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),15,1858 poststroke rehabilitation (9 cases),19,59,60 or movement disorders (84 cases), 22 of which were combined with DBS.17,6173 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.


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.

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.

Intraoperative Neurophysiologic Mapping

We use both somatosensory and motor mapping to determine the course of the central sulcus and the position of the M1 region. Somatosensory testing consists of placing the paddle electrode (Resume, Medtronic, Inc., Minneapolis, MN) on the dura in a variety of orientations, mostly perpendicular to the suspected precentral gyrus. Median or ulnar nerve somatosensory evoked potentials (SSEPs), or both, are then performed by using a 20- to 50-mA, 100-µsec monopolar square pulse at a rate of 4.32 Hz. The SSEPs are recorded from the lead in both a bipolar (e.g., contacts 0-1, 1-2, and 2-3 for a 4-contact lead) and monopolar (all referenced to the 10-20 location of Fz) recording montage. The central sulcus is defined as the point at which the N20 response phase reverses polarity (Fig. 93-2). Mapping is performed epidurally over the entire exposed area and for short distances under the bone if needed. Typically, 7 to 10 recordings are obtained, which takes no more than 10 minutes of operative time. Early experience with this technique was gained with use of the 4-contact Resume lead (Medtronics, Minneapolis, MN); however, recently, we have used a 16-contact lead connected to a rechargeable implantable pulse generator (IPG) system (Precision Plus, Boston Scientific, Niatick, MA), a constant-current system that in our initial experience has yielded quicker onset of pain relief. Long-term results with this system still need to be evaluated.

Motor mapping is performed with a 5-mm ball probe (Model E1564, Valleylab, Gosport, UK) that is applied on the dura over the suspected M1 area. The probe functions as the anode and is referenced to a cathode placed at Fz. Electromyographic recording needles are placed in bipolar fashion in the orbicularis oculi, orbicularis oris, trapezius, deltoid, biceps, triceps, flexor carpi ulnaris, abductor pollicis brevis, first dorsal interosseus, quadriceps, tibialis anterior, and abductor hallucis muscles. Stimulation consists of short trains of five to nine stimuli at a rate of one train per second, a pulse width of 500 µsec, and a 4-msec interspike interval. Stimulation is begun at each location starting at 5 mA and increased in 1-mA steps until a motor response is elicited or the maximal stimulus of 25 mA is reached. Ice-cold saline is kept ready in the field to irrigate the dura should a seizure occur. Barbiturates may be given intravenously as well if necessary.

In our experience, the mean stimulation amplitude required to generate an evoked response is 13.0 ± 4.2 mA (range, 7 to 22.4 mA). Stimulation is halted when the first electromyographic response is noted. Figure 93-3

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