Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011551 (depersonalization)
 1,117 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phencyclidine (PCP) and ketamine can induce a model psychosis in drug addicts and exacerbate the symptoms of chronic schizophrenics. The model psychoses these drugs induce mimic a variety of schizophrenic symptoms, including flattened affect, dissociative thought disorder, depersonalization and catatonic states. These symptoms can persist for prolonged periods and chronic PCP and ketamine addicts have persisting memory deficits. Dizocilpine (MK-801) is a simpler drug than PCP or ketamine in its actions, but it shares with both the property of blocking in a non-competitive manner the N-methyl-D-aspartate (NMDA) ion-channel. Behavioral observations and drug-discrimination studies in animals indicate that PCP and dizocilpine are similar in their effects and they both have a neurotoxic effect on neurons in posterior cingulate cortex. Recent studies have indicated that both of these drugs, when given continuously for several days, further induce neuronal degeneration in other limbic structures. These include brain regions of rats related to olfaction, associated limbic structures such as piriform cortex and posterior regions of entorhinal cortex and in it's projections, through the perforant pathway, to dentate gyrus and other cells in ventral hippocampus. These degenerative consequences may be excitatory neurotoxic effects, for these compounds also induce an elevation in glucose metabolism maximal in just those structures where degeneration is observed and the degeneration involves entire cells, with all of their processes. It has been suggested these non-competitive NMDA antagonists induce an increase in firing rate in a limbic circuit which includes the perforant pathway. At least some competitive NMDA antagonists induce the same pattern of degeneration and altered glucose utilization. There is anatomical and functional evidence that alterations in these same limbic structures are present in the dementia syndrome manifested by some schizophrenics and most Alzheimer's patients. This suggests that these non-competitive NMDA antagonists may provide a more complete model of psychoses and memory disturbances than previously recognized, in that they can mimic both persisting symptomatology and neuroanatomical abnormalities. While the neurochemical underpinnings of this effect remain elusive, it appears to be both age and sex dependent. Further studies of the mechanisms by which NMDA antagonists induce increased glucose utilization and neurotoxicity in these limbic structures may clarify these alterations in this simplified Papez-like circuit.
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PMID:The N-methyl-D-aspartate antagonists phencyclidine, ketamine and dizocilpine as both behavioral and anatomical models of the dementias. 779 58

Aging is a physiological process that shares many behavioral, biochemical and neuroendocrine phenomena with the pathophysiological situation of unresolved stress, as well as with a pharmacologically induced syndrome resulting from chronic benzodiazepine (BZ) consumption. Behavioral findings include symptoms such as drowsiness, ataxia, fatigue, confusion, weakness, dizziness, vertigo, syncope, reversible dementia, depression, impairment of intellectual, psychomotor and sexual function, agitation, auditory and visual hallucinations, paranoid ideation, panic, delirium, depersonalization, sleepwalking, aggressivity, orthostatic hypotension, and insomnia. Neuroendocrine findings include: central depletion of noradrenaline (NA), dopamine, adrenaline (AD), and serotonin (5-HT); reduction in the ratio of circulating NA/AD as well as platelet 5-HT and increase of AD, plasma free 5-HT and cortisol. These disturbances together with the increased platelet aggregability observed in the three groups are typical of unresolved-stress situations. Immunological findings include significant reduction of peripheral T lymphocytes (CD3, CD4, CD8) and the CD4/CD8 ratio, CD16 and gamma-delta cells. On the other hand, the three groups (elderly subjects, subjects faced with unresolved stress, and BZ consumers) show increase of the CD57 lymphocyte subset as well as natural killer cytotoxicity. Alterations of several biological markers have also been found, specifically in the oral glucose tolerance test, the intramuscular clonidine test, and the supine/orthostasis/exercise test. From a clinical point of view, the three groups appear to be more susceptible to the appearance and progression of many acute and chronic diseases (infectious and malignant diseases). As a result, chronic consumption of BZs should be avoided in both the elderly and subjects in unresolved-stress situations.
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PMID:Benzodiazepines: tolerability in elderly patients. 884 97

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74

There is little systematic research on the cross-cultural validity of the dissociative disorders, especially in non-western countries. This study evaluates the fit of the DSM-IV classification and concepts of these disorders with local concepts, experiences and local presentations in south-west Uganda. We conducted focus group discussions with medical students, traditional healers, religious leaders, counselors, community members and other health workers (n=48). They were supplemented by key informant interviews with religious people, traditional healers and leaders (n=11). The responses were subjected to thematic analysis. Dissociative amnesia and depersonalization were generally recognized and seen as the result of traumatic experiences and were useful categories in Uganda. However, dissociative fugue did not match local concepts and was confused with spirit possession and other conditions such as alcoholic fugues and dementia. The description of dissociative identity disorder was always interpreted as a possession trance disorder by the local healers. We found only partial support for the validity of the DSM-IV classification of dissociative disorders in Uganda.
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PMID:The validity of DSM-IV dissociative disorders categories in south-west Uganda. 1611 84

Corticosteroids are widely used in modern medicine but can result in troubling psychiatric side-effects. Physicians and other medical professionals should be aware of the potential for these side-effects, possible means of prevention, and efficacious treatments. Herein, we review adult case report data published during the past quarter-century on adverse corticosteroid-induced psychiatric effects, and present a case of corticosteroid-induced psychotic depression. PubMed and PsychLit databases were searched using the terms 'corticosteroids', 'steroids', and the generic names of corticosteroid medications with terms for psychiatric symptoms or syndromes, including psychosis, mania, hypomania, depression, apathy, anxiety, panic, depersonalization, delirium, confusion, hallucinations, delusions, paranoia, cognitive impairment and dementia. Fifty-five cases and a number of clinical trials investigating the incidence and treatment of these psychiatric symptoms and syndromes were identified. Data on incidence, drug dose, risk factors, course of illness and treatment (when present) were tabulated. We conclude that the cumulative data indicate that psychiatric complications of corticosteroid treatment are not rare and range from clinically significant anxiety and insomnia, to severe mood and psychotic disorders, delirium and dementia. While tapering or discontinuation of the corticosteroid treatment may remedy these adverse side-effects, psychotropic medications are often required because of the medical necessity of the corticosteroid or the severity of the psychiatric symptom. Further studies are needed to better understand the deleterious psychiatric effects associated with corticosteroids.
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PMID:Psychiatric complications of treatment with corticosteroids: review with case report. 2200 87

Population aging has increased age-related diseases such as dementia, Alzheimer's disease (AD) being the most common in older adults (50%-60%). It is one of the most feared conditions for its irreversible and incurable, by its chronicity and it consists of a long process of depersonalization. The clinical diagnosis is mainly based on DSM-IV and NINCDS-ADRDA. Definitive diagnosis is post-mortem, as it requires histopathological confirmation. However, there have been new diagnostic criteria based EA biomarkers, which can be done in life, anticipating the course of several years before dementia. Thus, physicians are increasingly exposed to AD patients in early stages, having to face the dilemma of communicating the diagnosis to a patient with cognitive failures and disease awareness, with the implications that generates about him and his family. The objectives of this paper will analyze the ethical problem of communication of clinical diagnosis of AD in prodromal stages (pre-dementia) in our country, based on the analysis of ethical principles (autonomy and non maleficence) involved in decision making.
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PMID:[Ethical considerations regarding the communication of diagnosis of prodromal Alzheimer's disease]. 2515 75

How deep are the historical roots of our concept of major depression (MD)? I showed previously that psychiatric textbooks published in 1900-1960 commonly described 18 characteristic depressive symptoms/signs that substantially but incompletely overlapped with the current DSM (Diagnostic and Statistical Manual of Mental Disorders) MD criteria. I here expand that inquiry to the key years of 1880-1900 during which our major diagnostic categories of manic-depressive illness (MDI) and dementia praecox were developed. I review the symptoms of depression/melancholia in 28 psychiatric textbooks and 8 other relevant documents from this period including monographs, reviews and the first portrayal of melancholia Kraepelin in 1883. Descriptions of melancholia in the late nineteenth and twentieth century textbooks closely resembled each other, both reporting a mean of 12.4 characteristic symptoms, and emphasizing core features of mood change and alterations in cognitive content and psychomotor behavior. The detailed monographs, reviews and the early description of Kraepelin were more thorough, reporting a mean of 16.6 of these characteristic symptoms. These nineteenth century texts often contained phenomenologically rich descriptions of changes in mood and cognition, loss of interest and anhedonia and emphasized several features not in DSM including changes in volition/motivation, posture/facial expression and derealization/depersonalization. In the early nineteenth century, melancholia was often defined primarily by delusions or as the initial phase of a unitary psychosis transitioning to mania and then dementia. By 1880, the concept of depression as an independent mood disorder with characteristic symptoms/signs and a good prognosis had stabilized. Kraepelin incorporated this syndrome into his diagnostic concept of MDI, changing its name to 'Depressive States', but did not alter its underlying nature or clinical description.
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PMID:The genealogy of major depression: symptoms and signs of melancholia from 1880 to 1900. 2878 9

There is increasing evidence and recognition that Lyme borreliosis (LB) causes mental symptoms. This article draws from databases, search engines and clinical experience to review current information on LB. LB causes immune and metabolic effects that result in a gradually developing spectrum of neuropsychiatric symptoms, usually presenting with significant comorbidity which may include developmental disorders, autism spectrum disorders, schizoaffective disorders, bipolar disorder, depression, anxiety disorders (panic disorder, social anxiety disorder, generalized anxiety disorder, posttraumatic stress disorder, intrusive symptoms), eating disorders, decreased libido, sleep disorders, addiction, opioid addiction, cognitive impairments, dementia, seizure disorders, suicide, violence, anhedonia, depersonalization, dissociative episodes, derealization and other impairments. Screening assessment followed by a thorough history, comprehensive psychiatric clinical exam, review of systems, mental status exam, neurological exam and physical exam relevant to the patient's complaints and findings with clinical judgment, pattern recognition and knowledgeable interpretation of laboratory findings facilitates diagnosis. Psychotropics and antibiotics may help improve functioning and prevent further disease progression. Awareness of the association between LB and neuropsychiatric impairments and studies of their prevalence in neuropsychiatric conditions can improve understanding of the causes of mental illness and violence and result in more effective prevention, diagnosis and treatment.
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PMID:Neuropsychiatric Lyme Borreliosis: An Overview with a Focus on a Specialty Psychiatrist's Clinical Practice. 3014 26