ERP P300, a biological marker of obsessive-compulsive disorder

1997 ◽  
Vol 103 (1) ◽  
pp. 213
Author(s):  
M Derouaux
2011 ◽  
Vol 26 (S2) ◽  
pp. 977-977 ◽  
Author(s):  
H. Olbrich ◽  
S. Olbrich ◽  
I. Jahn ◽  
U. Hegerl ◽  
K. Stengler

Neurophysiological hyperactivation of cortical and subcortical brain areas has been reported in obsessive-compulsive disorder (OCD) using functional imaging techniques and electroencephalography (EEG). Also sleep disturbances and delayed sleep phases have been associated with OCD symptomatology. However, vigilance regulation in OCD during the transition phase from wakefulness to sleep onset remains unclear. Therefore the aim of this study was to analyze EEG-source estimates and EEG vigilance regulation in OCD patients in comparison to healthy controls.A 15 minute resting EEG was recorded in 30 unmedicated OCD patients and 30 healthy, age and gender matched controls. EEG power source estimates of the whole time series were computed by exact Low Resolution Brain Electromagnetic Tomography (eLORETA). Each consecutive one second EEG-segment was classified into one out of seven EEG-vigilance stages (0, A1, A2, A3, B1, B2/3, C) using Vigilance Algorithm Leipzig (VIGALL). The eLORETA analysis (log of F-ratios, p < 0.05, corrected for multiple comparison) revealed significantly increased delta power in the right superior frontal gyrus for OCD patients in comparison to healthy controls. Vigilance analysis yielded significantly increased amounts of high vigilance stage A2 (Mann-Whitney test, p < 0.001, corrected for multiple comparison) for OCD patients.This study repeated findings of altered EEG-power in frontal areas in OCD patients. Alterations of EEG-vigilance regulation were found with increased amounts of high vigilance stage A2. This is in line with a hypothesis of cortical hyperactivation in OCD. The value of EEG-vigilance as a possible biological marker for e.g. treatment response should be focus of further studies.


2006 ◽  
Vol 36 (9) ◽  
pp. 1321-1326 ◽  
Author(s):  
NIC J. van der WEE ◽  
HANS H. HARDEMAN ◽  
NICK F. RAMSEY ◽  
MATHIJS RAEMAEKERS ◽  
HAROLD J. VAN MEGEN ◽  
...  

Background. Oculomotor studies have found saccadic abnormalities in obsessive–compulsive disorder (OCD), lending support for models postulating a central role for inhibition in OCD. Saccadic abnormalities in OCD may also be potential candidates for a biological marker, important for more endophenotype-oriented research. Saccadic abnormalities have not been examined in psychotropic-naive patients with OCD without co-morbidity.Method. We compared the error rates and latencies of 14 carefully selected adult psychotropic-naive patients with OCD with no co-morbid diagnosis and 14 pairwise matched healthy controls on a fixation task, on a prosaccade task and on an antisaccade task.Results. Patients with OCD showed normal error rates on all tasks, but latencies on the antisaccade task were significantly increased.Conclusions. Our results indicate that patients with OCD have no gross impairment of oculomotor inhibitory capacities, but may have a disturbed capacity to deliberately initiate a saccade to an imagined target.


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