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Abstract Details

Hypercalcemia-associated PRES and Status Epilepticus
General Neurology
P2 - Poster Session 2 (8:00 AM-9:00 AM)
6-005
To describe a rare cause of Posterior Reversible Encephalopathy Syndrome (PRES)

Hypercalcemia-associated PRES (Posterior Reversible Encephalopathy Syndrome) is a rare phenomenon and there have only been a few case reports describing it. The mechanism of hypercalcemia-associated PRES is still unknown. Here we present a patient who presented with status epilepticus and supra-physiological level of calcium with MRI showing PRES-like changes.

Case description

A 61-year-old man was admitted in the hospital for altered mental status and new-onset convulsive seizures who had been accidentally taking Vitamin D3 50,000 units every day rather than once a week as prescribed. He had frequent seizures and was intubated for airway protection. He was normotensive, however was unarousable on his exam. The basic metabolic panel was mostly unremarkable except for hypercalcemia (Ca 17.3 mg/dl). Extensive CSF serology studies, including the viral tests, failed to show any evidence of meningoencephalitis. A continuous EEG study showed abundant 1 Hz generalized spike slow waves. CT scan of the head was negative for acute process. A brain MRI study showed areas of hyperintensity in the cortical and sub-cortical regions of bilateral parietal and occipital lobes. The calcium level gradually normalized after 3 days of treatment, as well as the EEG abnormalities.

NA

PRES is a neurological entity characterized by seizures, headache and reversible subcortical vasogenic edema. The typical MRI findings of PRES are reversible vasogenic edema that mainly affects the posterior cerebral lobes. The diagnosis of PRES consists of typical image findings and clinical presentation. Common causes of PRES include hypertension, acute or chronic renal disease, eclampsia, vasculitis. Hypercalcemia is rarely associated with PRES. The underlying pathophysiological process for hypercalcemia-induced PRES are not well elucidated yet. However, several mechanisms have been proposed such as vasospasm or endothelial dysfunction.

Authors/Disclosures
Fransisca Indraswari, MD (Brown Neurology/The Miriam Hospital)
PRESENTER
Dr. Indraswari has nothing to disclose.
Hai Chen, MD, PhD Dr. Chen has nothing to disclose.