Introduction

Alcohol consumption is a mattern of concern world-wide and a major problem of public health in many countries. The estimated overall prevalence of alcohol dependence is 0.5–3% of the population in Europe or in the USA. The central and peripheral nervous systems are the two principal targets. Chronic alcohol ingestion can impair the function and morphology of most, if not all, brain structures (Fadda and Rossetti, 1998). In particular, alcohol is an important toxic agent for the cerebellum (see also Chapter 21). This chapter describes the effects of alcohol consumption in humans, focusing on cerebellar function.

Clinical findings

Both acute and chronic ingestion of alcohol result in cerebellar dysfunction (Gilman et al., 1981). The main complaint in patients presenting alcohol-induced cerebellar dysfunction is difficulty in standing and walking. The majority of patients report a lack of coordination in the lower extremities (Gilman et al., 1990). Table 22.1 summarizes the neurological signs, both cerebellar and extracerebellar, which are observed in adult alcoholic patients.

During acute alcohol intoxication, patients exhibit slurred speech, gaze-evoked nystagmus, anterior–posterior oscillations in Romberg's test, and broad-based ataxic gait. These ataxic signs tend to become chronic features with chronic alcohol abuse (Gilman et al., 1981). Gait difficulties either worsen progressively over weeks or months, or may rapidly turn to a debilitating deficit, particularly in the case of malnutrition. A third pattern of progression is encountered rarely and comprises relatively unpredictable exacerbations. In alcoholic patients, legs appear stiff during gait but not when the patient is in a lying position. This ‘stiff appearance’ was well observed in the syndrome of ‘alcoholinduced cerebellar degeneration’, described by Victor and colleagues in 1959.