CHAPTER 168 Motor Cortex Stimulation
Electrical stimulation of the nervous system has been known since antiquity to have analgesic effects. Intermittent application of electricity for the treatment of pain has a long and colorful history, culminating in the development of modern systems for the chronic administration of therapeutic electrical current.1 Following the introduction of spinal cord stimulation in 1967, electricity has been used successfully to modulate pain by stimulation of peripheral nerves and central nervous system structures, including the spinal cord, brainstem, thalamus, and most recently the cerebral cortex.
In the early 1990s, motor cortex stimulation (MCS) was introduced as a treatment for central deafferentation pain. This severe pain syndrome occurs with interruption of the spinothalamic pathway, most commonly following hemorrhagic or ischemic stroke. The primary sensory cortex was initially targeted as the final relay in the spinothalamic system; however, it was soon realized that stimulation of the motor cortex was more effective in controlling pain.2 Chronic stimulation of the precentral cortex for the treatment of pain was first introduced by Tsubokawa and colleagues in 1991.3,4 Subsequently, there has been growing corroborative evidence derived from case reports and individual case series to suggest that epidural MCS can be an effective treatment for many patients with intractable neuropathic pain. Poststroke pain, phantom limb pain, multiple sclerosis, spinal cord injury pain, postherpetic neuralgia, and neuropathic pain of the limbs or face have all been reported to respond favorably to MCS.5 Most clinical studies focus on the use of MCS in poststroke pain, for which there are few other treatments. Poststroke pain responds variably to MCS, with about 50% of patients achieving adequate relief. However, some studies have documented excellent results in the treatment of trigeminal neuropathic pain, with 75% to 100% of patients achieving good or excellent pain relief.6–10 MCS thus appears to hold promise for patients with intractable and otherwise difficult-to-treat pain syndromes.
Surgical Technique
Following Tsubokawa’s initial report,4 several studies were published using a similar technique of introducing an epidural electrode through a bur hole under local anesthetic.3,6,8,11–15 In several cases, groups that started out using a bur hole technique later switched to performing electrode placement through craniotomy,6,8,9,14 and most surgeons now perform a craniotomy either under local6–8,10,13,14,16–21 or general anesthesia.22–29 Nearly all investigators place the electrodes epidurally, although subdural placement has been described.30,31 Image-guided neuronavigation is used to precisely identify the motor cortex intraoperatively,9,20,27–29,32 and proper placement is confirmed with physiologic testing.
Fiducials are placed preoperatively on the scalp, and volumetric magnetic resonance imaging (MRI) is obtained. The central sulcus, sylvian fissure, and inferior and superior frontal sulci are identified. The “hand knob,” a distinctive area of motor cortex, can usually be easily identified in oblique sections (Fig. 168-1). For facial pain, the optimal target is often identified anterior to the central sulcus adjacent to or below the inferior frontal sulcus. Some investigators have used functional MRI (fMRI) to assist in identifying the appropriate areas for stimulation (Fig. 168-2). Prophylactic antibiotic medication is given along with anticonvulsant agents. The patient is placed in a supine position with a roll beneath the shoulder and the head rotated to the ipsilateral side of the pain. The target is mapped onto the contralateral scalp, and an incision centered over the central sulcus is made.
When the appropriate cortical target has been confirmed, the diagnostic grid is removed, and a 4-contact paddle electrode is positioned over the motor cortex, parallel to the central sulcus. Some investigators have described placement of the electrode perpendicular to the central sulcus, with the two central contacts of the electrode array over the target point in the motor cortex. A second electrode may be placed posteriorly over the central sulcus to allow for transsulcal stimulation and increased programming options (Fig. 168-3). Each electrode is sutured to the outer layer of the dura. If an externalized trial is to be performed, the lead wire is tunneled out through a separate stab incision, and the craniotomy bone flap is secured.
Stimulation Parameters
There is tremendous variation in reported stimulation parameters for MCS. Pain relief can occur at amplitudes from 0.5 to 10 V, rates from 5 to 130 Hz, and pulse widths from 60 to 450 microseconds.33 Although most studies have used rates of about 40 Hz, others have found higher rates to be necessary in some cases. There is also no agreement on whether wide or narrow pulse widths provide more effective stimulation. Amplitudes have in many cases been empirically chosen, whereas other investigators base stimulation amplitude on a percentage of motor threshold.
Pain relief is most commonly achieved at amplitudes of 6 V or less, with average amplitudes of 5 V or less in most studies. Amplitudes greater than 6 V are more likely to be associated with seizures during programming, with seizures commonly induced at amplitudes approaching 9 V.34
Many investigators have noted that MCS frequently produces a period of poststimulus pain relief that can range from minutes to hours. Thus, most publications report the use of a cycling mode of stimulation, with 10 minutes to 3 hours on stimulation followed by 15 minutes to 6 hours off stimulation. In one study, switching from a continuous to cycling mode (in addition to other programming changes) may have contributed to improvement in pain relief.34
Indications and Results
Central Deafferentation Pain
MCS was originally developed in response to the lack of effective treatments for central deafferentation pain. In Tsubokawa’s first published report, 5 of 12 patients had complete resolution of their pain at 1 year of follow-up, with another 3 exhibiting significant decrease in pain.3 These encouraging early results led many other investigators to pursue this technique for treatment of this otherwise difficult-to-treat condition.9,11,12,17,22,23,28,29,35–38
Nguyen and colleagues9 reported 13 patients with central deafferentation pain from ischemic and hemorrhagic stroke as well as trauma (1 case) and abscess (1 case). Ten patients (77%) had “significant improvement,” classified as more than 40% reduction in pain. In a large series of 31 patients with poststroke pain (3 bulbar, 20 thalamic, and 8 suprathalamic), Katayama and associates17 obtained “satisfactory” pain relief in 15 (48%) with follow-up periods of more than 2 years. In 20 patients with central neuropathic pain, including 16 with poststroke pain, Mertens and colleagues achieved “excellent” pain relief in 25% and “good” pain relief in 35%. Other series have generally corroborated these results, with about 50% to 60% of patients achieving significant pain relief.
Trigeminal Neuropathic Pain
Trigeminal neuropathic facial pain is a syndrome of severe, constant facial pain related to disease of, or injury to, the trigeminal nerve or ganglion. Causes of trigeminal neuropathic pain can include injury from sinus or dental surgery, skull or facial trauma, or intentional destruction for therapeutic reasons (deafferentation), as well as intrinsic pathology of any part of the trigeminal system.39 Patients who fail surgical treatment for trigeminal neuralgia may sometimes develop trigeminal neuropathic pain (also called trigeminal deafferentation pain),39 for which there are few, if any, effective treatments. Few significant advances have occurred in pharmacologic therapy, and anticonvulsant and antidepressant medications remain the mainstay of treatment. Deep brain stimulation of well-defined targets in the sensory thalamus and periaqueductal or periventricular gray matter has had generally disappointing results.40
MCS has shown some promise in the treatment of trigeminal neuropathic pain, beginning with the 1993 publication by Meyerson and colleagues.6 In a group of 10 patients with different types of neuropathic pain, all 5 patients with trigeminal neuropathic pain obtained between 60% and 90% pain relief at 8 to 28 months. A follow-up study by Herregodts and associates41 showed 50% to 100% reduction in visual analog scale pain scores in 4 of 5 patients with trigeminal neuropathic pain.
In a 1996 study by Ebel and coworkers,7