical therapy, and antidepressants may help.
Corticobasal Degeneration (CBD)
CBD is the least common of the atypical causes of parkinsonism. It often affects patients quite asymmetrically and progresses more rapidly than Parkinson’s disease. The initial symptoms of CBD usually develop after age 60 and include asymmetric bradykinesia, rigidity, limb dystonia (abnormal postures), postural instability, and disturbances of language (speech expression or comprehension). There is often marked and disabling apraxia, i.e., it becomes difficult or impossible to use the affected limb even though there is no weakness or sensory loss.
There is no specific treatment for CBD. Supportive treatment such as botulinum toxin for dystonia, antidepressant medications and speech and physical therapy may help. Levodopa and dopamine agonists seldom offer benefit.
Multiple System Atrophy (MSA)
MSA is a neurodegenerative disease of unknown cause. Initially it may be difficult to distinguish from Parkinson’s disease, but it is far less common and progresses more rapidly. The mean age of onset is in the mid-50s. Clinically, it presents with bradykinesia, poor balance, abnormal autonomic function, rigidity, difficulty with coordination, or a combination of these features. Abnormalities of autonomic function include impotence, low blood pressure upon standing, excessive or reduced sweating, and constipation. There are three subtypes of the illness, each affecting different systems.
Striatonigral degeneration (SND) is characterized by parkinsonism, but without much tremor and with poor response to Sinemet. In the Shy-Drager syndrome, parkinsonism and autonomic abnormalities are conspicuous. In olivopontocerebellar atrophy (OPCA), patients have lack of coordination and clumsiness which affect balance and gait.
As MSA progresses, other symptoms and signs develop that reflect involvement of a different system. Patients with the parkinsonian presentation typically have an asymmetrical tremor, bradykinesa, rigidity and postural instability. Men often develop impotence; both men and women often experience urinary urgency and incontinence. Patients with Shy-Drager syndrome present with more prominent symptoms of autonomic dysfunction.
Although 30% of patients with MSA obtain a definite but short-lived benefit from levodopa and dopamine agonists, the parkinsonism is typically poorly responsive to medications. Dyskinesias and dystonia emerge in half of treated patients. There is not much experience of using deep brain stimulators (DBS) for MSA, but some researchers have found a modest benefit of DBS that persisted for over two years in a few patients.
Vascular Parkinsonism
Multiple small strokes can cause parkinsonism. Patients with this disorder are more likely to present with gait difficulty than tremor and are more likely to have symptoms that are worse in the lower than upper limbs. Some will also report the abrupt onset of symptoms or give a history of step-wise deterioration (symptoms get worse, then plateau for a period). Treatment is the same as for Parkinson’s disease, but the results are often disappointing.
Dementia with Lewy bodies (DLB)
This disorder is characterized by early dementia, prominent hallucinations, fluctuations over the day in cognitive status, and parkinsonism. The neuropsychological profile is characterized by deficits in attention, executive function (problem solving, planning) and visuospacial function (the ability to produce and recognize figures, drawing or matching figures).
Treatment with cholinesterase inhibitors may reduce delusions, apathy, agitation and hallucinations. A severe reaction to antipsychotic medication is another feature of this disease. If behavioral problems do not respond to cholinesterase inhibitors, low-dose treatment with atypical antipsychotic medications (quetiapine, resperidone, or clozapine) may be considered. Although motor symptoms may respond to levodopa, hallucinations may become worse with its use.
The above information was contributed by Mariann Di Minno, RN, MA, and Michael J. Aminoff, MD, DSc, of the Parkinson’s Disease Clinic and Research Center at the University of California, San Francisco. Added to this site from the National Parkinson’s Foundation.
More information can be found at WebMD Parkinson’s Disease Center.
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Glossary of Terms
Acetylcholine
A chemical messenger released by cholinergic nerves. Normally in many parts of the body, including the brain, and necessary to normal body functioning. There appears to be a reciprocal seesaw relationship between acetylcholine and do pamine and their respective nerve cell systems.
Action Tremor
Rhythmic, involuntary movement of a limb when movement is initiated, e.g., when writing or lifting a cup. Not usually seen in the earlier stages of Parkinson’s.
Adrenaline (epinephrine)
The neurotransmitter of the adrenal gland which is secreted in moments of crisis. It stimulates the heart to beat faster and work harder, increases the flow of blood to the muscles, causes an increased alertness of mind, and produces other changes to prepare the body to meet an emergency.
Agonist
A chemical or drug that mimics neurotransmitter activity.
Akinesia
Absence of body movements.
Alpha-Tocopherol
Chemical name for biologically active form of Vitamin E.
Amantadine
A drug which stimulates the release of available dopamine in the brain.
Anticholinergic
Adjective applied to a substance (medication) that reduces the action of acetylcholine.
Anticholinergic Parkinson’s Drugs (Artane, Cogentin)
The group of drugs which decreases the action of acetylcholine. The specified drugs may help reduce rigidity, tremor, and drooling in Parkinson’s.
Antihistamines
Drugs opposing the actions of histamine; commonly used to treat allergies. Used in the past for Parkinson’s as they sometimes had beneficial effects on symptoms due to their anticholinergic properties.
Apomorphine
A derivative of morphine and a dopamine agonist. Currently experimentally used as injectable treatment for severe Parkinson’s.
Ataxia
Loss of balance
Athetosis
Dyskinesias in which there are slow, repetitive, sinuous involuntary movements.
Autonomic Nervous System
The branch of the nervous system that controls internal organs in the body, e.g., heart, lungs.
Basal Ganglia or Nuclei
Deeper structures in the brain, concerned with normal movement and walking. The caudate nucleus, putamen and Substantia Nigra are basal ganglia affected in Parkinson’s.
Benign Essential Tremor
A condition characterised by tremor of the hands, head, voice, and sometimes other parts of the body. Essential tremor often runs in families and is sometimes called familial tremor. It is sometimes mistaken for a symptom of Parkinson’s. However, this is an action tremor and there is no rigidity or bradykinesia.
Beta-Blockers (ß-Blockers)
Drugs which block the action of epinephrine at certain sites. Usually used to treat hypertension and heart disease, they may be effective in the treatment of benign essential tremor.
Bilateral
Occurring on both sides of the body.
Blepharospasm
Spasmodic blinking or involuntary closing of the eye lids; a type of dystonia.
Bradykinesia
Slowing down of a movement. Bradykinesia involves slowness of initiating and executing movements and fine motor movements and difficulty in performing repetitive movements. It is a major symptom of Parkinson’s.
Carbidopa
The ingredient in Sinemet which prevents the breakdown of the levodopa in the body before it can reach the brain.
Central Nervous System (CNS)
Consists of the brain and spinal cord.
Cerebellum
Part of the brain that is involved in coordination.
Cerebral Cortex
The largest part of the brain; responsible for thought, reasoning, memory, sensation, voluntary movement.
Choline
A naturally occurring substance which is a precursor of acetylcholine.
Chorea
A type of dyskinesia (abnormal movement), characterised by continuing, rapid, dance-like movements. May result from high doses of levodopa and/or long term levodopa therapy.
Choreoathetosis
A dyskinesia characterised by choreic and athetoid movements.
Cogwheel Rigidity
Stiffness in the muscles, with a jerky quality when arm and leg joints are repeatedly moved.
Constipation
Diminished ability of intestinal muscles to move feces (stool), often resulting in very hard stool. A common problem in Parkinson’s.
Deprenyl
(Eldepryl, Selegiline, Jumex) A drug that slows the breakdown of chemicals like dopamine by inhibiting the action of certain enzymes. It increases effects of dopamine in the brain.
Dopa Decarboxylase Inhibitors
Drugs that block the conversion of levodopa to dopamine outside the brain.These include carbidopa and benserazide.
Dopamine
A chemical produced by the brain; it assists in the effective transmission of electrochemical messages from one nerve cell to the next. It is deficient in the basal ganglia and Substantia Nigra of a person with Parkinson’s. It governs actions of movement, balance and walking.
Dopamine Agonist
Drugs that mimic the effects of dopamine and stimulate the dopamine receptors.
Dopaminergic
An adjective used to describe a chemical, a drug, or a drug effect related to dopamine.
Drug Holiday
A 3 to 14 day withdrawal of a drug after long term treatment.
Drug Induced Parkinsonism
Parkinson’s symptoms which have been caused by drugs used to treat other conditions, e.g., neuroleptic drugs, and reserpine, used to be used to treat hypertension.
Dysarthria
Speech difficulties caused when the muscles associated with speech are affected.
Dyskinesia
Abnormal movement of voluntary muscles. Dystonia, athetosis, and chorea are types of dyskinesia.
Dysphagia
Difficulty in swallowing.
Dystonia
Involuntary spasms of muscle contraction that cause abnormal movements and postures. May appear as a side effect of long term drug treatment in Parkinson’s and may worsen in response to stress.
Encephalitis
Inflammation of the brain usually caused by a virus infection.
Encephalitis Lethargica
(Sleeping Sickness) A specific kind of encephalitis which occurred in scattered epidemics throughout the world during the period 1916 to 1926; it usually caused sleepiness, double vision, trouble swallowing, and drooling. Many of those affected developed advanced Parkinsonism as depicted in the movie Awakenings.
Ethopropazine
(Parsidol/Parsitan) A drug sometimes used in the past for Parkinson’s due to its anticholinergic effects.
Extrapyramidal Nervous System
Refers to the caudate, putamen, and Substantia Nigra. It is affected in Parkinson’s.
Festination
Walking in rapid, short, shuffling steps.
Flexion
A bent, curved posture.
Freezing
Temporary, involuntary inability to move
Glaucoma
A sustained increase of pressure within the eyeball which can injure the optic nerve and cause impaired vision or blindness. Treatment with anticholinergics may exacerbate glaucoma.
Globus pallidus
The inner part of the lenticular nucleus. The lenticular nucleus and the caudate nucleus form the Striatum.
Heimlich Maneuver
A form of first aid for people who are choking.
Hypokinesia
Abnormally diminished motor activity.
Idiopathic
An adjective meaning “of unknown cause”. The usual form of Parkinson’s is idiopathic Parkinson’s.
Intention Tremor
One occurring when the person’s attempts voluntary movement.
Lenticular nucleus
This group of cells along with the caudate nucleus form the Striatum or Corpus Striatum.
Levodopa
The international generic name for the medicinal formulation of L-Dopa. It is contained in Sinemet and Prolopa.
Levodopa-Induced Dyskinesias
A side effect of medication which may occur with prolonged use. These abnormal, involuntary movements may be alleviated by reducing the amount of medication.
Lewy Body
Pink, staining spheres on damaged brain cells; markers for Parkinson’s.
Livido Reticularis
A purplish or bluish mottling of the skin seen usually below the knee and sometimes on the forearm in persons under treatment with the drug amantadine (Symmetrel).
Micrographia
The tendency to have very small handwriting due to difficulty with fine motor movements in Parkinson’s.
MPTP
A toxic chemical, exposure to which can lead to Parkinson’s.
Myoclonus
Jerking, involuntary movement of arms and legs, usually occurring during sleep.
Neostriatum
Vital part of the brain comprised of two basal ganglia (caudate and putamen).
Neuroleptic Drugs
(Also called major tranquilizers) A class of drugs which act as dopamine antagonists (by blocking some dopamine receptors). They can aggravate symptoms of Parkinson’s. This class includes Haloperidol (Haldol), and the phenothiazines, e.g., Compazine, Stelazine, Chlorpromazine, etc.
Neuron
A nerve cell.
Neurotransmitter
A specialized chemical produced in nerve cells that permits the transmission of information between nerve cells.
Nigrostriatal Degeneration
Degeneration of the nerve pathways from Substantia Nigra to the striatum. These pathways are normally rich in dopamine and are those affected in PD.
Norepinephrine (Noradrenalin)
Chemical transmitter found mainly in two areas of the brain involved in governing the involuntary autonomic nervous system.
On-Off Fluctuations
Fluctuations that occur in response to levodopa therapy in which the person’s mobility changes suddenly and unpredictably from a good response (on) to a poor response (off).
Orthostatic Hypotension
A drop in blood pressure during rapid changes in body position (e.g., from sitting to standing).
Palilalia
A symptom of Parkinsonism, especially the postencephalitic form, in which a word or syllable is repeated and the flow of speech is interrupted.
Pallidectomy
Excision or destruction of the Globus Pallidus, which is part of the Lenticular Nucleus, which is part of the Striatum.
Paresthesia
Sensations, usually unpleasant, arising spontaneously in a limb or other part of the body, variously experienced as “pins and needles” or a feeling of warmth or coldness (thermal paresthesias).
Parkinson’s Disease
That form of Parkinsonism originally described by James Parkinson as a chronic, slowly progressive disease of the nervous system characterized clinically by the combination of tremor, rigidity, bradykinesia, and stooped posture, and pathologically by loss of the pigmented nerve cells of the Substantia Nigra in the brain.
Parkinson’s Facies
A stolid masklike expression of the face, with infrequent blinking; it is characteristic of Parkinson’s.
Parkinsonism
A clinical state characterised by tremor, rigidity, bradykinesia, stooped posture, and shuffling gait. The more common causes of Parkinsonism are Parkinson’s Disease, striatonigral degeneration, and a reversible syndrome induced by ma jor tranquillizing drugs.
Paralysis agitans
The Latin form of the older, popular term shaking palsy, which was used to designate Parkinson’s in James Parkinson’s time.
Parlodel (Bromocriptine)
A dopamine agonist useful in treating all of the primary symptoms of Parkinson’s. It may be used alone or with other antiparkinson medications.
Permax (Pergolide)
A drug similar in action to Parlodel but more potent.
Postural Deformity
Stooped posture.
Postural Instability
Difficulty with balance.
Postural Tremor
Tremor that increases when hands are stretched out in front.
Precursor
Something that precedes, e.g., a sign or symptom that forewarns of another, such as muscle aching may be the precursor of a tremor.
Progressive Supranuclear Palsy (PSP)
A degenerative brain disorder sometimes difficult to distinguish from Parkinson’s especially in the early stages. PSP symptoms are rigidity and akinesia, difficulty looking up and down, speech and balance problems. Those with PSP often have poor response to antiparkinson medications.
Prolopa
Trade name for the antiparkinson drug composed of levodopa and benserazide. This drug combination contains a ratio of 4 mg. of levodopa to 1 mg. of benserazide (Prolopa 50-12.5, 100-25, 200-50).
Propulsive Gait
Disturbance of gait typical of Parkinsonism in which, during walking, steps become faster and faster with progressively shorter steps that pass from a walking to a running pace and may precipitate falling forward.
Range of Motion
The extent that a joint will move from being fully straightened to completely bent.
Receptor
A sensory nerve ending that responds to a stimulus.
Resting Tremor
Shaking that occurs in a relaxed and supported limb.
Retropulsive Gait
Walking that is propelled backwards.
Rigidity
Refers in medical usage to a type of muscular stiffness encountered when examining people with Parkinson’s. It is characterized by a constant, even resistance to passive manipulation of the limbs.
Seborrhea
Increased discharge of the oily secretion sebum from the sebaceous glands of the skin.
Seborrheic Dermatitis
Inflammation of the skin sometimes associated with seborrhea.
Shaking Palsy
Old popular term which James Parkinson employed to designate the specific disorder we now call Parkinson’s.
Shy-Drager Syndrome
This is a condition in which the symptoms are the result of abnormalities in motor function and problems in the autonomic nervous system. A person with Shy-Drager Syndrome has Parkinsonism, extremely low blood pressure which worsens upon standing, bladder problems, severe constipation, and decreased sweating. This condition is quite rare.
Sialorrhea
Drooling of saliva.
Side Effect
A drug’s effect that is different from the beneficial effect for which the drug is being taken.
Sinemet
Trade name for the antiparkinson drug that is a mixture of levodopa and carbidopa. This drug combination contains a ratio of levodopa 4 mg. or 10 mg. to carbidopa 1 mg. (Sinemet 100/25, Sinemet 250/25).
Sinemet CR
Controlled-release Sinemet. 200 mg. Levodopa with 50 mg. Carbidopa in a capsule contained in a matrix (outer layer) releasing the drug more slowly in the body. These capsules are not to be taken all at once, but rather in separate doses over the course of a day.
Stereotactic Surgery
Surgical technique that involves placing a small electrode in an area of the brain to destroy a tiny amount of brain tissue.
Striatonigral Degeneration
This is a degeneration of the nerve pathways travelling from the striatum to the Substantia Nigra. People with this degeneration also appear to have Parkinsonism. However, they respond differently to drug therapy than people with Parkinson’s.
Striatum
Area of brain controlling movement, balance, and walking. Connects to and receives impulses from Substantia Nigra.
Substantia Nigra
Black pigmented area of the midbrain where cells manufacture the neurotransmitter dopamine.
Sustention or Postural Tremor
Tremor that increases when hands are stretched out in front.
Symmetrel (Amantadine)
A drug that releases dopamine and is useful in PD.
Tardive Dyskinesia
This is a movement disorder associated with long-term use of neuroleptic drugs such as Chlorpromazine, Haloperidol, Loxapine, etc. Movements of a person with tardive dyskinesia are similar in appearance to those of a person with levodopa induced dyskinesias, but the causes of the two conditions are different.
Thalamotomy
Operation in which a small region of the thalamus is destroyed, achieved by stereotactic techniques. Tremor and rigidity in Parkinsonism and other conditions may be relieved by thalamotomy.
Thalamus
Anatomical term designating a mass of grey matter centrally placed deep in the brain near its base and serving as a major relay station for impulses travelling from the spinal cord and cerebellum to the cerebral cortex.
Toxin
A poisonous substance.
Tremor
Rhythmic shaking and involuntary movement of part(s) of the body as a result of sequential muscle contractions.
Unilateral
Occurring on one side of the body. Parkinson’s symptoms usually begin unilaterally.
Vomiting Center
Term referring to an area of the brain where the nausea and vomiting reflex may be triggered by some medications.
“Wearing Off” Phenomenon
Waning of the effect of the last dose of levodopa, associated with abrupt reduction or loss of mobility.
Modified from the glossary published by The Parkinson’s Society of Southern Alberta
Special thanks to Simon J. Coles
