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There are high rates of obesity and low self-esteem in patients with psychosis. The occurrence of negative voice content directly about appearance is therefore plausible. Derogatory comments about appearance are likely to be distressing, increase depression and contribute to social withdrawal.
To systematically assess the occurrence of voice content regarding appearance and identify correlates.
Sixty patients experiencing verbal auditory hallucinations at least once a week in the context of non-affective psychosis completed a measure assessing positive and negative voice content about appearance. They also completed assessments about body image, self-esteem, psychiatric symptoms and well-being.
Fifty-five (91.7%) participants reported hearing voices comment on their appearance. A total of 54 (90%) patients reported negative voice content about their appearance with 30 (50%) patients experienced negative appearance comments on a daily basis. The most common negative comment was ‘the voices tell me that I am ugly’ (n = 48, 80%). There were 39 (65%) patients who reported positive voice content on appearance. The most frequent positive comment was ‘I look as nice as other people’ (n = 26, 43.3%). Negative voice content about appearance was associated with body image concerns, paranoia, voice hearing severity, depression, worry, negative self-beliefs and safety-seeking behaviours. Positive appearance voice content was associated with greater body esteem and well-being and lower levels of depression and insomnia.
Voice content about appearance is very common for patients seen in clinical services. Negative voice content may reflect – and subsequently reinforce – negative beliefs about one's appearance, low self-esteem, worry and paranoia.
The period before the formation of a persecutory delusion may provide causal insights. Patient accounts are invaluable in informing this understanding.
To inform the understanding of delusion formation, we asked patients about the occurrence of potential causal factors – identified from a cognitive model – before delusion onset.
A total of 100 patients with persecutory delusions completed a checklist about their subjective experiences in the weeks before belief onset. The checklist included items concerning worry, images, low self-esteem, poor sleep, mood dysregulation, dissociation, manic-type symptoms, aberrant salience, hallucinations, substance use and stressors. Time to reach certainty in the delusion was also assessed.
Most commonly it took patients several months to reach delusion certainty (n = 30), although other patients took a few weeks (n = 24), years (n = 21), knew instantly (n = 17) or took a few days (n = 6). The most frequent experiences occurring before delusion onset were: low self-confidence (n = 84); excessive worry (n = 80); not feeling like normal self (n = 77); difficulties concentrating (n = 77); going over problems again and again (n = 75); being very negative about the self (n = 75); images of bad things happening (n = 75); and sleep problems (n = 75). The average number of experiences occurring was high (mean 23.5, s.d. = 8.7). The experiences clustered into six main types, with patients reporting an average of 5.4 (s.d. = 1.0) different types.
Patients report numerous different experiences in the period before full persecutory delusion onset that could be contributory causal factors, consistent with a complex multifactorial view of delusion occurrence. This study, however, relied on retrospective self-report and could not determine causality.
Cerebral cavernous malformation (CCM) is a form of intracranial vascular disease that may arise sporadically or be dominantly inherited. Linkage studies have revealed genetic heterogeneity among the dominantly inherited forms suggesting the existence of at least three loci called CCM1, CCM2 and CCM3.
In the present study, we screened five families with dominantly inherited CCM for CCM1 gene mutations with denaturing high performance liquid chromatography (DHPLC). Then, we performed linkage analysis and haplotyping on these five families using highly polymorphic markers at the candidate CCM loci.
None of the five families tested with DHPLC were found to have mutations in the CCM1 gene. Based on haplotyping, we identified three families segregating alleles for CCM2, while two families segregated alleles for CCM3. Using linkage analysis, we could confirm that one family (IFCAS-1) had a positive Lod score of 2.03 (p<0.0001) at the CCM2 locus using marker D7S678.
The present study is the first one to replicate linkage at the CCM2 locus and provides a fifth family identified as such. It also supports the concept of genetic heterogeneity in CCM, identifying four other families that showed no mutations in the CCM1 gene.
The aim of the present study was to identify the mutations in the connexin 32 gene in French-Canadian families with X-linked Charcot-Marie-Tooth disease (CMTX).
Molecular analysis was performed by nonisotopic single strand conformation polymorphism (SSCP) analysis and sequencing. Clinical evaluation was carried out according to the scale defined by the European Hereditary Motor and Sensory Neuropathy Consortium.
In one family, the mutation Arg142Trp was located in the transmembrane domain III whereas, in four other families we identified a novel mutation (Ser26Trp) located in the transmembrane domain I of the connexin 32 gene. Haplotype analysis revealed that these four families are related and suggests a founder mutation. Sixteen patients from these four families were studied. As expected, all the affected males were more clinically affected than the females and all affected patients exhibited some electrophysiological characteristics of demyelination.
Our study suggests that the Ser26Trp mutation may cause a primary demyelinating neuropathy that is not associated with a specific clinical phenotype. We also find evidence that the majority of kindreds share a common ancestor.
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