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Definitions of Delirium Tremens (DT) and related clinical states are discussed together with the concepts of aetiology and pathogenesis in relation to psychiatric disease. The withdrawal theory which considers reduction or cessation of alcohol intake as an important precipitating factor in DT is discussed; this theory is supported by experimental studies of ethanol withdrawal in man and by studies indicating cross dependence between ethanol and several other CNS depressors; the arguments in the literature for and against the withdrawal theory are discussed. Other possible aetiological factors such as type of liquor, hypovitaminosis, liver disease, dysfunction of the adrenals and fat emboli are reviewed, and it is concluded that these factors are unimportant as precipitating or specific aetiological factors in DT. Possible pathophysiological mechanisms are discussed, especially concerning electrolyte metabolism and cerebral blood flow and oxygen consumption. It is concluded that the pathophysiology of the disease is poorly understood, and some possibilities for future research are indicated. The discussion about treatment of DT is concentrated on drug treatment, and the literature concerning antipsychotics and sedatives is reviewed. It is concluded that barbital, a long-acting barbiturate, is the most effective treatment; diazepam can be recommended as an acceptable alternative. Finally, practical recommendations concerning treatment are given.

Tremor measurements were obtained from 12 male volunteers before and during ethanol intoxication. The tremor recorded during extension and flexion of the hand is called physiological action tremor (PAT) and shares many of the same frequency, amplitude, and electromyographic characteristics reported for withdrawal tremor (WT). This report focuses on the relationships of these two tremors and presents further evidence to consider that PAT and WT might be controlled by the same mechanisms.

BAEP studies hint at different neurophysiological findings between gamma and delta alcoholics. On the first day of withdrawal gamma alcoholics show slight vegetative withdrawal symptoms in the form of CNS hyperexitability trough the shortening of the early IPL. However delta alcoholics show prolongations of the late IPL which can be interpreted as a consequence of brain stem transmission disorders resulting from chronic intoxication. After four weeks the BAEP deviations found in both groups indicate a clear tendency of recovery which points to functional disorders.

There has been speculation that a kindling model may have applicability to alcohol withdrawal syndromes and seizures, suggesting that repeated alcohol withdrawals may lead to increased severity of subsequent withdrawals. We evaluated historical and clinical variables of a group of male alcoholics with (n = 25) and without (n = 25) alcohol withdrawal seizures. We found that the number of detoxifications appeared to be an important variable in the predisposition to withdrawal seizures. The withdrawal seizure group had 12 of 25 (48%) patients with 5 or more previous detoxifications, compared to only 3 of 25 (12%) of the control group. A relationship between alcohol use history and withdrawal seizures was not supported by the data. These findings support the concept that previous alcohol withdrawals may "kindle" more serious subsequent withdrawal symptomatology, ultimately culminating in withdrawal seizures.

Auditory brainstem responses were obtained from 52 alcoholic patients with or without neurological complications of alcoholism. Almost half of the patients had abnormal auditory brainstem responses manifested by a prolonged central conduction time (Wave I to V interval) without significant alterations in morphology. The incidence of abnormal auditory responses was related to the type and the number of neurological complications. Patients with Wernicke-Korsakoff syndrome, dementia or cerebellar degeneration had high incidence of brainstem abnormalities. All patients with 3 or more neurological complications had abnormal auditory brainstem responses.

42 alcoholic patients were grouped together according to the symptom-sign clusters derived from original classification variables of AMDP-rating scale system: (1) mild withdrawal, (2) severe withdrawal, (3) Korsakoff's syndrome, and (4) the clinical syndrome of dementia. Groups determined by clusteranalysis were subjected to a discriminant function analysis. Total cerebral blood flow (CBF) and the cerebral metabolic rates of oxygen, carbon dioxide, glucose and lactate were investigated. Patients with mild withdrawal tended to display increased oxygen uptakes reflecting 'pseudonormal' mean values with a wide range of the single data but predominantly elevated over the normal range. In mild withdrawal lactate production showed a tendency to increasing derangement of metabolism. There was much evidence of disturbance of brain oxidative metabolism with progressively decreasing cerebral metabolic rates of glucose, lactate, oxygen, and CBF from mild to severe withdrawal, Korsakoff's syndrome and dementia. Progression of both clinical phenomenology and cerebral dysfunction and/or damage culminates in simplified (reduced, "burnt-out") neuronal functional levels in advanced cases.

The sleep pattern of 13 alcoholics was recorded for five consecutive nights after the cessation of alcohol intake. In six of the 13 patients, delirium tremens occurred after hospitalization. A decrease of total sleep time and slow wave sleep was more pronounced in the patients with delirium tremens than in those without. REM sleep had slightly decreased in both groups. Rebound increase in REM sleep had not been observed in all the patients with delirium tremens. Stage 1-REM with tonic EMG was observed in these two groups. From these results we are inclined to hypothesize that a deficiency of cerebral 5-HT in alcoholics may lead to a pronounced decrease in slow wave sleep, with rapid eye movements appearing in stage 1 sleep.

Tolerance to ethanol, as assessed by loss of the righting reflex or by improved performance in the aerial righting reflex test, was only observed in animals which did not show signs of a withdrawal reaction. With long exposure periods to ethanol vapor, tolerance was no longer present in animals exhibiting withdrawal reactions. These data are consistent with the hypothesis that a reversal of tolerance precedes prior to the development of physical dependence on ethanol.

Based on a series of known facts on clinical findings and changes in the metabolism of chronic alcoholics and delirious people the possible pathomechanism of cerebral imbalances is presented according to a synopsis. The clinical symptomatology, in particular vegetative symptoms and the coordination of reflexes - to which more attention should be paid than has been up to now - make delirium appear a diencephalic illness, the sympathicotonic and ergotropic development of which together with a preponderance of noradrenergic-adrenergic mechanisms, remains unexplained to this day.