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Involuntary Movements 

Involuntary Movements
Chapter:
Involuntary Movements
Author(s):

Chizoba Umeh

DOI:
10.1093/med/9780190609917.003.0032
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A 69-year-old woman presents to the neurology clinic for evaluation of involuntary movements. She has a 19-year history of Parkinson’s disease (PD) and history of hypertension, hyperlipidemia, and peripheral arterial disease. She developed involuntary choreiform movements of the head, trunk, and limbs, gradually worsening over the past five years. The involuntary movements occur during 50% of her waking hours and result in fatigue. Her medications for PD include carbidopa/levodopa/entacapone, rasagiline, ropinirole, and amantadine.

On exam, she has a blood pressure of 130/58 and pulse of 77. She has decreased facial expression, reduced voice volume, and cogwheel rigidity in the upper extremities. Her gait is stooped and severely slowed with freezing steps. She has severe-intensity choreiform movements of the face, trunk, and legs.

What do you do now?

Levodopa-Induced Dyskinesia

The term chorea, stemming from the Greek word for dance (“choreia”) describes brief, irregular, non-rhythmic, flowing, involuntary movements. In a patient presenting with choreic movements, the differential diagnosis is broad and includes hereditary causes of chorea such as Huntington’s disease and Wilson’s disease, in addition to acquired causes (stroke, paraneoplastic, infectious, drug-induced). There is no family history in this case to support a hereditary etiology. The slow clinical course argues against an acute vascular etiology such as an infarct or hemorrhage. If focal neurological signs are present, MRI of the brain should be considered to rule out a lesion in the basal ganglia. Vascular causes of chorea can often result in contralateral hemichorea or hemiballismus as opposed to generalized chorea.

A brain MRI in this patient showed incidental finding of moderate white matter disease of the cerebral hemispheres and pons consistent with chronic microvascular ischemic disease.

If there is family history of chorea, genetic testing can be considered as part of the workup. In younger patients presenting with chorea, tremor, and psychiatric symptoms, serum copper/ceruloplasmin, liver function tests, and 24-hour urine copper may be obtained as initial evaluation for Wilson’s disease.

The patient’s history of neurodegenerative PD and chronic levodopa treatment is an important clue that the likely cause of the movement disorder is levodopa-induced involuntary choreic movements, also termed “dyskinesia.” Patients often report “peak dose dyskinesia” in the evening when the total daily levodopa dose accumulates and the dyskinesia may be the most severe.

It is important to note that not all Parkinson’s patients on levodopa therapy develop dyskinesia. Certain risk factors have been identified: younger age of onset of PD, greater disease severity, higher levodopa dose, and longer duration of levodopa treatment. For unclear reasons, women have been shown in some studies to be more likely to develop dyskinesia.

Patients can have varying severity of dyskinesia. The decision to treat the dyskinesia depends on the degree of disability to the patient. While some patients exhibit anosognosia, and are unaware of the dyskinesia, others have severe, disabling dyskinesia that may impact their coordination, gait, and quality of life.

For patients with troublesome dyskinesia, various treatments options are available. One approach is to decrease the likelihood of peak dose dyskinesia by lowering the per-dose amount of levodopa (i.e., reduce from 200 mg to 150 mg per dose) while increasing the number of times the levodopa therapy is taken daily (i.e., from three times daily to four times daily). Amantadine, an antiviral and antiparkinsonian agent, has shown efficacy in reducing dyskinesia. Intraduodenal levodopa directly delivers levodopa to the duodenum and jejunum and has been shown to reduce dyskinesia. Surgical treatment with placement of a deep brain stimulator in the subthalamic nucleus or globus pallidus interna is another approach to managing dyskinesia. This patient received a deep brain stimulator to the globus pallidus interna with reduction of the dyskinesia.

Once levodopa-induced dyskinesia develops, it generally remains present at varying frequency and severity, depending on the daily dose of levodopa and adjunctive treatments for PD.

Key Points to Remember

  • Choreiform involuntary movements, “dyskinesia,” are a manifestation of chronic levodopa treatment in PD.

  • Vascular causes such as infarct or hemorrhage should be excluded in patients with acute onset hemi-chorea.

  • Pharmacological or surgical treatment should be considered in PD patients with disabling dyskinesia.

References

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2.Thanvi B, Lo N, Robinson T. Levodopa-induced dyskinesia in Parkinson’s disease: clinical features, pathogenesis, prevention and treatment. Postgrad Med J. 2007;83:384–388.Find this resource:

3.Mazzucchi S, Frosini D, Bonuccelli U, Ceravolo R. Current treatment and future prospects of dopa-induced dyskinesias. Drugs Today (Barcelona). 2015;51:315–329.Find this resource:

4.Lundqvist C. Continuous levodopa for advanced Parkinson’s disease. Neuropsychiatric Dis Treat. 2007;3:335–3348.Find this resource: