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Neurosurgical Approaches to the Treatment of Pain
SUMMARY
The neurosurgeon is often consulted for the treatment of pain. With many patients in chronic pain, an opportunity exists to intervene and eliminate the pain in a definitive manner. Since the 1970s there have been significant changes in the neurosurgical approach to the treatment of pain. In this chapter we address the various surgical lesioning procedures performed on the supratentorial structures of the brain, as well as procedures targeting the brain stem, spinal cord, spinal root, and peripheral nerve.
Pain management is dependent on the type of pain. Nociceptive pain arises from stimulation of peripheral nociceptors and is transmitted to the central nervous system via intact somatosensory pathways. This type of pain represents innate protective sensation. Clinical examples of nociceptive pain include the pain of acute trauma, postoperative incisional pain, and cancer pain following bony invasion. This type of pain may respond well to opioid analgesics ( ). Neuropathic pain arises following injury to the nervous system peripherally (e.g., post-herpetic neuralgia), centrally (e.g., Dejerine–Roussy post–thalamic stroke pain), or both (e.g., brachial plexus avulsion pain). This type of pain may be refractory to opioid analgesics and may require complex multimodality interventions.
Surgical approaches to treating pain fall within four broad classes: decompression, reconstruction, ablation, and modulation. Compression or entrapment of sensory structures such as peripheral nerves or dorsal roots may disrupt function and lead to the development of pain. Decompression procedures are commonly performed by neurosurgeons to release entrapped sensory structures and potentially relieve pain. We briefly discuss some common entrapment neuropathies. Reconstruction refers to attempts to directly repair injured neural elements. An example would be nerve grafting following peripheral nerve transection or nerve root replantation following brachial plexus avulsion. This class of treatment is not described further in this chapter. Ablation procedures aim to disrupt the pain-signaling pathways in the periphery (e.g., peripheral neurectomy, dorsal rhizotomy, dorsal root ganglionectomy), spinal cord (e.g., cordotomy, myelotomy, lesioning of the dorsal root entry zone [DREZ]), brain stem (mesencephalotomy), or supratentorial pain-processing centers in the diencephalon and telencephalon. These procedures are discussed in detail. Modulation aims to alter pain signaling or processing either electrically (nerve stimulators) or pharmacologically (intrathecal drug pumps). Stimulation and drug delivery procedures have largely replaced many of the ablative procedures and are discussed in detail in Chapter 41 .
Decompression Procedures
Compression or entrapment of neural structures may disrupt function and cause pain. Neural elements may be compressed by various adjacent structures, including but not limited to hypertrophic ligaments, scar tissue, fibrous bands, anomalous bony overgrowth, and blood vessels. There may be several anatomic locations along the course of a peripheral nerve where entrapment is more likely to occur (e.g., carpal tunnel for the median nerve and fibular head for the common peroneal nerve). Entrapment may be static, dynamic, or the result of chronic repetitive movements. Severe pain may be the only symptom of neural compression. However, severe entrapment neuropathies do not always result in pain, and the degree of pain does not always correlate with the severity of entrapment. A classic illustrative example is thoracic outlet syndrome. The rare patient with neurogenic thoracic outlet syndrome as a result of compression of the lower trunk of the brachial plexus is typically initially seen late in the course with severe motor and sensory deficits and muscle atrophy but no significant pain. However, the vast majority of patients in whom thoracic outlet syndrome is diagnosed primarily have complaints of pain and typically minimal to no weakness or sensory loss. Table 40-1 describes several entrapment syndromes that may be encountered.
Table 40-1
Nerve Entrapment Syndromes
| NERVE | LOCATION OF ENTRAPMENT | SYMPTOMS AND SIGNS |
|---|---|---|
| Brachial plexus (C8, T1; thoracic outlet syndrome) | Junction of first rib and brachial plexus | Shoulder, arm, hand numbness, tingling; pain made worse with the spear-throwing position; supraclavicular tenderness |
| Suprascapular | Suprascapular notch | Posterior shoulder pain along the border of the trapezius muscle, scapular notch tenderness, pain with arm hyperadduction |
| Axillary | Quadrangular space | Shoulder or upper arm pain and tenderness in the quadrangular space |
| Intercostobrachial | Axilla, lateral thoracic wall | Posteromedial arm pain, anterior chest wall pain |
| Ulnar | Cubital tunnel retinaculum | Ulnar distribution, pain with tenderness of the ulnar nerve |
| Posterior interosseous branch of the radial nerve | Arch of the supinator muscle (arcade of Fröhse) | Pain in the dorsal forearm, discrete tenderness over the brachial radialis muscle distal to the lateral epicondyle |
| Median | Pronator teres | Volar forearm pain, discrete tenderness in the region of the pronator teres |
| Superficial radial | Brachioradialis tendon | Paresthesias of the dorsal wrist and thumb, without weakness |
| Lateral femoral cutaneous | Inguinal ligament or fascia lata | Numbness, burning pain in the anterolateral thigh |
| Saphenous | Subsartorial (Hunter’s) canal | Medial knee and anterior tibial pain, tenderness over the adductor canal |
| Sciatic | Piriformis muscle | Sacral or gluteal pain, discrete tenderness between the greater trochanter and ischium |
| Common peroneal | Fibular head | Knee pain extending down the anterolateral tibial area: tenderness just below the fibular head (lateral knee) |
| Deep peroneal | Anterior tarsal tunnel (inferior extensor retinaculum) | Pain and tenderness in the dorsum of the foot |
| Posterior tibial nerve | Medial tarsal tunnel | Burning pain and numbness over the bottom of the foot |
Painful entrapment neuropathies are often diagnosed clinically on the basis of symptoms and findings on physical examination. In some instances pain may be elicited by percutaneous stimulation of the nerve at the location of entrapment. Electrophysiological and imaging studies may be useful in some instances to confirm the clinical diagnosis and evaluate the severity of injury and level of pathology along the neuraxis. However, these studies are of limited utility for diagnosing entrapment of smaller cutaneous nerves, which are difficult to study with routine electrodiagnostic or imaging evaluations. In general, decompression of entrapped nerves is associated with low morbidity and offers the possibility of a definitive cure for pain.
Ablative Procedures
Peripheral Neurectomy
Transection of peripheral nerves, or neurectomy, may be indicated to treat both nociceptive and neuropathic pain. Neurectomy procedures interrupt transmission between peripheral nociceptors or injured nerves and the central nervous system. An example of a neurectomy procedure for nociceptive pain is selective denervation for the treatment of joint pain. Beneficial results have been reported for treatment of painful disorders of the knee, elbow, and wrist. The challenge of joint denervation is balancing the need to transect enough nerve branches to the joint to interrupt pain signaling without completely denervating the joint and rendering it ineffective and prone to destruction by overuse or contraction. Presacral neurectomy may be an option for the treatment of nociceptive chronic pelvic pain. This procedure has been shown to benefit patients with chronic pain from endometriosis and secondary dysmenorrhea. However, as a recent meta-analysis demonstrated, there is a lack of sufficient evidence from randomized controlled trials to support the use of this intervention ( ).
Peripheral neurectomy is commonly used for the treatment of neuropathic pain that arises following nerve injury. The rationale for neurectomy in these circumstances is based on the hypothesis that the neuropathic pain state is being driven by aberrant input from injured afferent fibers in the injured nerve. Under normal physiological conditions the afferent fibers in a peripheral nerve transmit signals only in response to stimulation of their distal terminals; however, following peripheral nerve injury, mechano- and chemosensitivity may arise at the nerve end neuroma, along the nervi nervorum, or in the dorsal root ganglion (DRG). Thus, internal or external stimulation of the injured nerve may produce pain. In addition, hyperalgesia may develop in the areas of denervation and at places where intact and degenerating nerve fibers overlap. The surgical goal for management of a painful neuroma is to perform a neurectomy proximal to the area of injury and thus interrupt the connection between the neuroma and the central nervous system. Inevitably, a new neuroma will form at the proximal transection site and may become a pain generator. Neuroma relocation surgery aims to relocate the proximal nerve stump to a new area, usually in muscle or bone, without nerve tension, away from joints (to avoid tethering), free of scar, and sufficiently insulated from external pressure ( Fig. 40-1 ). The new neuroma that forms at the proximal transection site is insulated from excessive mechanical and chemical stimulation and thus less likely to become a pain generator. Histologically, “relocated neuromas” have less connective tissue and less nerve fascicle disarray than classic nerve-end neuromas do. Success rates as high as 80% have been reported for neuroma relocation surgery ( ).
Dorsal Rhizotomy and Ganglionectomy
The pseudo-bipolar cell bodies of primary sensory afferents reside in DRGs and project distally to innervate the periphery and proximally (via the dorsal root) to form synapses in the dorsal horn of the spinal cord. The traditional belief established by the “law of Bell and Magendie” is that for a given spinal nerve, sensory and motor functions are segregated in the dorsal and ventral roots, respectively. Dorsal rhizotomy and ganglionectomy procedures take advantage of this anatomical functional segregation by selectively interrupting sensory transmission without injuring the motor pathways. Unlike peripheral neurectomy, dorsal rhizotomy and ganglionectomy interrupt the sensory pathway without the risk of painful neuroma formation because the distal afferent fibers remain intact in the case of rhizotomy and degenerate following ganglionectomy.
Electron microscopy has demonstrated that up to 29% of fibers in human ventral roots are small unmyelinated (presumably afferent) fibers ( ). Some of these fibers course from the periphery into the ventral root and loop back into the dorsal root to enter the dorsal horn ( ), but others bypass the dorsal root and enter the spinal cord directly through the ventral root ( ). The rationale for dorsal root ganglionectomy is that removal of the DRG leads to degeneration of the afferents coursing in both the dorsal and ventral horn and is thus a more comprehensive lesion than rhizotomy. However, sensory cell bodies may be located outside the DRG in the dorsal root, in the ventral root, or distally along the nerve. One theoretical disadvantage of ganglionectomy is that it leads to wallerian degeneration of peripheral afferents and target tissue denervation, which may contribute to pain and dysesthesias ( , ).
Dorsal rhizotomy is performed through an intradural approach, whereas ganglionectomy is performed extradurally. For dorsal rhizotomy, a laminectomy is performed, the dura is opened, and the dorsal rootlets are identified at the intervertebral foramen, traced proximally, and divided sharply. An extradural rhizotomy can be performed if the lateral facet is removed, and the nerve roots may be exposed laterally, traced proximally, and divided. For ganglionectomy, the DRG is exposed in the foramen, dissected free from the ventral root, and removed. It may be challenging to dissect the ventral root off the DRG, and this structure may be injured or need to be removed with the DRG.
As is the case for most pain procedures, careful patient selection is essential. There is significant sensory overlap among adjacent dermatomes. A monoradicular pain syndrome may be suggested by a positive nerve root block; however, nerve blocks have not proved to be a reliable predictor of outcome, and the validity of peripheral nerve blocks has been brought into question ( ). The predictive value of diagnostic blocks may be improved if they are performed with a placebo control. A positive block occurs when good pain relief is achieved with a small volume of local anesthetic injected into the neural foramen and no pain relief after placebo injection or injection at the nerve root above or below in blinded fashion. Even when a single dermatome is identified as the pain generator, the question of how many segments need to be denervated for pain relief remains. To achieve a clinical effect, the adjacent segments above and below the target level may be included in the surgical procedure. Ablation of multiple roots (more than six) may compromise spinal cord blood flow and poses a risk for spinal cord infarction. In addition, extensive loss of sensory function in an extremity may severely compromise function.
Reported response rates with dorsal rhizotomy and ganglionectomy vary greatly (19–69% for rhizotomy, 0–100% for ganglionectomy) and are confounded by heterogeneous patient populations, inadequate length of follow-up, and variability in the number of levels interrupted, use of preoperative diagnostic nerve blocks, and outcome measures. Clinical efficacy tends to decrease with time. The problem of late pain recurrence may be less of an issue in patients with limited life expectancy. For pain from cancer, reported success in 70% of patients at an average 10.5-month follow-up. There are few indications for rhizotomy or ganglionectomy for the treatment of extremity pain. reported successful treatment of diffuse upper extremity pain in 50% (7/14) of patients with 3 years’ median follow-up. A similar response rate was reported for lower extremity pain. published their results of dorsal rhizotomy performed on 51 patients with chronic lumbar radiculopathy. At 6 months after surgery, 55% were believed to have good or excellent outcomes. However, favorable long-term (2–4 years) outcomes were obtained in only 19% of patients. Similar deterioration in outcomes has been observed in several series and has led many to favor ganglionectomy over rhizotomy. The most impressive results following ganglionectomy have been reported for the treatment of thoracic and occipital pain, with some series reporting long-term success rates as high as 68% for thoracic ( ) and 80% for occipital neuralgia ( ). For treatment of refractory pain states, such as failed back surgery syndrome (FBSS), the results have been much less favorable. reported that treatment success was achieved in only 2 of 13 patients with FBSS at 2 years after surgery and in none at 5.5 years.
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