2 -  Causes and clinical course
Wernicke’s encephalopathy is usually associated with
alcoholism.  Because the same pattern of brainstem
damage is seen in alcoholism and thiamine deficiency,
deficiency of thiamine has long been thought to be
the cause of neurological dysfunction in people who
abuse alcohol and do not eat a balanced diet
(Dreyfus & Victor 1961).  Excessive use of alcohol is
also damaging to the gastrointestinal tract, which
might then prevent absorption of essential nutrients
and vitamins such as thiamine.

Neubürger (1937) described Wernicke
encephalopathy in patients with gastrointestinal
disorders not related to alcoholism, and he suggested
a connection between intestinal health and the brain.  
Sulfuric acid damaged the gastrointestinal tract in one
of Wernicke’s three cases; diminished consciousness
may also have lead to nutritional deficiencies in this
and the case of Gayet.  Gayet’s patient would fall
asleep while eating and could not be aroused.

Somnolence is one of the characteristic features of
Wernicke's encephalopathy.  However, this
somnolence is less the drifting in and out of true sleep
than failure to maintain a conscious state.  Fisch
(1970) pointed out that the auditory system keeps us
in touch with our environment even during sleep, but
the clock radio, alarm clock, and even prolonged
ringing of the telephone can be useless in rousing a
person who is "sleeping off" intoxication.   
Consciousness and general awareness seem clearly
linked to the auditory system of the brain, and it is well
documented by now that Wernicke-like impairments of
the brain include the auditory system and lead to
auditory deficits.

Decreased level of consciousness can also be linked
to involvement of other brainstem autonomic centers,
and deficits in short- to long-term memory to
involvement of the mammillary bodies.  The affected
brainstem sites reported by Wernicke and subsequent
investigators also include gray matter in the floor of
third and fourth ventricles.  That this damage included
oculomotor nuclei was largely inferred from clinical
observations.  Impairment of eye movements was one
of the clinical signs described by Wernicke and
oculomotor disturbances have long been recognized
as characteristic of Wernicke's encephalopathy
(Cogan et al. 1985, Victor et al. 1989).

Ataxia and weakness are also prominent in
Wernicke's encephalopathy, and can be attributed to
involvement of cerebellar function (Butterworth 1993).

The difference between asphyxia and chronic hypoxia
was first clarified by Myers (1972).  A similar
difference is evident in circumstances of toxic injury.  
Acute alcohol intoxication can be fatal, as is too often
evident in newspaper reports of binge drinking among
college students.  In most cases the effects of alcohol
are less catastrophic.  Likewise the effects of airway
impairment, malabsorption and decline in liver
function will lead to more chronic conditions, and more
widespread effects in the brain.

1. Dreyfus PM, Victor M (1961)
   Effects of thiamine deficiency
   on the central nervous system.
   
2. Neubürger K (1937)  
   Wernickesche Krankheit bei
   chronischer Gastritis.  Ein
   Beitrag zu den Beziehungen
   zwischen Magen und Gehirn.
   
3. Gayet M (1875) Affection
   encéphalique (encéphalite
   diffuse probable) localisée
   aux étages supérieurs des
   pédoncules cérébraux et aux
   couches optiques, ainsi qu’au
   plancher du quatrième
   ventricule et aux parois
   latérales du troisième.
   
4. Fisch L (1970) The selective
   and differential vulnerability of
   the auditory system.
   
5. Cogan DG et al. (1985) Ocular
   signs in thiamine-deficient
   monkeys and in Wernicke's
   disease in humans.
   
6. Victor M et al. (1989) The
   Wernicke-Korsakoff syndrome
   and related neurologic
   disorders due to alcoholism
   and malnutrition, 2nd ed.
   
7. Myers RE (1972) Two patterns
   of perinatal brain damage and
   their conditions of occurrence.
   

Full References

References

1. Dreyfus PM, Victor M (1961) Effects of thiamine deficiency on the central nervous system.  
   American Journal of Clinical Nutrition 9: 414-425.
   
2. Neubürger K (1937) Wernickesche Krankheit bei chronischer Gastritis.  Ein Beitrag zu den
   Beziehungen zwischen Magen und Gehirn.  Zeitschrift für die gesamte Neurologie und
   Psychiatrie 160:208-225.
   
3. Gayet M (1875) Affection encéphalique (encéphalite diffuse probable) localisée aux étages
   supérieurs des pédoncules cérébraux et aux couches optiques, ainsi qu’au plancher du
   quatrième ventricule et aux parois latérales du troisième. Archives de physiologie normale et
   pathologique série 2, 2:23-351.
   
4. Fisch L (1970) The selective and differential vulnerability of the auditory system.  In GEW
   Wolstenholm and J Knight, (Eds), Sensorineural Hearing Loss:  A Ciba Foundation
   Symposium (pp 101-116). London: Churchill.
   
5. Cogan DG, Witt ED, Goldman-Rakic PS (1985) Ocular signs in thiamine-deficient monkeys
   and in Wernicke's disease in humans. Archives of Ophthalmology 103:1212-1220.
   
6. Victor M, Adams RD, Collins GH (1989) The Wernicke-Korsakoff syndrome and related
   neurologic disorders due to alcoholism and malnutrition, 2nd ed, Contemporary Neurology
   Series v30. Philadelphia, PA : F.A. Davis Co.
   
7. Myers RE (1972) Two patterns of perinatal brain damage and their conditions of occurrence.  
   American Journal of Obstetrics and Gynecology 112:246-276.
   

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