Is antipsychotic medication stigmatizing for people with mental illness?

Antipsychotic medications are clearly identified as important in the treatment of individuals with schizophrenia and with bipolar disorder. However, negative societal reaction related to having a serious mental illness and the socially undesirable side effects associated with antipsychotic medication treatment may combine to worsen stigma associated with treatment for mental illness. Specific stigmatizing effects of antipsychotic therapy may be difficult to evaluate independently from factors such as symptoms, insight into illness and side effects. Attitudes towards antipsychotic medication may be positive in individuals who recognize therapeutic drug effects, however other individuals may view medications negatively due to a sense of stigma. Stigma among individuals with bipolar disorder in relation to treatment with antipsychotic medication has not been well addressed in the literature. An additional concern among individuals with bipolar disorder who receive antipsychotic medications may be the notion that antipsychotics are 'schizophrenia drugs', and thus an inappropriate treatment for their condition. Antipsychotic medications can be stigmatizing for patients with serious mental illness, however the roots of stigma are extensive, and efforts to minimize stigma can only be successful when addressed by the individual with illness, their families and loved ones, treatment providers and society at large.     

Do people recognise mental illness?

BACKGROUND: Mental health literacy has been defined as the public's knowledge and the beliefs about mental disorders enhancing the ability to recognise specific disorders. AIMS: Firstly, to determine whether the public recognises a person depicted in a vignette as mentally ill or as experiencing a crisis. Secondly, to reveal the factors influencing the correct recognition. METHODS: Multiple logistic regression analysis of an opinion survey conducted in a representative population sample in Switzerland (n=844). RESULTS: The depression vignette was correctly recognised by 39.8% whereas 60.2% of the respondents considered the person depicted as having a 'crisis.' The schizophrenia vignette was correctly identified by 73.6% of the interviewees. A positive attitude to psychopharmacology positively influenced the recognition of the two vignettes whereas a positive attitude to community psychiatry had the inverse effect. Moreover, for the depression vignette previous contact to mentally ill people had a positive influence on the recognition. For the schizophrenia vignette instead, rigidity and interest in mass media had a negative influence, respectively. CONCLUSIONS: The low knowledge about mental disorders, particularly depression, confirms the importance and the need to increase mental health literacy. Furthermore, professionals must openly discuss illness models with their patients, especially emphasising the differences between illness and crisis.     

Genetic bases of mental illness -- a cure for stigma?

An increased emphasis on biological causes of mental illness has been viewed as having the potential to significantly reduce stigma. From this perspective, the current genetics revolution can be seen as a source of hope. However, some have argued that biological attributions could increase stigma, for example by making the ill person seem 'defective' or 'physically distinct' -- 'almost a different species'. In this paper, I use a multicomponent conceptualization of stigma as a guide in forming hypotheses about the likely impact of genetic attributions on the stigma of mental illness.     

From whence comes mental illness stigma?

BACKGROUND: This paper seeks to answer two fundamental questions: What is the basis of the current form of mental illness stigma? and Why do western cultures stereotype people with mental illness as dangerous, incompetent and blameful, rather than something else? MATERIAL AND DISCUSSION: We argue that a motivational model called system-justification offers several benefits for answering these questions. System-justification portrays stigma as a way of making sense of economic and political differences between the majority and stigmatized subgroups. We contrast system-justification with two cognitive models of stigma that seem to have strong support from naive psychology: mental illness stigma results as the normal perception of a group of people who are dangerous and/or blameworthy and there is a kernel of truth to the stigmatizing attitudes about people with mental illness. Although research supporting the latter two models is mixed, there are significant limitations to the models, as well as concerns that normal perception and kernel of truth might actually promote stigma. CONCLUSIONS: As an alternative, system-justification combines three paradigms that suggest its worthiness for future research: 1) a review of historical and economic forces that influence social phenomena; 2) the need of humankind to understand these forces and organize them into a unitary framework; and 3) the cognitive mechanisms that are essential for this comprehension. Implications of this model for stigma change are discussed.     

Is late onset depression a prodrome to dementia?

BACKGROUND: Recent research suggests there are clinical and biological differences between late onset depression (LOD) and early-onset depression (EOD). OBJECTIVES: In this paper we review clinical, epidemiological, structural neuroimaging and genetic investigations of late life depression that have been performed over the past two decades and offer evidence that LOD is often a prodromal disorder for dementia. RESULTS: LOD patients are more likely to have cognitive impairment and to have more deep white matter lesions (DWMLs). Evidence concerning cortical and temporal lobe atrophy is conflicting, while the ApoE 4 allele is not associated with LOD. CONCLUSIONS: It is likely that LOD is not a prodrome for a particular type of dementia, but the majority of patients who do develop dementia will acquire Alzheimer's disease (AD) or a vascular dementia, as these are by far the most common causes of dementia. This issue requires further clarification with follow-up of patients over the long term.     

Is there a protective effect of normal to high intellectual function on mental health in children with chronic illness?

Background

The aims of this study are to describe the methodological challenges in recruiting a follow-up sample of children referred to an interdisciplinary hospital child protection team (CPT) and to compare participating versus non-participating groups on several demographic variables and maltreatment characteristics.

Methods

Of the 319 in- and outpatients referred to the CPT at University Children's Hospital Zurich from 2005–2006 a sample of 180 children was drawn to contact for a follow-up. The children and their parents were asked to participate in a face-to-face interview at the hospital; in 42 cases the children and parents consented to do so. Alternatively, the parents could take part in a telephone interview (n = 39). Non-participation resulted because no contact or adequate communication in German, French, or English could be established (n = 49) or because the parents or children refused to participate (n = 50).

Results

Participants and non-participants did not differ significantly in mean child age at follow-up, gender, family status, place of residence, certainty and type of maltreatment, and type of perpetrator. However, the child's nationality had a significant impact: Percentages of foreign nationals were higher in the fully participating group (45%; n = 19) and the non-contactable group (53%; n = 26) and significantly lower in the refusal (26%; n = 10) and the telephone interview group (18%; n = 9). Although a high percentage of families had moved in the few years since the CPT intervention (32%; n = 57), the percentage of moves was not significantly higher in non-participants compared to participants.

Conclusions

Further research is needed to support these results in different national backgrounds and to test for biases in variables not included – especially socioeconomic status. This includes gathering more detailed information on non-participants, while respecting ethical boundaries. Overall, the fact that only child's nationality was unevenly distributed between participants and non-participants is encouraging.     

Is mental retardation a defect of synapse structure and function?

Mental retardation is believed to be a result of alterations in molecular pathways underlying neuronal processes involved in cognitive functions. It is not fully understood, however, which molecular pathways are critical for cognitive mechanisms. Furthermore, whether mental retardation is a developmental or ongoing disorder of cognitive functions is unknown. Answering these questions will help elucidate the etiology of mental retardation and possibly lead to new therapies. Several recently published studies suggested that mental retardation might be caused by defects in synapse structure and function. Four genes mutated in families with mental retardation encode proteins known as Rho guanine nucleotide exchange factor 6, oligophrenin-1, p21-activated kinase, and guanine dissociation inhibitor 1. Each of these interacts with various guanine nucleotide-binding proteins involved in signaling pathways that regulate the actin cytoskeleton, neurite outgrowth, neurotransmitter release, and dendritic spine morphology. The goal is to understand the roles of these genes in normal cognitive functions.