Austin J Clin Neurol 2015;2(4): 1034
Hyperosmolar Hyperglycemia Associated With Central Pontine Myelinolysis, Seizure, and Cerebral Venous Thrombosis
Nirav H Shah*, Tatjana Rundek, and Ralph Sacco
Department of Neurology, University of Miami, USA
*Corresponding author: Nirav H. Shah, Department of Neurology, Miller School of Medicine, University of Miami, 1120 NW 14th Street, CRB 1365, Miami, FL 33136, USA
Received: March 21, 2015; Accepted: April 08, 2015; Published: April 11, 2015
A 55 year-old right-handed man developed left-gaze deviation and a generalized tonic-clonic seizure. Labs demonstrated glucose of 678mg/dL, sodium of 130mg/dL, and a serum osmolality of 300mg/dL. There was no evidence of alcohol intoxication. Brain MRI demonstrated central pontine and middle cerebral peduncle restriction on diffusion-weighted imaging consistent with central pontine myelinolysis [A,B]. Seven days after event, sagittal (◊) and left transverse sinus thrombosis (*) was suspected on MRI-FLAIR [C] and confirmed with MR Venogram [D] (Figure 1). The patient was anticoagulated and discharged without neurological deficitten days after event.
Figure 1: Brain MRI of central pontine and middle cerebral peduncle restriction.
This patient serves as are minder of neurological consequences and treatment implications of hyperosmotic states. Hyperosmolar hyperglycemia and electrolyte imbalance can cause osmotic demyelination even in the absence of alcohol intoxication. Impaired venous drainage may in part account for extra-pontine demyelination [1,2]. Hyperosmotic hyperglycemia has also been associated with seizures, focal neurological deficits, and cerebral venous thrombosis [3-5].
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Citation: Shah NH, Rundek T and Sacco R. Hyperosmolar Hyperglycemia Associated With Central Pontine Myelinolysis, Seizure, and Cerebral Venous Thrombosis. Austin J Clin Neurol 2015;2(4): 1034. ISSN : 2381-9154