Cognitive performance predicts treatment decisional abilities in mild to moderate dementia.

OBJECTIVE: To examine the contribution of neuropsychological test performance to treatment decision-making capacity in community volunteers with mild to moderate dementia. METHODS: The authors recruited volunteers (44 men, 44 women) with mild to moderate dementia from the community. Subjects completed a battery of 11 neuropsychological tests that assessed auditory and visual attention, logical memory, language, and executive function. To measure decision making capacity, the authors administered the Capacity to Consent to Treatment Interview, the Hopemont Capacity Assessment Interview, and the MacCarthur Competence Assessment Tool--Treatment. Each of these instruments individually scores four decisional abilities serving capacity: understanding, appreciation, reasoning, and expression of choice. The authors used principal components analysis to generate component scores for each ability across instruments, and to extract principal components for neuropsychological performance. RESULTS: Multiple linear regression analyses demonstrated that neuropsychological performance significantly predicted all four abilities. Specifically, it predicted 77.8% of the common variance for understanding, 39.4% for reasoning, 24.6% for appreciation, and 10.2% for expression of choice. Except for reasoning and appreciation, neuropsychological predictor (beta) profiles were unique for each ability. CONCLUSIONS: Neuropsychological performance substantially and differentially predicted capacity for treatment decisions in individuals with mild to moderate dementia. Relationships between elemental cognitive function and decisional capacity may differ in individuals whose decisional capacity is impaired by other disorders, such as mental illness.

The P3 auditory event-related brain potential indexes major personality traits.

BACKGROUND: The amplitude of the auditory P3 event-related potential is reduced in patients with axes I and II disorders. Data regarding P3 amplitude and normal personality traits in healthy individuals have been inconsistent, however, although more extreme variants of dimensional traits such as neuroticism and extraversion are associated with psychiatric morbidity. METHODS: Male subjects (n = 18) recruited from the community completed the NEO Five-Factor Inventory, which consists of five scales: Neuroticism, Extraversion, Openness, Agreeableness, and Conscientiousness. P3 potentials were generated using an auditory discrimination paradigm to which a third, novel stimulus was added. Partial least squares analysis, a multivariate statistical procedure, was used to test the relationship, in both stimulus conditions, between P3 amplitude at six electrode sites and the five personality dimensions. RESULTS: P3 amplitude across conditions and sites was positively related to Extraversion, Openness, Agreeableness, and Conscientiousness and negatively related to Neuroticism. CONCLUSIONS: Previous studies have shown that both reduced P3 amplitude and a high Neuroticism/low Extraversion-Openness-Agreeableness-Conscientiousness trait pattern are associated with the presence of, and risk for, substantial psychiatric morbidity. Our results suggest that processes indexed by auditory P3 amplitude are related to these broad personality dimensions in healthy individuals.

Personality traits in schizophrenia: comparison with a community sample.

The objective of this study was to compare personality trait profiles in patients with schizophrenia and healthy controls. Male outpatients with schizophrenia (N = 24) and a male nonpsychiatric community sample (N = 46) completed the NEO-FFI personality questionnaire. Multivariate analyses were used to compare mean scale scores and scale profiles for each group. The overall personality profile of clinically stable patients with schizophrenia differed significantly from that of a community sample. On individual scales, patients scored significantly higher on neuroticism and significantly lower on conscientiousness. These results confirm and extend those of previous studies that used normative data for comparison and a much longer version of the same personality questionnaire. Prospective studies of populations at risk are needed to determine whether group differences reflect a premorbid diathesis for schizophrenia or a secondary effect of serious mental illness.

Sympathoadrenal hyperactivity and the etiology of neuroleptic malignant syndrome.

OBJECTIVE: The author's goal was to develop a pathophysiological model for neuroleptic malignant syndrome with greater explanatory power than the alternative hypotheses of hypothalamic dopamine antagonism (elevated set point) and direct myotoxicity (malignant hyperthermia variant). METHOD: Published clinical findings on neuroleptic malignant syndrome were integrated with data from human and animal studies of muscle physiology, thermoregulation, and autonomic nervous system function. RESULTS: The data show that the sympathetic nervous system's latent capacity for autonomous activity is expressed when tonic inhibitory inputs from higher central nervous system centers are disrupted. These tonic inhibitory inputs are relayed to preganglionic sympathetic neurons by way of dopaminergic hypothalamospinal tracts. The sympathetic nervous system mediates hypothalamic coordination of thermoregulatory activity and is a primary regulator of muscle tone and thermogenesis, augmenting both of these when stimulated. In addition, the sympathetic nervous system modulates all of the other end-organs that function abnormally in neuroleptic malignant syndrome. CONCLUSIONS: There is substantial evidence to support the hypothesis that dysregulated sympathetic nervous system hyperactivity is responsible for most, if not all, features of neuroleptic malignant syndrome. A predisposition to more extreme sympathetic nervous system activation and/or dysfunction in response to emotional or psychological stress may constitute a trait vulnerability for neuroleptic malignant syndrome, which, when coupled with state variables such as acute psychic distress or dopamine receptor antagonism, produces the clinical syndrome of neuroleptic malignant syndrome. This hypothesis provides a more comprehensive explanation for existing clinical data than do the current alternatives.

Diaphoresis and dehydration during neuroleptic malignant syndrome: preliminary findings.

Serum osmolality and its relationship to diaphoresis and polydipsic behavior were examined in a series of 38 episodes of neuroleptic malignant syndrome (NMS) in 29 patients. Clinical variables were associated with significantly higher serum osmolality, and diaphoresis tended to emerge earlier than polydipsia in the course of NMS. The findings of this study are consistent with the hypothesis that, at least in some NMS patients, diaphoresis leads to dehydration followed by physiologically appropriate thirst and increased oral water intake. It appears that intravenous hydration is often necessary to correct the significant free water deficit that can occur during the course of NMS.

Thermoregulatory dysfunction in neuroleptic malignant syndrome.

Hyperthermia is the central feature of neuroleptic malignant syndrome (NMS), but its etiology remains elusive. Two competing hypotheses implicate either hypothalamic dysfunction (inappropriate "set point") or direct myotoxicity (excessive peripheral heat production). These two models have distinct implications for thermoregulatory activity in NMS. The first predicts that the individual should respond as to a hypothermic threat or infection (the hypothalamus signals the body to raise its temperature). The second implies that an excessive heat load is perceived by the hypothalamus, which responds to this hyperthermic threat (it signals the body to lower its temperature). To assess the validity of these two hypotheses the thermoregulatory responses of a series of NMS patients (36 patients, 46 episodes) were examined using standard statistical methods. In contrast to normal mammalian thermoregulatory behavior, thermoeffector responses were not organized into either mode, but appeared to function somewhat independently and paradoxically. We conclude that neither hypothesis is sufficient to explain altered thermoregulation in NMS, and that the loss of integrated thermoeffector activity may be unique to this disorder.

Platelet monoamine oxidase activity and deficit syndrome schizophrenia.

Measures of affective flattening that combine self-reported emotional experience with observed affect may identify deficit syndrome patients better than ratings based on observed affect alone. In this study, we examined 23 clinically stable but chronically ill schizophrenic patients, 15 of whom were found to have a deficit syndrome. After exclusion of patients with self-reported depressed mood from the deficit syndrome group, the remaining patients with a deficit syndrome not accompanied by self-reported depressed mood showed a strikingly homogeneous distribution of platelet monoamine oxidase activity. Results suggest that inclusion of self-reported emotional experience in clinical definitions of the deficit syndrome will increase the specificity of diagnosis.

Enzyme elevations in the neuroleptic malignant syndrome.

Enzyme elevations are frequently observed in neuroleptic malignant syndrome (NMS), but their significance is unknown and their source is uncertain. In this study the relationship of serum enzymes to creatine phosphokinase (CPK) in NMS is examined. Thirty-seven patients with at least one probable episode of NMS were studied, and 83 consecutive newly admitted psychiatric patients constituted a comparison group. Serum levels of lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT), aldolase, and alkaline phosphatase (AP) were compared to serum CPK levels in each patient group. Except for AP, all enzymes were significantly correlated with CPK in both groups. However, correlations were much higher in the NMS group, and regression lines for CPK-LDH and CPK-GOT pairs differed significantly between patient groups. These data strongly suggest that a common process underlies the enzyme elevations frequently seen in NMS, that these enzymes originate in muscle tissue, and that these findings are not caused solely by agitation or psychological stress. It is likely that increased production and selective "leakage" of enzymes from myocytes play a role in this process.

Sensation seeking and novelty seeking. Are they the same?

Responses to Zuckerman's Sensation Seeking Scale (SSS) and Cloninger's Tridimensional Personality Questionnaire (which consists of novelty seeking, harm avoidance, and reward-dependence dimensions) have been linked to a variety of behavioral and psychiatric variables. The relationship of these two measures to one another has not been examined previously and, in the present study, is evaluated in a group of men briefly hospitalized for treatment of alcohol and chemical dependence. Total sensation seeking scale scores were significantly correlated (Pearson r) with total novelty seeking scale scores. Set correlation analysis revealed significant overall relationships between sensation seeking and both high novelty seeking and low harm avoidance. Most of these overall relationships were attributable to six subscales, although broad relationships were observed between the SSS disinhibition and novelty seeking subscales, and between a harm avoidance subscale and all SSS subscales. Neither statistical approach identified an association between reward dependence and sensation seeking.

Sympathoadrenomedullary activity in the neuroleptic malignant syndrome.

Many clinical features of the neuroleptic malignant syndrome suggest that sympathetic nervous system hyperactivity is involved in the pathophysiology of this disorder. Only a few studies have examined levels of catecholamines or their metabolites in patients with NMS; results so far have been inconclusive. In the present study urinary catecholamine metabolites obtained during the course of NMS were studied with respect to frequently reported signs and symptoms of NMS. The principal findings are that (1) elevated urinary catecholamines and metabolites are a frequent but inconstant feature of NMS; (2) it is likely that sympathetic nervous system hyperactivity contributes to the picture of fulminant NMS; and (3) the role of the adrenal medulla in producing excess catecholamines during NMS is uncertain.

A comparison of diagnostic criteria for neuroleptic malignant syndrome.

BACKGROUND: A variety of diagnostic criteria for neuroleptic malignant syndrome (NMS) have been used in clinical studies of this disorder, but it is not known if different criteria consistently identify NMS. This study examines agreement between three frequently used sets of diagnostic criteria in a series of possible NMS episodes. METHOD: All clinically suspected NMS episodes occurring at a large tertiary psychiatric facility during a 6-year period were evaluated by three different sets of diagnostic criteria. Agreement among these criteria was quantified statistically by means of the kappa and intraclass correlation coefficients. RESULTS: The NMS diagnostic criteria examined generally demonstrated only fair agreement with one another in the diagnosis of NMS. Agreement was best among these criteria when the "probable" category was employed. A complex interaction involving both definition and structure of individual diagnostic criteria and designation of criteria as major or minor appears to contribute to these findings. CONCLUSION: The published diagnostic criteria used in this study do not consistently identify NMS episodes and demonstrate different thresholds for assigning this diagnosis. These differences are not due solely to different definitions of individual criteria (e.g., fever). Possible implications of these findings for clinical practice and research are discussed.

Some biological and behavioral features associated with clinical personality types.

The author reviews supporting evidence for the existence of two personality prototypes that correspond to two DSM-III-R personality "clusters." These hypothetical personality prototypes are characterized by extreme variations along several interrelated personality trait dimensions and by differences in two biological measures. The possibility that individual differences in central serotonin and/or catecholamine activity may underlie some of the features associated with these prototypes is discussed in light of current data. The usefulness of this conceptualization as a supplemental axis of personality classification is suggested.