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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Information which has emerged thus far relates to the overall transmitter mechanisms of sleep. The data, while conflicting, point to the involvement of many neuroregulators at numerous integrative levels of the process. However the long term question still remain: what triggers and maintain sleep, what stops sleep, what occurs to the body and brain during sleep--in essence, why sleep? These questions are now problems for behavioral neurochemists, whereas in a previous era, they were problems for philosophers. Unfortunately, our answers to date, while in another idiom, have hardly been more complete or satisfying. To answer these questions, it will be necessary to understand, in detail, the manner in which neurobiochemical processes relate to the functional physiology of sleep. Although existing studies have given invaluable insight into the neurochemical anatomy of sleep, we have only recently acquired the technical and biochemical expertise necessary to investigate sleep as it occurs normally. Future research must focus on the dynamic changes associated with the regulatory mechanisms of neurotransmitters. Many questions can be asked. With sleep transitions, what changes occur in transmitter content, synthesis, or release? Are there changes in metabolic pathways, reflecting a shift from intra- to interneuronal metabolism? What changes occur in pre- and postsynaptic neurotransmitter receptors to affect sensitivity? What constraints do genetic (245) and environmental (246) factors impose upon these mechanisms? Knowledge of such parameters will allow us to construct more complete models of the neuroregulatory basis of sleep and waking. However, as we acquire this knowledge, we must avoid the temptation of assuming causation when the evidence merely shows correlation. Neuroregulation are involved in the control of number different behaviors; and, at present, we have few, if any, methods of establishing causative links between a specific neuroregulator and a specific behavioral state. Yet, even without an understanding of what "causes" sleep, we may be able to develop pharmacological agents which permits discrete alteration of sleep mechanisms in a more physiological and specific manner. This potential for manipulation of sleep is of obvious importance in illnesses such as insomnia, narcolepsy, and sleep apnea (247, 248). In addition, it may be valuable in the treatment of such conditions as psychosis and depression, where sleep disturbances are an important component of the illness. For example, delirium tremens might be best understood as a psychotic episode which is the result of an aspect of sleep emerging into wakefulness. The range and breadth of both the basic questions and the potential application of sleep research portend an exciting future for this field.
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PMID:Neuroregulators and sleep mechanisms. 16 54

Delirium tremens is linked with a chronic depression of the central nervous system by alcohol and a compensatory hyperactivity of neurotransmitters. A sudden stoppage of alcohol intake induces excessive production of these transmitters. Firstly appearing is a noradrenergic hyperactivity which may be responsible not only for reducing the magnesium blood level but also for activating the other transmitter systems. A magnesium blood level lower than 1 mmol.l-1 involves a risk of seizures and requires IV magnesium sulfate. Noradrenergic hyperactivity can be prevented by IV alcohol associated with sedation best achieved by IV clomethiazole in alcoholic solution. Should these preventive measures fail, noradrenaline action in the central nervous system can be blocked by clonidine. Should hallucinations become manifest, linked to dopaminergic hyperactivity, haloperidol is indicated. Benzodiazepines may be useful, particularly carbamazepine, for their depressing effect on gaba-ergic hyperactivity.
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PMID:[Delirium tremens. Recent neurophysiologic concepts and therapeutic outlook]. 151 60

Benzodiazepines are generally well tolerated (compared to barbiturates or antidepressants, their side-effects are milder). They may be used safely, their toxicity is low. Benzodiazepine overdosage may be lethal only if the drug is taken simultaneously with other drugs or alcohol. They act primarily through inhibiting the GABA system, their anxiolytic and sedative effects are of primary importance from the psychiatric aspect. Their classification is based on the difference in their receptor affinity (potency) and kinetics. Derivatives of low, medium and high potency are known. The introduction of high potency benzodiazepines in psychiatry has increased the therapeutic means. The major field of indication of benzodiazepine therapy is DSM-III anxiety disorders and insomnias but they may be successfully used in the treatment of manic conditions, schizophrenia, delirium tremens, clinical conditions accompanied by anxiety-depression, acute restlessness, neuroleptic-induced acute distonias, and akathisias. Even if therapeutic doses are used, tolerance to benzodiazepines may develop after some weeks of therapy. The general withdrawal symptoms are not severe, but the rebound symptoms often hinder the discontinuance of the drug or the reduction of doses. When prescribing benzodiazepines the risk of long-term therapy and the prevention of the development of drug addiction have to be considered.
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PMID:Use of benzodiazepines in psychiatry. 181 22

This paper examines severity of depressive symptoms, as measured by the Beck Depression Inventory, in chronic alcoholics with and without a history of hallucinations. We found a) alcoholics entering alcohol treatment who have experienced hallucinations during detoxification report higher levels of subjective depression than alcoholics who have never experienced hallucinations, b) the level of subjective depression in alcoholics with a history of hallucinations remains higher at the end of inpatient alcohol treatment than in alcoholics without hallucinations, and c) hallucination is the important variable; alcoholics with blackouts, seizures, and delirium tremens, do not experience higher levels of depression during detoxification. The reporting of a significantly higher level of depressive symptoms by alcoholics with a history of experiencing hallucinations during withdrawal suggests that in some alcoholics, there exists a vulnerability for mood abnormalities which includes a predisposition toward other abnormal mental phenomena such as perceptual distortions.
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PMID:Dysphoria in male alcoholics with a history of hallucinations. 186 70

Patients with alcohol dependence commonly experience symptoms of anxiety, depression, and insomnia. It is essential that clinicians recognize and treat anxiety disorders in alcoholic patients. Panic attacks with and without agoraphobia are especially prevalent among alcoholics and their families. Treatments of choice for panic disorder are the monoamine oxidase inhibitors, as well as tricyclic antidepressants and the benzodiazepine alprazolam. Benzodiazepines seem to be effective in controlling two pathophysiologic characteristics of alcohol withdrawal--noradrenergic and hypothalamic-pituitary-adrenocortical overactivity. They also can be used to prevent and treat withdrawal seizures and delirium tremens. They are not indicated for the treatment of alcohol dependence per se.
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PMID:Anxiety and alcoholism. 268 Nov 71

After undergoing replantation and revascularization surgery for a complex hand injury, a 25-yr-old male developed florid delirium tremens. Over a 5-day period, he received 2850 mg of midazolam as a constant infusion of varying rates. The midazolam controlled his severe agitation without respiratory depression and the hand reconstruction survived undamaged.
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PMID:Massive doses of midazolam infusion for delirium tremens without respiratory depression. 334 36

A sequential sample of 101 patients hospitalized for ethanol withdrawal and requiring sedation for evolving withdrawal syndromes was assigned randomly according to a double-blind protocol to treatment with either alprazolam or chlordiazepoxide administered orally. The data from one patient were unevaluable due to acute bleeding, leaving a sample of 100 (50 in each condition). At discharge, three independent ratings of diaphoresis, tremor, hallucinations, nausea/vomiting, and overall severity of withdrawal were obtained, and the occurrence of delirium tremens and grand mal seizures was noted. Patients also completed the Beck Depression Inventory, and their disposition following discharge was recorded. There were no statistically significant differences between the two treatment groups on any of the dependent variables studied. It was concluded that the choice between alprazolam and chlordiazepoxide for managing ethanol withdrawal should be based on criteria other than efficacy of control. Potential antidepressant effects and drug kinetics were suggested as the basis for rational decision-making.
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PMID:Double-blind trial of alprazolam and chlordiazepoxide in the management of the acute ethanol withdrawal syndrome. 388 64

A forty-two year old female with known alcoholic liver disease was given intravenous lorazepam and diazepam for delirium tremens. This resulted in a comatose state with depression of some brainstem reflexes. Her initial EEG showed a pattern of spindle coma with some responsivity of the background. Clinical improvement occurred with cessation of the benzodiazepines and the EEG showed a return to normal patterns. A review of the literature showed no previous description of this pattern in benzodiazepine coma. Two reports of spindle coma are noted with alcohol and imipramine. The prognostic significance of this pattern in drug overdose is therefore not definitive by itself. Outcome is probably more dependent on the clinical condition of the patient and the reversibility of the drug toxicity.
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PMID:Spindle coma in benzodiazepine toxicity: case report. 407 34

One hundred patients, aged between 60 and 92 years, were treated with tiapride for neurological disorders (abnormal movements, buccofacial dyskinesias, dopa therapy complications, ballism, eyelid tics, senile tremor, post-traumatic headache, delirium tremens), psychiatric disorders with more or less marked agitation and of various types (hysteria, depression, mood disturbances, hypochondria, delusions, hallucinations), or for mental deficiency, senile dementia, or arteriopathic dementia. Results were excellent, being satisfactory in 70 p. cent, and even more marked in some groups. Tolerance was very good, with some rare cases of somnolence. The efficacy and safety of tiapride makes it of particular value for treating neuropsychiatric disorders in geriatric patients.
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PMID:[Tiapride in the treatment of neurological and psychiatric disorders in the elderly (author's transl)]. 627 32

Cluster analysis was carried out on a sample of 92 patients with behavior disorders caused by degenerative, vascular, (alcohol) toxic, and other diseases of the brain. Rating variables of the AMDP system concerning mental state, social behavior, need for special care, sleep disorders, autonomic, physical, and neurologic symptoms were used in the absence of severe degrees of disordered consciousness such as stupor, coma, delirium tremens, and gross cerebral lesions. Results suggested the existence of four major groups of global cognitive impairment combined with neurasthenia and irritability in the first, hypochondriasis and depression in the second, withdrawal symptoms in the third, and severe disorientation in the fourth. At the seven-group level the groups were further distinguished according to severe withdrawal, amnestic syndrome, and dementia by various social and illness behaviors, sleep-wakefulness pattern, hypo- or hyperactivity, additional physical, and neurologic symptoms. Other minor types of organic brain syndromes were identified as individual cases by hallucinations or other circumscribed cognitive, psychomotor, affect, motivation, personality, and/or behavior disorder, symptomatic manic, or schizophreniform psychosis. The findings lent support to old classifications and new ones of organic mental syndromes (DSM-III).
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PMID:Classification of organic brain syndromes by cluster analysis. 742 21


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