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PURPOSE OF REVIEW: Bipolar disorder has the highest rate of suicide of all psychiatric conditions and is approximately 20-30 times that of the general population. The purpose of this review is to discuss findings relevant to bipolar disorder and suicide. RECENT FINDINGS: Risk factors include male gender, living alone, divorced, no children, Caucasian, younger age (< 35 years), elderly age (> 75 years), unemployment, and a personal history of suicide attempt and family history of suicide attempt or suicide completion, as well as predominant depressive polarity. Suicide is associated with the depressed or mixed subtypes, not mania. Although there are emerging treatments for bipolar depression, such as ketamine and TMS, lithium remains the only medication associated with lowered suicide rates in bipolar disorder. Understanding clinical and demographic risk factors for suicide in bipolar disorder remains the best way to prevent suicidal behavior. Early intervention and treatment with anti-suicidal medications, such as lithium, along with close observation and follow-up is the best way to mitigate suicide in patients with bipolar disorder.
Subject(s)
Bipolar Disorder/drug therapy , Bipolar Disorder/psychology , Suicidal Ideation , Suicide, Attempted/prevention & control , Suicide, Attempted/psychology , Humans , Risk FactorsABSTRACT
BACKGROUND: Schizoaffective disorder (SAD) is a chronic, potentially disabling psychotic disorder common in clinical settings. SAD often has been used as a diagnosis for individuals having an admixture of mood and psychotic symptoms whose diagnosis is uncertain. Its hallmark is the presence of symptoms of a major mood episode (either a depressive or manic episode) concurrent with symptoms characteristic of schizophrenia, such as delusions, hallucinations, or disorganized speech. METHODS: A literature search in PubMed and Google Scholar was conducted to identify articles on SAD. We also reviewed major textbooks and DSM-5 to identify pertinent information. RESULTS: This review begins with the history and classification of SAD. Debate continues to swirl around the concept, as some experts view SAD as an independent disorder, while others see SAD as either a form of schizophrenia or a mood disorder. The disorder is more common in women and its course follows the middle ground between schizophrenia and bipolar disorder. SAD appears to have high heritability. Most patients appear to benefit from antipsychotics plus antidepressants and/or mood stabilizers, depending on whether the patient has the depressive or bipolar subtype. Electroconvulsive therapy can also be effective. CONCLUSIONS: SAD is a chronic psychotic disorder that continues to be controversial. There has been inadequate research regarding its epidemiology, course, etiologic factors, and treatment.
Subject(s)
Psychotic Disorders/diagnosis , Psychotic Disorders/history , Schizophrenia/diagnosis , Antipsychotic Agents/therapeutic use , Australia , History, 20th Century , History, 21st Century , Humans , Psychotic Disorders/classification , Schizophrenia/classification , Schizophrenia/drug therapy , Schizophrenic PsychologyABSTRACT
Background : Widely reported by bipolar disorder (BD) patients, cognitive symptoms, including deficits in executive function, memory, attention, and timing are under-studied. Work suggests that individuals with BD show impairments in interval timing tasks, including supra-second, sub-second, and implicit motor timing compared to the neuronormative population. However, how time perception differs within individuals with BD based on BD sub-type (BDI vs II), mood, or antipsychotic medication-use has not been thoroughly investigated. The present work administered a supra-second interval timing task concurrent with electroencephalography (EEG) to patients with BD and a neuronormative comparison group. As this task is known to elicit frontal theta oscillations, signal from the frontal (Fz) lead was analyzed at rest and during the task. Results : Results suggest that individuals with BD show impairments in supra-second interval timing and reduced frontal theta power compared during the task to neuronormative controls. However, within BD sub-groups, neither time perception nor frontal theta differed in accordance with BD sub-type, mood, or antipsychotic medication use. Conclusions : his work suggests that BD sub-type, mood status or antipsychotic medication use does not alter timing profile or frontal theta activity. Together with previous work, these findings point to timing impairments in BD patients across a wide range of modalities and durations indicating that an altered ability to assess the passage of time may be a fundamental cognitive abnormality in BD.
ABSTRACT
BACKGROUND: Widely reported by bipolar disorder (BD) patients, cognitive symptoms, including deficits in executive function, memory, attention, and timing are under-studied. Work suggests that individuals with BD show impairments in interval timing tasks, including supra-second, sub-second, and implicit motor timing compared to the neuronormative population. However, how time perception differs within individuals with BD based on disorder sub-type (BDI vs II), depressed mood, or antipsychotic medication-use has not been thoroughly investigated. The present work administered a supra-second interval timing task concurrent with electroencephalography (EEG) to patients with BD and a neuronormative comparison group. As this task is known to elicit frontal theta oscillations, signal from the frontal (Fz) lead was analyzed at rest and during the task. RESULTS: Results suggest that individuals with BD show impairments in supra-second interval timing and reduced frontal theta power during the task compared to neuronormative controls. However, within BD sub-groups, neither time perception nor frontal theta differed in accordance with BD sub-type, depressed mood, or antipsychotic medication use. CONCLUSIONS: This work suggests that BD sub-type, depressed mood status or antipsychotic medication use does not alter timing profile or frontal theta activity. Together with previous work, these findings point to timing impairments in BD patients across a wide range of modalities and durations indicating that an altered ability to assess the passage of time may be a fundamental cognitive abnormality in BD.
ABSTRACT
Myotonic dystrophy type 1 is the most common form of muscular dystrophy in adults, and is primarily characterized by muscle weakness and myotonia, yet some of the most disabling symptoms of the disease are cognitive and behavioral. Here we evaluated several of these non-motor symptoms from a cross-sectional time-point in one of the largest longitudinal studies to date, including full-scale intelligence quotient, depression, anxiety, apathy, sleep, and cerebral white matter fractional anisotropy in a group of 39 adult-onset myotonic dystrophy type 1 participants (27 female) compared to 79 unaffected control participants (46 female). We show that intelligence quotient was significantly associated with depression (P < 0.0001) and anxiety (P = 0.018), but not apathy (P < 0.058) or hypersomnolence (P = 0.266) in the DM1 group. When controlling for intelligence quotient, cerebral white matter fractional anisotropy was significantly associated with apathy (P = 0.042) and hypersomnolence (P = 0.034), but not depression (P = 0.679) or anxiety (P = 0.731) in the myotonic dystrophy type 1 group. Finally, we found that disease duration was significantly associated with apathy (P < 0.0001), hypersomnolence (P < 0.001), IQ (P = 0.038), and cerebral white matter fractional anisotropy (P < 0.001), but not depression (P = 0.271) or anxiety (P = 0.508). Our results support the hypothesis that cognitive deficits, hypersomnolence, and apathy, are due to the underlying neuropathology of myotonic dystrophy type 1, as measured by cerebral white matter fractional anisotropy and disease duration. Whereas elevated symptoms of depression and anxiety in myotonic dystrophy type 1 are secondary to the physical symptoms and the emotional stress of coping with a chronic and debilitating disease. Results from this work contribute to a better understanding of disease neuropathology and represent important therapeutic targets for clinical trials.
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OBJECTIVE: We tested the hypothesis that variant repeat interruptions (RIs) within the DMPK CTG repeat tract lead to milder symptoms compared with pure repeats (PRs) in myotonic dystrophy type 1 (DM1). METHODS: We evaluated motor, neurocognitive, and behavioral outcomes in a group of 6 participants with DM1 with RI compared with a case-matched sample of 12 participants with DM1 with PR and a case-matched sample of 12 unaffected healthy comparison participants (UA). RESULTS: In every measure, the RI participants were intermediate between UA and PR participants. For muscle strength, the RI group was significantly less impaired than the PR group. For measures of Full Scale IQ, depression, and sleepiness, all 3 groups were significantly different from each other with UA > RI > PR in order of impairment. The RI group was different from unaffected, but not significantly different from PR (UA > RI = PR) in apathy and working memory. Finally, in finger tapping and processing speed, RI did not differ from UA comparisons, but PR had significantly lower scores than the UA comparisons (UA = RI > PR). CONCLUSIONS: Our results support the notion that patients affected by DM1 with RI demonstrate a milder phenotype with the same pattern of deficits as those with PR indicating a similar disease process.
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BACKGROUND: Few adequately-powered studies have systematically evaluated brain morphology in adult-onset myotonic dystrophy type 1 (DM1). OBJECTIVE: The goal of the present study was to determine structural brain differences between individuals with and without adult-onset DM1 in a multi-site, case-controlled cohort. We also explored correlations between brain structure and CTG repeat length. METHODS: Neuroimaging data was acquired in 58 unaffected individuals (29 women) and 79 individuals with DM1 (50 women). CTG repeat length, expressed as estimated progenitor allele length (ePAL), was determined by small pool PCR. Statistical models were adjusted for age, sex, site, and intracranial volume (ICV). RESULTS: ICV was reduced in DM1 subjects compared with controls. Accounting for the difference in ICV, the DM1 group exhibited smaller volume in frontal grey and white matter, parietal grey matter as well as smaller volume of the corpus callosum, thalamus, putamen, and accumbens. In contrast, volumes of the hippocampus and amygdala were significantly larger in DM1. Greater ePAL was associated with lower volumes of the putamen, occipital grey matter, and thalamus. A positive ePAL association was observed for amygdala volume and cerebellar white matter. CONCLUSIONS: Smaller ICV may be a marker of aberrant neurodevelopment in adult-onset DM1. Volumetric analysis revealed morphological differences, some associated with CTG repeat length, in structures with plausible links to key DM1 symptoms including cognitive deficits and excessive daytime somnolence. These data offer further insights into the basis of CNS disease in DM1, and highlight avenues for further work to identify therapeutic targets and imaging biomarkers.