ABSTRACT
This review approaches the topic of childbirth and mental illness using a model of perinatal health which takes into consideration the multiple determinants of health, approached from a lifespan perspective. The paper seeks to answer four broad questions using this model and available literature: (1) What is the relationship between childbirth and mental disorders? (2) How common are mental disorders during childbearing, and what is the perinatal course of illness? (3) What are the effects of mental illness during childbearing on foetal and infant developmental outcomes? (4) How do you approach the detection and treatment of mental disorders during the perinatal period?
Subject(s)
Child Development , Mental Disorders/epidemiology , Mental Disorders/psychology , Mothers/psychology , Parturition/psychology , Psychology, Child , Female , Humans , Infant , Pregnancy , Risk Factors , Time FactorsSubject(s)
Depressive Disorder, Major/therapy , Electroconvulsive Therapy/adverse effects , Electroconvulsive Therapy/methods , Takotsubo Cardiomyopathy/etiology , Aged , Cerebral Ventriculography/statistics & numerical data , Depressive Disorder, Major/drug therapy , Female , Functional Laterality/physiology , Humans , Iatrogenic Disease , Psychotropic Drugs/therapeutic use , September 11 Terrorist Attacks/psychology , Takotsubo Cardiomyopathy/diagnostic imaging , Treatment OutcomeABSTRACT
INTRODUCTION: One in a hundred people will develop schizophrenia; about 75% of people have relapses and continued disability, and a third fail to respond to standard treatment. Positive symptoms include auditory hallucinations, delusions, and thought disorder. Negative symptoms (demotivation, self-neglect, and reduced emotion) have not been consistently improved by any treatment. METHODS AND OUTCOMES: We conducted a systematic review and aimed to answer the following clinical questions: Which interventions reduce relapse; and improve adherence rates? Which interventions are effective in people resistant to standard antipsychotic drugs? We searched: Medline, Embase, The Cochrane Library, and other important databases up to October 2007 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA). RESULTS: We found 45 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions. CONCLUSIONS: In this systematic review we present information relating to the effectiveness and safety of the following interventions: behavioural therapy, clozapine, cognitive behavioural therapy (CBT), compliance therapy, continuation of antipsychotic drugs (reduce relapse rates), first-generation antipsychotic drugs in treatment-resistant people, multiple-session family interventions, psychoeducational interventions, second-generation antipsychotic drugs in treatment-resistant people, and social-skills training.
Subject(s)
Antipsychotic Agents , Schizophrenia , Antipsychotic Agents/therapeutic use , Chronic Disease , Clozapine/therapeutic use , Humans , Schizophrenia/diagnosis , Treatment OutcomeABSTRACT
During neuromuscular junction formation, extracellular matrix-mediated signals cause muscle surface acetylcholine receptors (AChRs) to aggregate at synaptic sites. Two extracellular matrix proteins, agrin and laminin, have each been shown to initiate signaling pathways that culminate in AChR clustering in cultured muscle cells. Here we present evidence that laminin-induced AChR clustering is mediated by the activation of the Rho GTPases Cdc42, Rac and Rho. Clustering in response to laminin is blocked by the dominant negative mutants Cdc42N17, RacN17 and RhoN19, as well as by the Rho inhibitor C3 transferase. Moreover, laminin-induced AChR clustering is impaired by the Rho kinase inhibitor Y-27632. Agrin-induced AChR clustering has previously been shown to require activation of Cdc42, Rac and Rho. Therefore, although agrin and laminin use distinct transmembrane receptors to initiate AChR clustering, their signaling pathways converge at the level of Rho GTPase activation.
