TOPIRAMATE COULD AGGRAVATE COMPLEX PARTIAL SEIZURE IN THE ADVANCED SECONDARY EPILEPTOGENESIS
Abstract number :
3.128
Submission category :
Year :
2002
Submission ID :
82
Source :
www.aesnet.org
Presentation date :
12/7/2002 12:00:00 AM
Published date :
Dec 1, 2002, 06:00 AM
Authors :
Hisanori Hasegawa. Neurology Service, Aleda E. Lutz Saginaw VA Medical Center, Saginaw, MI
RATIONALE: Topiramate (TPM) is frequently used for treatment of partial complex seizure with good response. However, in the clinical practice, there seems a group of patients in which TPM aggravate the symptom although the number is small. Reason of seizure aggravation has not been studied. This is a pilot study to find out likely correlation with EEG findings and adverse seizure control by TPM.
METHODS: Electroencephalogram (EEG) was reviewed for those whose seizure frequency increased after starting TPM. TPM was continued at least one month prior to discontinuation. Six patients were identified in consecutive 127 intractable complex partial seizure patients in epilepsy clinic. In all of the cases, EEG studies were done before TPM was introduced.
RESULTS: Common EEG feature of these six patients was bilateral neocortical epileptic activities. None of them had mesial temporal involvements at T1-T2 electrodes in sleep and awake EEG. MRI findings are normal for all of these cases.
[underline]Case 1[/underline]: 37 year old veteran presented episodic macropsia with spacial distortion. EEG showed frequent epileptiform discharges in bilateral posterior synchrony in parietal head region. TPM aggravated symptom. Gabapentin (GPN) eliminated the recurrence.
[underline]Case 2[/underline]: 45 year old woman having frequent IID and electrographic seizure pattern in bilateral temporal neocortex, with bilateral synchronous seizure onset at T3 and T4 in EEG. FBM had no benefit. TPM worsened seizure frequency, but GPN decreased frequency of seizure.
[underline]Case 3[/underline]: 42 year old woman with intractable CPS. EEG showed bilateral frontal IID. Topiramate aggravated symptom, but it was alleviated by gabapentin.
[underline]Case 4[/underline]: 42 year old woman with frequent CPS due to head injury. EEG showed bilateral independent multifocal IID. Symptom was aggravated by TPM but alleviated by GPN.
[underline]Case 5[/underline]: 10 year old girl of intractable frontal lobe epilepsy. EEG showed frequent bifrontal synchrous IID with left side preponderence. TPM and FBM increased seizure frequency, but improved by GPN.
[underline]Case 6[/underline]: 35 year old man. EEG showed 4 Hz bilateral frontal spike and wave discharges with left temporal neocortical IID. TPM increased seizure frequency by 50% in one month. Subsequently he was treated with GPN with moderate improve in seizure control.
CONCLUSIONS: These observations suggest that bihemispheric epileptiform activities are common denominator in those patients whose symptomatology was aggravated by TPM. Neocortical bilateral synchrony is the advanced stage of the secondary epileptogenesis according with classification by Morrell ([italic]Morrell, F, 1985[/italic]). Unlike hippocampal seizure, neocortical bilateral synchrony primarily involves synaptic connection via corpus callosum. However the mechanism of TPM aggravation is unknown, the clinical correlations suggest that TPM may not decrease the contralateral synaptic transmissions but rather enhance them in bilateral synchrony. It seems worth trying GPN if TPM or FBM failed or aggravate the symptomatology for patients who have bilateral neocortical epileptogenicity. Further studies will be planned.