PURPOSE: Reversible cerebral vasoconstriction has been hypothesized to be the etiology of seizures due to hypercalcemia, but angiographic studies documenting vasoconstriction have not previously been available. METHODS: We present a 43-year-old woman who had frequent seizures that later evolved to status epilepticus with marked hypercalcemia at the time of the seizures. RESULTS: Magnetic resonance imaging (MRI) of the patient's brain revealed high signal changes in T(2)-weighted imaging, fluorescence-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) over the bilateral occipital and thalamic areas. Cerebral angiography showed blood vessels narrowing, disappearing altogether over the right posterior cerebral artery (PCA) branch, which is compatible with vasoconstriction. Vasoconstriction caused the MRI high signal in the occipital area, which was associated with subsequent periodic lateralized epileptic discharges. The patient's clinical condition improved with management of seizures and hypercalcemia. A second brain MRI 2 weeks later revealed complete resolution of the high-signal lesions. Follow-up cerebral angiography study also showed total recovery of vasoconstriction. CONCLUSIONS: The sequence of events suggests the hypothesis that reversible cerebral vasoconstriction may play a role in hypercalcemia-induced seizures.
PURPOSE: Reversible cerebral vasoconstriction has been hypothesized to be the etiology of seizures due to hypercalcemia, but angiographic studies documenting vasoconstriction have not previously been available. METHODS: We present a 43-year-old woman who had frequent seizures that later evolved to status epilepticus with marked hypercalcemia at the time of the seizures. RESULTS: Magnetic resonance imaging (MRI) of the patient's brain revealed high signal changes in T(2)-weighted imaging, fluorescence-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) over the bilateral occipital and thalamic areas. Cerebral angiography showed blood vessels narrowing, disappearing altogether over the right posterior cerebral artery (PCA) branch, which is compatible with vasoconstriction. Vasoconstriction caused the MRI high signal in the occipital area, which was associated with subsequent periodic lateralized epileptic discharges. The patient's clinical condition improved with management of seizures and hypercalcemia. A second brain MRI 2 weeks later revealed complete resolution of the high-signal lesions. Follow-up cerebral angiography study also showed total recovery of vasoconstriction. CONCLUSIONS: The sequence of events suggests the hypothesis that reversible cerebral vasoconstriction may play a role in hypercalcemia-induced seizures.