• Energy Research
• clinical medicine close
• German close
• Neuroinformatics close

This paper reviews and discusses basic knowledge of biochemical mechanisms of action of ethanol upon the central nervous system, the emphasis being on effects upon cerebral membrane structures and processes as well as mechanisms of chemical synaptic transmission. Results of detailed studies into material and steric changes in membranes, ion-dependent adenosine triphosphatases, variations in ion balance, effects upon cyclic nucleotides, influences on special transmitter systems, and mechanisms of formation of morphine-analogous condensation products are presented. In addition, open questions are derived and formulated in problem complexes.

The incidence and prevalence of alcoholism in the elderly population are tendentially underestimated. There are some reasons for this fact. The pathway to the diagnosis of alcoholism may be considerably compromised in the often comorbid or multimorbid patient. To live up to an advanced age seems to be a good argument against chronic substance abuse. Elderly people and their relatives are often still more reluctant to report about socially stigmatizing disorders. On top of that, the amount of social control is reduced after the end of employment and upon entering retirement. Yet, if alcohol-withdrawal symptoms occur, e.g., following an admission of the addicted patient to a hospital, the missed diagnosis of alcoholism means a delay of the correct interpretation of such complications and of the necessary treatment. Aged patients with reduced physical and mental reserve capacity are at special risk of developing further serious complications. Progressive, sometimes irreversible decay of the cognitive functions in long lasting delirious states or, as an aftermath of withdrawal, epileptic seizures are of particular importance.

In a total of forty-five cases of masturbation practiced by children EEG derivations were made before, during, and after anticonvulsive treatment. The results obtained confirm the clinical experience showing that the observed seizure-like phenomena have no relation whatever to forms of epilepsy.

This review describes the following results of human genetic research on the "normal" human EEG: As shown by comprehensive studies on mono- and dizygotic twins, interindividual variability of the human EEG under "normal" conditions is largely genetically determined. This was mainly shown for the resting EEG, but holds true also for the sleeping EEG, the reaction to ethanol, and for visually and auditory evoked potentials. Some fairly common EEG variants have been described which follow simple Mendelian modes of inheritance. Hence, they must go back to correspondingly simply differences in certain genes and gene-determined proteins. These variants have been useful as model systems for a neurobiologically founded research strategy in behaviour genetics of man. Comparative studies using psychological, neurophysiological (visual and auditory evoked potentials) and biochemical methods revealed group difference especially between carriers of the low-voltage EEG, the EEG with monomorphic alpha-waves and an EEG variant containing, in addition to alpha-waves, numerous diffuse beta-waves. Utilizing concepts from basic research in neurophysiology, they could be explained by corresponding differences in central information processing. Individual differences of EEG reaction are also observed after a controlled ethanol load. They have a genetic basis, too. An especially clearcut reaction of the EEG to alcohol can be seen in individuals with irregular alpha-activity of low amplitude in the resting EEG. Moreover, these persons appear to be especially susceptible for "learning" to become alcohol addicts. Individual variability in maturation during childhood and youth of brain structures responsible for EEG production are also under genetic control. This EEG maturation influences intellectual and psychic maturation.

For some little time it has been known that hyperosmolar coma is a clinical condition which may arise from various causes and yet is based on a fundamental pathophysiological disturbance: extracellular hyperosmolarity, usually accompanied by hyperglycemia or hypernatremia. The clinical and biological picture is easily recognizable and requires immediate and massive rehydration with hypotonic solutions. Many pathological uncertainties still exist, but one thing is certain and of great importance: in many cases, hyperosmolar coma is the result of errors or negligence: for this reason it is essential know this syndrome so that it may be better avoided.