• Energy Research
• 3. Good health 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.

The effects of spontaneous respiration and mechanical ventilation on ICP were examined by investigating the interaction between elevated pressure and alcohol intoxication. 200 ml ethanol 48% were infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (Group 1), 7 young pigs with elevated intracranial pressure during spontaneous respiration (Group 2), and 4 young pigs without elevated intracranial pressure during spontaneous respiration (Group 3). While the behaviour of intracranial pressure during mechanical ventilation in the animals from Group 1 was inhomogeneous with a tendency to rise (29 mmHg to 34 mmHg), intracranial pressure (28 mmHg to 55 mmHg) increased dramatically in Group 2. This increase was associated with a sharp rise of paCO2 (37.6 mmHg to 73.3 mmHg) and a decline of paO2 (74 mmHg to 13 mmHg). None of the animals in Group 2 survived. paCO2 also rose in alcoholized animals without elevated ICP (Group 3) (41.9 mmHg to 63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in Group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory centre. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure can be generally avoided.

The mobilization of xenobiotics is, in common with their persistence and accumulation, a latent problem of our chemicalized society. Possible sequels connected with the chronic consumption of alcohol were demonstrated by results from animal experiments. After a 10-week exposition to DDE (50 p.p.m. given with the diet), followed by a time of nonexposition, rats were mated and their reproductiveness was brought in relation to the results from residue analyses. Half of the animal received 20% alcohol instead of drinking water during pregnancy and lactation. An alcohol-induced increase in the mobilization of DDE was evidenced on determining residues in the maternal brain, the placentae and the foetus, and also by the excretion in milk and urine. There was a significance increase in prenatal and postnatal mortality (reduced survival index). By analogy to DDT, an oestrogenic action is assumed to be causative.

We used the effect of ethanol on the convulsion threshold as model of injuriousness to analyse the CNS protective efficacy of nootropics. The CD50 of picrotoxine in mice was significantly diminished in comparision with the controls between 5 and 6 hours after 66 mmol/kg ethanol administered intraperitoneally and between 7 and 8 h after 92.4 mmol/kg. In this moment the administered ethanol was already eliminated; the effect is explained as a reversible consequence of the previous ethanol exposition. The influence of nootropics was examined. Piracetam (0.7 mmol/kg i.p.) as well as methylglucaminorotate (MGO) (0.68 mmol/kg-1 i.p.) suppressed the ethanol effect on the convulsibility, pyritinol (0.82 mmol/kg) was ineffective, and meclophenoxate (1.02 mmol/kg) by itself decreased the convulsions threshold.

Under the acute influence of alcohol with blood alcohol concentrations (BAK) ranging between 0.62 to 2.04%, the IPL prolongations of our subjects were within standard deviations compared with normal data. Depending on the BAK, these minor IPL alterations hint at a special vulnerability in the pontomesodiencephal area. The increase in BAK significantly correlates with the reduction of body temperature. The BAEP proves to be suitable for defining undear states of coma different origin.

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.

After remarks about the history of pediatric electroencephalography some particularly important neurophysiological and especially electroencephalographical studies out-of the last ten years are reviewed: polygraphic studies in healthy and sick newborns, spectralanalytical investigations of the EEG in twins, infants and older children. The review is closed by some critical considerations about possibilities and limitations of the automatic analysis of the childhood EEG.

Oromandibular dystonia is a neuromuscular disorder characterized by tonic or clonic involuntary spasms of the masticatory and lingual muscles. We treated 50 patients with this movement disorder by injection of lidocaine and alcohol into the masticatory or tongue muscles to block muscle afferents from muscle spindle. The patients were divided according to clinical features into four groups: jaw-closing, jaw-opening, jaw-deviation, and tongue dystonias. Objective evaluation of the symptoms before and after therapy was based on a clinical scaling protocol in terms of four parameters (mastication, speech, pain, and discomfort scales). Symptoms improved in all patients without major side effects. The overall objective improvement (60.2+/-29.5%) was significantly (P<0.005, ANOVA) lower in tongue dystonia (14.1%) than in jaw-closing dystonia (67.6%) and jaw-opening dystonia (68.3%). Although the response of the muscle afferent block to tongue dystonia was hardly satisfactory, this treatment is suggested to be effective for oromandibular dystonia.

This article deals with the effects of alcohol on sleep and sleep EEG of healthy individuals and alcohol-dependent patients during different phases of alcohol dependency. Healthy individuals initially experience an improvement in sleep, although a greater quantity of alcohol can lead to problems of sleep maintenance during the second half of the night. Pre-existing sleep deprivation or sleep restriction potentiates the effects of alcohol. Alcohol-dependent patients are found to be more prone to sleep problems than healthy individuals, which can facilitate the development of alcoholism. These patients experience difficulty falling asleep and suffer from a reduced total sleep time during all phases of the disorder, often accompanied by other sleep disorders such as sleep apnea syndrome or periodic leg movements during sleep. Certain predictors for the risk of relapse in abstinent alcoholics have been identified. Neurobiological findings in sleep and alcohol dependency are discussed. The cholinergic-aminergic reciprocal interaction model of REM and non-REM sleep regulation is significant in this context. Therapeutic implications are discussed.