The relationship between personality and DSM-III axis I disorders in the population: results from an epidemiological survey.

OBJECTIVE: The aim of this study was to assess the relationships between specific personality disorders and DSM-III axis I conditions in a community sample. METHOD: A total of 810 subjects were examined by psychiatrists in the second stage of the Eastern Baltimore Mental Health Survey, part of the Epidemiological Catchment Area Program of the National Institute of Mental Health. A semistructured examination, the Standardized Psychiatric Examination, was employed to assess axis I and axis II conditions. Scales for compulsive and antisocial personality disorders were derived from DSM-III criteria. The relationships between scores on these personality disorder scales and the presence of generalized anxiety disorder, alcohol use disorders (alcohol abuse and alcohol dependence), and simple phobia were evaluated by using logistic regression. RESULTS: Higher compulsive personality scores were associated with a greater odds of generalized anxiety disorder and simple phobia but a smaller odds of alcohol use disorders. In contrast, higher antisocial personality scores were associated with a greater odds of alcohol use disorders but a smaller odds of generalized anxiety disorder. There was no relationship between antisocial personality scores and simple phobia. CONCLUSIONS: Personality disorders have specific relationships to axis I conditions, which suggests different vulnerabilities but also different protective influences.     

Neuronal loss in layers V and VI of cerebral cortex in Huntington's disease.

Neuronal loss in the cerebral cortex in Huntington's disease (HD) has not been well documented, nor has its laminar pattern been definitively established. We therefore counted neurons in individual cortical laminae in the dorsal frontal cortex of 5 HD and 5 control autopsy brains. Significant neuronal loss (to 57% of control, P = 0.002) was found in layer VI of HD brains. These cells project principally to the thalamus, the claustrum and other regions of cerebral cortex; thus their loss is unlikely to be the result of retrograde degeneration secondary to striatal pathology. Layer V neurons were also decreased (to 71% of control, P = 0.034). Degeneration of cerebral cortical neurons may be at least partly responsible for some of the non-choreic symptoms of HD, such as dementia, irritability, apathy, and depression.     

Results of a high-resolution genome screen of 437 Alzheimer's disease families

Alzheimer's disease (AD) is a devastating neurodegenerative disorder of late life with complex inheritance. Mutations in three known genes lead to the rare early-onset autosomal dominant form of AD, while a common polymorphism (epsilon 4) in the gene encoding apolipoprotein E (APOE ) is a risk factor for more typical late-onset (>60 years) AD. A recent study concluded that there are up to four additional genes with an equal or greater contribution to the disease. We performed a 9 cM genome screen of 437 families with AD, the full National Institute of Mental Health (NIMH) sample, which has been carefully ascertained, evaluated and followed by our group over the last decade. Performing standard parametric and non-parametric linkage analyses, we observed a 'highly significant' linkage peak by Lander and Kruglyak criteria on chromosome 19q13, which probably represents APOE. Twelve additional locations-on 1q23, 3p26, 4q32, 5p14, 6p21, 6q27, 9q22, 10q24, 11q25, 14q22, 15q26 and 21q22-met criteria for 'suggestive' linkage [i.e. two-point lod score (TLS) >/=1.9 and/or multipoint lod score (MLS) >/=2.2] in at least one of our analyses. Although some of these will surely prove to be false positives, these linkage signals should provide a valuable framework for future studies aimed at identifying additional susceptibility genes for late-onset AD.     

Quantitative assessment of psychologic state of patients with anorexia nervosa or bulimia: response to caloric stimulus

Hospitalized patients with anorexia nervosa (N = 17) or bulimia (N = 11) were given a standard liquid meal containing 400 calories. Using analogue scales, bulimic patients were found to have greater anxiety, lower mood, lower sexual arousal, and more fear of fatness than either control or anorectic patients. This finding of increased general "dysphoria" in bulimic patients persisted after the meal without any significant premeal to postmeal changes. Anorectic patients also differed from controls, but less than the bulimic patients. Some measures of anxiety correlated significantly with body mass index before the meal in bulimic patients, whereas in anorectic patients the correlation was significant only after the meal.     

Pedigree study of familial Alzheimer disease

Twenty-one families with familial Alzheimer disease were ascertained in a dementia clinic and assessed by multiple family interviews. Eight autopsies were reviewed. The age of onset varied from 25 to 85. Seven pedigrees showed evidence of 3 generation transmission. Paternal age of the founders of 4 lines which could be assessed was higher than controls.     

Familial aggregation in Alzheimer dementia--II. Clinical genetic implications of age-dependent onset

A biomathematical genetic model for the age-specific risk of Alzheimer Dementia (AD) was applied to two problems in the clinical genetics of this disorder. In a test of the ability of a clinical marker specifically to identify genetic AD, cases grouped by the phenotype of amnesia with aphasia or apraxia (aaa) were shown to have familial risk that suggested a pure genetic illness, and differed significantly (p = 0.006) from cases without this phenotype. The model was also used in a Bayesian paradigm to assess the probability that individual cases had hereditary disease, given their family history. Here the results were surprisingly ambiguous: Even with no affected relatives, there is a substantial likelihood that many AD cases may have a genetic illness. Hence, one cannot reliably classify individual cases as "familial" or "sporadic" from family history alone. The phenotype of aaa (or other suitable marker) appears to be more reliable than the degree of manifest familial aggregation as an indicator of genetic AD.     

Neuropsychological correlates of brain atrophy in Huntington's disease: a magnetic resonance imaging study

Summary Magnetic resonance imaging and a comprehensive cognitive evaluation were carried out in a series of 29 patients with mild to moderate Huntington's disease (HD). A factor analysis of the neuropsychological test scores provided three factors: a memory/speed-of-processing factor, a frontal factor, and a response inhibition factor. The memory/speed factor correlated significantly with measures of caudate atrophy, frontal atrophy, and atrophy of the left (but not the right) sylvian cistern. There were no significant correlations between the frontal or response inhibition factors and measures of cortical or subcortical brain atrophy. Our findings confirm that subcortical atrophy is significantly correlated with specific cognitive deficits in HD, and demonstrate that cortical atrophy also has important association with the cognitive deficits of patients with HD.