It is associated primarily with alcohol abuse and malnutrition. As alcoholism is 3-4 times more frequent in men than in women, incidence of Wernicke encephalopathy is greater in male than in female alcoholics. Wernicke encephalopathy is found largely in the alcoholic population, although it is not restricted to this group. Thiamine depletion can occur because of poor diet or impaired absorption. Only one third of patients with acute Wernicke encephalopathy present with the classic clinical triad.
Ocular abnormalities are the hallmarks of Wernicke encephalopathy.
Horizontal nystagmus and paralysis of lateral rectus muscles are common. Less frequently noted are pupillary abnormalities such as sluggishly reactive pupils, ptosis, and anisocoria. Global confusional state Apathy Impaired awareness of the immediate situation Spatial disorientation Inattention Inability to concentrate Ataxia, the loss of equilibrium seen in the early stages of the disease, results from vestibular paresis, which is uniformly found yet often poorly appreciated. Wide-based, ataxic gait seen in the subacute and chronic phases of the illness results from cerebellar dysfunction, either alone or combined with vestibular dysfunction. Hypothermia, from involvement of the temperature-regulating center, is characteristic.