European Journal of Neurology 2005, 12: 75–76
LETTER TO THE EDITOR Seizure suppression after left anterior temporal lobectomy in a patient with an ipsilateral parietal lesion C. Barbaa, D. Policicchiob, F. Dogliettob, F. Papaccib and G. Colicchiob a
Fondazione Santa Lucia, IRCCS, Rome, Italy; and bInstitute of Neurosurgery, Catholic University, Rome, Italy Correspondence: Carmen Barba, Fondazione Santa Lucia, IRCCS, Via Ardeatina, 306, 00179, Rome, Italy (e-mail:
[email protected]). Keywords: epilepsy surgery, invasive recordings, lesional epilepsy Received 7 June 2004 Accepted 27 June 2004 Sir, Epilepsy surgery can provide a solution for drug-resistant patients (Revlyn, 2003). Non-lesional epilepsies account for 20–30% of patients in major epilepsy surgery centres (Cascino, 2001). When a lesion is evident, a presurgical protocol,
Figure 1 On the left: Preoperative functional MRI showing the primary motor area activation and the left parietal lesion extending to insula and T1. No hippocampal abnormality was disclosed. On the right: Stereotatic X-ray with 10 implanted electrodes indicated by letters: four located in left temporal lobe: anterior hippocampus (B), posterior hippocampus (C), inferior and superior temporal gyrus (E and U); four near to the lesion: two anteriorly (G and R) and two posteriorly (N and P), one in the posterior parietal region (W), one in the parieto-occipital area (V). In each electrode the first contact was the deepest one. including both non-invasive and invasive investigations, might be needed to assess whether the lesion is the cause of epilepsy (Morris, 2001). We present the case of a drug-resistant patient with a wide left parieto-temporal
lesion, seizure-free after left temporal lobectomy. A 38-year-old female was submitted to presurgical evaluation in our Epilepsy Surgery Centre. Neurological examination was fully normal. Family history was
Figure 2 Ictal discharge during SEEG recordings (four consecutive traces): the spiky activity at electrode B stopped for 7 s (first arrow) and then it seemed to retrieve for a few seconds. Then, a low amplitude rapid activity was observed at electrode B and less consistently at electrode C, G (second arrow). Only after 30 s spikes and spikes and waves involved all other electrodes (third arrow) preceeded by lowering of background activity. At this moment, the patient prevents about epigastric aura. The last arrow indicates the occurrence of impairment of consciousness.
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negative for epilepsy. Delivery and psychomotor development were not problematic. Seizures began at the age of 6 years; they occurred monthly, mostly concomitant with the menstrual cycle. Their semiology was stereotyped: cephalic confusion and inability to speak, followed by eyes and head turning towards the left side, left simple gestual automatisms and right arm dystony. Finally, the so-called Ôfencing postureÕ was assumed. The patient presented both production and comprehension post-ictal aphasia for several minutes. MRI showed a lesion (possibly due to a perinatal ischaemic damage) in the left parietal lobe, extending to the first temporal gyrus and insula (Fig. 1). Functional MRI showed the MI (primary motor area) just in front of the lesion (Fig. 1). Median nerve SEPs were fully normal. Neuropsycological assessment disclosed slight mental retardation with left hemisphere predominance. Wada test demonstrated left dominance for language. Five seizures were recorded during prolonged video-EEG monitoring. Interictal and ictal EEG were characterized by left temporal abnormalities with diffusion to the right hemisphere. As electroclinical correlations suggested a left temporal onset of seizures and
MRI showed a wide parieto-temporal lesion, invasive recordings were performed in order to precisely define the epileptogenic zone and clarify its correlation to the lesion. Stereoelectroencephalography (SEEG) was recorded using 10 intracranial electrodes (Fig. 1). The interictal EEG was characterized by very slow activity at the contacts implanted in the temporal lobe. Six spontaneous seizures were recorded: the ictal discharge (Fig. 2) began at electrode B (anterior hippocampus) at least 10 s before the first clinical sign. No complete seizure was provoked by cortical stimulations but auras were induced at electrodes B, C (posterior hippocampus) and U (T1). A left anterior temporal lobectomy with hippocampectomy was performed sparing T1 and a part of T2 without any post-surgical deficits. Histological examination did not show clear hippocampal sclerosis but only minimal gliotic reactions. Neuropsychological assessment showed an improvement in all examinations except for a verbal test. Eighteen months after surgery the patient is in Engel’s class Ia. In this patient the decision to perform a temporal lobectomy was guided by electroclinical correlations suggesting a left
temporal origin of seizures and a secondary involvement of the parietal lesional area. SEEG proved crucial in this case, being the only invasive presurgical procedure allowing the investigation of mesial regions and intra-sulcal areas (Tassi et al., 2002). Precise identification of the epileptogenic zone, possibly using invasive procedures, may be helpful in obtaining a good outcome even in patients whose MRI findings might exclude a surgical solution. References Cascino DG (2001) Epilepsy surgery in nonsubstrate-directed partial epilepsy. In: Luders HO, Comair YC, eds. Epilepsy Surgery, 2nd edn. Lippincott Williams and Wilkins, Philadelphia, pp. 1020–1033. Morris III HH. (2001) Lesionectomy as a treatment for chronic epilepsy: is it sufficient for a good outcome? In: Luders HO, Comair YC, eds. Epilepsy Surgery, 2nd edn. Lippincott Williams and Wilkins, Philadelphia, pp. 967–971. Revlyn P. (2003). Beyond pharmacotherapy: surgical management epilepsia. 44(Suppl. 5):23–28. Tassi L, Colombo N, Garbelli R et al. (2002). Focal cortical dysplasia: neuropathological subtypes, EEG, neuroimaging and surgical outcome. Brain 125:1719–1732.
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