Treatment of Refractory Status Epilepticus with Hemispherectomy: A Note of Caution
Article first published online: 1 SEP 2005
Volume 46, Issue 9, page 1553, September 2005
How to Cite
Derakhshan, I. (2005), Treatment of Refractory Status Epilepticus with Hemispherectomy: A Note of Caution. Epilepsia, 46: 1553. doi: 10.1111/j.1528-1167.2005.18205_1.x
- Issue published online: 1 SEP 2005
- Article first published online: 1 SEP 2005
To the Editor:
The report by Duane et al. (1) on the treatment of status epilepticus with hemispherectomy contains several significant laterality and technical items (not mentioned by the respected authors) deserving comments:
The (presumably) right-handed boy that they described had silent status for several days before the process was interrupted by the injection of pentobarbital (PTB) into the right carotid artery. Injection in the left carotid seems to have affected only the activity in the left hemisphere (see Fig. 3b of their article). This asymmetry corroborates the assertion that the influence of the major hemisphere (in this case, the right) on the minor (the left) via the callosum is one way and that the said influence is excitatory in nature (2–4).
The technical aspect relates to the fact that the EEG run at higher speed showed the temporal precedence of the epileptic events occurring in the major hemisphere compared with those in the minor by an estimated 50–60 ms (p. 1002, and Fig. 2). This corresponds to the interhemispheric transfer time (IHTT). The EEG at lower speed did not provide such information. Rather, the EEG at conventional speed was misleading in suggesting a “bilateral independent spike” on two different occasions (p. 1001, and Fig. 2A). According to the callosal circuitry just delineated and described in detail elsewhere (2–4), this patient was right hemispheric in his laterality of motor control (including that of speech, as the most obvious task in indicating such characteristics). This is evident from the fact that postoperatively the patient “had paucity of speech for 1 month, although the patient's speech was presumed to be left hemisphere dominant.” We were not informed whether this assumption was based on the patient's behavioral handedness or the result of the amytal testing. At any rate, the speech impediment (aphasia) showed that it was an incorrect assumption. Similar examples may be found in the recent literature reviewed elsewhere (2). We were not informed as to the resolution of the language problem.
According to the anatomy under discussion, only the major hemisphere is capable of initiating seizures (excluding those instances with a nondominant lesion causing increased intracranial pressure, thus affecting the major hemisphere) (2). Therefore in the case described by the authors, no need exists for continuation of anticonvulsants after the removal of the major hemisphere (p. 1004).
Given the panorama of procedures used in this case, it is obvious that (with the exception of high-speed EEG) none of them provided secure guidance in bringing the situation to successful conclusion. Elsewhere I have shown that such guidance can be obtained noninvasively by determining the reaction time of two similar effectors on each side of the body (4). The side closer to the command center will have a shorter reaction time by an amount commensurate to IHTT (see earlier).
I would be grateful to the authors for answers regarding the issue of language recovery in this patient.