Relationship between Cavum Septum Pellucidum and Epilepsy.
- Author:
Ki Young CHOI
1
;
Jong Pil EUN
;
Ha Young CHOI
Author Information
1. Department of Neurosurgery, Research Institute of Clinical Medicine, Chonbuk National University Medical School and Hospital, Jeonju, Korea. jp-eun@hanmail.net
- Publication Type:Original Article
- Keywords:
Cavum septum pellucidum;
Epilepsy
- MeSH:
Anticonvulsants;
Classification;
Epilepsy*;
Epilepsy, Temporal Lobe;
Headache;
Humans;
Magnetic Resonance Imaging;
Neuronal Migration Disorders;
Septum Pellucidum*
- From:Journal of Korean Neurosurgical Society
2004;36(1):13-17
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: The authors study a relationship between the presence of cavum septum pellucidum(CSP) and the development of epilepsy by comparing the presence of CSP, which has been known to be a normal variation, in normal control group and epilepsy patients. METHODS: This study included 377 patients with epilepsy and 252 controls without epilepsy. Of epilepsy patients, 168 patients underwent surgery due to intractability and 209 patients was on medication of antiepileptic drugs. Control group had only headache and no visible lesion in MRI. Of 168 surgical patients, 102 patients had temporal lobe epilepsy and 66 patients had extratemporal lobe epilepsy. Ninty five patients showed a neuronal migration disorder in histopathologic findings. Definition of "CSP" and "partial CSP" was followed by Pauling's classification. RESULTS: CSP was present 8.2% of epilepsy patients and 1.6% of control group(p<0.01). CSP was detected in 11.3% of patients with surgical treatment and in 5.7% of patients with medical treatment. CSP was noticed in 8.9% of temporal lobe epilepsy, in 15.2% of extratemporal lobe epilepsy, in 13.7% of patients with neuronal migration disorder, and in 8.2% of patients with no neuronal migration disorder. CONCLUSION: Presence of CSP is statistically higher in epilepsy patients than in control group. This results indicates that the presence of CSP may not be a simple normal variation, and it can be considered a developmental anomaly that may contribute to epileptogenesis.
