CHAPTER 164 Neurosurgical Management of Intractable Pain
Prelude to Surgical Treatment
Acute pain is a signal of actual or impending tissue injury and is generated by activation of nociceptors in tissue that has sustained an injury or insult. Acute pain resolves as injured tissue heals. Chronic pain, conversely, outlasts the typical period required for healing of an acute injury. Some definitions of chronic pain are based on the duration of pain (e.g., pain that lasts longer than 3 or 6 months). This is not an accurate distinction, however, because different types of acute injury require different lengths of healing time, and the transition of acute pain to chronic pain can vary according to the nature of the injury.1
Although sometimes difficult to make, the distinction between acute and chronic pain is important. Treatment of acute pain should be aimed at achieving analgesia while promoting tissue healing. This treatment might include rest or immobilization, analgesics, and passive physical therapy.2 In contrast, chronic pain does not serve a useful physiologic purpose (unless tissue injury is ongoing). In some cases, chronic pain no longer reflects disease but instead is considered a disease itself.3 Physical deconditioning is also a common accompaniment of many chronic pain disorders, such as failed back surgery syndrome (FBSS). Thus, many patients with chronic pain require physical reactivation and rehabilitation rather than the rest and relaxation recommended in the treatment of acute pain. This means that chronic pain often requires a treatment program opposite that used to treat acute pain and that the distinction between acute and chronic pain is critical because treating chronic pain as acute pain only promotes further disuse and deconditioning.2 The differentiation of acute and chronic pain is also important because psychological and social factors that can complicate a pain complaint might be more common in patients with chronic as opposed to acute pain. In fact, in some cases, psychosocial factors can be the predominant cause of a complaint of chronic pain.
The distinction between nociceptive and neuropathic pain is also important because the two types of pain usually respond differently to specific treatments. Nociceptive pain is generated when injury or disease (e.g., a broken arm, cancer pain with local tissue invasion) activates the nociceptors that stimulate central nervous system nociceptive pathways. Nociceptive pain, which patients describe as “throbbing,” “aching,” or “dull,”4 is thus a normal, protective response of the nociceptive systems. In contrast, neuropathic pain is the result of a pathologic process (injury or disease) affecting the peripheral or central nervous system. Such neuronal injury leads to abnormal neuronal excitability, spontaneous discharges, and ephaptic transmission, which might, in turn, lead to generation of pain with or without peripheral, let alone nociceptive, input. Thus, in contrast to nociceptive pain, neuropathic pain reflects abnormal neuronal activity. Neuropathic pain, which patients describe as “burning,” “shooting,” “tingling,” or “shock-like,”4 can be continuous or paroxysmal (lancinating). Although nociceptive pain usually responds to opioids (e.g., the pain of a broken arm can be treated with morphine), neuropathic pain tends to resist opioid treatment (at least at typical doses) and frequently requires treatment with nonopioid medications.
Surgical treatment of intractable pain is not usually the first treatment option. In most cases, treatment of intractable pain should follow a rational process with the simplest, safest methods used first and interventional treatments reserved for later use.4 A simple way of picturing this approach is a pain treatment ladder, similar to the one proposed by the World Health Organization.5 On the lowest rungs are the simplest, safest measures. Each higher rung reflects a more invasive treatment, which, just like climbing to higher rungs on a ladder, entails greater risk should complications arise. Medical therapy, beginning typically with nonopioids (e.g., nonsteroidal anti-inflammatory medications) in conjunction with adjuvant therapies when appropriate, should generally precede surgical intervention. If adequate pain control is not obtained with nonopioids, mild opioids might be required, to be replaced by strong opioids if necessary. In most cases, pain relief is most readily achieved using scheduled rather than “as needed” analgesic dosing.6,7 Neuropathic pain frequently requires treatment with nonopioid medication, although opioids can be helpful for some patients. For continuous neuropathic pain (e.g., constant burning, dysesthetic pain), useful adjuvant medications include antidepressants (e.g., tricyclic antidepressants such as amitriptyline), clonidine, local anesthetics (e.g., mexiletine), and capsaicin cream.7 Paroxysmal, lancinating, or evoked neuropathic pain might improve with anticonvulsants (e.g., carbamazepine, phenytoin, gabapentin) or baclofen.7 Nonpharmacologic adjuvant therapy, including psychological support, relaxation therapies, coping strategies, passive physical therapy (e.g., massage, heat/cold), transcutaneous electrical nerve stimulation, and orthoses)6,7 can be useful in the treatment of nociceptive or neuropathic pain.
Patient Selection for Surgical Pain Therapies
In most cases, surgical intervention is reserved for patients in whom conservative therapies result in inadequate pain relief or are associated with unacceptable side effects or risks; no absolute contradictions to surgery exist; and treatment of the underlying cause of pain is not possible, practical, or appropriate.4,8 For example, radicular leg pain from lumbar spinal stenosis can be treated with decompressive lumbar laminectomy; however, if a patient also has severe coronary artery disease that increases operative risk or has persistent pain after prior spinal surgery that reduces the potential benefit of surgery, SCS might be the safest and most appropriate treatment.8,9
The pain should have a definable organic cause. It is especially important to identify the cause of chronic pain of nonmalignant origin in order to reduce the likelihood of significant underlying or primary psychological dysfunction. Psychological dysfunction can be common in patients with chronic pain disorders and might preclude a good outcome to surgical treatment. Thus, a formal psychological evaluation might be appropriate for many (or most) patients being considered for surgical treatment of intractable pain. Contraindications to surgical intervention include overt psychological dysfunction, such as active psychosis, suicidal or homicidal behavior, major uncontrolled depression or anxiety, serious alcohol or drug abuse, or serious cognitive deficits. Other psychological problems, which may be viewed as “risk factors,” include somatization disorder, personality disorders (e.g., borderline or antisocial), history of serious abuse, major issues of secondary gain, nonorganic signs on physical examination, unusual pain ratings (e.g., 12 on a 10-point scale), inadequate social support, unrealistic outcome expectations, and, in the case of implantable augmentative devices, an inability to understand the device or its use. Patients with psychological risk factors are not necessarily precluded from surgical treatment, but the treatment program should address the psychological issues to facilitate a good outcome.10
Neurosurgical Therapies for Intractable Pain
Neurosurgeons can use anatomic, augmentative (or neuromodulation), and ablative therapies (Table 164-1).11 The treatment offered should be tailored to meet the needs of each individual patient and the skills of the treating physician. Specific interventions vary in their appropriateness as a treatment for pain in specific body regions (Tables 164-2 through 164-5). Patient-related factors that must be taken into consideration when selecting a therapy include the etiology, distribution, and characteristics (nociceptive or neuropathic) of the pain; life expectancy; and psychological, social, and economic issues relevant to the pain complaint. The relative advantages and disadvantages of anatomic, augmentative, and ablative therapies should be weighed in view of these factors, and a choice among these three general approaches should be made before choosing a specific intervention. Selecting the right treatment for the right patient at the right time increases the likelihood of a successful outcome.
ANATOMIC | AUGMENTATIVE | ABLATIVE |
---|---|---|
Correction of structural deformity |
DREZ, dorsal root entry zone.
Modified from North RB. Neurosurgical procedures for chronic pain: general neurosurgical practice. Clin Neurosurg. 1992;40:182-196.
AUGMENTATIVE |
ABLATIVE |
AUGMENTATIVE |
ABLATIVE |
AUGMENTATIVE |
ABLATIVE |
AUGMENTATIVE |
ABLATIVE |
Ablative therapies, however, have a role in the treatment of certain pain syndromes12,13 and can target almost every level of the peripheral and central nervous systems. Thus, ablative therapies can be directed at preventing transmission of nociceptive information into the central nervous system at the level of peripheral nerves (neurectomy, neurotomy), roots (ganglionectomy, rhizotomy), and the spinal cord dorsal horn (DREZ, including nucleus caudalis DREZ). Ascending nociceptive pathways can be disrupted at the level of the spinal cord or brainstem (cordotomy, myelotomy, tractotomy) or within the brain (thalamotomy, cingulotomy).
Augmentative Therapies
Stimulation therapies approved for use in the United States include SCS and PNS. The major indication for SCS is for treatment of neuropathic pain in an extremity. The pain should be relatively focal (e.g., localized to one or two extremities or focal on the trunk) and static in nature. Common applications include treatment of persistent radicular pain associated with FBSS8,9,14–19 or neuropathic pain related to complex regional pain syndrome (“reflex sympathetic dystrophy”).20,21 In the FBSS population, the success rate (defined typically as 50% or greater reduction in pain) is about 60% at 5 years.8,15,16 Patients with complex regional pain syndromes have similar outcomes, although success rates as high as 70% to 100% have been reported.20,21 SCS can also be effective for neuropathic pain affecting the trunk (e.g., postherpetic neuralgia and some types of postthoracotomy pain) and for extremity pain due to peripheral neuropathy,22 root injury, phantom limb syndrome (but not necessarily postamputation stump pain), and peripheral vascular disease.23,24 SCS is widely used in Europe as a successful treatment of refractory angina pectoris,25,26 but this indication does not have specific U.S. Food and Drug Administration (FDA) approval.
The indications for PNS are similar to those for SCS, except that the distribution of pain should be limited to the territory of a single peripheral nerve.27 Overlap exists between the application of SCS and PNS. Extremity pain that might be appropriate for PNS can sometimes be treated equally well with SCS, and many surgeons find it easier to implant a percutaneous SCS electrode than to implant a PNS electrode (which usually requires an open procedure). Some situations clearly require PNS rather than SCS, for example, treatment of occipital neuralgia or cranial postherpetic neuralgia.28
Intracranial stimulation therapies include DBS of the somatosensory thalamus, hypothalamus, and periventricular-periaqueductal gray29–34 or MCS.35–38 These therapies are used primarily for treating pain of nonmalignant origin, such as pain associated with FBSS, neuropathic pain following central or peripheral nervous system injury, or trigeminal pain or cluster headache. Neither DBS nor MCS is approved by the FDA for the treatment of pain, although DBS has been used for more than two decades.
Targets for focal electrical stimulation of the brain include the ventrocaudal nucleus (nucleus ventroposterolateralis and ventroposteromedialis) and the periventricular-periaqueductal gray (PVG-PAG). Stimulation sites for DBS are generally chosen on the basis of the pain characteristics. Nociceptive pain and paroxysmal, lancinating, or evoked neuropathic pain (e.g., allodynia, hyperpathia) tend to respond to PVG-PAG stimulation, which might activate endogenous opioid systems. Continuous neuropathic pain responds most consistently to paresthesia-producing stimulation of the sensory thalamus (nucleus ventrocaudalis).32