1. What is the diagnosis? A. Pontine Glioma B. Marchiafava-Bignami C. Wernicke encephalopathy D. Central pontine myelinolysis 2. What is th...
1. What is the diagnosis?
A. Pontine Glioma
B. Marchiafava-Bignami
C. Wernicke encephalopathy
D. Central pontine myelinolysis
2. What is the pathophysiology?
A. Rapid correction of Thiamine
B. Rapid correction of Na+
C. Correction of Na+was too slow
D. Autoimmune Demyelination
3. What is the earliest sign?
A. Restricted diffusion in the lower pons
B. T2 Hypointensity
C. Homogeneous Contrast Enhancement
D. Blooming on Gradient
ANSWERS
1. What is the diagnosis?
Central pontine myelinolysis
2. What is the pathophysiology?
Rapid correction of Na+
3. What is the earliest sign?
Restricted diffusion in the lower pons
CPM
This is an acute demyelination of the white matter tracts of the pons. It’s seen in the setting of acute osmotic changes, classically described with the rapid correction of hyponatremia.
KEY FEATURES
– The classic history is a chronic alcoholic (nursing home patient or transplant patient), who had a rapidly corrected Na+. He/She felt much better after the correction, then returns to the ED 3 days later with spastic quadriparesis and pseudobulbar palsy (hyperactive gag reflex, and dysarthria).
– The first sign is restricted diffusion in the lower Pons.
– Low signal on T1 and high signal on T2 in the same region (lower pons) may not show up for two weeks.
It can enhance like an acute MS plaque (but doesn’t have to). Peripheral fibers are classically spared.
