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Acute/subacute/chronic toxic effects of EtOH on CNS
Wernicke encephalopathy (WE)
Marchifava-Bignami disease (MBD)
EtOH: Disproportionate superior vermian atrophy, enlargement of lateral ventricles, sulci with chronic EtOH
WE: Mammillary body, medial thalamus, hypothalamus, periaqueductal gray abnormal signal/enhancement/diffusion restriction
MBD: Abnormal signal and later necrosis in corpus callosum
Nonalcoholic atrophy
Demyelination (toxic, acquired/inherited metabolic)
Corpus callosal hyperintensity
Status epilepticus
Drug toxicity
Encephalitis
Hypoglycemia
EtOH: Causes both direct/indirect neurotoxicity
WE: Thiamine (vitamin B1) deficiency
WE can be alcoholic or nonalcoholic
MBD: Chronic EtOH abuse, anecdotal association with red wine
WE: Triad of ataxia, oculomotor abnormalities, confusion
Classic clinical triad present in only minority of patients
EtOH: Cessation, establishment of adequate nutrition
WE: Immediate administration of IV thiamine → quick response
50% of WE cases occur in nonalcoholics, including children!
Nutritional deficiency, after gastric bypass, etc.
, as well as necrosis in the mid-corpus callosum
related to alcoholic toxicity. Mammillary body
, periaqueductal gray necrosis
is seen with Wernicke encephalopathy.
, markedly enlarged cerebellar fissures
.
. Note that the genu, body, and splenium are all involved.
in this patient with acute Wernicke encephalopathy.
Alcoholic (EtOH) encephalopathy
Wernicke encephalopathy (WE)
Marchiafava-Bignami disease (MBD)
Acute, subacute, or chronic toxic effects of EtOH on CNS
Can be primary (direct) or secondary (indirect)
Primary (direct) effects of EtOH = neurotoxicity
Cortical/cerebellar degeneration, peripheral polyneuropathy
Secondary (indirect) effects
Trauma, malnutrition, coagulopathy
Rare treatable complication = WE
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