This review presents data showing that apathy is common across a number of disorders. Apathy is not only common, but is also associated with significant problems: reduced functional level, decreased response to treatment, poor illness outcome, caregiver distress, and chronicity. Preliminary evidence of treatment efficacy exists for dopaminergic drugs and for amphetamines. Strong evidence of efficacy exists for acetylcholinesterase inhibitors in Alzheimer's disease, and for atypical antipsychotics in schizophrenia. Frontal-subcortical system(s) dysfunction is implicated in the causation of apathy; apathy subtypes based on the various frontal-subcortical loops may thus exist. Further research involving diagnosis, pathophysiology, and treatment is suggested.

Objective Apathy is highly prevalent among neuropsychiatric populations and is associated with greater morbidity and worse functional outcomes. Despite this, it remains understudied and poorly understood, primarily due to lack of consensus definition and clear diagnostic criteria for apathy. Without a gold standard for defining and measuring apathy, the availability of empirically sound measures is imperative. This paper provides a psychometric review of the most commonly used apathy measures and provides recommendations for use and further research. Methods Pertinent literature databases were searched to identify all available assessment tools for apathy in adults aged 18 and older. Evidence of the reliability and validity of the scales were examined. Alternate variations of scales (e.g., non-English versions) were also evaluated if the validating articles were written in English. Results Fifteen apathy scales or subscales were examined. The most psychometrically robust measures for assessing apathy across any disease population appear to be the Apathy Evaluation Scale and the apathy subscale of the Neuropsychiatric Inventory based on the criteria set in this review. For assessment in specific populations, the Dementia Apathy Interview and Rating for patients with Alzheimer’s dementia, the Positive and Negative Symptom Scale for schizophrenia populations, and the Frontal System Behavior Scale for patients with fronto-temporal deficits are reliable and valid measures. Conclusion Clinicians and researchers have numerous apathy scales for use in broad and disease-specific neuropsychiatric populations. Our understanding of apathy would be advanced by research that helps build a consensus as to the definition and diagnosis of apathy, and further refine the psychometric properties of all apathy assessment tools.

This prospective follow-up study addresses whether impulsivity versus other aspects of borderline personality disorder (BPD) are (1) stable over a 7-year follow-up period; (2) able to predict the persistence versus remittance of BPD over 7 years of follow-up, and (3) more predictive of the level of borderline psychopathology on follow-up than other aspects of the disor der. When the cohort was assembled, 88 of 130 subjects scored seven or higher on the Diagnostic Interview for Border lines (DIB), indicating a definite diagnosis of BPD. The cohort was reassessed at 2 and 7 years after the index admission. At the 7-year follow up, 81(62.3%) of the original cohort were re examined, two (1.6%) were deceased, six (4.6%) suicided, 36 (27.7%) refused to participate and five (3.8%) could not be lo cated. The results indicated that the initial impulse action subscale score was highly correlated with the 7-year follow-up score (r = 0.53). Using a stepwise multiple regression tech nique, the impulse action subscale score from the DIB best pre dicted borderline psychopathology at the 7-year follow up, with an r2 of 0.24, F= 24.84, p < 0.001. This prospective study of subjects with BPD indicates that impulsivity is stable over time and highly predictive of borderline psychopathology over 7 years follow up. These results suggest the treatment of impul sivity may impact the course of BPD.Predicting the course of borderline personality disorder (BPD) has provided an ongoing challenge to researchers and yielded diverse findings. Paris (1988) concluded that empirical studies following BPD subjects for more than 2 years showed a lack of consistency in determining predictors of outcome for BPD. Even though some research has shown that certain aspects of borderline psychopathology predict poor global outcome, few studies have examined whether any of the factors predict remittance or From the St.

Substantial psychological and neurobehavioural evidence is available to support the hypothesis that traumatic brain injury (TBI) is a risk factor for subsequent psychiatric disorders. However, studies utilizing established psychiatric diagnostic schemes to study these outcomes after TBI are scarce, and no studies have included an assessment of personality disorders in addition to the major psychiatric disorders. This study utilizes structured psychiatric interviews to measure the prevalence of DSM-III(R) disorders in a sample of 18 subjects derived from a TBI rehabilitation programme. Results revealed high rates for major depression, bipolar affective disorder, generalized anxiety disorder, borderline and avoidant personality disorders. Co-morbidity was also high. A preliminary study of postulated predictive factors revealed possible roles for sex and for initial severity of injury. The study supports the association between TBI and psychiatric disorder, and suggests the need for monitoring, for prevention, and for treatment of psychiatric disorders after TBI.

Infection with several important pathogens could constitute risk factors for cognitive impairment, dementia, and Alzheimer's disease (AD) in particular. This review summarizes the data related to infectious agents that appear to have a relationship with AD. Infections with herpes simplex virus type 1, picornavirus, Borna disease virus, Chlamydia pneumoniae, Helicobacter pylori, and spirochete were reported to contribute to the pathophysiology of AD or to cognitive changes. Based on these reports, it may be hypothesized that central nervous system or systemic infections may contribute to the pathogenesis or pathophysiology of AD, and chronic infection with several pathogens should be considered a risk factor for sporadic AD. If this hypothesis holds true, early intervention against infection may delay or even prevent the future development of AD.