Editorial: Supplementary motor resections

Abstract

In the following article, Kim et al.1 attempted to understand the factors that influence outcomes in the resection of the medial frontal lobes. As the authors indicate in their introduction, since Penfield and Welch,2 neurosurgeons treating epilepsy have noted this interesting phenomenon of temporary postoperative deficits in motor and possibly speech function associated with resection of the medial frontal cortex immediately anterior to the central gyrus. The term “supplementary motor area,” or SMA, has been used to describe this region. They detail their experience in treating 43 adults with a variety of pathological lesions of the medial frontal lobe as a means of controlling pharmacoresistant epilepsy. They found that transient new neurological deficits occurred in approximately half of their patients and that these deficits affected a mixture of motor, sensory, and speech functions. Only 3 (7%) of the 43 patients had what they considered to be permanent deficits, and all deficits involved motor loss: 1 case involving the upper extremity; 1 case, the lower extremity; and 1 case, the upper and lower extremities. While this series adds a significant number of patients to the literature on this important topic, it does not yet give neurosurgeons what they would like to know regarding surgery in this brain region. What has been difficult to determine is which patients are more likely to experience these deficits and, even more importantly, which patients are at higher risk for permanent deficits. Kim et al. found that, in general terms, patients who demonstrated temporary deficits had resections that were farther posterior (true SMA) and more inferior, including the cingulate gyrus. The authors performed a multivariate analysis and found that resection of the cingulate gyrus was the only factor that was predictive of a new deficit.1 There were no predictors of which patients would have permanent deficits, possibly because the risk was so low (7%). Nevertheless, these data should be helpful to surgeons who are planning to resect medial frontal cortex, both for the treatment of pharmacoresistant epilepsy and for the resection of cortical brain tumors. Like the findings of Kim et al., the review by Rostomily et al.3 indicated that permanent deficits are exceedingly rare. Similarly, Tate et al.4 described a large series of patients who had undergone resection of lesions from the cingulate gyrus. Once again, permanent deficits were exceedingly rare, and temporary deficits were more likely to occur if SMA tissue was also resected, which implies that although resection of the cingulate gyrus is a factor, it is not the only explanation for new deficits. The take-home message from this series of cases is that patients and families should be informed in advance about the possibility of new, probably transient deficits when this region of the brain is approached, and a 50% likelihood seems reasonable. What the report by Kim et al. does not do is help us to understand whether there was something different about the injury in cases in which permanent deficits developed. For example, could there have been a vascular injury that caused damage to primary motor cortex (for example, a pericallosal arterial branch or a venous infarction), or is there something intrinsically different about the SMA in a small subset of patients? Presumably, with enough experience and with the addition of tools such as functional MRI and fiber tract imaging, these questions will eventually be answered. Until then, surgeons must give patients as much advance information as possible and continue to wait expectantly each time an SMA syndrome occurs to see if the deficits resolve. (http://thejns.org/doi/abs/10.3171/2013.1.JNS121986)