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Alcohol-related neurological disorders

Alcohol and other drugs play a signifi cant role in the onset and course of neurological disorders. As toxic agents, these substances directly affect nerve cells and muscles, and therefore have an impact on the structure and functioning of both the central and peripheral nervous systems. For example, long-term use of ethanol is associated with damage to brain structures which are responsible for cognitive abilities (e.g. memory, problem-solving) and emotional functioning. In people with a history of chronic alcohol consumption the following abnormalities have been observed: cerebral atrophy or a reduction in the size of the cerebral cortex, reduced supply of blood to this section of the brain which is responsible for higher functions, and disruptions in the functioning of neurotransmitters or chemical messengers. These changes may account for defi cits in higher cortical functioning and other abnormalities which are often symptoms of alcohol-related neurological disorders.

Fetal alcohol syndrome

The role of alcohol in fetal alcohol syndrome has been known for many years: the condition affects some children born to women who drank heavily during pregnancy. The symptoms of fetal alcohol syndrome include facial abnormalities, neurological and cognitive impairments, and defi cient growth with a wide variation in the clinical features .Not much is known about the prevalence in most countries but, in the United States, available data show that the prevalence is between 0.5 and 2 cases per 1000 births. Though there is little doubt about the role of alcohol in this condition, it is not clear at what level of drinking and during what stage of pregnancy it is most likely to occur. Hence the best advice to pregnant women or those contemplating pregnancy seems to be to abstain from drinking, because without alcohol the disorder will not occur.

Alcohol-related polyneuropathy

A typical example of a toxiconutritional disorder, alcohol-related polyneuropathy is elicited by a combination of the direct toxicity of alcohol on the peripheral nerve and a relative defi ciency of vitamin B1 and folate. In its usual form it starts in an insidious, progressive way with signs located at the distal ends of the lower limbs: night cramps, bizarre sensations of the feet and the sufferer is quickly fatigued when walking. Examination reveals pain at the pressure of the muscular masses. This polyneuropathy evolves to a complete form with permanent pain in the feet and legs. The signs of evolution of alcoholic polyneuropathy are represented by the defi cit of the leg muscles leading to abnormal walk, exaggerated pain (compared to burning, at any contact) and skin changes. At the latest stage, ulcers may occur. The onset of the peripheral neuropathy depends on the age of the patient, the duration of the abuse and also the amount of alcohol consumed. The excessive abuse of this substance determines the central and/or peripheral nervous lesions.

Wernicke’s encephalopathy

Wernicke’s encephalopathy is the acute consequence of a vitamin B1 defi ciency in people with severe alcohol abuse. It is due to very poor diet, intestinal malabsorption and loss of liver thiamine stores. The onset may coincide with an abstinence period and is generally marked by somnolence and mental confusion; which gradually worsens, together with cerebellar signs, hypertonia, paralysis and/or ocular signs. The prognosis depends on how quickly the patient is given high-dose vitamin B1 (by intravenous route, preferably). A delay or an absence of treatment increases the risk of psychiatric sequelae (memory disorders and/or intellectual deterioration). If the treatment is too late, the consequences could be an evolution to a Wernicke–Korsakoff syndrome, a dementia.

Alcohol and epilepsy

Alcohol is associated with different aspects of epilepsy, ranging from the development of the condition in chronic heavy drinkers and dependent individuals to an increased number of seizures in people already with the condition. Alcohol aggravates seizures in people undergoing withdrawal and seizure medicines might interfere with tolerance for alcohol, thereby increasing its effect. Though small amounts of alcohol might be safe, people suffering from epilepsy should be advised to abstain from consuming this agent. After an episode of weeks of uninterrupted drinking, sudden abstinence may lead to epileptic seizures and severe coma, “delirium tremens”. Detoxifi cation should be under medical supervision and possibly with medication to decrease the risk of this potentially life-threatening condition. In terms of relative risk, much more is known about alcohol and epilepsy than other conditions. There is little difference between abstainers and light drinkers in the risk for chronic harmful alcohol- related epilepsy. Risk is highest at levels of consumption which exceed 20 g of pure alcohol (or two drinks) per day for women and 40 g for men. For example, the WHO project on comparative risk assessment has shown more than a sevenfold increase in risk among those who consume these high volumes or are dependent on alcohol when compared with abstainers for both male and female drinkers .

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