Treatment Applications of Cortical Stimulation

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CHAPTER 93 Treatment Applications of Cortical Stimulation

Since initial reports in the early 1990s, motor cortical stimulation (MCS) of the primary motor cortex (M1) has been used to treat chronic refractory pain conditions and a variety of movement disorders. In this chapter we report several of our own cases in which MCS was used to treat poststroke and non-poststroke pain syndromes and movement disorders, Parkinson’s disease (PD), essential tremor, and corticobasal degeneration. In addition, we cover the essential history of MCS and details on how the basic aspects of the procedure can be achieved.

Although some attempts to use cortical stimulation for the treatment of neurological disorders were made in the latter half of the 20th century, only recently has chronic MCS been investigated seriously as a surgical treatment of both chronic pain and medically refractory movement disorders. Before the advent of viable chronically implanted stimulation systems, disorders of central nervous system function were treated by ablation or extirpation of the offending tissue. In 1909, Horsley reported suppression of athetosis by resection of the motor cortex.¹ Interestingly, he localized the upper limb region of M1 by direct cortical stimulation. In the 1930s and 1940s, Bucy extirpated the motor cortex to treat PD and other tremor disorders.¹^,² In 1954, Penfield and Jasper resected a patient’s primary sensory cortex (S1) to treat burning pain but did not achieve complete resolution of symptoms until they also resected the precentral gyrus.³ Later that same decade, White and Sweet reported minimal success treating refractory pain with postcentral resection.⁴

The contemporary history of nervous system stimulation as a treatment modality perhaps begins with Heath, who in 1954 stimulated the septal area with the goal of activating pleasure centers and alleviating pain.⁵ Twenty-five years later, Woolsey and colleagues demonstrated inhibition of tremor and rigidity in PD patients via precentral stimulation,⁶ although permanent implantation of electrodes was not attempted. It was not until the 1970s, when Mundinger stimulated the sensory thalamic nuclei to treat spasticity and athetosis, that chronic stimulation of the brain was used to treat movement disorders.⁷^,⁸ Since then, deep brain stimulation (DBS) at several sites, including the thalamus,⁹ cingulum,¹⁰ periventricular and periaqueductal gray areas,¹¹ and more recently the globus pallidus pars interna¹² and subthalamic nucleus,¹³ has been attempted to treat a variety of functional brain disorders. During the mid-1980s, Hosobuchi implanted electrodes subcortically in the somatosensory region in 76 chronic deafferentation pain patients and noted beneficial results in 44.¹⁴ In 1985 and 1991, Tsubokawa and colleagues reported their results with chronic stimulation of the M1 region for the treatment of post-thalamic stroke pain.¹⁵^,¹⁶ In 1998, Ngyuen and coauthors reported using stimulation of M1 to treat PD.¹⁷ A MEDLINE review of articles from 1991 to 2008 revealed 512 cases in which MCS was used for the treatment of pain (422 cases),^15,¹⁸^–⁵⁸ poststroke rehabilitation (9 cases),^19,^59,⁶⁰ or movement disorders (84 cases), 22 of which were combined with DBS.^17,⁶¹^–⁷³ Some studies included previously reported cases from earlier references that the authors tried to differentiate but may have missed.

As of May 2008, Tsubokawa and associates at Nihon University had the largest published experience with MCS, 88 cases in all.^29,^33,^65,⁶⁶ Their work included comparisons of DBS and spinal cord stimulation (SCS) to MCS, predominantly for the treatment of chronic pain and movement disorders. They reported that 59% of patients who underwent DBS or MCS for involuntary movements resulting from stroke experienced some benefit, mostly relief of hemichorea and resting tremor.³⁰ Nineteen percent of patients who underwent MCS primarily for pain control also showed improvement in their movement problems, which consisted of hemiparesis predominantly. The results for treating phantom limb pain were less promising.³³ Only 6 of 19 patients had good pain relief from SCS alone. Ten of those who failed SCS eventually underwent ventrocaudal thalamic DBS. Of these, 6 patients had good long-term pain control. Of another 5 patients who failed SCS, only 1 experienced greater pain relief when subsequently treated with MCS. Nevertheless, this patient still experienced only moderate pain reduction. In another study of 12 patients with various brain lesions (6 with thalamic stroke, 3 with stroke in the posterior limb of the internal capsule, 1 with pontine stroke, 1 with multiple sclerosis, and 1 with postrhizotomy pain), 6 achieved “excellent” outcomes (defined as 100% pain improvement) at 1 year, with 5 of 11 patients maintaining this response after 2 years.¹⁵^,⁵¹ Three patients whose responses were initially categorized as “good” (60% to 80% improvement) were recategorized as either “fair” (40% to 60% improvement) or “poor” (<40% improvement) at 1 year. In 1998, Katayama and coauthors reported that although satisfactory pain control could be achieved in 23 of 31 poststroke patients initially, at 2 years pain control was still satisfactory in only 8 of these initial 23 patients.³¹

Several groups in Italy have developed a moderate experience with the use of MCS primarily for the treatment of movement disorders.^24,^39,^61,^62,^64,^68,⁷¹ Early results from these studies were promising, but as time progressed the benefits diminished. In a study sponsored by the Italian Neurosurgical Society,⁶⁸ 10 patients were monitored for 3 to 30 months after MCS for PD. All but 1 patient were ineligible for DBS because of age, findings on magnetic resonance imaging (MRI), or neurocognitive difficulties. The mean duration of disease was 12.4 years. Three patients improved less than 25%, 6 improved 25% to 50%, and 1 improved more than 50% as measured with a global rating scale. The stimulation parameters were as follows: 2.5 to 6 V, 150 to 180 µsec, and 25 to 40 Hz. Over time, these beneficial effects were lost, as reported in later presentations.⁷⁴^,⁷⁵

Programming and Complications

Historically, stimulation parameters for the treatment of chronic pain have varied widely. Stimulation amplitudes have ranged from a minimum of 0.5 V to the device’s maximal output of 10.5 V, stimulation frequencies from 5 to 210 Hz, and pulse widths from 1 to 500 µsec.* The most common adverse effect is induction of seizures, the majority of which occur during the initial testing phases. Hardware failure and infection are the second and third most likely complications, respectively. Both Myerson and colleagues³⁵ and Nguyen and associates⁷⁷ reported postoperative hematomas; one was asymptomatic and one required surgical intervention. Three groups have described subdural instead of epidural electrode placement.^47,^53,⁵⁴ In one of these reports two of nine patients suffered hemorrhages, one of which was fatal.⁴⁷ The other patient was left in a persistent vegetative state.

Physiologic and Clinical Rationale for Motor Cortical Stimulation

M1 is the final common link between the deeper circuitry that coordinates movement and the part of the spinal cord through which the movement is realized. Moreover, M1 is one of the few brain regions where the pyramidal and extrapyramidal systems interact directly. Because the symptoms of extrapyramidal disorders require a functioning pyramidal system to become manifest, it is reasonable to hypothesize that movement disorders such as PD, tremor, and dystonia may respond to therapeutic electrical stimulation at this target, particularly in light of the clinical precedents noted earlier.

On a practical level, MCS is potentially safer than DBS in that penetration of the brain parenchyma (and in the case of epidural stimulation, even exposure of the brain) is avoided. It may be performed with general anesthesia, does not require frame-based stereotactic guidance or technically advanced neurophysiologic mapping, and virtually eliminates the possibility of intraparenchymal hemorrhage. Consequently, it is important to consider MCS as an alternative or even preliminary procedure to DBS, particularly in patients with PD and refractory pain syndromes involving the face or upper extremity because these conditions are represented on the more accessible lateral convexity of the M1 cortex.

Methods

Surgical and Cortical Mapping Technique

Although the M1 region can be accessed via bur hole,^24,^39,^40,^64,^68,^74,⁷⁵ we prefer a small craniotomy, which allows us to perform detailed electrophysiologic mapping of the region and to suture the stimulating electrode to the dura so that it remains in place. The operation is performed with the patient supine. The anesthetic technique must be tailored so that neurophysiologic mapping can be performed. We prefer a complete total intravenous anesthetic protocol using a continuous infusion of propofol combined with either fentanyl or remifentanil. Standard doses are in the range of 75 to 150 µg/kg/min of propofol and 0.05 to 0.5 µg/kg/min of fentanyl or remifentanil. Inhaled agents are avoided, particularly nitrous oxide, because of their detrimental effects on motor evoked potentials. No muscle relaxants are used except during induction/intubation.

We do not use three-point cranial fixation because rigid fixation is unnecessary and could cause injury to the patient if a seizure is induced during cortical stimulation/mapping. To center the incision over the M1 region, the midpoint from nasion to inion is determined,* and a curved incision extending from approximately 1 cm behind this midpoint toward the anterior margin of the tragus is marked on the scalp before preparing and draping the surgical field (Fig. 93-1). This incision allows a 5- to 6-cm craniotomy, which can be adjusted superiorly or inferiorly along the convexity to map the hand or face, respectively. Even though the craniotomy lies mainly above the superior temporal line, the superior edge of the temporalis muscle may be detached when access to the facial region of M1 is required. One may leave a cuff of temporalis fascia for reattachment of the muscle during closure.

FIGURE 93-1 Schematic drawing denoting the external landmarks and measurements for planning craniotomy for motor cortical stimulation. Nasion-inion (N-I line) measurements are often about 36 cm. The surgeon then makes an imaginary line between a point approximately 1 to 2 cm behind the midpoint of the N-I line and the outer canthus. A curvilinear incision may then be made over this imaginary line, more superior for the hand and arm areas and more inferior along the convexity to access the face region. This should allow a small craniotomy approximately 5 to 6 cm in diameter centered over the M1 region of interest. The lead may be manipulated for mapping and then secured to the dura as shown. The lead wire may then exit through the posterior and inferior bur hole.

Some surgical teams advocate using functional MRI (fMRI) to localize M1 preoperatively.^37,^40,^43,⁵⁰ In our experience, these studies provide no information that cannot be obtained by intraoperative mapping; however, validation of fMRI might one day obviate the need for a small craniotomy or intraoperative mapping, or both. Nevertheless, the potential for target inaccuracies as a result of brain shifting, the desire to better secure the electrode to the dura, and the potential for misrepresentation of functional activity on fMRI have kept us from adopting this technique to date.