pain

One learns quickly in dealing with such patients that not all pain is the consequence of serious disease. Every day, healthy persons of all ages have pains that must be taken as part of normal sensory experience. To mention a few, there are the “growing pains” of children; the momentary hard pain over an eye or in the temporal or occipital regions, which strikes with such suddenness as to raise the suspicion of a ruptured intracranial aneurysm; the more persistent ache in the fleshy part of the shoulder, hip, or extremity that subsides spontaneously or in response to a change in position; the fluctuant precordial discomfort of gastrointestinal origin, which conjures up fear of cardiac disease; the breathtaking “stitch in the side,” due to intercostal or diaphragmatic cramp. These normal pains, as they should be called, tend to be brief and to depart as obscurely as they came. Such pains come to notice only when elicited by an inquiring physician or when experienced by a patient given to worry and introspection. They must always be distinguished from the pain of disease.
Whenever pain—by its intensity, duration, and the circumstances of its occurrence—appears to be abnormal or when it constitutes the chief complaint or one of the principal symptoms, the physician must attempt to reach a tentative decision as to its mechanism and cause. This is accomplished by a thorough interrogation of the patient, with the physician carefully seeking out the main characteristics of the pain in terms of

1.
Location

2.
Mode of onset

3.
Provoking and relieving factors

4.
Quality and time-intensity attributes

5.
Duration

6.
Severity
Knowledge of these factors in every common disease is the lore of medicine. The severity of pain is often difficult to assess. Extreme degrees of pain are betrayed by the patient's demeanor, but lesser degrees can be roughly estimated by the extent to which the pain has interfered with the patient's sleep, work, and other activities or by the patient's need for bed rest. Some physicians find it helpful, particularly in gauging the effects of analgesic agents, to use a “pain scale,” i.e., to have the patient rate the intensity of his pain on a scale of zero (no pain) to ten (worst pain) or to mark it on a line. Needless to say, this general approach is put to use every day in the practice of internal medicine. Together with the physical examination, including tests designed to reproduce and relieve the pain, and ancillary diagnostic procedures, it enables the physician to identify the source of most pains and the diseases of which they are a part.
Once the pains due to the more common and readily recognized diseases of each organ system are eliminated, there remain a significant number of chronic pains that fall into one of four categories: (1) pain from an obscure medical disease, the nature of which has not yet been disclosed by diagnostic procedures; (2) pain associated with disease of the central or peripheral nervous system (i.e., neurogenic or neuropathic pain); (3) pain associated with psychiatric disease; and (4) pain of unknown cause.
Pain due to Undiagnosed Medical Disease
Here the source of the pain is usually peripheral and caused by a lesion that irritates and destroys nerve endings. Hence the term nociceptive pain is often used, but it is ambiguous. It usually means an involvement of structures bearing the termination of pain fibers. Carcinomatosis is the most frequent example. Osseous metastases, peritoneal implants, invasion of retroperitoneal tissues or the hilum of the lung, and implication of nerves of the brachial or lumbosacral plexuses can be extremely painful, and the origin of the pain may remain obscure for a long time. Sometimes it is necessary to repeat all diagnostic procedures after an interval of a few months, even though at first they were negative. From experience one learns to be cautious about reaching a diagnosis from insufficient data. Treatment is directed to the relief of pain, at the same time instilling in the patient a need to cooperate with a program of expectant observation.
Neurogenic, or Neuropathic, Pain
These terms are generally used interchangeably to designate pain that arises from direct stimulation of nervous tissue itself, central or peripheral, exclusive of pain due to stimulation of sensitized C fibers (i.e., the nociceptive pain described above). This category comprises a variety of disorders involving single and multiple nerves, notably trigeminal neuralgia and those due to herpes zoster, diabetes, and trauma (including causalgia); a number of polyneuropathies of diverse type; root irritation, e.g., from a prolapsed disc; spinal arachnoiditis and spinal cord injuries; the thalamic pain syndrome of Déjerine-Roussy; and rarely parietal lobe infarction (Schmahmann and Leifer). The clinical features that characterize central pain have been reviewed by Schott. As a rule, lesions of the cerebral cortex and white matter are associated not with pain but with hypalgesia. Particular diseases giving rise to neuropathic pain are considered in their appropriate chapters. The following remarks are of a general nature, applicable to all of the painful states that compose this group.
The features that characterize neurogenic and neuropathic pain are their persistence and generally poor response to analgesic medication; their burning, gnawing, aching, and often shooting or lancinating quality; their frequent association with hyperesthesia, hyperalgesia, allodynia, and hyperpathia (see above); the presence in many cases of a sensory deficit and some autonomic dysfunction; and the variable temporal relationship of the pain to the disease of which it is an expression.
Peripheral Nerve Pain Painful states that fall into this category are in most cases related to disease of the peripheral nerves, and it is to pain from this source that the term neuropathic is more strictly applicable. Pain states of peripheral nerve origin far outnumber those due to spinal cord, brainstem, thalamic, and cerebral disease. Although the pain is localized to a sensory territory supplied by a nerve plexus or nerve root, it often radiates to adjacent areas. Sometimes the onset of pain is immediate on receipt of injury; more often it appears at some point during the evolution or recession of the disorder. The disease of the nerve may be obvious, expressed by the usual sensory, motor, reflex, and autonomic changes, or these changes may be undetectable by standard tests. In the latter case, the term neuralgia is the preferred term.
The postulated mechanisms of peripheral nerve pain are diverse and probably differ from those of central diseases. In peripheral nerve, one mechanism is denervation hypersensitivity, first described by Walter Cannon. He noted that when a group of neurons is deprived of its natural innervation, they become hyperactive. Some neurologists point to a reduced density of certain types of fibers in nerves supplying a causalgic zone as the basis of the burning pain, but the comparison of nerves from painful and nonpainful neuropathies has not proved to be consistently different. Dyck and colleagues, in a study of painful versus nonpainful axonal neuropathies, concluded that there was no difference between them in terms of the type of fiber degeneration. The occurrence of ectopic impulse generation all along the surface of injured axons and the possibility of ephaptic activation of unsheathed axons seems applicable particularly to causalgic states in which nerve pain appears to be abolished by sympathetic denervation. Stimulation of the nervi nervorum of larger nerves by an expanding intraneural lesion or a vascular change was postulated by Asbury and Fields as the mechanism of nerve trunk pain. Regenerating axonal sprouts, as in a neuroma, are also hypersensitive to mechanical stimuli. On a molecular level, it has been shown that sodium channels accumulate at the site of a neuroma and all along the axon after nerve injury, and this gives rise to ectopic and spontaneous activity of the sensory nerve cell and nerve fiber. Such firing has been demonstrated in humans after nerve injury. This mechanism is concordant with the relief of neurogenic pain by sodium channel–blocking anticonvulsants. Spontaneous activity in nociceptive C fibers is thought to give rise to burning pain; firing of large myelinated A fibers is believed to produce dysesthetic pain induced by tactile stimuli. The abnormal response to stimulation is also influenced by sensitization of central pain pathways. Hyperalgesia is proposed to result from such a mechanism (see Woolf and Mannion). Possibly more than one of these mechanisms is operative in a given peripheral nerve disease.
Central Pain In central lesions, deafferentation of secondary neurons in the posterior horns or of sensory ganglion cells that terminate on them may cause the deafferented cells to become continuously active and, if stimulated by a microelectrode, to reproduce pain. In the patient whose spinal cord has been transected, there may be intolerable pain in regions below the level of the lesion. It may be exacerbated or provoked by movement, fatigue, or emotion and projected to areas disconnected from suprasegmental structures (akin to the phantom pain in the missing part of an amputated limb). Here, and in the rare cases of intractable pain with lateral medullary or pontine lesions, loss of the descending inhibitory systems seems a likely explanation. This may also explain the pain of the Déjerine-Roussy thalamic syndrome described on page 172. Altered sensitivity and hyperactivity of central neurons is an alternative possibility.
Further details concerning the subject of neuropathic pain can be found in the writings of Scadding and of Woolf and Mannion (see References).
Pain in Association with Psychiatric Diseases
It is not unusual for patients with endogenous depression to have pain as the predominant symptom. And most patients with chronic pain of all types are depressed. Wells and colleagues, in a survey of a large number of depressed and chronic pain patients, have convincingly corroborated this clinical impression. Fields has elaborated a theoretical explanation of the overlap of pain and depression. In such cases one is faced with an extremely difficult clinical problem—that of determining whether a depressive state is primary or secondary. In some instances the diagnostic criteria cited in Chap. 57 provide the answer, but in others it is impossible to make this distinction. Empiric treatment with antidepressant medication or, failing this, with electroconvulsive therapy is one way out of the dilemma.
Intractable pain may be the leading symptom of both hysteria and compensation neurosis. Every experienced physician is familiar with the “battle-scarred abdomen” of the woman with hysteria (so-called Briquet disease) who has demanded and yielded to one surgical procedure after another, losing appendix, ovaries, fallopian tubes, uterus, gallbladder, etc., in the process (“diagnosis by evisceration”). The recognition and management of hysteria are discussed in Chap. 56.
Compensation neurosis is often colored by persistent complaints of headaches, neck pain (whip-lash injuries), low-back pain, etc. The question of ruptured disc is often raised, and laminectomy and spinal fusion may be performed (sometimes more than once) on the basis of dubious radiologic findings. Complaints of weakness and fatigue, depression, anxiety, insomnia, nervousness, irritability, palpitations, etc., are woven into the clinical syndrome, attesting to the prominence of psychiatric disorder. Long delay in settlement of litigation, allegedly to determine the seriousness of the injury, only enhances the symptoms and prolongs the disability. The medical and legal professions have no certain approach to such problems and often work at cross-purposes. We have found that a frank, objective appraisal of the injury, an assessment of the psychiatric problem, and encouragement to settle the legal claims as quickly as possible work in the best interests of all concerned. While hypersuggestibility and relief of pain by placebos, etc., may reinforce the physician's belief that there is a prominent factor of hysteria or malingering (see Chap. 56), such data are difficult to interpret and are not acceptable in court.
Chronic Pain of Indeterminate Cause
This is the most difficult group of all—pain in the thorax, abdomen, flank, back, face, or other part that cannot be traced to any visceral abnormality. Supposedly all neurologic sources, such as a spinal cord tumor, have been excluded by repeated examinations and imaging procedures. A psychiatric disorder to which the patient's symptoms and behavior might be attributed cannot be discerned. Yet the patient complains continuously of pain, is disabled, and spends a great deal of effort and money seeking medical aid.
In such a circumstance, some physicians and surgeons, rather than concede their helplessness, may resort to extreme measures such as exploratory thoracotomy, laparotomy, or laminectomy. Or they may injudiciously attempt to alleviate the pain and avoid drug addiction by severing roots and spinal tracts, often with the result that the pain moves to an adjacent segment or to the other side of the body.
This type of patient should be seen frequently by the physician. All the medical facts should be reviewed and the clinical and laboratory examinations repeated if some time has elapsed since they were last done. Tumors in the hilum of the lung or mediastinum, in the retropharyngeal, retroperitoneal, and paravertebral spaces, or in the uterus, testicle, kidney, and prostate offer special difficulty in diagnosis, often being undetected for many months. Neurofibroma causing pain in an unusual site, such as one side of the rectum or vagina, is another type of tumor that may defy diagnosis for a long time. Neurologic pain is almost invariably accompanied by alterations in cutaneous sensation and other neurologic signs, the finding of which facilitates diagnosis; the appearance of the neurologic signs may be long delayed, however. The possibility of drug addiction as a motivation should be eliminated. It is impossible to assess pain in the addicted individual, for the patient's complaints are woven into his need for medication. Temperament and mood should be evaluated carefully from day to day; the physician must remember that the depressed patient often denies being depressed and may occasionally smile. When no medical, neurologic, or psychiatric disease can be established, one must be resigned to managing the painful state by the use of nonnarcotic medications and frequent clinical re-evaluations. Such a course, though not altogether satisfactory, is preferable to prescribing excessive opioids or subjecting the patient to ablative surgery.
Because of the complexity and difficulty in diagnosis and treatment of chronic pain, most medical centers have found it advisable to establish pain clinics. Here a staff of internists, anesthesiologists, neurologists, neurosurgeons, and psychiatrists are able to review each patient in terms of drug dependence, neurologic disease, and psychiatric problems. Success is achieved by treating each aspect of chronic pain, with emphasis on increasing the patient's tolerance of pain by means of biofeedback, meditation and related techniques, by using special invasive anesthetic special procedures (discussed later in the chapter), by establishing a regimen of pain medication, and by controlling depressive illness.
Rare and Unusual Disturbances of Pain Perception
Lesions of the parieto-occipital regions of one cerebral hemisphere sometimes have peculiar effects on the patient's capacity to feel and react to pain. Under the title of pain hemiagnosia, Hecaen and Ajuriaguerra described several cases of left-sided paralysis from a right parietal lesion which, at the same time, rendered the patient hypersensitive to noxious stimuli. When pinched on the affected side, the patient, after a delay, became agitated, moaned, and seemed distressed but made no effort to fend off the painful stimulus with the other hand or to withdraw from it. In contrast, if the good side was pinched, the patient reacted normally and moved the normal hand at once to the site of the stimulus to remove it. The motor responses seem no longer to be guided by sensory information from one side of the body.
There are also two varieties of rare individuals who from birth are totally indifferent to pain (“congenital insensitivity to pain”) or are incapable of feeling pain (“universal analgesia”). The former have an uncertain congenital deficiency of a neurotransmitter or an equally obscure peculiarity of the central receptive apparatus (see Chap. 9), and the second group suffers from either a congenital lack of pain neurons in dorsal root ganglia, a polyneuropathy, or a lack of pain receptors in the primary afferent neuron.
The phenomenon of asymbolia for pain is another rare and unusual condition, wherein the patient, although capable of distinguishing the different types of pain stimuli from one another and from touch, is said to make none of the usual emotional, motor, or verbal responses to pain. This patient seems totally unaware of the painful or hurtful nature of stimuli delivered to any part of the body, whether on one side or the other. The current interpretation of asymbolia for pain is that it represents a particular type of agnosia (analgagnosia) or apractagnosia (cf. Chap. 22), in which the organism loses its ability to adapt its emotional, motor, and verbal actions to the consciousness of a nociceptive impression. “Le sujet a perdu la compréhension de la signification de la douleur.” We have been unable to corroborate the existence of this syndrome from our own clinical experience.
Treatment of Intractable Pain
Once the nature of the patient's pain and underlying disease have been determined, therapy must include some type of pain control. Initially, of course, attention is directed to the underlying disease, with the idea of eliminating the source of the pain by appropriate medical, surgical, or radiotherapeutic measures.
If the patient is ridden with disease and will not live more than a few weeks or months, is opposed to surgery, or has widespread pain, surgical measures are out of the question. However, pain from widespread osseous metastases, even in patients with hormone-insensitive tumors, may be relieved by radiation therapy or by hypophysectomy. Pain confined to a restricted area of the jaw or face may be relieved by nerve root blocks; by radiofrequency destruction of the trigeminal nerve, roots, or ganglion; or in some cases by decompressive surgery of an aberrant vascular loop that abuts a root in the posterior fossa. Usually, nerve section is not a satisfactory way of relieving restricted pain of the trunk and limbs because the overlap of adjacent nerves prevents complete denervation. Another procedure to be considered before undertaking the section of several contiguous sensory roots is the regional delivery of narcotic analogues, such as fentanyl or ketamine, by means of an external pump and a catheter that is implanted percutaneously in the epidural space in proximity to the dorsal nerve roots in the affected region; this device can be used safely at home.
If radiation therapy and other medical and surgical measures are not feasible or fail to relieve the pain, a program utilizing analgesic medication must be undertaken. Central to such a program is the use of opioids, which to this day represent the most effective analgesic agents for the management of severe chronic pain due to medical disease.
A useful way in which to undertake the management of chronic pain that affects several parts of the body, as in the patient with metastases, is with codeine, oxycodone, or propoxyphene taken together with aspirin, acetaminophen, or another nonsteroidal anti-inflammatory agent. The analgesic effects of these two types of drugs are additive, which is not the case when narcotics are combined with diazepam or phenothiazine. Antidepressants may have a beneficial effect on pain, even in the absence of overt depression. This is true particularly in cases of neuropathic pain (painful polyneuropathy and some types of radicular pain). Sometimes these nonnarcotic agents may in themselves or in combination with other treatment modalities be sufficient to control the patient's pain, and the use of narcotics can be kept in reserve.
Use of Opioids and Opiates Should the foregoing measures prove to be ineffective, one must turn to more potent narcotic agents. Methadone and levorphanol are the most useful drugs with which to begin, because of their effectiveness by mouth and the relatively slow development of tolerance. The oral route should be utilized whenever possible, since it is more comfortable for the patient than the parenteral route. Also, the oral route is associated with less side effects, except for nausea and vomiting, which tend to be worse than with parenteral administration. Should the latter become necessary, one must be aware of the ratios of oral to parenteral dosages required to produce equivalent analgesia. These are indicated in Table 8-1.




Table 8-1 Common drugs for the management of chronic pain


If oral medication fails to control the pain, the parenteral administration of codeine or more potent opioids becomes necessary. Again, one may begin with methadone, dihydromorphone (Dilaudid), or levorphanol, given at intervals of 4 to 6 h, because of their relatively long duration of action (particularly in comparison to meperidine). Alternatively, one may first resort to the use of transdermal patches of drugs such as fentanyl, which provide relief for 24 to 72 h and which we have found particularly useful in the treatment of pain from brachial or lumbosacral plexus invasion by tumor. Long-acting morphine preparations are useful alternatives. Should long-continued injections of opiates become necessary, the optimal dose for the relief of pain should be established and the drug then given at regular intervals around the clock, rather than “as needed.” The administration of morphine (and other narcotics) in this way represents a laudable shift in attitude among physicians. For many years it was taught that the drug should be given in the smallest possible doses, spaced as far apart as possible, and repeated only when severe pain reasserted itself. It has become clear that such usage of the drug results in unnecessary discomfort and, in the end, the need to use larger doses. The fear of creating narcotic dependence and the expected phenomenon of increasing tolerance must be balanced against the overriding need to relieve pain. The most pernicious aspect of addiction, that of compulsive drug-seeking behavior and self-administration of the drug, occurs only rarely in this setting and usually in patients with a previous history of addiction or alcoholism, with depression as the primary problem, or with certain character defects that have been loosely referred to as “addiction proneness.” Even in patients with severe acute or postoperative pain, the best results are obtained by allowing the patient to determine the dose and frequency of intravenous medication, so-called patient-controlled analgesia, or PCA. Again, the danger of producing addiction is minimal.
Excellent guidelines for the use of orally and parenterally administered opioids for cancer-related pain are contained in the article of Cherny and Foley and in the publication of the U.S. Department of Health and Human Services (see References).
The regimen outlined above conforms with current information about pain-control mechanisms. Aspirin and other nonsteroidal anti-inflammatory analgesics are believed to prevent the activation of nociceptors by inhibiting the synthesis of prostaglandins in skin, joints, viscera, etc. Morphine and meperidine given orally, parenterally, or intrathecally presumably produce analgesia by acting as “false” neurotransmitters at receptor sites in the posterior horns of the spinal cord—sites that are normally activated by endogenous opioid peptides (see Fig. 8-5). The separate sites of action of nonsteroidal analgesics and opioids provide an explanation for the therapeutic usefulness of combining these drugs. Yet another mechanism, described earlier in this chapter, consists of the physiologic activation of the intrinsic analgesic system (descending pathways from brain to spinal cord) by electrical stimulation, administration of placebo, and possibly acupuncture; short bursts of transcutaneous electrical stimulation may also suppress pain in this way. Not only do opioids act directly on the central pain-conducting sensory systems but they also exert a powerful action on the affective component of pain. Serotoninergic neurons are also thought to play a role in pain modulation.
Other Supplemental Medications Tricyclic antidepressants, especially the methylated forms (imipramine, amitriptyline, and doxepin), block serotonin reuptake and thus enhance the action of this neurotransmitter at synapses and putatively facilitate the action of the intrinsic opiate analgesic system. As a general rule, relief is afforded with tricyclic antidepressants in the equivalent dose range of 75 to 125 mg daily of amitriptyline, but little benefit accrues with higher doses. The newer serotoninergic antidepressants seem not to be as effective for the treatment of chronic neuropathic pain (see review by McQuay and colleagues), but these agents have not yet been extensively investigated in this clinical condition.
Anticonvulsants have a beneficial effect on many central and peripheral neuropathic pain syndromes but are generally less effective for causalgic pain due to partial injury of a peripheral nerve. The mode of action of phenytoin, carbamazepine, neurontin, and other anticonvulsants in suppressing the lancinating pains of tic douloureux and certain polyneuropathies as well as pain after spinal cord injury and myelitis is not understood. The biphosphate compound pamidronate, known to relieve several painful bone disorders, is being adopted increasingly for the treatment of causalgic pain, but the precise indications for its use remain to be defined.
The use of analgesic (nonnarcotic and narcotic), anticonvulsant, and antidepressant drugs in the management of chronic pain are summarized in Table 8-1.
Treatment of Neuropathic Pain
The treatment of pain induced by nerve root compression or intrinsic peripheral nerve disease utilizes several special techniques, some of which fall in the province of the anesthesiologist. If the pain is regional and has a predominantly burning quality, capsaicin cream can be applied locally, care being taken to avoid contact with the eyes and mouth. The irritative effect of this chemical seems in some cases to mute the pain. Concoctions of “eutectic” mixtures of local anesthetic creams (EMLA) and the simpler lidocaine gel preparation may provide relief in postherpetic neuralgia and painful peripheral neuropathies.
Injections of epidural corticosteroids or mixtures of analgesic and steroids are helpful in selected cases of lumbar or thoracic nerve root pain and occasionally in painful peripheral neuropathy, but precise criteria for the use of this measure are not well established. Root blocks with lidocaine or with longer-acting local anesthetics are helpful at times in establishing the precise source of radicular pain. Their main therapeutic use in our experience has been for thoracic radiculitis from shingles, chest wall pain after thoracotomy, and diabetic radiculopathy. Similar local injections are used in the treatment of occipital neuralgia.
The infusion of lidocaine has a brief beneficial effect on many types of pain, including neuropathic varieties, localized headaches, and facial pain, and it is said to be useful in predicting the response to longer-acting agents such as its oral analogue, mexiletine, although this relationship has been erratic in our experience (see Table 8-1). Mexiletine is given in an initial dose of 150 mg per day and slowly increased to a maximum of 300 mg three times daily; it should be used very cautiously in patients with heart block.
Finally, reducing sympathetic activity within somatic nerves by direct injection of the sympathetic ganglia in affected regions of the body (stellate ganglion for arm pain and lumbar ganglia for leg pain) has met with mixed success in neuropathic pain, including that of causalgia and reflex sympathetic dystrophy. A variant of this technique utilizes regional intravenous infusion of a sympathetic blocking drug (bretylium, guanethidine, reserpine) into a limb that is isolated from the systemic circulation by the use of a tourniquet. It is known as a “Bier block,” after the developer of regional anesthesia for single-limb surgery. The use of these techniques, and the intravenous infusion of the adrenergic blocker phentolamine, is predicated on the concept of “sympathetically sustained pain,” meaning pain that is mediated by the interaction of sympathetic and pain nerve fibers (“false synapse” or “ephapsis”) or by the sprouting of adrenergic axons in partially damaged nerves. This form of treatment is still under study, but the most consistent responses to sympathetic blockade are obtained in cases of true causalgia that results from partial nerve injury and in reflex sympathetic dystrophy. These pain syndromes have been referred to by a number of different names, most recently as the “complex regional pain syndrome,” but all refer to the same constellation of burning and other regional pains that may or may not conform to a nerve or root distribution (see page 1438). A number of other treatments have proven successful in some patients with reflex sympathetic dystrophy, but the clinician should not be sanguine about their chances of success over the long run. Perhaps the most novel and promising of these has been the use of bisphosphonates (pamidronate, alendronate), which have been beneficial in painful disorders of bone, e.g., Paget disease and metastatic bone lesions. Another treatment of last resort is the epidural infusion of drugs such as ketamine; sometimes this has a lasting effect on causalgic pain.
The therapeutic approaches enumerated here are usually undertaken in sequence. They reflect the general ineffectiveness of currently available treatments and our uncertainty as to the mechanisms of neuropathic pain. There are occasional successes, most of them temporary. Further references can be found in the article by Katz.
Use of Ablative Surgery in the Control of Pain
It is the authors' considered opinion that a program of medical therapy should always precede ablative surgical measures. Only when a variety of analgesic medications (including opioids) combined with phenothiazines and anticonvulsants, and only when certain practical measures, such as regional analgesia or anesthesia, have completely failed should one turn to neurosurgical procedures. Also, one should be very cautious in suggesting a procedure of last resort for pain that has no established cause, as, for example, limb pain that has been incorrectly identified as causalgic because of a burning component of the pain but in which there has been no nerve injury.
The least destructive procedure consists of implantation of an electrical stimulator, usually adjacent to the posterior columns. This procedure, which enjoyed a brief period of popularity, affords only incomplete relief and is difficult to maintain in place; it is now little used. The use of nerve section and dorsal rhizotomy as definitive measures for the relief of regional pain has already been discussed, under “Treatment of Intractable Pain,” above.
Spinothalamic tractotomy, in which the anterior half of the spinal cord on one side is sectioned at an upper thoracic level, effectively relieves pain in the opposite leg and lower trunk. This may be done as an open operation or as a transcutaneous procedure in which a radiofrequency lesion is produced by an electrode. The analgesia and thermoanesthesia may last a year or longer, after which the level of analgesia tends to descend and the pain to return. Bilateral cordotomy is also feasible, but with greater risk of loss of sphincteric control and, at higher levels, of respiratory paralysis. Motor power is nearly always spared because of the position of the corticospinal tract in the posterior part of the lateral funiculus.
Pain in the arm, shoulder, and neck is more difficult to relieve surgically. High cervical transcutaneous cordotomy has been used successfully, with achievement of analgesia up to the chin. Commissural myelotomy by longitudinal incision of the anterior or posterior commissure of the spinal cord over many segments has also been performed, with variable success. Lateral medullary tractotomy is another possibility but must be carried almost to the midline to relieve cervical pain. The risks of this latter procedure and also of lateral mesencephalic tractotomy (which may actually produce pain) are so great that neurosurgeons have to all intents abandoned these operations.
Stereotactic surgery on the thalamus for one-sided chronic pain is still used in a few clinics, and the results have been instructive. Lesions placed in the ventroposterior nucleus are said to diminish pain and thermal sensation over the contralateral side of the body while leaving the patient with all the misery or affect of pain; lesions in the intralaminar or parafascicular-centromedian nuclei relieve the painful state without altering sensation (Mark). Since these procedures have not yielded predictable benefits to the patient, they are now seldom practiced. The same unpredictability pertains to cortical ablations. Patients in whom a severe depression of mood is associated with a chronic pain syndrome have been subjected to bilateral stereotactic cingulotomy or the equivalent, subcaudate tractotomy. A considerable degree of success has been claimed for these operations, but the results are difficult to evaluate. Orbitofrontal leukotomy has been virtually discarded because of the personality change that it produces (see Chap. 22).
Unconventional Methods for the Treatment of Pain
Included under this heading are certain techniques such as biofeedback, meditation, imagery, acupuncture, some forms of spinal manipulation, as well as transcutaneous electrical stimulation. Each of these may be of value in the context of a comprehensive pain management program, conducted usually in a pain clinic, as a means of providing relief from pain and suffering, reducing anxiety, and diverting the patient's attention, even if only temporarily, from the painful body part. Attempts to quantify the benefits of these techniques—judged usually by a reduction of drug dosage in response to a particular form of treatment—have given mixed results. Nevertheless, it is unwise for physicians to dismiss these methods out of hand, since well-motivated and apparently well-balanced persons have reported subjective improvement with one or another of these methods and, in the final analysis, this is what really matters. Conventional psychotherapy in combination with the use of medication and, at times, of electroconvulsive therapy can be of great benefit in the treatment of associated depressive symptoms, as discussed above