Abstract Details

Title Acute Onset Chorea in Profound Hypophosphatemia with Bilateral Basal Ganglia Lesions

Topic Movement Disorders

Presentation(s) P13 - Poster Session 13 (5:30 PM-6:30 PM)

Poster/Presentation
Number 3-011

Objective Chorea is a hyperkinetic movement disorder with irregular non-stereotyped movements of the limbs, likely due to abnormal activity within the globus pallidus. Various metabolic derangements are implicated in chorea, but hypophosphatemia has not been reported. We present a case of acute onset chorea in the setting of profound hypophosphatemia.

Background Patient is a 69 year old man with a history of hypertension, diabetes mellitus type 2, peripheral vascular disease, and end-stage renal disease on hemodialysis living in a nursing home. During dialysis, he became acutely altered with continuous neck and truncal writhing movements as well as asynchronous non-stereotyped movements of all limbs. He did not have any recent illness, fever, change in medication regimen, or toxin ingestion.

Design/Methods NA

Results Work-up revealed profound hypophosphatemia (0.8mg/dL), but normal calcium, magnesium, glucose, hepatic panel, antinuclear antibodies, antiphospholipid antibodies, iron, copper, B12, ceruloplasmin, thyroid stimulating hormone, parathyroid hormone, ESR/CRP, HIV, syphilis, urine drug screen, and smear acanthocytes. Cerebrospinal fluid studies were unremarkable. Hemodynamics and oxygenation were normal peri-dialysis. CT scan of the brain revealed chronic cerebral atrophy and diffuse ventriculomegaly. MRI of the brain revealed T2-hyperintense lesions confined to the bilateral basal ganglia. Mentation improved and abnormal movements resolved over the course of several days with aggressive phosphate repletion. On one month follow-up, he was at neurologic baseline.

Conclusions Extensive literature review reveals chorea described in auto-immune, vascular, infectious, toxic, and most commonly, metabolic pathologies. Chorea has been described with abnormal above-mentioned studies as well as hyperphosphatemia (classically in hypoparathyroidism), but not hypophosphatemia. The resolution with treatment suggests a causal relationship between phosphate depletion and chorea. Further study is required to elucidate the role of hypophosphatemia in chorea possibly due to catastrophic mitochondrial energy failure within the highly metabolic basal ganglia structures.

Authors/Disclosures
Chaitanya Medicherla, MD PRESENTER	Dr. Medicherla has nothing to disclose.
Robert Staudinger, MD, F�鶹��ýӳ��	Dr. Staudinger has nothing to disclose.

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