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)

lsd (lysergic acid diethylamide) is a powerful bio-active substance related to serotonin in structure. Its actions generally affect autonomic, sensory and psychological functions. Autonomic stimulation is varied. Sensory responses are usually visual, involving heightened and distorted color perception and fusion of sensory impressions. Psychological responses include a feeling that a unique experience is occurring; feelings of depersonalization; pronounced fluctuation of mood; time and space distortions; autistic phenomena; fluctuation of aggressive drives (usually reduction); and spontaneous reoccurrence of the lsd experience. THE SUBJECTIVE RESPONSES CAN BE RELATED TO THREE BASIC PHENOMENA: (1) expectation; (2) loss of characteristic modes of perceptual and cognitive patterning; and (3) hypersuggestibility. THE MAJOR ADVERSE REACTIONS ARE: (1) chronic drug dependence including subsequent personality changes and depressive reactions; and (2) acute ego dissolution. These reactions usually occur in already emotionally ill people. Most of these users fall into two groups, those with unresolved identity problems and those with severe ego abnormality. The majority of adverse reactions are of the chronic drug dependence type and are usually seen in adolescents and young adults who have not negotiated the age-appropriate tasks of forming and integrating the various identities that are the composite of their life experiences.lsd helps alleviate these stresses via some of its psychological properties as discussed. It also provides a nidus for the formation of a subculture where goals for social, sexual and vocational achievement are lower and idiosyncratic modes of adaptation are better tolerated. A smaller group of users who have serious reactions such as psychosis, rage reactions, homicidal and suicidal ideation are usually found to have preexisting ego abnormality such as ambulatory schizophrenia, chronic impulse disorders and borderline states. Although adverse reactions most often appear to be related to pre-morbid psychopathology, this is not invariably so. Further, there is as yet no reliable method to determine who will have an adverse reaction and what the nature of that reaction will be.
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PMID:The LSD syndrome. A review. 488 83

The high rate of benzodiazepines (BZD) consumption has been repeatedly confirmed by epidemiological surveys in most major western world countries. In a recent french survey 7% of chronic users of BZD (use in 5/7 days for the last 12 months) were found the general population (17% in the population aged above 65). It has been suggested that the high BZD consumption rate could be related to dependence. The existence of BZD dependence was described in the early sixties with very high dose of chlordiazepoxide but it has become a real concern for the medical community since the late seventies with increasing number of reports of withdrawal symptoms. The extend of the actual rate of withdrawal symptoms at BZD tapering is still very controversial and according to the different studies it varies from 39 to 90%. The between studies difference in parameters such as: the patient populations (psychopathology, treatment duration), the type of tapering employed (duration, nature of the medical and psychological support) and the used operational criteria for withdrawal definition most likely explain this wide variation in the rate of occurrence of withdrawal manifestations. According to the American Psychiatric Association Task Force on Benzodiazepine Dependence, Toxicity and Abuse three type of pathological events can happen after treatment discontinuation: rebound, withdrawal syndrome and recurrence. The rebound consists in the early and transitory reappearance of the anxiety symptoms pre-existing to the treatment but in an exacerbated from; the withdrawal syndrome associates the resurgence of the pre-existing anxiety symptoms and new symptoms as sensory disturbances (metallic taste, hyperosmia, cutaneous exacerbated sensitivity, photophobia...) nausea, headache, motor disturbance in some rare cases depersonalization, paranoid reaction, confusion, convulsion. Rebound or withdrawal syndrome appearance delay varies from hours to few days according mostly to compounds elimination half-life. The relapse develops later with a progressive reapparance of pre-treatment symptoms. In practice recurrence and rebound are often difficult to isolate: recurrence can follow rebound. Different operational criteria of definition for this different entities have been proposed but there is a need for a consensual position. The treatment length, a high daily dose, an alcohol abuse history, a dependent personality and the severity of the psychopathology of the patients have been found to be predictive for the occurrence of withdrawal symptoms. Behavioural therapies (individual or in group) have been proposed with some success for the treatment of benzodiazepine dependence; drug treatment with carbamazepine or imipramine have demonstrated some efficacy. Other drug as buspirone clonidine having anxiolytic properties have not demonstrated efficacy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Dependence on benzodiazepines. Clinical and biological aspects]. 791 65