Restoring effects of oxytocin on the attentional preference for faces in autism.

Reduced attentional preference for faces and symptoms of social anxiety are common in autism spectrum disorders (ASDs). The neuropeptide oxytocin triggers anxiolytic functions and enhances eye gaze, facial emotion recognition and neural correlates of face processing in ASD. Here we investigated whether a single dose of oxytocin increases attention to faces in ASD. As a secondary question, we explored the influence of social anxiety on these effects. We tested for oxytocin's effects on attention to neutral faces as compared to houses in a sample of 29 autistic individuals and 30 control participants using a dot-probe paradigm with two different presentation times (100 or 500 ms). A single dose of 24 IU oxytocin was administered in a randomized, double-blind placebo-controlled, cross-over design. Under placebo, ASD individuals paid less attention to faces presented for 500 ms than did controls. Oxytocin administration increased the allocation of attention toward faces in ASD to a level observed in controls. Secondary analyses revealed that these oxytocin effects primarily occurred in ASD individuals with high levels of social anxiety who were characterized by attentional avoidance of faces under placebo. Our results confirm a positive influence of intranasal oxytocin on social attention processes in ASD. Further, they suggest that oxytocin may in particular restore the attentional preference for facial information in ASD individuals with high social anxiety. We conclude that oxytocin's anxiolytic properties may partially account for its positive effects on socio-cognitive functioning in ASD, such as enhanced eye gaze and facial emotion recognition.

[Psychotherapy of Asperger syndrome in adults]. / Psychotherapie des Asperger-Syndroms im Erwachsenenalter.

There is an increase in awareness in professionals that the Asperger syndrome (AS) in adulthood is associated with specific problems and burdens which may well differ from those in childhood and adolescence. The core symptoms of AS generally persist into adulthood, however in contrast to childhood and adolescence there is no specific support system for adults in Germany. Also the environment of the afflicted patient changes thus producing different challenges and problems. In addition a subgroup of patients with high functioning AS primarily presents in adulthood generally due to secondary psychosocial problems, depression or anxiety. Difficulties in social interaction, problems with modified daily routines and unforeseen situations cause severe frustration for the majority of the patients. While several therapy programs have been developed and implemented for children and adolescents, for adults there are none. Also there is a lack of comprehensive concepts addressing the specific needs of adult patients with AS. From an economic perspective this is particularly unfortunate since affected people often have good or excellent partial abilities and might be very valuable employees. In this article existing therapeutic concepts for AS are summarized and a newly designed group therapy program for adult patients with Asperger syndrome in Freiburg is introduced (Freiburg Asperger-spezifische Therapie für Erwachsene, FASTER) which specifically addresses the needs and problems of adult patients with AS.

Subtle prefrontal neuropathology in a pilot magnetic resonance spectroscopy study in patients with borderline personality disorder.

The authors examined the brains of patients with borderline personality disorder (BPD) by using short echo time single voxel spectroscopy and found a significant 19% reduction of absolute N-acetylaspartate concentrations in the dorsolateral prefrontal cortex in BPD (P=0.01) compared with control subjects.

Reduction of frontal neocortical grey matter associated with affective aggression in patients with temporal lobe epilepsy: an objective voxel by voxel analysis of automatically segmented MRI.

BACKGROUND: Interictal episodes of aggression are often reported in patients with epilepsy. Some have characteristics of what has been referred to as episodic dyscontrol or intermittent explosive disorder (IED). Although structural brain abnormalities are thought to play a part in the pathophysiology of aggression, there are few in vivo studies of structural cerebral changes in patients with epilepsy and aggression. Using quantitative MRI, subtle structural brain abnormalities can be investigated in subgroups of patients with both epilepsy and episodes of affective aggression. METHODS: After automated segmentation of cerebral grey matter from T1 weighted MRI, the objective technique of statistical parametric mapping (SPM) was applied to the analysis of 35 control subjects, 24 patients with temporal lobe epilepsy (TLE) with a history of repeated, interictal episodes of aggression, and 24 patients with TLE without episodes of aggression. Both TLE patient groups were compared with each other and with the control subjects on a voxel by voxel basis for increases and decreases of grey matter. RESULTS: The patients with TLE with aggressive episodes had a decrease of grey matter, most markedly in the left frontal lobe, compared with the control group and with patients with TLE without aggressive episodes. CONCLUSION: These findings suggest that a reduction of frontal neocortical grey matter might underly the pathophysiology of aggression in TLE. These voxel by voxel comparisons can guide further in vivo studies into aggression.

Affective aggression in patients with temporal lobe epilepsy: a quantitative MRI study of the amygdala.

Recurrent episodes with interictal affective aggression are a rare but well-recognized problem in patients with temporal lobe epilepsy. They are referred to as episodic dyscontrol or, more precisely, as intermittent explosive disorder (IED). The amygdala play a crucial role in the affective evaluation of multimodal sensory input and the neurobiological mediation of aggressive behaviour. With hippocampal sclerosis, in the context of mesial temporal lobe sclerosis, being the most common cause of temporal lobe epilepsy, we hypothesized that the amygdala might be affected by the same pathogenic process in aggressive patients. We investigated 50 patients with temporal lobe epilepsy: 25 with and 25 without a history of IED. Data from clinical, electrophysiological, neuropsychological and psychometric investigations were obtained, as well as MRI scans for the quantitative assessment of possible amygdala pathology. We found no evidence of a higher prevalence of amygdala sclerosis in the aggressive patients. Hippocampal sclerosis was significantly less common in patients with temporal lobe epilepsy and IED. However, a significant subgroup of patients (20%) with temporal lobe epilepsy and aggressive behaviour had severe amygdala atrophy in the context of a history of encephalitis. Another subgroup of aggressive patients (28%) had different left temporal lesions affecting either the amygdala or periamygdaloid structures. IED was associated with left-sided or bilateral EEG and MRI abnormalities, low IQ and high scores in depression and anxiety.

On some clinical implications of the ventral striatum and the extended amygdala. Investigations of aggression.

In this paper, we have first reviewed the animal studies which suggest an association between the amygdala and aggressive behavior. This is followed by a review of the literature of aggression in epilepsy, emphasizing the less controversial peri-ictal aggressions, with the more controversial assertion that temporal lobe epilepsy in particular is associated with an increase in interictal aggression. We then go on to describe the results of some investigations using the MRI to examine amygdala pathology in a group of patients presenting with affective aggression in comparison with a control group. The main findings are that the patients with aggression tend to have lower IQs and more psychopathology than the control group. There is no difference in amygdala T2 and volumetric assessments between the groups, but a subgroup of patients are defined with aggression, left-sided amygdala atrophy, and a history of encephalitis.