Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0002622 (amnesia)
5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article discusses the development and validation of a paper and pencil screening measure, the Structured inventory of Malingered Symptomatology (SIMS), designed to detect malingering. Test items were constructed from a combination of revised validity questions from existing instruments and characteristics of malingerers noted by existing research. Items were organized on one of five subscales by experienced clinical psychologists. College students (N = 476) were assigned to one of seven simulation conditions (i.e., psychosis, amnesia, neurologic impairment, mania, depression, low intelligence, and "fake bad") or an honestly responding group. All subjects were administered the SIMS, the F and K scales of the MMPI, 16PF Faking Bad scale, and portions of the malingering scale. The SIMS total score demonstrated the highest sensitivity rating (95.6%) for detection when compared with the other validity indices. Suggestions concerning further research using the SIMS as well as its potential utility in a complete evaluation process are discussed.
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PMID:Detection of malingering: validation of the Structured Inventory of Malingered Symptomatology (SIMS). 921 90

Psychosis has been recognized as a common feature in neurodegenerative disease for many years. Hallucinations, delusions, and other psychotic phenomena occur in a wide range of degenerative disorders including Alzheimer disease, Huntington disease, Parkinson's disease, diffuse Lewy body disease, "Parkinson plus" syndromes, Pikc's disease, and other frontotemporal degenerations, amyotrophic lateral sclerosis, and prion associated diseases. It is also interesting that neurodegenerative disease-type dementia may be a feature in some psychotic illnesses such as schizophrenia. Clinical evaluation of psychosis in the setting of dementia presents a significant challenge for clinicians and researchers. Amnesia, language or speech impairments, and behavioral problems amy distort and obscure the presentation of symptoms. However, recognition and understanding of the psychotic manifestations may lead to the institution of more effective therapeutic or preventive options that can serve to delay long term care placement and improve patient and caregiver quality of life. In addition, a more comprehensive understanding of the pathophysiology, neuroanatomical substrates, and distinctive pathological features underlying the development of psychotic symptoms in neurodegenerative diseases may provide important insights into psychotic processes in general.
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PMID:Psychosis in Neurodegenerative Disease. 1032 Apr 31

Glutamate is the principal excitatory neurotransmitter in brain. Our knowledge of the glutamatergic synapse has advanced enormously in the last 10 years, primarily through application of molecular biological techniques to the study of glutamate receptors and transporters. There are three families of ionotropic receptors with intrinsic cation permeable channels [N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate]. There are three groups of metabotropic, G protein-coupled glutamate receptors (mGluR) that modify neuronal and glial excitability through G protein subunits acting on membrane ion channels and second messengers such as diacylglycerol and cAMP. There are also two glial glutamate transporters and three neuronal transporters in the brain. Glutamate is the most abundant amino acid in the diet. There is no evidence for brain damage in humans resulting from dietary glutamate. A kainate analog, domoate, is sometimes ingested accidentally in blue mussels; this potent toxin causes limbic seizures, which can lead to hippocampal and related pathology and amnesia. Endogenous glutamate, by activating NMDA, AMPA or mGluR1 receptors, may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury. It may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's chorea. In animal models of cerebral ischemia and traumatic brain injury, NMDA and AMPA receptor antagonists protect against acute brain damage and delayed behavioral deficits. Such compounds are undergoing testing in humans, but therapeutic efficacy has yet to be established. Other clinical conditions that may respond to drugs acting on glutamatergic transmission include epilepsy, amnesia, anxiety, hyperalgesia and psychosis.
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PMID:Glutamate as a neurotransmitter in the brain: review of physiology and pathology. 1073 72

Alzheimer's disease (AD) has become recognised as a major cause of morbidity and mortality in the ageing population worldwide. Over 20 million people worldwide are affected by AD, which ensures that the disease imposes a major economic burden. Alzheimer's disease is a progressive neurodegenerative disorder with characteristic clinical and neuropathological features. Neurofibrillary tangles, neuritic plaques and amyloid angiopathy occur in varying severity in brains of patient's with Alzheimer's disease. Biological markers of AD allowing an early definitive premorbid diagnoses are currently not available. Memory loss for recent events is invariable and often the earliest prominent symptom. Language disorders, difficulties with complex tasks, depression, psychotic symptoms and behavioral changes are other common manifestations of AD. Diagnosis involves the early detection of cognitive decline and ruling out other causes of dementia like vascular dementia, Lewy body dementia, fronto-temporal degeneration or reversible causes like hypothyroidism. Acetylcholinesterase inhibitors have shown to be effective in mild to moderate AD in improving the cognitive function of patients in clinical trials. Caregiver intervention programs have considerable potential to improve both the caregiver and patient quality of life.
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PMID:Diagnosis and management of Alzheimer's disease--an update. 1107 82

Sigma (sigma) receptors have generated a great deal of interest on the basis of their possible role in psychosis, neuroprotection and various other behaviors including learning processes. The existence of at least two classes of sigma receptor binding sites (sigma(1) and sigma(2)) is now well established. The recent cloning of the mouse, guinea pig and human sigma(1) receptors has allowed the study of the discrete distribution of the sigma(1) receptor mRNA in rodent and human brain tissues using in situ hybridization. Overall, the sites of expression of specific sigma(1) receptor mRNA signals were in accordance to the anatomical distribution of sigma(1) receptor protein first established by quantitative receptor autoradiography. Specific sigma(1) receptor hybridization signals were found to be widely, but discretely distributed, in mouse and guinea pig brain tissues. The highest levels of transcripts were seen in various cranial nerve nuclei. Lower, but still high hybridization signals were observed in mesencephalic structures such as the red nucleus, periaqueductal gray matter and substantia nigra, as well as in some diencephalic structures including such as the habenula and the arcuate, paraventricular and ventromedial hypothalamic nuclei. Superficial (I-II) and deeper (IV-VI) cortical laminae were moderately labeled in the mouse brain. Moderate levels of sigma(1) receptor mRNA were also found in the pyramidal cell layer and the dentate gyrus of the hippocampal formation. Other structures such as the thalamus and amygdaloid body also expressed the sigma(1) receptor mRNA although to a lesser extent. In murine peripheral tissues, strong hybridization signals were observed in the liver, white pulp of the spleen and the adrenal gland. In the postmortem human brain, moderate levels of sigma(1) receptor mRNA, distributed in a laminar fashion, were detected in the temporal cortex with the deeper laminae (IV-VI) being particularly enriched. In the hippocampal formation, the strongest hybridization signals were observed in the dentate gyrus while all other subfields of the human hippocampal formation expressed lower levels of the sigma(1) receptor mRNA. Antisense oligodeoxynucleotides against the purported sigma(1) receptor were used next to investigate the possible role of this receptor in dizocilpine (MK-801)/NMDA receptor blockade-induced amnesia. Following a continuous intracerebroventricular infusion of a specific sigma(1) receptor antisense into the third ventricle (0.4 nmol/h for 5 days), sigma(1)/[3H](+)pentazocine binding was significantly reduced in mouse brain membrane homogenates while a scrambled antisense control was without effect. Moreover, the sigma(1) receptor antisense treatments (5 nmol/injection, every 12 hx3 or 0.4 nmol/h for 5 days) attenuated (+)MK-801/NMDA receptor blockade-induced cognitive deficits in the treated mice while a scrambled antisense control had no effect. Taken together, these results demonstrate the widespread, but discrete, distribution of the sigma(1) receptor mRNA in the mammalian central nervous system. Moreover, antisense treatments against the purported sigma(1) receptor gene reduced specific sigma(1)/[3H](+)pentazocine binding and modulated cognitive behaviors associated with NMDA receptor blockade providing further evidence for the functional relevance of the cloned gene.
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PMID:Expression of the purported sigma(1) (sigma(1)) receptor in the mammalian brain and its possible relevance in deficits induced by antagonism of the NMDA receptor complex as revealed using an antisense strategy. 1120 32

Gamma-hydroxybutyric acid (GHB) is gaining popularity as a drug of abuse. Reports of toxicity and lethality associated with GHB use have increased. This survey study was designed to identify patterns of GHB use, its effects, and withdrawal syndrome. A survey inquiring about the effects of GHB was administered to 42 users. The results showed that GHB was used to increased feelings of euphoria, relaxation, and sexuality. Adverse effects occurred more frequently in daily users and polydrug users than in occasional GHB users. Loss of consciousness was reported by 66%, overdose by 28%, and amnesia by 13% of participants during GHB use and by 45% after GHB use. Three daily users developed a withdrawal syndrome that presented with anxiety, agitation, tremor, and delirium. Participants described GHB intoxication as having similarities to sedative-hypnotic or alcohol intoxication. Regular use has been shown to produce tolerance and dependence. Participants dependent on GHB reported using multiple daily doses around the clock. High frequency users appeared at the greatest risk for developing withdrawal delirium and psychosis after abrupt discontinuation of GHB use.
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PMID:Gamma-hydroxybutyric acid: patterns of use, effects and withdrawal. 1157 21

Although dissociative phenomena are often transient features of mental states, existing measures of dissociation are designed to measure enduring traits. A new present-state self-report measure, sensitive to changes in dissociative states, was therefore developed and psychometrically validated. Fifty-six items were formulated to measure state features, and sorted according to seven subscales: derealization, depersonalization, identity confusion, identity alteration, conversion, amnesia and hypermnesia. The State Scale of Dissociation (SSD) was administered with other psychiatric scales (DES, BDI, BAI, SCI-PANSS) to 130 participants with DSM-IV major depressive disorder schizophrenia, alcohol withdrawal, dissociative disorders and controls. In these sample populations, the SSD was demonstrated as a valid and reliable measure of changes in and the severity of dissociative states. Discriminant validity, content, concurrent, predictive, internal criterion-related, internal construct and convergent validities, and internal consistency and split-half reliability were confirmed statistically. Clinical observations of dissociative states, and their comorbidity with symptoms of depression and psychotic illness, were confirmed empirically. The SSD, an acceptable, valid and reliable scale measuring state features of dissociation at the time of completion, was obtained. This is a prerequisite for further investigation of correlations between changes in dissociative states and concurrent physiological parameters.
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PMID:Psychometric validation of the State Scale of Dissociation (SSD). 1200 98

A review of research studies to date suggests that psychosis is a relatively rare, but serious, complication of traumatic brain injury (TBI). Psychotic syndromes occur more frequently in individuals who have had a TBI than in the general population. Onset of symptoms can be early or late. Psychosis can occur during the period of post-traumatic amnesia, in association with post-traumatic epilepsy, in association with TBI-related mood disorders, and as a chronic, schizophrenia-like syndrome. TBI can interact with genetic vulnerability to increase the risk of developing illnesses such as schizophrenia. Thorough diagnostic assessment is the foundation of rational and effective pharmacotherapy for psychosis after TBI. Atypical antipsychotic drugs have emerged as first line drugs for treatment of psychotic disorders from all causes, including TBI. Anticonvulsant, antidepressant or other drugs may also be needed in some cases. Medication approaches must be adjusted for the particular characteristics and vulnerabilities of the patient with a TBI.
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PMID:Evaluation and treatment of psychosis after traumatic brain injury. 1254 83

Zolpidem is a sedative and hypnotic drug belonging to imidazopyridine family. Zolpidem facilitates GABAA function more selectively than benzodiazepines, and produces a selective hypnotic effect. In comparison with benzodiazepines this mechanism could be reduce liability to induce dependence. Recently, some cases of zolpidem abuse and dependence have been published. The Authors report 2 cases of addiction to high dose of zolpidem and compare them with others described in the literature. Both patients had been reknown drug addicts before their first prescription of zolpidem and a borderline personality disorder was diagnosed. The patients rapidly developed over consumption and dependence of the molecule, when taking doses as high as 240 and 400 mg daily. To get zolpidem, one patient falsifies prescriptions. They don't suffer from the sedative effects while searching for anxiolytic and stimulating effects. They were also dysarthric, confused, high energy for mental and physical activity. The cases of zolpidem abuse and dependence in the literature describe these symptoms and others such as losing sense of orientation in time and space, amnesia and visual hallucinations. The most typical withdrawal symptom is high levels of anxiety. Moreover, one patient presents an epileptic seizure whereas the other display a severe psychiatric complication such a psychosis. In the literature, withdrawal was accompanied by confusion, suicidal ideas, nausea, vomiting, sweat, tremors, tachycardia and insomnia rebound. The epileptic seizures are described but acute psychosis complication is rare. Pharmacological hypotheses are described. The effects of zolpidem on GABAA receptor gene expression are consistent with the reduced tolerance liability of this drug as well as with other ability to induce both physical dependence and withdrawal syndrome. Through the review of the literature, the Authors noted that 50% of the cases of dependence on zolpidem are drug addicts, therefore concluding that drug addicts are more likely to become dependent on zolpidem.
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PMID:[Dependence on zolpidem: a report of two cases]. 1510 18

Anticholinergic agents have multiple CNS effects, even when used in therapeutic doses. These can include sedation, amnesia, delirium and, in rare cases, psychosis. While there is some symptom overlap between delirium and psychosis, psychotic patients will have a clear sensorium. We present the case of a 59-year-old male who became psychotic and required hospitalization after the administration of a large anticholinergic load from a smoking cessation clinic. We will review the literature regarding previous cases of anticholinergic medication induced psychosis, discuss treatment options and review the clinical effects of anticholinergic medications.
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PMID:Psychosis induced by smoking cessation clinic administered anticholinergic overload. 1551 50


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