Alcohol related disorders

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Experimentally, chronic alcohol consumption results in neuronal loss. CT evidence of atrophy and neuropsychological impairment is common in alcoholics. However, whether or not these result from the direct toxic and dementing effect of alcohol remains uncertain.


Probably the commonest cause of acquired ataxia, alcoholic patients may develop a chronic cerebellar syndrome either as a sequel of Wernicke's syndrome or as a district clinical entity. A long history of alcohol abuse is obtained. Males are predominantly affected.

Onset is gradual and symptoms often stabilise.

Ataxia of gait with lower limb inco-ordination predominates. The upper limbs are spared. Nystagmus is rarely present. Cerebellar dysarthria is usually mild. Coexistent signs of peripheral neuropathy are often found.

Investigations: - Abnormal liver function tests e.g. elevation of enzymes - y GT.

- Macrocytosis in peripheral blood film.

- CSF examination normal.

- CT and MRI reveal cerebellar vermal atrophy.

Progression —- may evolve rapidly and reverse with improved nutrition and alcohol withdrawal, may evolve subacutely.

may evolve chronically and slowly progress over many years.

Pathology: - Purkinje cell loss in cerebellar hemispheres and in superior cerebellar vermis.

Pathogenesis: - The disorder may be due to nutritional deficiency, especially thiamine, or else result from the direct toxic effect of alcohol or electrolyte disturbance on the cerebellum.

Differential diagnosis: - Distinguish from hereditary and other acquired ataxias, e.g. hypothyroidism, remote effects of carcinoma.

Treatment: - Alcohol withdrawal, a well balanced diet and adequate vitamin supplementation. CENTRAL PONTINE MYELINOLYSIS

Alcohol abuse, debilitating disease or rapid connection of hyponatraemia may precipitate presentation.

The lesion is one of demyelination with cavitation. Microscopically, myelin is lost, oligodendrocytes degenerate but neurons and axons are spared.

Clinically, an acute or subacute pontine lesion is suspected, evolving __

over a few days, with bulbar weakness and tetraparesis, (locked-in syndrome). Nv / / ^ \ \

The limbs are flaccid with extensor plantar responses. ^ ^

With progression of the lesion, eye signs become evident and conscious level becomes depressed -» coma -> death. Pons


Electrolytic disturbances (low sodium, low phosphate) are found. Liver function is normal. CSF examination is normal. MRI is more sensitive than CT showing an abnormality in the pons.

Recognition of this condition before death is important in view of its reversibility, though prior to CT/MRI availability it was diagnosed at autopsy. Vigorous supportive therapy with correction of metabolic abnormalities and vitamin supplementation is advised. In patients with severe hyponatraemia (<110 mmol/1), especially alcoholics, slow correction is essential.

CORPUS CALLOSUM DEMYELINATION (syn: Marchiafava-Bignami disease) This is a rare disorder occurring in malnourished alcoholics. Occasionally diagnosed premortum by MRI, progressing to death over some weeks. The clinical picture is that of personality change with signs of frontal lobe disease. The condition occurs most commonly in persons of Italian origin.

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