New PDF release: Adverse syndromes and psychiatric drugs: a clinical guide

By Peter M. Haddad, Serdar Dursun, Bill Deakin

ISBN-10: 0198527489

ISBN-13: 9780198527480

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Another theory that attempts to explain the pathophysiology of NMS centres on the role of sympathoadrenal hyperactivity (Gurrera and Romero 1992; Gurrera 1999; Gurrera 2000). According to this model, a predisposition to extreme sympathetic nervous system hyperactivity may act as a trait vulnerability for NMS. In the presence of state variables, such as neuroleptic-induced DA system hypoactivity or psychological distress, this leads to the clinical picture of NMS. This model needs to be tested in clinical studies to verify its validity.

1985). The reported incidence of NMS has varied widely in the past decades. This partly reflects methodological factors, including the diagnostic criteria adopted and whether these are restricted to the full syndrome or encompass partial cases. 4 per cent of patients treated with antipsychotics (Addonozio et al. 15 per cent (Keck et al. 07 per cent (Gelenberg et al. 2 per cent being widely accepted (Caroff and Mann 1993). Men outnumber women twofold (Caroff 1980; Addonizio et al. 1987) and this has been attributed to the tendency to medicate men with higher doses than women.

1960). qxd 5/5/04 5:37 PM Page 38 38 ADVERSE SYNDROMES AND PSYCHIATRIC DRUGS: A CLINICAL GUIDE toxic reactions. Similar reactions occurred when MAOIs were combined with the analgesic pethidine. Both reactions are now known to be examples of serotonin toxicity (Gillman 1998). Debate ensued concerning the safety of ‘combined antidepressant treatment’. Imipramine, the TCA involved in the early reports, possesses weak serotonin reuptake inhibitor (SRI) capacity which is usually insufficient to precipitate serotonin toxicity, even if combined with MAOIs.

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Adverse syndromes and psychiatric drugs: a clinical guide by Peter M. Haddad, Serdar Dursun, Bill Deakin


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