Transient increase of intact visual field size by high-frequency narrow-band stimulation.

Three patients with visual field defects were stimulated with a square matrix pattern, either static, or flickering at frequencies that had been found to either promote or not promote blindsight performance. Comparison between pre- and post-stimulation perimetric maps revealed an increase in the size of the intact visual field but only for flicker frequencies previously found to promote blindsight. These changes were temporary but dramatic - in two instances the intact field was increased by an area of ∼30 deg(2) of visual angle. These results indicate that not only does specific high-frequency stimulus flicker promote blindsight, but that intact visual field size may be increased by stimulation at the same frequencies. Our findings inform speculation on both the brain mechanisms and the potency of temporal modulation for altering the functional visual field.

Bandpass characteristics of high-frequency sensitivity and visual experience in blindsight.

Patient RP suffers a unilateral right homonymous quadrant anopia but demonstrates better than chance discrimination for stimuli presented in the blind field at temporal frequencies between 33 and 47Hz (all significant at p<.05, binomial). Examination of her reports of visual experience during blind-field discrimination suggests a more complex picture in which experiences particular to correct discrimination are not found at low-mid-gamma frequencies, but are significantly more likely than average (76%, p<.001) at a lower frequency (22Hz) at which blindsight is not observed. We believe that visual experience may serve to support blindsight if discrimination tasks are generally impaired at frequencies outside of the low-mid-gamma band. If this is so, although generally experienced as non-specific and unstructured light, the visual experience that accompanies discrimination performance must be based upon a neural representation which includes information on the visual features present in the stimulus.

Differences in hippocampal volume between major depression and schizophrenia: a comparative neuroimaging study.

Several studies have demonstrated that structural brain change is detectable in the hippocampus in both patients, with schizophrenia and major depression. Only few studies, however, compared both clinical disease entities directly and no larger study has tried to take different disease stages into account. The objectives of this study are to investigate whether hippocampal volumes are reduced in patients with schizophrenia and those with major depression with the same duration of illness compared to healthy controls and to assess further changes at different disease stages. A total of 319 inpatients and healthy controls were enrolled and investigated with magnetic resonance imaging (MRI). Hippocampal volumes were measured using the segmentation software BRAINS. Bilateral hippocampal volume reductions were detected in both schizophrenic and depressed patients compared to healthy control (HC) subjects. Although younger, schizophrenic (SZ) patients showed in their MRI scans significant bilaterally reduced hippocampal volumes compared to patients with major depression. Although the hippocampal reductions were similar at the onset of symptomatic manifestation of both diseases, there was a further significant reduction of the left hippocampus in the recurrently ill SZ subgroup. The data suggest rather dynamic structural brain alterations in schizophrenia compared to major depression. Here, the presented application of the comparative neuroscience approach, by the use of large neuroimaging MRI databases, seems highly valuable. In the field of psychiatry, with its still controversial operationalized descriptive diagnostic entities, the cross-nosological approach provides a helpful tool to better elucidate the still unknown brain pathologies and their underlying molecular mechanisms beyond a single nosological entity.

Hippocampal volume reduction and history of aggressive behaviour in patients with borderline personality disorder.

Disturbances of aggression and impulse control are important symptoms of borderline personality disorder (BPD). The hippocampus is part of the limbic system, which is involved in the control of these types of behaviour. The aim of our study was to investigate potential structural changes of the hippocampal formation in BPD and to evaluate if these are related to aggressive and impulsive behaviour. Twenty-five female and right-handed BPD patients (DSM-IV) and 25 healthy control subjects matched according to sex, age, handedness and educational status were examined. Magnetic resonance imaging (MRI) was performed using a 1.5-T Magnetom Vision system. The software program "BRAINS" was employed for segmentation and volumetry of the hippocampal formation. German versions of instruments were used to evaluate impulsive and aggressive behaviour. Hippocampal grey matter volume was significantly decreased in BPD patients: the reduction was more pronounced in patients with multiple hospitalizations. Hippocampal volume of the left hemisphere was inversely correlated with lifetime history of aggressive behaviour. However, no significant relationship was found between hippocampal volume and impulsive behaviour. Our study confirms previous results indicating a volume reduction of the hippocampal formation in BPD patients. Furthermore, this structural change might facilitate aggressive behaviour. Subsequent studies are required to clarify whether the reduction of hippocampal volume is a trait and risk factor for increased aggression.

Amygdala volume and depressive symptoms in patients with borderline personality disorder.

BACKGROUND: Borderline personality disorder (BPD) is characterized by a high prevalence of comorbid psychiatric disorders, including major depression (MD). The aim of this study was to examine whether a co-occurrence of MD is associated with structural changes in the amygdala of BPD patients. METHODS: Twenty-five right-handed, female patients with BPD and 25 matched healthy control subjects were examined. Diagnoses of BPD and MD were made according to DSM IV. Depressive symptomatology was determined with the Hamilton Depression Scale (HAMD). Magnetic resonance imaging scans were performed with 1.5 T Magnetom Vision (Siemens, Erlangen, Germany). The software program "BRAINS" was applied for brain volumetry and segmentation. The amygdala was delineated as "region of interest." RESULTS: Comparison of amygdala volumes between the whole group of BPD patients and control subjects revealed no significant difference. Amygdala volumes in both hemispheres were significantly larger in BPD patients with MD compared with those without MD. There was a significant correlation in BPD patients between left amygdala volume and depressive symptoms as measured by HAMD. CONCLUSIONS: Correlation of amygdala volume with depression in BPD patients might indicate a causal relationship. Future studies should clarify whether amygdala enlargement is a risk factor for MD in BPD patients or a consequence of the affective disorder.

Some facilitatory effects of lorazepam on dynamic visual binding.

RATIONALE: The benzodiazepine lorazepam enhances the potential for inhibitory gamma-aminobutyric acid (GABAA) synapses in the cortex to stabilize postsynaptic, excitatory activity by synchronizing discharge rates at frequencies of around 40 Hz. Treatment with lorazepam also affects contour integration processes, suggesting that GABAA-mediated synchronization plays a role in visuospatial organization. This conclusion is supported by other physiological studies that link visual feature integration with neuronal synchronization. OBJECTIVES: One experiment was conducted to assess variations in dynamic figural priming as a result of lorazepam administration. METHODS: Observers were presented a modified version of a figural priming paradigm designed to investigate the effects of dynamic synchronization on visual feature integration. The priming paradigm consisted of premask crosses presented in a square arrangement within the same phase of a multiphase premask matrix oscillating at 40 Hz. Observers responded to a subsequently presented target square. The modification consisted of line elements presented at various distances relative to the unspecified extension of the lines making up the premask crosses. It was expected that priming effects would be enhanced for lines terminating close to the unspecified extension but only following administration of lorazepam. RESULTS: As anticipated, priming was enhanced substantially when the premask crosses flickered around static lines that terminated adjacent to the unspecified extension between the premask crosses. This effect was maximal following treatment with lorazepam. CONCLUSIONS: This finding supports the idea that GABAA-enhanced inhibitory synchronization mediates continuity coding during early visual processing.