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Movement disorders often complicate systemic illnesses. They occur in conjunction with metabolic encephalopathy, infection, neoplasms, and disorders of the endocrine, immune, and hematological systems. Movement disorders associated with systemic illness run the gamut from an exaggerated physiological tremor to hemiballismus, and also include the akinetic-rigid syndromes. In some cases, the movement disorder is what causes the patient to consult a physician. The underlying disorder may or may not be known at the time the movement disorder becomes obvious. In some cases, the pathophysiology of the systemic disorder causing the movement disorder is known. In some cases, there is a structural lesion in the brain responsible for the neurological problem. In other cases, there is no clear explanation for the movement disorder in the context of the systemic disease.




Endocrine abnormalities are commonly recognized causes of hyperkinetic movement disorders. Hyperthyroidism is associated with an exaggerated physiological tremor. Up to 97% of patients with hyperthyroidism will exhibit a tremor,1 the oscillatory frequency of which is the same as a physiological tremor, but the amplitude is greater. The hands are predominantly affected, although the feet, tongue, and eyelids can be affected as well. The pathophysiology is thought to be mediated by changes in peripheral β-adrenergic receptor tone. This theory is supported by the fact that β-blockers, including propranolol, will dampen the tremor. It is unclear whether there is a central generator for tremor. Positron emission tomography (PET) studies of patients with essential tremor reveal abnormal bilateral cerebellar, red nuclear, and thalamic activation.2 When thyrotoxicosis is the etiology of the tremor, the tremor is reversible by returning thyroid function to normal.


Chorea is a rare complication of hyperthyroidism, occurring in less than 2% of patients with thyrotoxicosis.1 The pathophysiology is not well understood, but the chorea is reversible with treatment of the hyperthyroidism.1,35 Baba and colleagues described a young woman with unilateral chorea and thyrotoxicosis with normal computed tomography (CT), magnetic resonance imaging (MRI), and single-photon emission CT (SPECT) scans.3 Autopsy studies of patients with hyperthyroid chorea reveal no pathological lesion within the basal ganglia.1,6 Measurements of dopamine metabolites in the cerebrospinal fluid (CSF) of patients with and without hyperthyroidism reveal lower levels of homovanillic acid (HVA) in patients with hyperthyroidism than in normals.6 Decreased HVA levels suggest an alteration in dopamine metabolism in hyperthyroid individuals.6 Thyroid abnormalities may alter the sensitivity of dopaminergic receptors.1,6 An alteration in basal ganglia metabolism or function, such as heightened sensitivity of dopamine receptors in the basal ganglia of hyperthyroid individuals, is one postulated mechanism for the chorea.6 It is possible that there may need to be preexisting damage to the basal ganglia to predispose a hyperthyroid individual to develop chorea. Fischbeck and Layzer described a patient who had an anoxic event prior to the development of hyperthyroidism and later developed chorea.7 The initial insult ...

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