JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
pontine myelinolysis and extra pontine myelinolysis involving the bilateral putamen/external capsule.
nutritional or electrolyte stress, such as alcoholism, liver disease, immunosuppression after transplantation, malnourishment with underlying medical disease, gastrointestinal disease with acute electrolyte abnormalities, the syndrome of inappropriate secretion of ADH (SIADH), renal disease, cancer, pregnancy, and in high-endurance exercise. During acute onset of hyponatremia, water moves from the blood into the brain cells which causes them to swell. These cells then adapt by losing electrolytes to reestablish their normal volume. If the hyponatremic state is corrected during this acute phase, the brain can quickly accumulate electrolytes to restore normal osmotic equilibrium. If the hyponatremic state persists, brain cells must also expel organic osmolytes in addition to electrolytes to fully restore normal cell volume. Movement of these osmolytes is much slower than movement of electrolytes. 3 In the chronic hyponatremic state, brain-cell volume is normal, but the intracellular osmolality is low to allow the brain to be in osmotic equilibrium with the blood. At this point, it is important
The patient continued to decline. An NG-tube followed later by a PEG tube was placed for nutrition. His sodium continued to correct with jevity feeds but his neurological status did not improve. On hospital day 25, the patient developed seizures and neurology was consulted. An Electroencephalography (EEG) showed two frequent spikes primarily in the left temporal central region consistent with status epilepticus. The patient was started on Keppra and Dilantin, which resolved the seizures, thought to be related to his brain’s structural abnormality. At discharge, his sodium was stable and he was sent to a nursing home with hospice.
LITERATURE REVIEW AND PATHOPHYSIOLOGY
The most common cause of CPM is an overly-rapid correction of hyponatremia in patients with conditions leading to
FINAL REPORT
EXAM: MRI Brain w/wo Contrast, 8/13/2015, 3:11 PM COMPARISON: None HISTORY: Encephalopathy. Suspected pontine myelinolysis TECHNIQUE: Multiplanar, multisequence MR images of the brain were performed before and after the IV administration of 20mL Omniscan. FINDINGS: There is restricted diffusion and associated increased T2 signal within the central pons. There is faint associated enhancement. There is also linear increased T2 signal within the lateral putamen/external capsule bilaterally corresponding increased signal on diffusion-weighted imaging although less significant signal dropout on ADC map. There is mild diffuse parenchymal atrophy with proportionate ventricular enlargement. There are mild chronic ischemic small vessel degenerative white matter changes. No mass or mass effect. Corpus callosum is normal. Pituitary and optic chiasm are grossly normal. Cerebellar tonsils are appropriately positioned. The major intracranial arterial flow voids are patent. There is no parenchymal hemorrage. IMPRESSION: Findings are compatible with osmotic demyelination syndrome with central pontine myelinolysis and extrapontine myelinolysis involving the bilateral lateral putamen/external capsule.
44 J La State Med Soc VOL 170 MARCH/APRIL 2018
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