Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Psychogenic (dissociative) amnesia is a psychiatric disorder characterised by a sudden loss of memory which is too extensive to be explained by ordinary forgetfulness, but which has no organic disease or explanation. Psychogenic amnesia is categorised among the dissociative disorders in DSM-IV and ICD-10 and begins suddenly, usually after severe psychosocial stress. The prognosis is good with complete recovery, and there is seldom relapse. This article describes a man, 45 years of age, who developed severe depression and amnesia following a very troublesome divorce. He did not talk, he communicated by signs and gestures, and he isolated himself in his mother's home. After being admitted to a psychiatric ward he became anorectic and developed erosive eoesophagitis/gastroduodenitis. Initially he was given perfenazin (Trilafon) 24 mg/day. The psychiatric treatment produced no results for the first three weeks, but the patient gradually recovered when the therapist and the patient recapitulated the conflicts associated with the divorce, using documents from the patient's lawyer as a guide. This method is called "therapeutic anamnesis" and is similar in many ways to psychiatric treatment of post-traumatic stress reactions.
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PMID:[Treatment of patients with psychogenic amnesia with the help of therapeutic anamnesis]. 983 Mar 45

We have recently reported a new protocol for inducing long-term depression through activation of GABAA receptors in the hippocampal slices. This long-term depression is reversed by bicuculline and potentiated by neurosteroids such as alphaxalone. It was also shown that glutamate receptor activity or extracellular calcium are not involved in the induction of this type of long-term depression. The present study investigated the possible relation between muscimol-induced long-term depression and barbiturates/benzodiazepine-induced amnesia and attempts to determine the possible effect of pregnenolone sulfate on muscimol-induced long-term depression. Extracellular recordings were made in the CA1 pyramidal cell layer of rat hippocampal slices following orthodromic stimulation of Schaffer collateral fibres in stratum radiatum (0.01 Hz). It was observed that pentobarbital, benzodiazepines and pregnanolone at concentrations that did not have any effect themselves on the population spike, potentiate the ability of muscimol to induce long-term depression. In addition to this, the long-term depression was either blocked or reversed by pregnenolone sulfate at concentrations (10 microM) where pregnenolone sulfate did not induce any multiple burst or increase of spike size. The results suggest that the potentiation of this type of long-term depression by benzodiazepines and barbiturates can explain the main adverse effect of these drugs, amnesia and cognitive impairment. Moreover, the prevention or reversal of this type of long-term depression by pregnenolone sulfate, may suggest a clinical application of this agent in the management of amnesia or dementia.
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PMID:Potentiation of muscimol-induced long-term depression by benzodiazepines and prevention or reversal by pregnenolone sulfate. 999 Jun 52

Use of the elevated plus-maze experiment and activity and traction tests in mice have revealed that seven daily treatments with 0.2 mg kg(-1) and higher doses of honokiol, a neolignane derivative extracted from Magnolia bark, had an anxiolytic effect without change in motor activity or muscle tone. Diazepam, 1 mg kg(-1), had the same anxiolytic potential as 0.2 mg kg(-1) honokiol but induced muscle relaxation. The aim of this study was to determine whether honokiol had diazepam-like side-effects. Mice treated with 1-10 mg kg(-1) diazepam, but not those treated with 0.1-2 mg kg(-1) honokiol, for 12 days showed withdrawal symptoms characterized by hyperactivity and running-fit when they were challenge-administered intraperitoneal flumazenil (10 mg kg(-1)) 24 h after the last treatment with diazepam. Oral diazepam (0.5-2 mg kg(-1), 10 min before) dose-dependently prolonged hexobarbital (100 mg kg(-1), i.p.)-induced sleeping, disrupted learning and memory, and inhibited (+)-bicuculline (40 mg kg(-1), i.p.)-induced death. Honokiol (0.2-20 mg kg(-1), p.o., 3 h before) had no such effects. The prolongation by diazepam (1 mg kg(-1)) of hexobarbital-induced sleeping was not modified by honokiol (0.2-20 mg kg(-1)). These results suggest that honokiol is less likely than diazepam to induce physical dependence, central depression and amnesia at doses eliciting the anxiolytic effect. It is also considered that honokiol might have no therapeutic effect in the treatment of convulsion.
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PMID:Honokiol, a putative anxiolytic agent extracted from magnolia bark, has no diazepam-like side-effects in mice. 1019 25

Adjuvant therapy with interferon for malignant melanoma causes neurotoxic side effects such as depression. The biochemical mechanisms are unknown. We report two cases with both depression and amnesia. In one case, attempted suicide was accompanied by 7 h of amnesia. The diagnostic classification and possible explanations for the amnesia secondary to interferon therapy are reviewed.
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PMID:[Depression and suicidal intentions as a side effect of high dosage interferon-alpha therapy--two cases]. 1035 18

A patient (PC) with severe and chronic retrograde amnesia for world knowledge (tested with famous events and famous faces), but unimpaired autobiographical memory is described. The 64-year-old man had traumatic brain injury four years prior to the present evaluation. Current brain imaging showed principally damage involving the infero-lateral prefrontal and the lateral temporal regions of the left-hemisphere. PC was of average intelligence, had no depression and only minor language problems, but manifested some additional anterograde memory deficits and performed subaverage in various frontal lobe-sensitive tests. Patient PC represents one of the very few cases with a preserved retrograde episodic and an impaired retrograde knowledge system, showing a dissociation between preserved retrieval of autobiographical events and amnesia for nonpersonal famous events. It is hypothesized that the sparing of autobiographical memories can be linked to the integrity of the right frontal and temporo-polar cortices.
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PMID:Retrograde amnesia for world knowledge and preserved memory for autobiographic events. A case report. 1036 96

Discoveries made over the past 20 years have greatly improved our understanding of how the brain functions. This article focuses on the relation between memory and cellular mechanisms of neuronal and synaptic plasticity in the hippocampus. Several studies indicate that the hippocampal formation is a crucial element of the neurobiological bases of higher cognitive function. Severe damage to the hippocampal formation is known to produce seemingly permanent anterograde amnesia. A generally accepted hypothesis in neurobiology has been that long-lasting activity-dependent changes in the efficacy of synaptic transmission in the mammalian brain are considered to be of fundamental importance for the development of neural circuitry and for the storage of information. The most compelling and reliable model for such changes has been long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus. Therefore, the possibility of the discovery and development of compounds that, by modulating hippocampal synaptic plasticity, would be useful for the management of dementia and amnesia.
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PMID:Hippocampal synaptic plasticity and cognition. 1047 82

The electroconvulsive therapy (ECT), which provokes a generalized epileptic seizure by an electrical stimulus, was first administered in 1938 and performed without anesthesia during thirty years. Nowadays, ECT is carried out using brief anesthesia (preferably methohexital) and skeletal muscle relaxation (succinylcholine) to avoid fearful complications like bone and muscle fractures. ECT is a safe treatment without absolute contraindications; the treatment risk corresponds to the risk of general anesthesia. ECT is indicated in depression, mania and schizophrenia. It plays an important role in the treatment of therapy resistant, severely ill patients with affective disorders, suicidal drive, delusional symptoms, vegetative dysregulation, inanition and catatonic symptoms. The response rate (remission or marked improvement) is about 70%. Usually ECT is performed 3 times per week, resulting in an ECT course with a total number of 6 to 12 single treatments. Within 2 or 3 weeks a substantial improvement can be expected. Further controlled studies are required with regard to antidepressive and/or antipsychotic continuation therapy after successful ECT course. Brief pulse stimulation, unilateral nondominant electrode placement and individual stimulus titration with respect to seizure threshold (EEG monitoring is required!) can minimize cognitive side effects. The apprehension that ECT could cause prolonged amnesia and structural brain damage has not been confirmed by the available scientific data. Modern brain imaging methods could elicit the until now unknown mode of action of ECT.
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PMID:[Clinical value of electroconvulsive therapy in treatment of depression]. 1063 58

Alzheimer's disease is a cortical dementia with an insidious onset and relatively slow progression. In the early stages and throughout most of the disease, memory impairment is the primary problem. Any manifestation of psychiatric symptoms is generally secondary to the amnesia, the paramount symptom of early Alzheimer's disease. The psychiatric symptoms emanate from the memory impairment. Therefore, testing memory is essential. The first stage of Alzheimer's disease commonly is marked by anxiety and depression secondary to memory impairment, and delusions. In the second stage, delusions often become more bizarre. Impairment of visuospatial memory, improper advances, and obscene language begin to replace disinhibited behavior, often to the point of violence directed at others. Increasing agitation requires restraints. In the third and final stage, screaming, banging, and cursing are common features. Verbal and behavioral perseverations are very common. Fecal and urinary incontinence and gait apraxia are other features of the final stage, again with restraints often necessary. In addition to outlining the progression of Alzheimer's disease through these stages, this article summarizes the available pharmacotherapy for the various psychiatric manifestations of the illness prevalent at each stage.
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PMID:Psychiatric disorders associated with Alzheimer's disease. 1073 May 8

Nocturnal eating disorder (NED) is a rare syndrome that includes disorders of both eating and sleeping. It is characterized by awakening in the middle of the night, getting out of bed, and consuming large quantities of food quickly and uncontrollably, then returning to sleep. This may occur several times during the night. Some patients are fully conscious during their nocturnal eating, while some indicate total amnesia. The etiology of NED is still unclear, as research findings are contradictory. Those suffering from NED exhibit various levels of anxiety and depression, and many lead stressful life-styles. Familial conflict, loneliness and personal crises are commonly found. Recently, a connection has been discovered between NED and unclear self-definition, faulty interpersonal communication, and low frustration threshold. Several authors link it to sleepwalking, leg movements during sleep, and sleep apnea. Treatment is still unclear and there have been trials of pharmacotherapy, psychotherapy, or a combination of both. However, pharmacological treatment has generally been found to be the most effective, although each case must be considered individually. In 1998, 7 women referred to our Eating Disorders Clinic, 5% of all referrals, were subsequently diagnosed as suffering from NED. Of these, 3 suffered from concurrent binge-eating disorder and 4 also from bulimia nervosa. 2 case studies representative of NED are presented.
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PMID:[Nocturnal eating disorder--sleep or eating disorder?]. 1088 92

Inhaled and other anesthetics profoundly affect the central nervous system, causing amnesia, immobility in the face of noxious stimulation, and depression of thermoregulation. Nonimmobilizers, inhaled compounds whose lipophilicity suggests that they should be anesthetics, do not produce immobility, but they do cause amnesia. Their effects on thermoregulation were the subject of the present study. We gave eight rats isoflurane on one occasion and the nonimmobilizer 2N (1,2-dichlorolhexafluorocyclobutane) on another. We measured the effect of various concentrations of each compound on thermoregulation provoked by body cooling. The specific outcome was increased metabolism, as reflected in increased output of carbon dioxide. Isoflurane decreased the temperature threshold for such increases and the maximum response intensity, doing so in a concentration-dependent manner, whereas 2N had a minimal or no effect at any concentration up to 0.9 minimum alveolar concentration (estimated from its lipophilicity). Thus, 2N may be a useful tool for studies of the mechanisms mediating the thermoregulatory depression produced by anesthetics: 2N should not affect such a mechanism.
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PMID:The nonimmobilizer 1,2-dichlorohexafluorocyclobutane does not affect thermoregulation in the rat. 1100 66


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