- Wernicke C (1881a) Die acute, haemorrhagische Poliencephalitis superior. Lehrbuch der
Gehirnkrankheiten für Ärzte und Studirende,Band II. Kassel: Theodor Fischer, pp 229-242.
- Rosenblum WI, Feigin I. (1965) The hemorrhagic component of Wernicke's encephalopathy.
Archives of Neurology 13:627-32.
- Hakim AM (1986) Effect of thiamine deficiency and its reversal on cerebral blood flow in the rat.
Observations on the phenomena of hyperperfusion, "no reflow," and delayed hypoperfusion.
Journal of Cerebral Blood Flow and Metabolism 6:79-85.
- Chen Q, Okada S, Okeda R (1997) Causality of parenchymal and vascular changes in rats with
experimental thiamine deficiency encephalopathy. Pathology International 47:748-756
- Torvik A (1987) Topographic distribution and severity of brain lesions in Wernicke's
encephalopathy. Clinical Neuropathology 6:25-29.
- 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.
- d'Avella D, Cicciarello R, Albiero F, Mesiti M, Gagliardi ME, Russi E, d'Aquino A, Princi P, d'Aquino S
(1991) Effect of whole brain radiation on local cerebral glucose utilization in the rat. Neurosurgery
28:491-495.
- d'Avella D, Cicciarello R, Gagliardi ME, Albiero F, Mesiti M, Russi E, D'Aquino A, Tomasello F (1994)
Progressive perturbations in cerebral energy metabolism after experimental whole-brain radiation
in the therapeutic range. Journal of Neurosurgery 81:774-779.
- d'Avella D, Cicciarello R, Zuccarello M, Albiero F, Romano A, Angileri FF, Salpietro FM, Tomasello F
(1996) Brain energy metabolism in the acute stage of experimental subarachnoid haemorrhage:
local changes in cerebral glucose utilization. Acta Neurochirurgica (Wien) 138:737-743.
7 - Mechanisms of damage
Wernicke (1881) described symmetric bilateral
hemorrhagic lesions within the brainstem in the three
cases he reported, and that they occurred in a
pattern of almost mathematical bilateral symmetry. If
a nucleus was damaged on the right, the nucleus on
the left was equally involved. Bilateral symmetry has
been noted as remarkable by many investigators, but
whether the lesions in Wernicke’s encephalopathy are
hemorrhagic in origin or not has been the subject of
considerable discussion. Rosenblum and Feigin
(1965) investigated this issue and found hemorrhages
in 60 percent of 43 cases that they investigated; of
these five were old hemorrhages identified only by
hemosiderin-laden macrophages viewable only by
microscopic examination.
Alcohol is a vasodilator, and the autoradiographic
method has shown an increase in blood flow is often
the first response to impairment of energy metabolism
(Hakim 1986, Chen et al 1997). If blood vessels are
compromised by arteriosclerosis or weakened by any
other cause, small hemorrhages are likely to occur
with increased blood flow. A ruddy face is commonly
viewed as characteristic of alcoholics and indicates
that circulatory adjustments to the skin take place with
habitual alcohol use. However, brain lesions
observed in most chronic alcoholics are old lesions
that usually predate death by many years and
therefore would not give evidence of their original
hemorrhagic origin. The alcoholic men whose brains
were examined by Wernicke died within two weeks of
episodes of acute intoxication.
The mammillary bodies are usually most prominently
affected in Wernicke’s encephalopathy caused by
alcohol abuse; the inferior colliculi are sometimes
damaged, but often show no visible signs of
involvement (Torvik 1987, Victor et al. 1989). The
reason for differences in vulnerability and variability in
brain sites damaged should yield to research using
the methods to measure changes in blood flow and
deoxyglucose uptake, which demonstrate metabolic
changes that precede visible damage. Investigations
on effects of alcohol and other toxic substances
indicate that many biofeedback mechanisms are
initiated to compensate for perturbations in
homeostasis. Increased blood flow is a common
response, a response usually greatest in the inferior
colliculi that may leave somewhat less active nuclei
such as the mammillary bodies more vulnerable to
early damage (Hakim 1986).
For example, D’Avella et al. (1991) used the
deoxyglucose method to clarify a syndrome of mental
deterioration observed in cancer patients after whole-
brain radiotherapy (WBR). Decreases in metabolic
activity were measured in about half of the brain
regions investigated after radiation of the brain in
laboratory rats. Significant decreases were found in
the auditory cortex and medial geniculate bodies, but
not in the inferior colliculus after radiation. This study
provides one of many examples that high metabolic
demand within the inferior colliculus may in some
circumstances allow it to benefit from vasodilation and
increased circulation to obtain oxygen and nutrients at
the expense of other areas of the brain.
It should be of interest to use the deoxyglucose
method to investigate the effects on the brain of
drugs, anoxia, radiation, vitamin deficiencies, head
trauma, and any other factor associated with altered
brain function. Factors or conditions that would
diminish rather than completely block metabolic
function would be expected to preserve the brainstem
nuclei of high metabolic rate, and lead to damage of
areas of the cerebral cortex that are less active from
moment to moment. Catastrophic insults such as
aerobic poisons (like pyrithiamine) would be expected
to produce a prominent form of Wernicke's
encephalopathy as in the experiments of Chen et al.
(1997).
- Wernicke C (1881a) Die acute,
haemorrhagische
Poliencephalitis superior.
- Rosenblum WI, Feigin I.
(1965) The hemorrhagic
component of Wernicke's
encephalopathy.
- Hakim AM (1986) Effect of
thiamine deficiency and its
reversal on cerebral blood flow
in the rat. Observations on the
phenomena of hyperperfusion,
"no reflow," and delayed
hypoperfusion.
- Chen Q et al. (1997) Causality
of parenchymal and vascular
changes in rats with
experimental thiamine
deficiency encephalopathy.
- Torvik A (1987) Topographic
distribution and severity of
brain lesions in Wernicke's
encephalopathy.
- Victor M et al. (1989) The
Wernicke-Korsakoff syndrome
and related neurologic
disorders due to alcoholism
and malnutrition, 2nd ed.
- d'Avella D et al. (1991) Effect of
whole brain radiation on local
cerebral glucose utilization in
the rat
- d'Avella D et al. (1994)
Progressive perturbations in
cerebral energy metabolism
after experimental whole-brain
radiation in the therapeutic
range.
- d'Avella D et al. (1996) Brain
energy metabolism in the
acute stage of experimental
subarachnoid haemorrhage:
local changes in cerebral
glucose utilization.