- These case reports describe two patients undergoing surgery for brain tumors in which the thalamocortical tract was mapped electrophysiologically as well as the corticospinal tract
- Sudden drops in cortical evoked responses at N20, a postcentral potential, or P22, a precentral potential, alerted the surgeon to the proximity of thalamocortical fibers projecting to the precentral or postcentral gyri
- In each case, postoperative analysis using MATLAB software confirmed a significant decrease in the magnitude of the median evoked responses during direct stimulation of the thalamocortical tract versus in its absence
- This method allowed redirection of the surgical plane to avoid injury of thalamocortical afferent fibers
When supratentorial surgery is performed under general anesthesia, neurophysiologic methods are used intraoperatively to map the corticospinal tract (CST), the neural pathway that controls skilled use of the extremities. Mapping permits more accurate identification of functional areas, helping surgeons avoid neurologic injury.
While mapping the CST in two cases, researchers at Massachusetts General Hospital recently found that they were able to electrophysiologically map thalamocortical fibers projecting separately to the precentral and postcentral gyri.
Mirela V. Simon, MD, MSc, of the Department of Neurology and an expert in intraoperative neurophysiologic mapping techniques at Mass General; William T. Curry, MD, co-director of Mass General Neuroscience and director of neurosurgical oncology in the Department of Neurosurgery; and colleagues describe the procedures in Operative Neurosurgery.
"Collision techniques" for mapping the CST rely on temporarily disturbing the conduction of electrical volleys through motor and/or sensory pathways as they are stimulated. The authors believe they are the first to attempt to use a collision technique to map the thalamocortical tract under general anesthesia.
Both patients were undergoing surgery for brain tumors. The central sulcus was localized using the somatosensory evoked potential (SSEP) phase reversal technique, and standard motor mapping and electrocorticography were performed. In addition, the resection cavity was electrically stimulated as N20, a postcentral potential, and P22, a precentral potential, were triggered. The resulting waveforms were continuously recorded.
Patient 1, a 24-year-old male, presented with right arm sensory deficit and pronator drift. MRI demonstrated a left parietal lesion. When the surgeon stimulated the inferior margin of the resection cavity, the N20 amplitude suddenly dropped. This change reversed promptly on subsequent trials as the stimulation was stopped, and the amplitude remained stable until the end of the resection.
Postoperative analysis using MATLAB software confirmed the clinical observation: 63% decrease in the magnitude of the median evoked responses during direct stimulation of the thalamocortical tract versus in its absence (P=0.02). Postoperatively, the patient had normal muscle strength and sensation in all limbs.
Patient 2, a 65-year-old woman, developed progressive left upper and lower limbs weakness, more severe in the proximal muscles and was found to have a lesion within the right central sulcus, invading the precentral gyrus. Electrical stimulation triggered no motor responses. Instead, the P22 amplitude suddenly dropped, with prompt recovery after readjustment of the position of the stimulator. Computer analysis confirmed an 88% decrease in evoked responses during subcortical stimulation (P<0.001).
In the immediate postoperative period, the patient displayed worsening of the strength in the proximal left arm and leg, but she recovered full motor function by the one-month follow-up visit.
Promising Clinical Benefit
The sudden drop in the cortical evoked responses alerted the surgeon to the proximity of thalamocortical fibers. Readjusting the surgical plane permitted avoidance of damage to the fibers, with preservation of the SSEP at the end of the resection.
These findings indicate that concentrating exclusively on mapping the motor cortex and CST is insufficient for preventing a clinically significant deficit in motor control, let alone a sensory deficit.
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