Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines twenty-four cases of amok, believed the largest number of cases ever collected. They were observed in Sarawak, East Malaysia. They occurred in all indigenous groups in Sarawak, excluding the Chinese, such as Malay, Sea Dayak, Land Dayak, Kayan, Punan and Melanau at frequencies more or less following the proportion of these groups in the total population. No differences were found according to religion, the Malay being Muslim and the other groups either predominantly Christian like the Iban or animistic. Only slight diminution in the frequency was observed from 1954 to 1968. The education level of the amok runners was much lower than that of the average population. The weapons used were those immediately at hand be it parang (short sword), ax, sticks, knives, guns, bare hands or a lorry. The classical four stages were largely present: (a) brooding and withdrawal, (b) homicidal paroxysm, (c) continuation of homicidal behaviour until killed, restrained or falling into stupor of exhaustion, (d) complete or partial amnesia. While in 14 no motive could be ascertained, insult, jealousy and paranoid ideation was present in the others. Both family history of mental illness and personal psychiatric history were predominant. All cases fell into accepted diagnostic categories from organic and endogenous psychosis to neurosis and behaviour disorder.
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PMID:Running amok. 60 13

The conception of a specific association between maturity-onset diabetes and manic-depressive psychosis, on a common basis with diencephalic functional obesity, has been recently taken again in consideration by the psychiatric literature. Investigations on this problem from diabetological point of view have been so far completely lacking, and are proposed with the present study. Symptomatic depressive conditions in diabetes are frequent and should be primarily separated from depressive endogenous psychosis. The pathogenesis of the association between diabetes of the adult-obese type and psychosis might be discussed according to a transactional theoretical model, assuming a positive feed-back mechanism of the two relationships: diabetes-psychosis and psychosis-diabetes. With these criteria, 4 observations of the clinical association were collected out of 274 admissions for diabetes, during 1976. Diabetes is intended as overt diabetes; obesity presented with the stenic picture; psychosis had a monopolar melancholic course. Similar clinical features were characteristic in all cases. The relationship diabetes-psychosis showed no evidence, unless importance should be given to a potential diabetes in 3 cases. On the contrary, the relationship psychosis-diabetes could be demonstrated in the four cases. A psychosomatic scheme connecting the neuro-hormonal correlations to a genetically conditioned exhaustion of the beta-function, is postulated. During melancholic recurrences, diabetes proved to be insulin-dependent and even insulin-resistent in 2 cases. Tricyclic antidepressant theraphy did not modify the metabolic situation.
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PMID:[Association of adult obese-type diabetes and depressive psychosis (clinical cases)]. 61

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

Paradoxical or "forced" normalization of the EEG of patients with epilepsy was first described by Landolt in 1953. It refers to conditions where disappearance of epileptiform discharge from the routine scalp EEG is accompanied by some kind of behavioral disorder. The best known of these is a paranoid psychotic state in clear consciousness, which is also known as "alternative" psychosis. Thus, the issue is related to much older observations which indicated a "biological antagonism" between productive psychotic symptomatology and epileptic seizures, which led to the therapy of psychoses with artificially induced convulsions. Apart from psychotic episodes, the clinical manifestations of PN comprise dysphoric states, hysterical and hypochondriacal syndromes, affective disorders, and miscellanea. PN can be observed in both generalized and localization-related epilepsies as a rare complication. A subset where it is more frequently seen are in adults with persistent absence seizures when the latter become finally controlled by succinimide therapy. These seem to be the drugs with the highest hazard of precipitation of PN, but all other AEDs have also been suspected. Sleep disturbance by succinimide treatment may play a crucial role, but a variety of other factors are also involved, including psychosocial factors. The pathogenesis of this condition has given rise to some debate but remains still unresolved. Eleven of the most important hypotheses have been discussed and seem to converge into a more comprehensive hypothesis which basically assumes that, during PN, the epilepsy is still active subcortically, perhaps with spread of discharge along unusual pathways. This activity is supposed to provide energy and, possibly, some of the symptoms included in the psychotic syndrome. A critical clinical condition results, usually with a dysphoric symptomatology, where a development towards psychosis is impending but still depends on the presence or absence of a variety of risk factors. Along with neurophysiological factors such as powerful inhibition of the spread of epileptic discharge, these may also include biographic factors such as the repeated experience of ictal sudden, unexpected loss of consciousness. Because during PN there presumably is ongoing epileptic activity, the differences with respect to other psychotic conditions in epilepsy are probably subtle rather than fundamental. Thus, it could be that ictal psychosis is characterized by a direct expression of epileptic activity, whereas in postictal psychosis a momentum of exhaustion may be added; moreover, in PN the prevailing pathogenic factor could be an abnormally high level of balance between excitatory and inhibitory processes.
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PMID:Acute behavioral symptomatology at disappearance of epileptiform EEG abnormality. Paradoxical or "forced" normalization. 200 2

A 27-year-old woman with a post-partum psychosis developed NMS which proved difficult to diagnose because of the organic features of the presenting illness. Possible contributory factors to the development of NMS included exhaustion, a non-specific viral illness, and rapid loading with haloperidol.
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PMID:Neuroleptic malignant syndrome in a case of post-partum psychosis. 262 Feb 14

Lethal catatonia, a syndrome described several decades before the advent of neuroleptic drugs, has been regarded by many investigators as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, published case reports of the two syndromes indicate differences in mode of onset, signs and symptoms, and outcome. Lethal catatonia often begins with extreme psychotic excitement, which, if persistent, can lead to fever, exhaustion, and death. Neuroleptic malignant syndrome begins with severe extrapyramidally induced muscle rigidity. Because lethal catatonia often requires neuroleptic treatment and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics, their early clinical differentiation is important.
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PMID:Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome. 260 93

The term fear of flying (FOF) has been applied to many sets of symptoms. Confusion has resulted from the use of the term FOF to describe problems arising from anxiety disorders, traumatic stress, exhaustion, psychosis, and motivational changes. This literature review describes the history and development of the term FOF, and suggests an approach to its evaluation by clinicians and administrators. Representative works from the last 65 years are reviewed in their historical contexts.
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PMID:A historical review of the fear of flying among aircrewmen. 355 51

In the present study two groups of 30 patients were compared. The first group included 30 acute schizophrenic patients, who were rated immediately after admission and 3 months later under depot-neuroleptics. The second group consisted of chronic schizophrenic outpatients, who were rated at the beginning of Fluphenazindecanoat-medication and 8 months later. As documentation PSE (present state examination) was used. Psychotic symptoms of the acute schizophrenic patients could be influenced well by the treatment, not in the same way, however, depressive and neurotic symptoms. The frequency of psychotic symptoms is lower in chronic schizophrenics than in acute ones at the beginning of therapy. 8 months later there are little more psychotic symptoms in chronic patients than in acute schizophrenics; the depressive symptoms follow the same design in a lower extant however. The scores of depressive symptoms in the acute-group are similar to those of chronic schizophrenics and do not change significantly in the course of 8 months lasting depot-neuroleptic therapy. Another study could show 1982, that 67 outpatients from 87 in the year 1972 still were in psychiatric care and control, 23% of them received antidepressiva because of depressive symptoms in connection with residual syndromes and only 4% because of exhaustion-syndromes after remission of the disease.
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PMID:[Depressive syndromes within the scope of schizophrenic psychoses]. 393 87

Lethal catatonia is often regarded as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, the two syndromes reveal differences in the mode of onset, signs and symptoms, and outcome. Lethal catatonia often begins with extreme psychotic excitement, which, if persistent, can lead to fever, exhaustion, and death. Neuroleptic malignant syndrome begins with severe extrapyramidally induced muscle rigidity. Early clinical differentiation is important, because lethal catatonia often requires neuroleptic treatment, and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics.
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PMID:[Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome: a case report]. 765 87

Neuroleptic malignant syndrome (NMS) is a rare but potentially lethal form of drug-induced hyperthermia characterised by mental status changes, muscle rigidity, hyperthermia and autonomic dysfunction. Increased awareness and early recognition will lead to prompt management. The diagnosis of NMS presents a challenge because several medical conditions generate similar symptoms. The presentation and course of NMS can be quite variable ranging from a stormy and potentially fatal course to a relatively benign and self-limiting course. The most important aspect of treatment is prevention. This includes reducing risk factors (e.g. dehydration, agitation and exhaustion), early recognition of suspected cases and prompt discontinuation of the offending agent. All patients with psychosis should be monitored daily for dehydration and elevated temperature, have vital signs checked and agitation should be watched for. Antipsychotics should be used conservatively with gradual titration of doses. The management of NMS should be based on a hierarchy of symptom severity. Following an episode of NMS, the patient should be reassessed for further treatment with antipsychotics and rechallenge should not be attempted at least 2 weeks following resolution of symptoms of NMS. The patient and family should be educated about the episode and consent for further medication use obtained after a clear explanation of the risk-benefit analysis.
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PMID:Neuroleptic malignant syndrome. Recognition, prevention and management. 967 59


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