Subject(s)
Diagnostic Errors , Epilepsy, Temporal Lobe/diagnosis , Epilepsy, Temporal Lobe/surgery , Equipment Failure , Magnetoencephalography/instrumentation , Magnetoencephalography/methods , Preoperative Care/methods , Action Potentials , Artifacts , Brain Mapping/instrumentation , Brain Mapping/methods , Humans , Reproducibility of Results , Sensitivity and SpecificityABSTRACT
BACKGROUND: We describe frontotemporal paroxysmal rhythmic activity recorded by magnetoencephalography (MEG) in patients with obsessive-compulsive disorder (OCD). METHOD: Twelve patients with OCD (per ICD-10 and DSM-IV criteria), aged 18 to 65 years, were assessed using MEG. Patients' classification according to the Yale Brown OCD Scale was as follows: severe = 8, moderate = 3, and mild = 1. MEG findings were compared with those of 12 age- and sex-matched healthy subjects (control group) with no previous history of psychiatric or neurologic disorders. All study participants underwent neurologic and basic medical examinations, including magnetic resonance imaging, electrocardiograms (EEGs), and electrooculograms. The study was conducted between January 2001 and January 2002. RESULTS: Two types of MEG activity were observed in patients with OCD: (1) frontotemporal paroxysmal rhythmic activity with low-amplitude spikes (< 1 picoTesla) in 92% (11/12) of patients and (2) intermittent isolated spikes and sharp waves in all patients (12/12). The OCD group had paroxysmal rhythmic MEG activity in the cingulate cortex (12/12), insula (10/12), hippocampus (9/12), temporal superior gyrus and angular and supramarginal gyri (9/12), precentral and post-central gyri (8/12), orbitofrontal cortex (5/12), and parietal lobes (5/12). MEG recordings were normal in the control group, and EEG findings were normal in both the OCD and control groups. CONCLUSIONS: Frontotemporal paroxysmal rhythmic activity with a preferential limbic distribution is a sensitive MEG finding in patients with OCD. Although the pathophysiology of this abnormality remains unknown, a corticostriatal network dysfunction was hypothesized.
Subject(s)
Cerebral Cortex/physiopathology , Frontal Lobe/physiopathology , Gyrus Cinguli/physiopathology , Hippocampus/physiopathology , Limbic System/physiopathology , Magnetoencephalography , Obsessive-Compulsive Disorder/diagnosis , Temporal Lobe/physiopathology , Adult , Brain Mapping , Dominance, Cerebral/physiology , Electroencephalography , Evoked Potentials/physiology , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Obsessive-Compulsive Disorder/physiopathology , Obsessive-Compulsive Disorder/psychology , Signal Processing, Computer-AssistedABSTRACT
Cortical dysplasia is known to produce continuous epileptiform discharges (CEDs) on electrocorticogram (EcoG) and EEG recordings. The authors studied the incidence of CEDs on ECoGs and correlated this data with pathologic findings. Thirty ECoGs were reviewed that were performed on patients with parietal or occipital lobe epilepsy operated on since 1960. CED was classified as: (1) continuous or semicontinuous rhythmic spikes or sharp waves at frequencies ranging from 2 to 8 Hz, and (2) repetitive bursts of rhythmic polyspike activity lasting 2 to 10 s. All nontumoral pathologic specimens were reviewed. Epileptiform activity was classified using the following criteria: focal (one gyrus), regional (two gyri), lobar (three gyri), bilobar, or multilobar. Pathologic examination showed gliosis in eight specimens, focal cortical dysplasia in five specimens, tumoral lesions in eight specimens, and other pathology in nine specimens. CED was found in 11 ECoGs. In seven pathology specimens, significant gliosis was shown, and in the remaining four specimens, a dysplastic lesion was diagnosed. Epileptiform activity was widespread (lobar, bilobar, or multilobar) when gliosis or focal cortical dysplasia was present. Absence of epileptiform activity or a focal/regional distribution was found in tumors and other lesions. These data suggest that extensive gliotic lesions are highly epileptogenic and produce CEDs, which are morphologically undistinguishable from those produced by focal cortical dysplasia.
