It is recommended that as a general precaution all patients with a known history of chronic alcohol consumption encountered at emergency care are given thiamine 250 mg i.v. without delay.
Alcohol crosses the blood brain barrier and will always cause CNS symptoms that are usually caused by ethanol. Treatment of alcohol withdrawal symptoms: see Treatment of Alcohol Withdrawal.
A hangover is the mildest reaction to alcohol consumption. It is usually not associated with withdrawal seizures, unless the patient's seizure threshold is lowered by some other cause (scarring of the brain, tumour etc.).
The cessation of chronic alcohol consumption results in withdrawal symptoms that are more severe than a hangover and may be accompanied by seizures or delirium tremens.
The differential diagnosis of withdrawal symptoms includes brain contusion, intracranial bleeding and CNS infections.
Wernick's disease is the result of thiamine deficiency and can be prevented with vitamin B1 administration.
Convulsive seizures and epilepsy
When stopping excessive use of alcohol or certain centrally acting medicines (e.g. benzodiazepines), withdrawal-related convulsive seizures often occur as a sign of transient over-excitability of the brain. The seizures often come as a series of several attacks, in which case they are called serial seizures.
Illicit drugs (heroin, cocaine, amphetamines) only induce seizures as a result of intoxication (= overdose) and not during withdrawal.
The risk of seizures in alcohol-dependent individuals is 10-fold compared with the rest of the population.
Withdrawal seizures
Binge drinking clearly increases the risk of convulsive seizures.
The diagnosis is based on the time interval between the emergence of withdrawal symptoms and a sufficiently strong exposure.
One to two days after the cessation of prolonged (at least several days) excessive use of alcohol or sedative drugs the patient experiences primary generalized tonic-clonic seizures, or partial (focal) seizures, together with other withdrawal symptoms.
Where seizures do not occur until more time has elapsed from stopping alcohol consumption the cause is either the cessation of a sedative drug use or an organic brain disease (e.g. subdural haematoma Traumatic Cerebral Haemorrhages).
In epilepsy of post-traumatic or cerebrovascular aetiology, the withdrawal seizures may manifest as partial seizures.
If findings suggestive of a brain disorder are not present on presentation, the likelihood of a condition requiring medical attention (intracranial bleeding, brain contusion, cerebrovascular disorder) is about 6%.
Plasma sodium, potassium and glucose concentrations should be determined.
The first withdrawal seizure should prompt one CT scan of the brain. Scanning should be repeated in the event of recurrent similar seizures only if they have a new focal feature or if they are associated with a new neurological deficit.
Antiepileptics should not be started for an alcohol-dependent patient if all seizures are related to alcohol consumption; in this case the treatment consists of cessation of alcohol intake.
The patient often stops taking the medication during a period of high alcohol use, and irregular use increases the risk of seizures. This should be borne in mind particularly in alcohol-dependent patients with post-traumatic epilepsy.
Alcohol alters the metabolism of antiepileptics.
Moderate alcohol consumption with meals (1-2 standard units) does not increase the incidence of seizures in epilepsy or affect the metabolism of antiepileptics. Antiepileptics must be taken regularly even during alcohol consumption.
Alcohol, epilepsy and driving health
Country specific driving laws dictate whether the person is eligible to apply for a driving licence and under which conditions.
Alcohol withdrawal seizure(s), even when it has occurred only once, may make it impossible to obtain a driving licence for professional purposes.
Cerebellar atrophy
The most common cause of gait disturbance in an alcohol-dependent person; it is more common than for example advanced polyneuropathy.
Clinical manifestation
Symptoms develop subacutely as a result of abundant and long-term use of alcohol and are most evident during a hangover.
Wide-based gait, difficulty in walking a straight line (tandem gait).
Heel-knee test yields symmetrical ataxia.
Low-frequency (3 Hz) tremor of the lower limbs appears when a supine patient raises his/her leg and bends the knee to a 90° angle.
Differential diagnosis
The symptoms of alcoholic cerebellar degeneration are typically limited to the lower limbs. The symptoms of other cerebellar disorders (cerebrovascular disorders, multiple sclerosis, hereditary disorders) usually also involve the upper limbs and the cranial nerve region.
Treatment
Discontinuation of alcohol consumption
Cognition in an alcohol-dependent person
Diminished intellectual capacity is significantly more common in alcoholics than in the general population. Permanent abstinence may, however, halt the progression.
A diagnosis of alcoholic dementia should not be made until other causes of memory disorder have been ruled out.
Central pontine myelinolysis
An iatrogenic disorder caused by a rapid correction of profound hyponatraemia (Na < 120 mmol/l) Hyponatraemia.
Partial cause is also alcohol use, not merely the correction of hyponatraemia.
The patients are usually alcohol-dependent, but the condition may also develop in hyponatraemia arising from other causes.
Myelinolysis is not limited to the pons region alone. Instead, it can be detected also e.g. in the cerebellum, basal ganglia region and thalamus.
Clinical manifestation
Mild forms of the disorder often go unnoticed or only have a few observable symptoms, but in severe forms the symptom picture includes tetraparesis, diminished consciousness and cranial nerve symptoms (dysphagia, dysarthria, nystagmus, gaze paresis). Severe forms may be fatal. Clinical signs become manifest before radiological changes are observable.
Treatment
Hyponatraemia in alcohol-dependent patients should not be corrected with an intravenous infusion. A suggested safe rate of normalizing the plasma sodium level is < 0.5 mmol/l/hour, but even this may lead to myelinolysis Hyponatraemia.
If the patient's clinical condition worsens during the sodium correction, the administration must be stopped and reinduction of hyponatraemia attempted.
Wernicke's disease
Caused by vitamin B1 (thiamine) deficiency
In addition to undernourished alcoholics, the risk groups include elderly individuals with impaired nutritional status, patients with a history of vomiting, those receiving parenteral nutrition, cancer patients and those with a chronic intestinal disease.
Thiamine is required for carbohydrate metabolism, and the administration of glucose, for example, will therefore increase its demand.
Symptoms
All components of the listed symptoms are rarely seen together, and many mild cases remain undiagnosed. It is therefore always important to give consideration to the possibility of Wernicke's disease.
The condition can be fatal, and treatment must already be initiated on suspicion alone.
The patient should receive thiamine 200 mg i.v. at 8-hour intervals for 3-5 days and thereafter 250 mg i.v. or i.m. once daily for 5-7 days. Thiamine is not sufficiently absorbed in the intestine. Glucose infusion must not be given before administering thiamine (it may worsen the situation). A multivitamin preparation is recommended as further treatment.
Pellagra
A deficiency disease rarely encountered in alcoholics in the Western countries; caused by a deficiency of niacin or its precursor, tryptophan.
Symptoms
Dermatitis, memory disorder, and diarrhoea (or constipation), possibly also spastic paresis, polyneuropathy, primitive reflexes, loss of appetite, incontinence, tongue pain, epileptic seizures and confusion
The likelihood of an alcoholic developing any of the following neurological disorders is markedly increased:
Brain injury
Brain injuries are three times as common in alcoholics as in the general population on average. Mild injuries often go undetected.
Chronic subdural haematoma
Cerebral circulatory disorders
Continuous excessive use of alcohol (> 60 g of ethanol/day) has been shown to increase the risk for intracerebral haemorrhage, subarachnoid haemorrhage and stroke.
Hepatic encephalopathy
Caused by hepatic insufficiency.
Symptoms include loss of attention, postural tremor, asterixis (flapping tremor) and myoclonia. The EEG displays slow-wave activity, and MRI shows hyperintense lesions in the area of globus pallidus, which will disappear as the hepatic insufficiency improves
Movement disorders
An alcohol withdrawal state is characterised by postural tremor that resembles essential tremor. Parkinsonism Parkinson's Disease is sometimes seen during withdrawal from alcohol, but this does not lead to the development of actual Parkinson's disease. Cerebellar degeneration and hepatic encephalopathy are also associated with tremor (see above).
Sleep disorders
Intoxication increases apnoeic periods during sleep and worsens the quality of sleep.
Infections
Listeria and pneumococcal meningitis, in particular, are common in alcohol-dependent individuals.
Thiamine deficiency may also cause polyneuropathy, beriberi and Marchiafava-Bignami syndrome (corpus callosum necrosis)
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