Altering risky decision-making: Influence of impulsivity on the neuromodulation of prefrontal cortex.

The prefrontal cortex (PFC) subserves complex cognitive abilities, including risky decision-making; the modulation of this brain area is shown to alter the way people take risks. Yet, neuromodulation of the PFC in relation to risk-taking behavior remains relatively less well-studied. Moreover, the psychological variables that influence such neuromodulation remain poorly understood. To address these issues, 16 participants took part in 3 experimental sessions on separate days. They received: (i) left anodal-right cathodal transcranial direct current stimulation (tDCS); (ii) left cathodal-right anodal stimulation; or (iii) sham stimulation while they completed two risk-taking tasks. They also measured on several cognitive-affective abilities and personality traits. It was revealed that left cathodal-right anodal stimulation led to significantly reduced risk-taking under a context of haste. The reduction of risk-taking (relative to sham) correlated with state and trait impulsivity, such that the effect was larger in more impulsive individuals. For these individuals, the tDCS effect size was considered to be large (generalized partial η(2) > .17). The effect of prefrontal-neuromodulation in reducing risk-taking was influenced by baseline impulsivity, reflecting a state-dependent effect of neuromodulation on the PFC. The results of this study carry important insights into the use of neuromodulation to alter higher cognition.

Neurobiological underpinnings of sensation seeking trait in heroin abusers.

Neurobiological investigation of heroin revealed that abusers of this highly addictive substance show dysregulation in brain circuits for reward processing and cognitive control. Psychologically, personality traits related to reward processing and cognitive control differed between heroin abusers and non-abusers. Yet, there is no direct evidence on the relationship between these neurobiological and psychological findings on heroin abusers, and whether such relationship is altered in these abusers. The present study filled this research gap by integrating findings obtained via magnetic resonance imaging (structural volume and resting-state functional connectivity) and self-reported personality trait measures (Zuckerman׳s Sensation Seeking Scale and Barratt Impulsivity Scale) on 33 abstinent heroin users and 30 matched healthy controls. The key finding is a negative relationship between high sensation seeking tendency and midbrain structural volume in the heroin users. Importantly, there was stronger coupling between the midbrain and ventromedial prefrontal cortex and weaker coupling between the midbrain and dorsolateral prefrontal cortex in heroin users. Our findings offer significant insight into the neural underpinning of sensation seeking in heroin users. Importantly, the data shed light on a novel relationship between the mesolimbic-prefrontal pathway of the reward system and the high sensation seeking personality trait in heroin abusers.

Differential effects of left parietal theta-burst stimulation on order and quantity processing.

Numbers can be used to represent different meanings, including order information ('Steve lives at house number 24') and quantity ('Steve is paid 24 pounds'). The few previous neuroimaging studies that investigated order and quantity processing reported conflicting evidence as to whether same or partially overlapping brain systems are engaged in these processes. Such inconsistencies may be related to the use of neuroimaging techniques which do not allow causal inference regarding brain-behaviour relationships. To overcome this problem, the present study employed continuous theta-burst stimulation (TBS) to investigate whether interference to either the left or right parietal regions affected order and quantity in similar or different ways. Results revealed that following TBS to the left intraparietal sulcus, quantity processing was impaired and order facilitated; TBS to the contralateral brain region led to no specific effects in either order or quantity processing. These findings suggest that there are at least partially different neuronal populations involved in order and quantity processing, and that the left parietal cortex is critical for both processes.

Schizophrenia and risk-taking: impaired reward but preserved punishment processing.

Risky decision-making is subserved by the frontostriatal system, which includes a network of interconnected brain regions known to be dysfunctional in patients with schizophrenia. This study aimed to investigate whether and to what extent patients with schizophrenia display a different pattern of risk-taking behavior relative to matched healthy controls. The Balloon Analogue Risk Task (BART) and the Risky-Gains Task were used as naturalistic measures of risk-taking behavior in 25 patients with schizophrenia and 25 controls. Results of the BART revealed that patients behaved more conservatively, and this in turn led to suboptimal risky decision-making. Consistently, patients behaved more conservatively in the Risky-Gains Task. Interestingly, however, they adjusted the pattern of risk-taking following a punished trial similar to controls. These findings indicate that patients have impaired reward but preserved punishment processing. This study complements previous studies on decision-making in schizophrenia and suggests specific rather than widespread abnormalities along the frontostriatal system in schizophrenia.

The course of depressive symptoms over time for women who completed drug treatment.

The purpose of the present study was to (a) describe the trend in depressive symptoms in a sample of postpartum women who used cocaine and who completed drug treatment; and (b) to examine possible correlates of those trends including treatment type and selected pretreatment characteristics. Self-reported levels of depressive symptoms improved from treatment entry to discharge and remained relatively stable through three postdischarge follow-up points. Baseline level of depression was the only pretreatment factor that was correlated with the trend in depressive symptoms. And length of time in treatment, previous drug treatment, and baseline severity of drug use were not.

Computed tomography findings in clinically normal and abnormal thyroid patients.

Fifty normal volunteers had unenhanced thyroid computed tomography scans. A range of normal computed tomography densities and volumes was established for each age group. Pre- and postcontrast scans were done on 47 abnormal patients with hemorrhagic cysts, multinodular goiter, thyroiditis, papillary carcinoma, and benign adenomas. The computed tomography characteristics of each of the pathologic groups was noted for both the abnormal areas and the uninvolved part of the gland. Preliminary observations of the computed tomography characteristics of each abnormality are discussed.

Computed tomography in soft tissue calcification layering.

Soft tissue calcification occurs in a variety of disorders. When it is associated with an abnormal calcium phosphorous product, it may present as large, periarticular masses that demonstrate layering on horizontal beam radiographs or computed tomography (CT). Previous reports have shown this phenomenon in idiopathic tumoral calcinosis. We report two patients with metastatic calcification of different etiologies: one patient with tumoral calcinosis and one with secondary hyperparathyroidism complicating chronic renal failure. Both showed layering on CT. The pathology of this phenomenon as well as therapeutic implications are discussed.

Protective effect of hyperthermia against the cytotoxicity of actinomycin D on Chinese hamster cells.

Hyperthermia is being tested as an adjuvant to chemotherapy for clinical use. We elected to study the interaction of heat at 43 degrees C with actinomycin D (AMD) (0.5 microgram/ml) in tissue culture using plateau phase Chinese hamster cells. The simultaneous administration of 43 degrees C and AMD produces more than additive cytotoxicity if the duration of exposure is less than 30 minutes; however, this is quickly reversed with longer exposures with the cells developing resistance to further cytotoxicity of AMD. If heat (43 degrees C) is applied before AMD exposure, the cells also are rendered insensitive, with a greater protection observed for longer periods of heating. For example, for cells heated for 2 hours at 43 degrees C and then exposed to AMD (0.5 microgram/ml for 2 hours), cytotoxicity to AMD is decreased by a factor of 10. Heat-induced resistance to AMD persists for at least 18 hours before full recovery of AMD effect returns. The application of heat following AMD exposure also protects against the cytotoxicity of AMD. Studies using 3H-AMD demonstrate that the resistance does not correlate with reduced membrane permeability to AMD of heated cells. Attention must be given to the timing of hyperthermia when used clinically as adjuvant therapy in patients receiving AMD.