Recent studies have reported that cognitive inflexibility associated with impairments in a frontal-striatal circuit and parietal region is a core cognitive deficit of obsessive-compulsive disorder (OCD). However, few studies have examined progressive changes in these regions following clinical improvement in obsessive-compulsive symptoms. To determine if treatment changes the aberrant activation pattern associated with task switching in OCD, we examined the activation patterns in brain areas after treatment. The study was conducted on 10 unmedicated OCD patients and 20 matched controls using event-related functional magnetic resonance imaging. Treatment improved the clinical symptoms measured by the Yale-Brown Obsessive Compulsive Scale and behavioral flexibility indicated by the switching cost. At baseline, OCD showed significantly less activation in the dorsal and ventral frontal-striatal circuit and parietal regions under the task-switch minus task-repeat condition compared with controls. After treatment, the neural responses in the ventral frontal-striatal circuit in OCD were partially normalized, whereas the activation deficit in dorsal frontoparietal regions that mediate shifting attention or behavioral flexibility persisted. It is suggested that altered brain activation in ventral frontal-striatal regions in OCD patients is associated with their cognitive flexibility and changes in these regions may underlie the pathophysiology of OCD.
Adult ; Basal Ganglia/*metabolism ; Behavioral Symptoms/drug therapy ; Female ; Frontal Lobe/*drug effects/physiopathology ; Humans ; Magnetic Resonance Imaging ; Male ; Obsessive-Compulsive Disorder/*drug therapy/physiopathology ; Parietal Lobe/*drug effects/physiopathology

OBJECTIVEOur previous work suggested that sensitivity of hippocampal neurons is changed in process of epileptic activities, and closely parallel to the dynamic characteristic of epileptic activity of the neurons. This study investigated the sensitivity of epileptic brain to vagal nerve stimulation (VNS) in epileptic process.

METHODSEpileptic model was evoked by penicillin. Left vagal nerves were stimulated to inhibit the seizures induced by penicillin. The electrocorticography (ECoG) and electromyography (EMG) were recorded to analyze inhibiting effect of VNS in epileptic process.

RESULTSIt was found that VNS could inhibit the seizures caused by penicillin, and the inhibiting effect of VNS to seizures increased as the vagal nerve stimulating time prolonged. It was also found that the inhibiting effect of VNS to seizures decreased in epileptic process.

CONCLUSIONThe results suggested that the sensitivity of epileptic brain to VNS was different in epileptic process. The inhibiting effect of VNS to seizure decreased as the development of seizures.

Action Potentials ; physiology ; Animals ; Electric Stimulation ; Electroencephalography ; Electromyography ; Epilepsy ; chemically induced ; prevention & control ; Frontal Lobe ; physiopathology ; Male ; Motor Cortex ; drug effects ; physiopathology ; Neural Inhibition ; physiology ; Nonlinear Dynamics ; Parietal Lobe ; physiopathology ; Penicillins ; Rats ; Rats, Sprague-Dawley ; Seizures ; chemically induced ; prevention & control ; Vagus Nerve ; physiology