NEUROPATHOLOGY- ALCOHOL AND THE CNS
I. CNS TRAUMA
II. ALCOHOLIC SYNDROMES
III. TOXINS
IV. SPECIFIC DISEASES OF THE CNS RELATED TO
ALCOHOL ABUSE
VOCABULARY:
Terms you should be familiar with:
"Rum fits"
Delirium tremens
Brain atrophy
Fetal alcohol syndrome
Hepatic encephalopathy
Wernicke's encephalopathy
Thiamine
Korsakoff's psychosis
Marchiafava Bignami disease
Methanol poisoning
Central pontine myelinolysis Cerebellar degeneration
Subacute combined degeneration
Peripheral neuropathy
Myopathy
OBJECTIVES: The objectives of this hour are to recognize the prevalence
of alcoholism in the United States, to recognize that the neuropathology
of alcohol is largely the neuropathology of trauma, to become familiar with
some of the common and interesting lesions of the CNS related to alcohol,
and to recognize that some of these are treatable if recognized early enough.
I. CNS TRAUMA
Alcoholics are prone to serious central and peripheral nervous system
complications of their habit. One must always keep in mind that alcoholics
are frequently victims of CNS trauma. In particular, think about the possibility
of contusion, subdural hematoma, or epidural hematoma in an alcoholic with
an altered level of consciousness. That is to say, the neuropathology of
alcohol is first and foremost the neuropathology of trauma.
II. ALCOHOLIC SYNDROMES
Alcoholic syndromes of the CNS without obvious morphologic correlates.
- Simple Intoxication
- "Rum Fits": seizures in the alcoholic
- Usually occur 48-72 hours after cessation of drinking
- Usually uncomplicated, generalized seizure that requires no treatment
- If more than two, if complicated, if neurologic exam or tests abnormal,
or if patient develops status epilepticus, consider other underlying cause.
- Delirium Tremens: syndrome of hallucinations (usually visual) and
up regulated autonomic system. Fatal if not treated rapidly and correctly.
III. TOXINS
Alcohol as a direct toxin of the CNS. Evidence to support this concept
includes:
- Brain atrophy and neuronal loss in some chronic alcoholics
- Alcohol fed to rats causes simplification of dendritic arborization
- Fetal alcohol syndrome.
Back to Top
IV. SPECIFIC DISEASES OF THE CNS RELATED
TO ALCOHOL ABUSE
- Hepatic Encephalopathy: cirrhosis of the liver and declining liver
parenchymal function leads to elevated serum ammonia level. Ammonia directly
toxic to CNS and leads to a declining mental status and coma. CNS deals
with ammonia by metabolizing to glutamine, probably via an enzyme pathway
housed in the astrocyte.
- Wernicke's Encephalopathy
- Thiamine deficiency
- Clinical triad of ataxia, ophthalmoplegia, and mental confusion
of acute onset
- Treatment with thiamine may completely reverse the clinical syndrome
if given early in the course
- Pathology involves mammillary bodies (confusion), periaqueductal
gray (ophthalmoplegia), and floor of the 4th ventricle (ataxia), and includes
petechial hemorrhages, capillary vascular proliferation, and astrocytosis
- Grossly, one looks for atrophy and discoloration of the mammillary
bodies, but this may not be apparent in 50% of cases
- Korsakov's Psychosis: historically, considered to be a sequela of
untreated or partially treated Wernicke's. More recent evidence suggests
that Korsakoff's is a separate entity caused by neuronal loss and degeneration
in the dorsomedial nucleus of the thalamus. This is most likely a nutritional
disorder secondary to chronic alcohol abuse. The clinical syndrome is confabulatory
amnesia.
- Marchiafava Bignami Disease
- Degeneration with loss of myelin in the central aspect of the corpus
callosum
- Originally described in Italian men fond of drinking red "dago"
wine.
- Now known to be a complication of chronic alcoholism without race
or sex predilection.
- Presumably nutritional, although exact etiology unknown
- Clinical syndrome of personality change, seizures and dementia
- Methanol Poisoning: for economic reasons, alcoholics will turn to
other liquids to quench their thirst. A favorite is methanol. Causes severe
gastritis, pancreatitis, and CNS toxicity. Has a specific effect on the
putamen, causing a hemorrhagic necrosis. Optic nerves and subcortical white
matter are demyelinated. Patients present with visual changes, mental confusion,
severe vomiting, severe acidosis, and an unexplainable anion gap. Treatment
includes giving alcohol IV (alcohol and methanol compete for the same metabolic
pathway, and it is actually a metabolic derivative of methanol, formic
acid, that is toxic), alkalinization, and dialysis.
- Central Pontine Myelinolysis (CPM)
- Approximately 75% of cases seen in alcoholics who are hospitalized
for other reasons.
- Considerable clinical and experimental evidence suggests that the
pathogenesis of CPM is related to the excessively rapid correction of hyponatremia
(greater than 20 mEq in 24 hours).
- CPM is associated with a clinical syndrome of declining mental status,
quadriparesis and cranial nerve abnormalities.
- Recovery is rare.
- Excessively rapid correction of hyponatremia is thought to lead
to an osmotic instability in the pons with marked edema and secondary demyelination.
Macrophages containing digested myelin are a prominent pathologic feature.
- Midline Cerebellar Degeneration: probably nutritional. Superior
vermis is most often affected with loss of Purkinje cells and resultant
ataxia. May be a folic acid problem.
- Subacute combined degeneration of the spinal cord
- Alcoholic peripheral neuropathy
- Acute and chronic myopathy
Back to Top
Go Back to Course
Outline
Go Back to Neuropathology
[ Introduction and Objectives
| Basic Reactions of the CNS | Vascular
Disease | Trauma to the CNS | Alcohol
and the CNS | Infections of the CNS | Tumors of the CNS | Diseases
of the Myelin Sheath | Spinal Cord Disease
| Muscle Disease | Congenital
Anomalies of the CNS | Neuropathology of AIDS
| Degenerative Diseases of the CNS | Dementia and Related Issues | Unconventional
Transmissible Agent (Prion) Diseases ]
Questions?
Comments? Send a message to the CATS guru: jkessler@salus.uvm.edu