Movement Disorders

From WiserWiki

[edit] Movement Disorders

Nagagopal Venna

This chapter is devoted to disorders characterized by excessive abnormal involuntary movements (Box 163-1). Parkinson's disease and related conditions are discussed elsewhere. Recent advances in molecular genetics, neuropharmacology, and stereotactic neurosurgery have invigorated this long-neglected area of neurology, as evidenced by the emergence of movement disorder clinics worldwide. The biologic substrate of the various hyperkinetic movement disorders is not well understood. Current evidence suggests that perturbations in the complex neural networks of the basal ganglia, subthalamic nuclei, inferior olivary nuclei of the medulla, and dentate nuclei of the cerebellum, driven by neurochemical imbalances, underlie these disorders, which are illustrated in video demonstration on the CD-rom published with this edition.

[edit] TREMORS

Tremors are rhythmic, involuntary oscillations of body parts caused by abnormal synchronous or alternating contractions of antagonistic muscles. They are common manifestations of many neurologic and systemic diseases (Box 163-2).^[1] Tremors can be focal or multifocal and usually affect the hands, head, lips, jaw, and tongue but only infrequently involve the legs and trunk. They may occur at rest or only on maintaining certain postures or with certain voluntary movements and cease during sleep. Tremors are sources of social embarrassment and occasionally are incapacitating. Their clinical characteristics and other abnormalities accompanying them, such as rigidity or ataxia, help determine the nature and etiology of the tremor.

[edit] Enhanced Physiologic Tremor

The normal oscillations of voluntarily moving body parts cause a fine 8 to 12 Hz tremor, becoming clinically noticeable when exaggerated by toxic and metabolic causes and drug and alcohol withdrawal states (Box 163-3). The tremor is brought on by holding the arms outstretched with fingers extended and stops when limbs are at rest. The tremor has small amplitude and is most prominent in the fingers. A history of drug and alcohol use, a review of current medications, and, in the appropriate clinical context, laboratory tests for hyperthyroidism, hypoglycemia, and pheochromocytoma help in determining the etiology. Drug and alcohol withdrawal tremors are transient. Toxic tremors usually resolve after decreasing or stopping the drug, although they may be persistent in the case of lithium and amiodarone. Anxiety-related tremors in musicians and other performers may be suppressed by propranolol, 20 to 40 mg taken 1½ hours before a performance. Similarly, tremor of thyrotoxicosis is lessened by propranolol as antithyroid drugs take hold.

[edit] Essential Tremor

A community-based study from Canada showed prevalence of 14% for essential tremor (ET) in persons over the age of 65 years compared with a rate of 3% for Parkinson's disease. Onset peaks in the second and fifth decades, and in about 30% of patients it is inherited as an autosomal dominant trait. The etiology of ET is unknown. Brain imaging and pathologic studies are normal, but positron emission tomography (PET) studies reveal hypermetabolism in the cerebellum, red nuclei, and thalamic and inferior olivary nuclei. These studies, and tremor suppression by thalamic stimulation, suggest a putative deep-brain pacemaker for the generation of the tremor. Tremor appears in the fingers and hands while holding a posture or with other voluntary movements. Using utensils or drinking from a cup brings on the tremor, and writing becomes distorted. Tremor may spread to the head as a side-to-side nod and to the jaw, tongue, and voice, but lower limbs are rarely affected. When arms are held outstretched, adduction and abduction, flexion and extension of fingers, and less often, pronation and supination of forearm emerge. A writing sample and copy of a spiral are an easy way of monitoring the tremor. In contrast to Parkinson's disease, there is no rigidity, bradykinesia, or postural instability. In some, the tremor is markedly decreased by even small amounts of alcohol. The diagnosis of ET is clinical, and neuroimaging is not indicated. ET as a risk factor for Parkinson's disease remains unproven although they often coexist.

Reassurance that the tremor is not caused by Parkinson's disease often suffices for patients with mild tremor. When it interferes with social, occupational, recreational, or day-to-day activities, moderately effective treatment is available (Box 163-4).^[2] Over 25 randomized, placebo-controlled studies have established propranolol as the most effective treatment to decrease the amplitude of the tremor of the hands and tongue in about 50% to 60% of the patients. From 20 to 40 mg of propranolol 1½ hours before a social gathering, professional meeting, or public performance may be adequate in some cases. For continuous suppression, propranolol, titrated from 60 mg up to 320 mg/day, either in single dose of the long-acting preparation or in three divided doses, is recommended. Tolerance does not develop in long-term use. Metoprolol and nadolol have been shown to be effective in one controlled study each. They are indicated when propranolol is effective but not tolerated because of adverse side effects or asthma. Metoprolol, 100 to 200 mg/day in divided doses, is relatively safe despite bronchospasm. Nadolol has the advantage of once-a-day dosing at 120 to 240 mg. Incidentally, atenolol is ineffective and pindolol may worsen ET. After a serendipitous observation in a patient with epilepsy and ET, long-term efficacy of primidone, a barbiturate antiseizure drug, has been confirmed in several controlled trials and is similar in magnitude to propranolol. It is started at a dosage of 25 mg at bedtime and increased gradually up to 250 to 750 mg/day in three doses to minimize early drowsiness and ataxia. Severe ET may need combinations of primidone and propranolol. An uncontrolled study demonstrated marked benefit from clonazepam in a subset of ET predominantly seen with goal-directed movement (kinetic tremor). In one placebo-controlled study, alprazolam improved ET in 24 patients at doses of 0.75 mg to 2.75 mg/day. One well-designed study showed no benefit from gabapentin. A good short-term study showed that theophylline was as effective as propranolol. A recent double-blind study confirmed modest reduction of ET of the hand with minor finger weakness after forearm intramuscular injection of botulinum toxin. The benefit lasted up to 12 weeks after each injection. Another study of botulinum injections in 43 patients showed benefit in head tremor, a component of ET less responsive to propranolol. Several small series have demonstrated significant amelioration of contralateral hand tremor and improvement in disability with a recently FDA-approved treatment by stereotactically implanted electrical stimulator in the thalamus, comparable to the benefit in Parkinson's disease tremor, in selected incapacitating cases.

[edit] CHOREA AND CHOREOATHETOSIS

Chorea and choreoathetosis are involuntary movements caused by dysfunction of the networks of the caudate nuclei and putamen, resulting in excessive dopaminergic and decreased inhibitory γ-aminobutyric acid (GABA) neurotransmitter function. Many brain diseases, as well as systemic and toxic factors, can induce choreoathetosis (Box 163-5).^[3] In chorea, movements are quick, brief, nonrhythmic, and usually affect the proximal parts of the limbs, although the head, neck, and trunk may also be involved. Movements are often incorporated into voluntary activity to mask them, as in brushing the hair when the arm jerks. Axial chorea causes lurching gait. Limbs may be hypotonic, with pendular tendon reflexes best seen at the knees. Voluntary movements, although strong, may be unsustained. When a patient grips the examiner's fingers, intermittent give in the grip feels like milking movements (“milk maid grip”). Athetosis causes slow, writhing, twisting movements, most evident in hands and feet, although the trunk can be affected. Frequently there is a mixture of chorea and athetosis (choreoathetosis). Like most hyperkinetic movements, these are increased by anxiety, fatigue, and stress, decreased by relaxation, and cease in sleep.

[edit] Drug-induced Choreoathetosis

Many drugs induce reversible choreoathetosis (Box 163-6).^[4] A few drugs cause chorea regularly, whereas with most it is a rare side affect. Levodopa is a common cause of choreoathetosis when used to treat advanced Parkinson's disease, and cocaine is an under-recognized cause of chorea (“crack dance”). With some drugs there is an underlying individual susceptibility for chorea. Oral contraceptive drugs cause chorea, particularly in women with a history of rheumatic fever, chorea gravidarum, systemic lupus erythematosus (SLE), and the antiphospholipid antibody syndrome. Phenytoin brings out choreoathetosis in persons with cerebral palsy.

[edit] Chorea Caused by Systemic Disease

Choreoathetosis is the most frequent movement disorder in systemic diseases (Box 163-7).^[3] About 4% of patients with SLE develop chorea in the course of known disease or as a presenting symptom. The abnormal movements may last a few days to as long as 3 years and may remit and relapse, with relapses usually coinciding with systemic flare-up of SLE. Magnetic resonance imaging (MRI) scans of the brain may be normal or show nonspecific change. Some patients with SLE and chorea have antiphospholipid antibodies and are at risk for arterial and venous thrombosis, including cerebral infarction. Microvasculopathy or antineuronal cytotoxic autoantibodies are proposed pathogenic mechanisms. Treatment is with prednisone for lupus activity and haloperidol for chorea. Chorea is a feature of the recently recognized primary antiphospholipid antibody syndrome, especially with use of oral contraceptives or pregnancy. Thyrotoxicosis presenting with chorea in young women has long been recognized and may remit and relapse with the hyperthyroidism and responds to dopamine-blocking haloperidol. Excess exogenous thyroxine can provoke chorea. Paroxysmal unilateral or generalized choreoathetosis has been reported with idiopathic hypoparathyroidism and is reversed by correcting the hypocalcemia. Polycythemia vera is a well-documented cause of buccolingual and limb choreoathetosis, principally in women over the age of 50 years. The chorea may last weeks to years and fluctuate, with no clear relations to hematocrit level, although treatment of the polycythemia does ameliorate the chorea. Chorea caused by rheumatic fever (Sydenham's chorea) is still prevalent outside the United States and Western Europe. Generalized chorea develops in about 20% of children with rheumatic fever, often as a presenting symptom and mostly in girls. Encephalopathy with emotional lability is a common accompaniment. In 75% of the patients the movements remit spontaneously in about 6 months, but about 20% have recurrences. Oral contraceptives and pregnancy may induce relapse even several years after the rheumatic fever. MRI scans may show reversible abnormalities in the caudate, putamen, and globus pallidus. The chorea is probably caused by autoantibodies provoked by the streptococcal infection cross reacting with caudate neurons. Haloperidol and valproic acid help control the chorea as natural remission occurs over several months. Diabetic nonketotic hyperglycemia is recently recognized as a cause of acute hemibody chorea, sometimes with hemiballismus, in women over the age of 50. MRI scans show abnormalities in the contralateral striatum consistent with petechial hemorrhages or demyelination. The chorea stops in a few days to a month with correction of metabolic derangement and a short course of haloperidol or diazepam.

[edit] Paroxysmal Choreoathetosis

Paroxysmal choreoathetosis is a rare episodic disorder that has been better delineated in recent years. In this disorder, bursts of generalized chorea/dystonia lasting minutes, hours, or a few days occur spontaneously or are triggered by sudden or sustained voluntary movements. Most cases are idiopathic or familial but it can be caused by multiple sclerosis, stroke, brain trauma, or encephalitis. Affected persons are often misdiagnosed as psychogenic. Carbamazepine, phenytoin, clonazepam, and acetazolamide reduce the paroxysms in some cases.

[edit] Hemiballismus

Hemiballismus is a dramatic syndrome that usually appears in elderly patients with hypertension and diabetes mellitus as a result of small infarctions or hemorrhages in or around the subthalamic nucleus. Metastases and toxoplasmosis in AIDS are occasional causes. Violent flinging of the limbs on one side, accompanied by continuous hemibody choreoathetosis, appears abruptly. Injuries may occur as the limbs strike surroundings or because of falls. The MRI may show the lesions in the contralateral basal ganglia or subthalamic nucleus. Frail elderly patients become exhausted by the incessant hyperactivity, which abates only in sleep. Stroke-related hemiballismus gradually subsides within a few weeks to a few months. Dopamine-blocking haloperidol and GABA-ergic clonazepam ameliorate the movements in most cases and can be synergistic. Valproic acid and progabide, both GABA-ergic drugs, may also be helpful. The rare refractory hemiballismus cases may benefit from stereotactic pallidotomy.

[edit] Huntington's Chorea

Huntington's chorea is an autosomal dominant neurologic disease caused by mutation of a gene on chromosome 4 with expansion to above 40 CAG triplets coding for glutamine. By unknown mechanisms, this causes a progressive loss of GABA-ergic and substance P interneurons of the striatum. A combination of involuntary movements and neuropsychiatric changes appears insidiously and worsens steadily. Onset is in the fourth and fifth decades, with an incidence of 2 to 7/100,000. Chorea of the face, tongue, head and neck, trunk, and limbs is the dominant symptom, accompanied by lurching gait and early impairment of voluntary eye saccades. Irritability, paranoia, and antisocial behavior are common and occur early, followed by cognitive deterioration. Depression and suicide are prevalent. Rigidity and bradykinesia eventually supervene. Diagnosis is based on the clinical picture and family history and is supported on MRI scans by selective atrophy of the heads of caudate nuclei and confirmed by DNA testing. Unfortunately there is no specific treatment. Chorea, when functionally disabling, can be improved by dopamine blockers such as haloperidol, low-dose dopamine agonist bromocriptine, or benzodiazepines such as clonazepam. Depression and the commonly observed obsessive-compulsive behaviors may respond to serotoninergic drugs such as fluoxetine.

[edit] TARDIVE DYSKINESIA

Tardive dyskinesia (TD) has emerged as a common hyperkinetic syndrome with the widespread use of antipsychotic dopamine-blocking drugs (Box 163-8).^[5] Most patients with TD have schizophrenia but it can develop in patients with depression or anxiety. Approximately 20% of patients on chronic treatment with antipsychotic drugs develop TD, but prevalence is as high as 36% in institutionalized patients. Risk factors for TD are age over 40 years, high dose, early occurrence of drug-induced Parkinson's disease, and female gender. Routine chronic use of anticholinergic drugs to offset drug-induced parkinsonism and diabetes mellitus are other predisposing factors.

Clinical experience shows that TD is rare with the new atypical antipsychotic drugs such as clozapine, although long-term observation is needed to confirm this. TD is increasingly reported with chronic use of drugs to treat nausea, gastroesophageal reflux, and gastroparesis of diabetes. Certain calcium channel blockers with dopamine agonist properties are also implicated. Drugs with high incidence of TD block the D2 receptors almost exclusively, whereas the new atypical antipsychotics cause more equal D2 and D1 receptor blockade, suggesting the possible pathogenesis.

Restless protrusions and twisting movements of the tongue, smacking and puckering of lips, and chewing movements appear insidiously and progress to increased blinking and blepharospasm. Movements become continuous and stereotyped. Hyperkinesia spreads to limbs, causing abrupt jerky movements, piano-playing hand movements, and foot tapping. Pelvic thrusts and grinding movements may appear. Some patients develop breathing dyskinesias that cause grunting, sighing, irregular noisy breaths, shortness of breath, and even respiratory alkalosis. Persistent TD can cause abrasions of the lips and tongue; truncal dyskinesia can cause sacral ulcers and exhaustion. Diagnosis is clinical in the context of chronic antipsychotic drug treatment. In persons not currently on these drugs, careful inquiry into recent or remote exposure should be made. In patients without psychiatric history, exposure to drugs such as metoclopramide should be sought. In the absence of such drug exposure, other causes of choreoathetosis, such as Huntington's disease, need to be considered. If the neuroleptics are continued, TD is likely to persist indefinitely, or worsen, but may rarely improve (17%). When the drug is stopped, however, most patients get better in the long term, despite a temporary increase in the dyskinesia. Remission of TD may occur in 30% to 60% of patients by 5 years, but in some TD has been permanent. The smallest effective dosage for the shortest possible time and periodic reevaluation of the need to continue the drugs are prudent. If TD does emerge, decreasing the dose or discontinuation of drug should be considered whenever feasible. For patients with moderate to severe disability, switching to clozapine—the atypical antipsychotic—has been effective both for the psychosis and for TD, based on several large series and several case reports, in doses of 200 mg/day to 900 mg/day (Box 163-9).

[edit] DYSTONIA

Dystonia is the least common but the most disabling of the hyperkinetic movement disorders. It is defined by twisting involuntary movements and abnormal postures. The biologic substrate of most forms of dystonia is poorly understood, but hypofunction of the medial globus pallidus and thalamus appears to be a common theme. Major advances in molecular genetics and neurochemistry, highlighted by the recent discovery of l-dopa–responsive dystonia, new therapies with botulinum toxin, and deep brain stimulation are driving the resurgence of interest in these disorders.

[edit] Acute Dystonic Reaction

Acute dystonic reaction is an alarming syndrome that is commonly seen in psychiatric practice and affects 2% to 12% of patients taking neuroleptics. Less well recognized is its occurrence with drugs used to treat nausea and migraine (Box 163-10). Acute blockade of dopamine receptors (D2 type) and relative hyperactivity in the cholinergic environment of the basal ganglia appear to mediate the abnormal movements. The greatest risk of this reaction is with high doses of high-potency neuroleptics. Young age, male gender, previous reactions, cocaine addiction, and dementia related to acquired immunodeficiency syndrome (AIDS) are other risk factors. In over 90% of cases dystonia occurs within 5 days. With sumatriptan, used for migraine, it may appear within 3 to 6 hours.

The movements are acute, dramatic, and often bizarre and are likely to be mistaken for hysterical behavior. Blepharospasm, forced eye deviation (oculogyric crisis), torticollis or retrocollis, trismus, slurred speech, and even opisthotonus may occur. Rarely, laryngeal and pharyngeal spasms may cause difficulty with breathing. Anxiety is a common accompaniment. Even though the dystonia is self limited, it can recur for several days after withdrawal of the causative drug. Treatment with anticholinergic medications such as benztropine or diphenhydramine or with a benzodiazepine such as lorazepam quickly arrests the dystonia (Box 163-11). The treatment should be continued orally for several days to prevent recurrences. Exceptionally, laryngeal/pharyngeal dystonia requires repeated intravenous medications, close monitoring of breathing, and, rarely, tracheal intubation. Subsequently, decrease of the dose of the drug or replacement with a lower-potency neuroleptic is needed.

[edit] Generalized Chronic Dystonia

The striking clinical syndromes of generalized chronic dystonia (Box 163-12) present with contortions of the limbs, head, neck, and trunk and disintegration of voluntary movements by the dystonia. Many begin in the limbs and eventually become generalized. Despite grossly normal strength and sensation the patients often eventually become chair or bedbound, with difficulty in speech and swallowing. In Rochester, Minnesota, the incidence is estimated to be 2 per million per year.

[edit] Drug-induced Chronic Tardive Dystonia

Chronic treatment with commonly used dopamine receptor-blocking neuroleptic drugs can result in a generalized dystonia with opisthotonus, retrocollis, and oromandibular dystonia. Despite discontinuation of the drugs, movements persist for a long time. This disorder is about one tenth as common as TD and tends to affect young adults in particular. The clinical picture may be readily mistaken for primary generalized dystonias. Treatment consists of decreasing the dose or discontinuing the neuroleptic drug whenever feasible and treating the residual dystonia symptomatically (Box 163-13). Clozapine, the new antipsychotic drug, may also alleviate TD.

Generalized dystonia is common in congenital encephalopathy caused by perinatal trauma, or cerebral palsy. Dystonia appears in early childhood and may worsen over the years. History of difficult birth, floppy baby syndrome, or delayed developmental milestones indicates the diagnosis. The treatment is symptomatic. Primary generalized dystonias, whether sporadic or inherited, have a similar clinical picture. The vast majority of these belong to Oppenheim type DYT-1, an autosomal dominantly inherited dystonia (dystonia musculorum deformans) prevalent in Ashkenazi Jews. Recent studies have identified the abnormal gene on chromosome 9 and the gene product as torsin-A, similar to heat shock proteins and proteases. The mechanism by which the gene lesion causes dystonia is not known. Dystonia frequently begins in the legs and becomes generalized over a few years. Intelligence is unaffected. The disease can be identified by family history and confirmed by DNA testing. No specific treatment is available but significant advances have occurred in the symptomatic treatment (Box 163-13).

[edit] l-Dopa Responsive Dystonia (Segawa Disease, DYT-5)

The identification of a generalized dystonia relieved by l-dopa has been the most dramatic recent discovery in the field of dystonia. Symptoms appear in childhood with toe walking, foot and leg dystonia, and disturbed gait, and slowly spread to the upper limbs and trunk. Bradykinesia and rigidity are often superimposed. The lower limb dystonia may be nearly absent in the morning but be severe in the evening and with exercise. Many are misdiagnosed as having static cerebral palsy. The condition is inherited as an autosomal dominant trait caused by a mutant gene on chromosome 14 encoding an enzyme needed for the synthesis of biopterin, a cofactor for tyrosine hydroxylase required for dopamine synthesis. The result is severe deficiency of dopamine in the striatum. Striking reversal of the dystonia by l-dopa is a defining feature.^[6] Because of atypical presentations, a therapeutic trial of l-dopa is worthwhile in any dystonia of uncertain etiology.

[edit] Chronic Focal Dystonia

[edit] Torticollis (Cervical Dystonia).

Torticollis is the most common focal dystonia of adults, with an incidence of about 24/1 million/year as estimated in Rochester, Minnesota. Most cases are idiopathic and monosymptomatic, with a presumed neurophysiologic perturbation in the basal ganglia and upper brainstem. It typically begins as intermittent torticollis between 30 and 50 years of age and slowly becomes continuous. Only about 10% of patients have remissions, but relapse is the rule. Forceful rotation of the neck to one side is the chief symptom. Characteristically, this is temporarily relieved by sensory tricks such as supporting the back of the head on a wall, touching the chin, or lying down. Dystonia ceases in sleep and worsens with stress. After years of dystonia, cervical spondylosis and radiculopathy may develop, with neck and arm pain. Rarely, hypertrophy of the trapezius can cause thoracic outlet neurovascular compression. Lateral bending and retrocollis are less common. Diagnosis is clinical, and brain imaging is normal. Initially, drug-induced and other symptomatic dystonias should be considered. Rarely, pseudotorticollis occurs because of structural disorders of the neck (Box 163-14).

Before botulinum toxin treatment, high doses of anticholinergic drugs were the mainstay of treatment for torticollis and were unsatisfactory. The symptomatic treatment of torticollis has been dramatically improved with the use of botulinum toxin injections into the dystonic muscles and is now the treatment of choice except in the mildest cases.^[7] The toxin acts on the intramuscular nerve ending, causing presynaptic blockade of acetylcholine release (chemical denervation). Numerous open-label and double-blind controlled trials have established the efficacy and safety of botulinum toxin for cervical dystonia. About 80% of patients experience major relief lasting about 3 months, but repeated injections over many years continue to provide benefit. In the few patients not responding to botulinum, selective peripheral surgical denervation can be helpful by sectioning the spinal accessory nerve branch to the sternomastoid muscle. Support through dystonia organizations is also very helpful in coping with such a chronic and disfiguring condition (website www.wemove.org).

[edit] COMPLEX HYPERKINETIC MOVEMENT DISORDERS

[edit] Wilson's Disease

Many varieties of abnormal movements occur in Wilson's disease, singly in the beginning and in complex combinations later. It should be considered in the diagnosis of any movement disorder of uncertain cause (Box 163-15). This rare but global autosomal recessive genetic disease is caused by heterogeneous mutations of a gene on chromosome 13. Copper deposition is most dense in the putamen, but many other basal ganglia and the cerebellum are affected by copper-induced neuronal destruction years after copper overload of the liver.

Neurologic symptoms begin in childhood to about age 50, with or without overt liver disease. Combinations of chorea, dyskinesia, dystonia, and tremor occur, along with bradykinesia and rigidity. Dystonia of face and bulbar muscles is early, with distortion of facial expression, dysarthria, and drooling. A proximal, postural tremor of the arms (”wing-beating“ tremor) is characteristic. Neuropsychiatric symptoms range from subtle alteration, with irritability and impaired social judgment, to aggressive behavior and cognitive decline. Syndromes resembling manic-depression and schizophrenia may be seen. Over 90% of cases of Wilson's disease with neurologic abnormalities have diagnostically critical Kayser-Fleischer rings. In about 40% of cases they are grossly visible as golden brown rings around the corneal limbus, but slit-lamp examination is the most sensitive method of detection. MRI scans show nonspecific abnormal signals in the putamen, caudate, and white matter. Diagnosis is confirmed by a battery of tests of copper metabolism, with a serum ceruloplasmin level of less than 20 mg/dl, free serum copper of more than 8 μmol/L, and liver copper of over 250 μg/g of dry weight.

Treatment early in the course of neurologic symptoms can reverse brain dysfunction in 20% of cases and produce marked improvements in about 60% (Box 163-16).^[8] Early diagnosis is critical to preserve and restore brain function. Treatment is best done by specialists in this disease because of its rarity and complexity. In several cases of advanced disease, liver transplantation produced sustained dramatic improvement of cerebral function.

[edit] REFERENCES

[edit] RESOURCES

• Patient support group website www.wemove.org

[edit] Tremors

• The International Tremor Foundation, 833 West Washington Blvd., Chicago, IL 06607, 312-733-1893.

[edit] Tardive Dyskinesia

• Tardive Dyskinesia/Tardive Dystonia National Association, PO Box 45732, Seattle, WA 45732, 206-522-3166, e-mail: Skaertd/tdna@aolnet.com

[edit] Huntington's Disease

• Huntington Disease Society of America, 158 W. 29th Street, 7th Floor, New York, NY 10001, 800-345-4372, Website: http://hdsa.mgh.harvard.edu

[edit] Dystonia

• Dystonia Medical Research Foundation, 1 E. Wacher Drive, Suite 2430, Chicago, IL 60601-1905, 800-377-3978, Website: http://www.dystoniafoundation.org

[edit] Torticollis

• National Spasmodic Torticollis Association, PO Box 5849, Orange, CA 92863-5849, 800-487-8385, Website: http://www.blueheronweb.com.nsta/NSTA/htm

[edit] Wilson's Disease

• Wilson's Disease Association, 4 Navaho Drive, Brookfield, CT 0680, 800-399-0266, e-mail: Stork#2@aol.com

[edit] Physician Website

• www.movementdisorders.org