Clinical application of neuroimaging in epilepsy. Issue 4 (1st April 2003)

• Record Type: Journal Article
• Authors: Wieshmann, U C
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 74:Issue 4(2003)
• Page Start: 466
• Page End: 470
• Publication Date: 2003-04-01
• Subjects: epilepsy -- clinical practice -- neuroimaging -- magnetic resonance imaging -- computed tomography; IGE, idiopathic generalised epilepsy -- CT, computed tomography -- MRI, magnetic resonance imaging; Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp.74.4.466
• Languages: English
• ISSNs: 0022-3050

Abstract

Abstract : Objective: To evaluate the use of neuroimaging in clinical practice and to assess the prevalence of detected structural abnormalities in epilepsy patients in a clinical set up. Methods: 919 outpatients were identified and the scan results reviewed. A total of 677 patients had chronic active epilepsy (88 had idiopathic generalised epilepsy (IGE), 588 had localisation related epilepsy, one had symptomatic generalised epilepsy), 57 had a single epileptic seizure, 46 were in remission, and 139 had non-epileptic attacks. Results: 391 patients had no scan (53 patients in this group had IGE, 182 had localisation related epilepsy, one had generalised symptomatic epilepsy, 18 had single epileptic attacks, 21 were in remission, 116 had non-epileptic attacks). Altogether 528 patients had a scan, the results were not available in 33, 163 had x ray computed tomography (CT) only, 178 had standard magnetic resonance imaging (MRI) (slice thickness 5 mm), and 154 had high resolution MRI (including a T1 weighted sequence with 1.5 mm thick slices). Some 252 of 495 scans (51%) were abnormal. Abnormalities were hippocampal sclerosis (n=128), atrophy or non-specific white matter lesions (n=35), vascular abnormalities (n=27), tumours (n=25), brain damage (n=24), malformations of cortical development (n=13). Excluding atrophy and non-specific white matter lesions the prevalence of detected abnormalities was 54% in localisation related epilepsy, 18% in single seizure patients, 16% in epilepsy in remission, and 0% in IGE and non-epileptic attacks. Conclusions: Abnormalities were detected in more than half of all patients with localisation related epilepsy, and in about one in five patients with single seizures or epilepsy in remission. Many patients had no scan or only CT or standard MRI. The true prevalence of structural abnormalities may be have been higher. Scanning did not add any information in patients with IGE or non-epileptic attacks.