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Neuroleptics catatonia

Neuroleptic malignant syndrome is an acute iatrogenic condition caused by neuroleptics, characterized by tremor, catatonia, fluctuating consciousness, hyperthermia, and cardiovascular instability. It is relatively uncommon, occuring in 1-1.5% of patients but is fatal in 11-38%, most often due to cardiovascular collapse (Jahan et al. 1992). The pathogenesis of neuroleptic malignant syndrome is poorly understood, but it is believed to result from altered dopamine and serotonin transmission in the hypothalamus, spinal cord, and striatum. Treatment includes discontinuation of neuroleptics and administration of drugs that increase dopamine transmission bromocriptine or L-dopa (Jahan etal. 1992 Baldessarini 1996). [Pg.257]

The primary indication for ECT in adolescents is the short-term treatment of mood symptoms, depressive or manic (Walter et al., 1999). Mood symptoms in the course of major depression, psychotic depression, bipolar disorder, organic mood disorders, schizophrenia, and schizoaffective disorder respond well to ECT. Psychotic symptoms in mood disorders also respond well to ECT whereas the effectiveness of ECT in the treatment of psychotic symptoms in schizophrenia is doubtful. There are suggestions that other uncommon clinical conditions in adolescents such as catatonia and neuroleptic malignant syndrome also benefit from ECT. The effectiveness of ECT seems to lessen when there is a comorbid personality disorder or drug and/or alcohol problems. There are very few data about usefulness on prepubertal children. [Pg.378]

Other diagnostic indications. A few less well-known diagnostic indications for ECT exist. The use of ECT in patients with Parkinson s disease is receiving greater interest. ECT is an effective treatment for depressions associated with this illness and may also be of benefit for the motor manifestations [see C. H. Kellner et al. 1994 for review]. Other conditions in which the use of ECT may be appropriate include catatonia and the neuroleptic malignant syndrome [Sackeim et al. 1995]. [Pg.175]

Malignant catatonia associated with a low serum iron concentration carries a high risk of evolving into neuroleptic malignant syndrome, going by the results of a retrospective study, in which 39 catatonic episodes in patients with low (n = 17) or normal (n = 22) serum iron concentrations were compared (379). All had been exposed to neuroleptic drugs. Hypoferremia has previously been related to the neuroleptic malignant syndrome. [Pg.214]

Lee JW. Serum iron in catatonia and neuroleptic malignant syndrome. Biol Psychiatry 1998 44(6) 499-507. [Pg.246]

Neuroleptic malignant Catatonia, stupor, fever, unstable Weeks can persist for Antagonism of Stop neuroleptic immediately ... [Pg.304]

Northoff G. Catatonia and neuroleptic malignant syndrome psychopathology and pathophysiology. J Neural Transm 2002 109 1453-67. [Pg.32]

Cases cf Neurotoxicity Toxicity at therapeutic or subtherapeutic levels was reported in three cases. In two of these cases, the role of lithium is questionable. In one case of a rapidly fatal presentation of neuroleptic malignant syndrome (NMS) in a 72-year-old woman whose lithium level was 1.5 mM, the authors report a lithium-induced fatal NMS because she was not prescribed an antipsychotic [84 ]. However, her presentation is also consistent with fatal catatonia, sepsis, or unknown consumption of an antipsychotic, none of which were ruled out, and all of which are more likely than lithium-induced NMS. A second case in which a delirium with dyspraxia, but not ataxia in a 57-year-old man with a lithium level of 0.44 mM, that resolved after discontinuation of botii lithium and tricyclic antidepressant medication, was felt to be an interaction between the lithium and the antidepressant [85 ]. Lithium may have played a role, but he had been on lithium for years, and had developed anticholinergic problems with quetiapine previously, suggesting that the anticholinei c effects of the tricyclic antidepressant were more important in the delirium than the lithium. The third case of a 65-year-old man with multisystem atrophy becoming considerably worse with lithium at a level of 1.1 mM, is much more likely to represent lithium-related neurotoxicity at therapeutic levels [86 ]. [Pg.31]

Nervous System Parkinsonism was present in 46% of 150 elderly patients being treated with haloperidol and xmrelated to plasma concentrations or duration of use [151 ]. Two cases of neuroleptic-induced catatonia following the administration of intravenous haloperidol are described both patients recovered following discontinuation of haloperidol [152 ]. A case of neuroleptic malignant syndrome in a 48-year-old male is reported with index exposure to intravenous haloperidol that resolved on discontinuation [153 ]. Obsessive-compulsive symptoms are associated with a number of SGAs particularly clozapine however a case report describes the development of obsessive-compulsive symptoms in a learning disability patient treated with haloperidol [154 ]. [Pg.68]

Gugger JJ, Saad M, Smith C. Neuroleptic-induced catatonia in two hospitalized patients. J Pharm Pract 2012 25(2) 250-4. [Pg.80]

The cis-, but not the trans, aminoalcohol (15) was effective in several pharmacological tests for neuroleptic activity. In mice, the benzo-thlazlnone 16 was the most potent of a series of compounds in causing depression, catatonia and decreased SMA. ... [Pg.9]


See other pages where Neuroleptics catatonia is mentioned: [Pg.142]    [Pg.170]    [Pg.679]    [Pg.213]    [Pg.214]    [Pg.214]    [Pg.287]    [Pg.2459]    [Pg.2460]    [Pg.2460]    [Pg.2460]    [Pg.152]    [Pg.446]    [Pg.300]    [Pg.28]    [Pg.221]   
See also in sourсe #XX -- [ Pg.170 ]




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