Methanol is metabolized to formaldehyde and formic acid by
alcohol dehydrogenase in the liver. It has been reported that
these metabolites are responsible for the direct toxicity of
methanol
7. It has been reported that common early
symptoms of methanol intoxication are nausea, vomiting,
abdominal pain and diminution of vision
7. The present case had nausea and vomiting on admission. The most
common neurological sequela is visual impairment due to
optic nerve damage from retrolaminar demyelination and
probably also axonal damage
7. Our case developed visual
impairment 21 hours after ingestion. A loss of consciousness
has also been described and it may progress to obtundation,
and coma
7. In methanol intoxication, while the optic nerve,
the deep white matter such as the putamina, and the occipital
and frontal lobes are more commonly involved, the cerebral
cortex and cerebellar involvement are rare
7,9.
In WE, pathological changes affect the specific areas of
the brain, such as the medial dorsal thalamic nucleus and
mammillary bodies which are the strategic regions of
memory, the hypothalamus, the superior vermis of the
cerebellum, the periaqueductal region, the pontine
tegmentum, the reticular formation of the midbrain, the
posterior corpora quadrigemina, and the cerebral cortex2,5.
It has been reported that acute lesions caused by extreme
rapidity of thiamine deficiency show a symmetrical
distribution5. In WE, histopathologic findings include loss
of myelin, followed with axon damage, reactive gliosis,
sometimes hemorragies in involved1,2,5.
Common symptoms or signs at presentation of WE
include ocular abnormalities, mental status changes,
incoordination of gait and trunk ataxia2,5. Abnormal eye
movements are nystagmus, ophthalmoplegy due to often
abducens palsy, and impairment of the conjugated eye
movements1,2,5. The WE patients with altered mental
status may exhibite a disordered spontaneous speech, loss of
memory, disorientation, loss of attention, and decreased
awaking or lethargy2. Our case was global amnestic at
admission. A short time later, he exhibited altered mental
status (acute confusional state). At same time, in his
examination, we determined diplopia and horizontal
nystagmus. Diplopia was related to asymmetric paralysis of
lateral rectus muscle. Our case was presented with ataxic
walking.
In the etiology of WE inadequate thiamine intake or
deficiency underlies. Thiamine dependent enzymes include
the á-ketoglutarate-dehydrogenase complex and the
pyruvate-dehydrogenase complex in the tricarboxylic acid
cycle, and transketolase in the pentose-phosphate pathway5. It has been reported that thiamine also seems to have a
role in acetylcholinergic and serotoninergic synaptic
transmission, axonal conduction, and production of GABA5. It has been reported that changes in serum osmosis of
ethanol may lead to acute demyelination10. Similarly,
methanol may also be caused acute demyelination as a result
of changes in serum osmosis11. In the anamnesis of our
patient there were no other diseases except chronic
alcoholism. The patient had taken metylalcohol because he
could not have etylalcohol for a few days. This syndrome
may begin acute, subacute or chronic. For example it may
begin acutely due to excessive glucose intake4. Our case
had a history of chronic alcoholism which may cause
thiamine deficiency; however, before exposure to methanol
intoxication, he had no symptoms or complaints relate to WE.
Rotenstreich et al.8 reported that vitamin B-1 might well be
effective in methanol intoxication. We observed that vitamin
B-1 was highly effective in our case with methanol
intoxication. These reasons may explain the developing
acutelly of WE in our case and improving rapidly from WE
with thiamine of our case.
The diagnosis is clinical and is mainly supported by the
dramatic response of neurological signs to parenteral
thiamine5. Magnetic resonance imaging supports diagnosis
of WE5. Because of that acute confusional status, ataxia,
nystagmus, optic neuropathy, and amnesia followed methanol
ingestion and it improved completely with thiamine therapy.
Thus we thought that in our case, diagnosis was WE. Also the
brain MRI findings were consistent with WE.
Finally, methanol intoxication may cause WE.
Methanol induced WE may also be developed due to
thiamine deficiency, direct toxic effects of methanol, or both
of them at the same time. In a case of acute confusional status
following the ingestion of methanol, WE should also be
thought and early thiamine therapy should be started in ED.
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