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Speech arrest during seizures is often considered indicative of involvement of Broca’s area in the ictal discharge. Chee et al and Wieshmann et al recently reminded us that ictal speech arrest can also be seen during seizures originating from the posterior aspect of the dominant superior frontal gyrus (SFG).
Chee et al described two patients with astrocytomas in this region (adjacent to the interhemispheric fissure, immediately rostral to the premotor cortex and primary motor strip). In both cases, video-EEG recorded seizures and electrical stimulation of the brain with implanted intracranial electrodes produced arrest of speech. However, consciousness, comprehension, and movements of the tongue, palate, and pharynx were preserved. During seizures, the ability to produce crude vocalizations such as "ma" and "pa" was also preserved. This suggests that the SFG is important in controlling the complex integrated movements of language. No postoperative deficit occurred in one patient after tumor resection. In the other, only mild slowing of writing was seen postoperatively.
Wieshmann et al studied 10 patients with seizures due to MRI-demonstrated frontal lobe parasagittal lesions (7 gliomas, 1 meningioma, 1 cavernoma, and 1 "cystic tumor"). In each case, at least one seizure was observed and described by a physician. Furthermore, four patients had video-EEG ictal recordings. In six patients, lesions affected the left SFG. In all six of these, ictal speech arrest with preserved consciousness was observed. In the other four patients with lesions of the right SFG, seizures featured left arm or leg tonic or clonic activity, but ictal speech arrest never occurred. Unfortunately, Wieshmann et al did not report post-surgical outcomes in their patients.
In this study by Wieshmann et al, despite clearly localizing MRI and ictal semiology findings, EEGs were surprisingly nonlocalizing. Interictally, only three patients had focal slowing concordant with their lesions. No patient had interictal focal spike-waves. The EEG was normal in five and exhibited secondarily synchronous bilateral epileptiform discharges in the other two. Among the four video-EEG recorded seizures, only one was accompanied by an ictal electrographic discharge. The other cases had no change in the EEG, even with the clinical seizures.
These reports from Chee et al and Wieshmann et al highlight several aspects of the poorly understood and complex role of the dominant SFG in speech production. First, the authors agree that an epileptogenic zone in this region is sufficient to produce speech-arrest seizures. It is not necessary to invoke primary involvement of other, more traditional, lateral speech areas. Second, while fixed lesions in this region do not produce expressive aphasia, transient functional disturbances (seizures and electrical stimulation) cause cessation of verbal output. This is not simple oro-motor apraxia, since voluntary tongue and pharyngeal movements, and simple vocalizations, persist despite the speech arrests.
Finally, although only Chee et al commented on their post-surgical outcome, it appears that resection of this region can be carried out without producing permanent post-operative aphasia. This has also been reported previously by Rostomily et al (J Neurosurg 1991;75:62-68), although for the first post-operative week they described transient muteness in all of their five patients. Functional redundancy in central language systems may be able to compensate for the loss of the SFG due to progressive disorders such as brain tumors, and even compensate after SFG resection. However, functional redundancy may not be able to compensate for the instantaneous SFG inactivation that occurs with seizures and electrical stimulation of the brain. drl