Pain management in the patient with prostate cancer

1131

Pain Management in the Patient with Prostate Cancer Richard Payne, M.D.

Prostate cancer is common and often is associated with pain. Currently, neoplasms of the prostate include 23% of all new cases of cancer in men, and these are second only to lung cancer as the cause of cancer death in men.' Black men have the highest incidence of prostate cancer in the world, estimated to be 123.4 per 100,000 (compared with 87.7 per 100,000 in white men),2 and prostate cancer may have caused more deaths than even lung cancer in black men in 1991 in the United state^.^

Estimates from surveys of cancer centers and oncology practices suggest that the prevalence of pain in patients with prostate cancer ranges from 55-100% (mean, 72Y0).~ Pain in prostate cancer may be caused by many factors (Table 1). In a busy oncologic practice, the management of pain complicating prostate cancer is a daily concern and usually revolves around the management of metastatic bone pain. Several recent reviews have emphasized new antitumor and analgesic treatments for the management of bone pain in cancer, and these will be discussed. In addition, the known patho- physiologic mechanisms of pain in prostate cancer and the assessment of pain complaints in the patient with prostate cancer will be reviewed.

Pain Syndromes in Prostate Cancer

Tumors of the prostate gland may produce: (1) local rectal, urethral, suprapubic, and penile pain as a result of expansion and inflammation of the prostate gland itself; (2) pain referred to the back, lower extremities, and abdominal area resulting from tumor growth lo- cally within the pelvis; and (3) distant bone pain with associated neurologic dysfunction associated with long bone, vertebral, and skull metastases. The urethral and

Presented at the American Cancer Society National Conference on Prostate Cancer, San Francisco, California, February 13-15,1992.

From the University of Cincinnati College of Medicine and the Pain Service, VA Medical Center, Cincinnati, Ohio.

Address for reprints: Richard Payne, M.D., Neurology Service, VA Medical Center, 3200 Vine Street, Cincinnati, OH 45220.

Accepted for publication August 6 , 1992.

suprapubic pain produced by lesions in the gland itself is seldom an important clinical problem and will not be discussed further.

The causes of pain with local pelvic extension of the tumor or distant bone metastases usually are obvious, and appropriate first-line treatment of the pain always requires treatment of the tumor. Usually, radiation therapy plays an important role. External beam radiation therapy for local bone and metastasis is effective in approximately 80% of patient^.^ Although the fraction- ation protocols vary, current studies support the use of a single fraction of 8 G Y , ~ except when irradiating the vertebral column. However, this is controversial and seldom is used in the United States. This dose of radiation is likely to be toxic to the spinal cord, especially if r e ~ e a t e d . ~ Although single-fraction radiation may re- duce the discomfort, distress, and inconvenience associated with palliative radiation therapy, most current regimens are still given in 2-15 fractions with overall response rates for pain relief ranging from 48-100%. However, pain relief after radiation therapy usually is transient, and after these patients have received their tissue-tolerance doses of radiation, no additional treatment can be given. Furthermore, details of the degree and duration of pain relief, the field size and treatment regimens, and information relating to the concomitant use of analgesics seldom were reported in these clinical studies on the beneficial effects of radiation therapy on bone pain. The few published prospective studies suggest that there is a dose-response relationship between the radiation therapy dose and the relief of bone pain, beginning at 4 G Y . ~

Hormonal therapies, such as diethylstilbestrol or orchiectomy, have been the mainstay of treatment of metastatic prostate cancer for many years. Either treatment is associated with a median survival of approximately 3 years. More recently, the luteinizing hormone- releasing hormone agonist, leuprolide, has been shown to be at least as effective as orchiectomy and diethylstilbestrol treatment. Drawbacks to leuprolide treatment include its expense and the flare response, in which there is a temporary increase in bone pain and urinary

1132 CANCER Supplement February 1, 1993, Volume 71, No. 3

Table 1. Causes of Pain in Prostate Cancer Causes of uain Examples/clinical syndromes

Bone metastasis Single metastasis of pelvis or long bone Vertebral body metastasis, spinal cord

Base-of-skull metastasis, cranial nerve

Perineal pain syndromes Soft tissue metastasis Lurnbosacral plexopathy

Pelvic tension "rnyalgia" Pelvic visceral uain "Prostatitis" uain

compresssion

palsies

outlet obstruction associated with initiation of therapy.' This can be minimized or negated completely by ad- ministering flutamide. However, as is the case for many antitumor therapies that relieve pain as a result of their tumoricidal effects, the quality, duration, and degree of pain relief is not well characterized in any of the published studies.

Other pharmacologic agents used to treat metastatic prostatic tumor in bone, such as radionuclide pharmaceuticals, calcitonin, and bisphosphonate compounds, will be discussed in the following sections that discuss bone pain.

Bone Pain in Prostate Cancer

Approximately 40% of patients with prostate cancer have Stage D disease when seen initially, and most of these have bone metastasis. In general, the mechanisms by which tumor cells travel from their primary site and implant in the bone are not simple and involve at least seven steps.5 Most of the bone metastases that occur in prostate cancer involve the pelvis and vertebral spine. The high incidence of vertebral body metastasis in prostate cancer has been related to dissemination of the tumor cells through the Batson plexus, a valveless system of pelvic veins that communicates with the vertebral venous system and (eventually) with the great veins of the head and neck.' This hypothesis was supported by experimental work that demonstrated reversal of flow from the pelvic veins into the vertebral veins with abdominal pressure' and the superposition of vertebral metastasis with the anatomy and architecture of vertebral veins in the Batson plexus." However, the prostate gland contains abundant lymphatic drainage," and lymphatic spread of this tumor into surrounding soft tissue also is common and can be an important cause of intractable pain. Furthermore, the distribution of prostatic metastases also correlates with the arterial distribution of tumor emboli." Taken together, these observations suggest multiple modes of tumor dissemination to bone in prostate cancer.13

The pathophysiology of metastatic bone pain is un- derstood poorly. Although most patients with bone metastases report pain, there are some with well-established lesions who do not, and there are occasional patients who report bone pain at a time when radio- graphic lesions are not evident. This has been studied best in breast cancer,14 but it also occurs in prostate cancer. Tumor growth in bone may produce pain by several mechanisms, including the following. First, there may be relatively rapid growth, causing expansion of the marrow space and increased interosseal pressure (> 50 mmHg). This may activate mechanore- ceptive nociceptors in the bone. In addition, elevation or invasion of the periosteum also may activate the nociceptors that innervate this structure. Second, the associated weakening of the bone may cause fractures. Third, the edema and inflammation associated with tumor growth in the bone may liberate chemical media- tors that activate nociceptors. Finally, recent data regarding the mechanisms of bone destruction emphasize that osteoclasts may be stimulated by various humoral factors associated with tumors. For example, carci- nomas may secrete prostaglandin^,'^ which would play a dual role of activating osteoclasts and sensitizing nociceptors.I6 These observations have provided a ratio- nale for the use of corticosteroids and nonsteroidal antiinflammatory analgesics, such as naproxen, for the management of metastatic bone pain.17 Lymphomas and myelomas may secrete another chemical, osteoclast-activating factor. However, the effects of this substance on bone nociceptors are not known.

Metastatic bone pain often is associated with neurologic dysfunction because of the close anatomic rela- tionships between the brain and cranial nerves with the skull vault and the spinal cord with the vertebral column. Therefore, characteristic clinical syndromes may be identified by the site of bony involvement, the coex- istence of mechanical instability secondary to fractures, and the neurologic dysfunction caused by tumor infil- tration of contiguous neurologic structures. Bone metastasis to the hip and pelvis often produce local pain that is exacerbated by movement, especially during weight bearing. In addition to palliative radiation therapy, this type of "incident pain" may require specific orthopedic interventions, such as pinning and other mechanisms of mechanical stabilization of the bone for satisfactory control of pain. True incident pain is no- toriously difficult to manage with conventional analgesic therapy alone. Unilateral incident pain at or below the waist, which has not responded to management with hormonal and radiation therapy in addition to analgesic therapy, may require cordotomy as the ultimate means of treatment."

Pain Management/Payrre 1133

The spread of prostate cancer to the vertebral bodies and calvarium, especially the skull base, often produces distinctive neurologic syndromes. These are important to recognize early because prompt initiation of antitumor treatments (especially radiation) may avoid neurologic impairment. For example, local and radicular back or neck pain is the predominant symptom in epidural spinal cord compression complicating vertebral body metastasis in these locations." Pain may be the only symptom of impending spinal cord compression and often precedes motor weakness and bowel or bladder incontinence by days or weeks. The spinal cord is compromised by the growth of the tumor in an anterior direction from the vertebral body. Irreversible spinal cord injury may occur when the vascular supply is compromised as a result of severe compression. Tho- racic spine vertebral body metastases often produce bilateral radicular pain and sensory symptoms (a "band- like" squeezing sensation across the upper abdomen or chest) because of the close proximity of the thoracic nerve roots to the vertebral body. However, metastases to the cervical or lumbar spine may produce unilateral pain and sensory loss because the vertebral bodies are wider in these areas, and lateral extension of the tumor may compress only one root a t a time.

The onset of back pain in association with band- like tightening across the chest or upper abdominal or radicular arm or leg pain may be the first sign of impending spinal cord compression. Motor and sensory loss occurs later, and autonomic disturbances producing bladder and bowel incontinence occur later still. Thus, the evaluation of the patient should begin at the onset of pain for the best chance to preserve motor and sphincteric function. This should include plain radiographs of the entire spine, which are focused on the symptomatic area, and magnetic resonance imaging (MRI) or computed tomographic (CT) myelography methods to image the entire spine. This is necessary because there is an approximately 15% incidence rate of another (clinically silent) epidural lesion.'' Corticoste- roid therapy should be started even before the radio- logic evaluation because this may decrease pain and protect the spinal cord from additional compression caused by edema from the tumor or radiation therapy. Even if metastatic disease is found using plain spinal radiographs, MRI or CT myelography should be done to define the extent of tumor invasion in the epidural space because this will influence the size of the radiation therapy ports and determine the dose and duration of corticosteroid therapy. If anterior vertebral body subluxation has occurred and there is bony compression of the spinal cord, surgical decompression is indicated if the patient's medical condition permits it. This

usually is followed by radiation therapy. Surgery usually is not attempted as primary treatment because the results of radiation therapy and corticosteroid treatment usually equal surgical decompression." This is especially true if a simple posterior decompressive lami- nectomy is done. However, if patients have recurrent spinal cord compression in a previously irradiated port, then an anterior spinal approach with the removal of tumor from the vertebral body, decompression of the tumor from the spinal canal, and restructuring of the vertebral body with methymethacrylate should be considered.*'

Local invasion of tumor from the pelvis into the sacrum may produce the syndrome of perineal pain, which often is difficult to manage. This syndrome is characterized by local pain in the buttocks and perirec- tal area, which often is accentuated by pressure on the perineal region, such as that caused by sitting or lying prone. In its most extreme form, the patient cannot sit to eat his meals or lie flat to sleep. He may spend much of his time standing. Because of the critical role of para- sympathetic sacral innervation to normal bladder and rectal sphincter function, continence is impaired early in the course of this syndrome (in distinction to spinal cord compression with more rostrally placed lesions), perhaps even before significant weakness can be dis- cerned in the legs.

The spread of a prostatic tumor to the calvarium may produce neurologic symptoms by two mechanisms. Metastases to the skull vault, which grow and compress the sagittal sinus, may produce a syndrome of severe headache with associated papilledema and sei- zures caused by elevation in the intracranial pressure. If untreated, focal neurologic deficits may occur secondary to (hemorrhagic) venous infarction of the brain. The cause of metastatic sagittal sinus occlusion usually is obvious and can be confirmed easily by MRI of the brain. A gadolinium-enhanced scan will show, not only the tumor metastasis, but also the blood clot in the sagittal sinus. Nonmetastatic sagittal sinus occlusion also may occur in prostate cancer as a complication of a hy- percoagulable state induced by diethylstilbestrol treatment.

Tumor metastasis to the base of the skull may produce distinct neurologic syndromes.21 Bone metastasis to this portion of the skull often produces severe headache referred to the top of the head or the occiput. Also, single or multiple cranial nerve palsies usually accom- pany basal skull metastasis. For example, clival metastases often compress the hypoglossal nerve, producing unilateral weakness of the tongue and deviation of the tongue to the side of the lesion when protruded from the mouth. Bone metastasis to the middle cranial fossa


may compress and infiltrate the facial nerve, producing ipsilateral weakness of the upper and lower face. Tu- mor invasion of the jugular foramen will produce severe headache with associated dysphagia, dysphonia, and hoarseness caused by dysfunction of the glosso- pharyngeal and vagal nerves that exit the skull base through this foramen.

Small lesions at the skull base may not be seen by plain films or bone scans of the skull. It is mandatory that CT scans with bone windows and 5-mm sections (so-called thin cuts) be done to show the tumor. It is sometimes necessary to do MRI scans of the base of the skull when CT scans are negative.” Radiation therapy directed to the base of the skull is the preferred treatment. Again, prompt recognition of these syndromes and aggressive treatment is indicated to prevent irreversible cranial nerve palsies, which often produce de- vastating neurologic impairments.

Other Pain Syndromes in Prostate Cancer

Local spread of the tumor from the prostatic gland into other pelvic and abdominal structures often is associated with pain of visceral and neuropathic origin. Un- like bone pain, which is well localized and likely to respond (at least transiently) to conventional radiation therapy and analgesic treatments, the response of visceral and neuropathic pain to these first-line treatments is less predictable. Obstruction of hollow abdominal vis- cera, such as the large or small bowel, usually produces diffuse abdominal pain of a colicky nature. Metastasis to the liver, especially when associated with stretching of the liver capsule, may produce right upper quadrant abdominal pain in addition to pain that is referred to the right shoulder. Pain emanating from the visceral structures usually is localized poorly and referred to cutaneous structure^.'^ The physiologic explanation for this relates to the convergence of cutaneous and visceral nociceptive inputs into common pools of spinal cord neurons involved in the central nervous system’s en- coding of pain.

Pain of neural origin also accompanies invasion of the soft tissues contiguous to the prostate gland, especially the psoas muscle in which the lumbosacral plexus is embedded. Compression and invasion of the large peripheral nerve trunks that make up the lumbosacral plexus causes pain in the parasacral area of the lower back with radiating pain into the anterior thigh (and upper lumbar trunk involvement) or into the posterola- teral leg and buttocks (with lower lumbar and sacral trunk inv~lvement).’~ This pain often is described as burning in quality, and there may be superimposed par- oxysms of shooting pain that have an electrical quality.

The burning pain and lancinations often are perceived in an area of numbness or sensory loss.

Metastatic lumbosacral plexopathy may produce unilateral or bilateral pain. If the tumor grows to invade the sacrum or lumbar vertebral bodies or there are growths from the paraspinal space through the inter- vertebral foramina, cauda equina or spinal cord compression also may occur.

The lumbosacral plexus may be injured by radiation therapy delivered to the pelvis for the treatment of prostate cancer. Clinically, radiation-induced lumbosacral plexopathy may be difficult to distinguish from tumor-related plexopathy, although the pain usually is less severe in the former and electromyographic analy- sis of neuromuscular function may show characteristic changes such as myokymia with radiation injury.25 Ra- diation injury to the lumbosacral plexus, like metastatic plexopathy, may produce irreversible neurologic injury causing bilateral leg weakness, bowel and bladder dis- turbance, and rarely, impotence.

Although neuropathic pain responds to opioids, the doses required generally are higher than those needed to manage pain of somatic (i.e., bony) or visceral originz6 Furthermore, adjuvant analgesic drugs, such as tricyclic antidepressants, corticosteroids, carba- mazepine, clonidine, and mexiletine, may suppress burning and lancinating neuropathic pain in affected men more effectively than ~pio ids . ’~

Management of Pain in the Patient With Prostate Cancer

General Principles

Recently, guidelines have been written describing the approach to the pain management in the patient with cancer.” These guidelines emphasize the need to evaluate the extent of disease and use the appropriate antitumor therapies to treat the cancer whenever possible. The treatment of pain may be necessary to obtain appropriate diagnostic studies to define the extent of disease or to allow the patient to complete radiation therapy or other cancer treatments. For example, adequate titration of analgesics often is necessary to provide enough comfort for the patient to lie quietly so that CT or MRI imaging may be completed to evaluate spinal cord compression or lumbosacral plexopathy. Guide- lines established by the World Health Organization suggest titrating the analgesic therapy using a three- step ladder approach. This approach emphasizes the titration of analgesic therapy along a continuum from mild pain, in which nonsteroidal antiinflammatory analgesics and analgesic adjuvants are used, to moderate and severe pain, in which opioid drugs are added.”

Pain ManagementlPayne 1135

General guidelines regarding the appropriate use of opioid drugs for acute and chronic cancer pain also were published recently. These guidelines emphasize a basic knowledge of the clinical pharmacology of opioid analgesics, including the concepts of relative potency and dose titration to effect. Knowledge of these concepts will allow the selection of appropriate starting doses of opioids and provide a means for titrating these drugs. If unacceptable side effects intervene before pain relief is obtained (despite the use of adjuvant drugs to augment analgesia or to counteract side effects), then another opioid drug should be used, another route of administration, or an alternative surgical or anesthetic approach should be considered. Furthermore, it is clear that chronic opioid administration may produce physical dependence and tolerance, although the need to increase opioid doses in a given patient usually is caused by increasing pain associated with progressive disease rather than tolerance caused by a change in opioid re- ceptor responsiveness. l8 Physical dependence and tolerance must be distinguished from psychologic dependence (usually called "addiction"), in which drug-crav- ing behaviors dominate the patient's life, and opioids are taken not primarily for pain relief but rather to prevent the unpleasant effects of withdrawal or to produce other psychotomimetic effects. Since the occurrence of psychologic dependence is rare in patients with cancer who have not had a substance-abuse disorder before the diagnosis of cancer, the fear of iatrogenic addiction should never be used as an excuse to withhold opioids for the treatment of pain.

Antitumor Treatments

The role of radiation and hormonal therapies in the management of bone pain in prostate cancer has been discussed. Recently, interest has focused on the role of intravenous administration of radiopharmaceuticals, such as phosphorus-32, ytterium-90, and strontium-89 in the management of metastatic bone disease. Stron- tium-89 may have less myelotoxicity than the other compounds by virtue of its relative selectivity for bone, and overall response rates for pain relief are reported as high as 80% (mean, 68Y0).~ These agents are useful in treating pain in prostate cancer as a secondary effect to the lysis of tumor in the bone. However, they should not be considered substitutes for conventional radiation therapy in patients with vertebral body metastasis because their antitumor effects are seldom rapid or potent enough to prevent spinal cord compression.

Special Considerations in Bone Pain

Bone pain is a major problem in prostate cancer. Stan- dard approaches for the treatment of bone pain include

the use of nonsteroidal antiinflammatory drugs in com- bination with opioids. The former are said to be uniquely efficacious in bone pain.I7 There are data sug- gesting that, in lytic bone metastases such as those typi- cal of breast and lung cancer, nonsteroidal antiinflammatory drugs may decrease pain and aid in the inhibi- tion of bone destruction as a result of their ability to inhibit prostaglandin synthesis. Prostaglandins en- hance osteoclast function and activate and sensitize nociceptors. Several of the newer drugs, such as ketopro- fenz9 and ket~rolac,~' have analgesic potencies that are much greater than aspirin and approach that of 10-12 mg of intramuscular morphine. It These drugs appear to be as effective in the osteoblastic metastases occurring in prostate cancer as they are in osteolytic metastasis. Finally, even the most potent newer nonsteroidal antiinflammatory drugs should not be viewed as substitutes for morphine or other opioids in the management of severe pain because all drugs in this class have a ceiling to their analgesic efficacy.

Drugs in the bisphosphonate class are used to manage hypercalcemia associated with malignancy31 and may secondarily influence bone pain. Bisphosphonates, such as etidronate and pamidronate, have potent inhibi- tory effects on osteoclasts, thereby decreasing bone re- sorption. They are useful treatments for hypercalcemia and aid in bone remodeling in osteolytic metastasis. Al- though experience is limited, these agents do not appear to be as effective against the bone pain found in osteoblastic metastases from prostate cancer.32

Calcitonin also inhibits osteoclast function and is a treatment for hypercalcemia. It also has been observed that calcitonin has antinociceptive effects in the central nervous system,33 and limited clinical trials in humans found analgesia when calcitonin was given intraspin- ally. Currently, this should be considered experimental therapy for pain because it is not approved by the Food and Drug Administration for this indication, and the neurotoxicity of intrathecal calcitonin has not been studied fully. However, the use of these therapies for bone pain are attractive in patients who cannot obtain satisfactory relief from opioids because they provide a potential means to induce analgesia by nonopioid mechanisms. Therefore, they may be able to achieve pain relief in opioid-tolerant or opioid nonresponsive patients. More clinical trials are necessary.

Hypophysectomy has been used to manage general- ized bone pain that has not responded to hormonal and systemic analgesic therapies.34 The hypophysectomy is done by alcohol injection and may produce immediate pain relief in 35% of patients that, lasts as long as 20 weeks. Success rates of up to 90% also were reported by these authors. The use of levodopa as a predictor of response to hypophysectomy and as a treatment per se


for metastatic bone pain is controversial. Earlier reports noted a 33% response rate in metastatic bone pain from breast cancer,35 but a more recent study reported a response rate of only 7% (1 of 14) in patients treated with levodopa-carbidopa for bone m e t a ~ t a s i s . ~ ~

Titration of Therapies

A major challenge to the oncologist in managing the patient with intractable pain is the timing and selection of alternative therapies for pain management because such therapies often are more costly and invasive (thereby, posing more risks of morbidity to the patient) and often are not as convincingly efficacious as first- line treatments. It must be emphasized that standard analgesic therapies, such as oral morphine in combina- tion with nonsteroidal antiinflammatory and adjuvant drugs used in accordance with World Health Organiza- tion guidelines, almost always should be exhausted before alternative approaches are tried. In addition, the decision to initiate alternative analgesic therapies also suggests that no additional antitumor treatments will be effective for the management of the primary tumor. As stated before and repeated here for emphasis, treatment failure with conventional analgesic therapies suggests the titration of all drug therapies to their maxi- mum doses, such that the patient reaches dose-limiting side effects before adequate pain relief is achieved. For most patients with cancer pain, this also means that alternative routes of opioid administration, such as sub- cutaneous or intravenous infusion, transdermal administration of fentanyl, and patient-controlled administration, have been tried and failed.

When this occurs and the patient has bilateral or midline pain below the level of the midthorax, the administration of opioids and/or a dilute local anesthetic solution into the lumbar epidural or subarachnoid space should be attempted.37 However, the pharmacoki- netics of spinally administered morphine are such that supraspinal effects, such as sedation and nausea/ vomiting, might not be avoidable. A recent study showed that it was not possible to distinguish epidural morphine from systemic morphine in terms of its effects on cognitive function.38 Therefore, spinal morphine administration should not be considered first-line therapy for most patients with intractable cancer pain.

For patients with midline sacral or perineal pain who have not responded to systemic and spinal opioids, cordotomy may be an alternative. This can be accomplished safely by an experienced neurosurgeon using a percutaneous approach to cut the spinothalamic tract in the cervical cord." Most patients obtain immediate pain relief, and up to 60% maintain such relief for 6 months. Transient urinary retention and ipsilateral paralysis are the most common side effects. Less than 1%

of patients have uncomfortable postcordotomy paresthesia, generally occurring more than 18 months after the procedure. Percutaneous cordotomy should be considered early in the disease course for a patient with incident pain because the rapid increase in pain with movement usually does not allow adequate treatment with opioids, even when patient-controlled analgesia is attempted. However, new pain sites are unmasked in many patients after a unilateral c ~ r d o t o m y , ~ ~ and bilateral procedures are required for the management of midline or bilateral pain.

Patients with perineal pain who have not responded to cordotomy or are not candidates for cordotomy may obtain pain relief with neurolytic ablation of the cauda equina. This usually is done by injecting a hyperbaric solution of phenol into the lumbar subarachnoid or epidural space. The patient is monitored care- fully, particularly for the appearance of paresthesia in the soles of the feet ('31 dermatome), because this may herald the destruction of sacral roots important for the maintenance of bowel and bladder continence. Patients must be informed about the potential risk of incontinence, and some patients do not consent to the procedure despite their significant pain when so informed. However, if the patient is paralyzed already and has lost bowel and bladder function because of cauda equina or bilateral lumbosacral plexus lesions, then the potential benefits of this procedure may outweigh any other remaining risks.

Interface of Pain Management and Quality-of- Life Considerations

It is intuitive that pain degrades the quality of life, and the assessment of suffering and quality of life are important considerations in the comprehensive management of the patient with cancer and pain.4o In the patient with prostate cancer, pain not only impairs function by impeding mobility, but it often is an accom- paniment of neurologic impairments, including cranial nerve deficits, paralysis, incontinence of bowel and bladder, and impotence. These impairments may result directly from the prostatic tumor destroying peripheral nerves and the spinal cord or indirectly from radiation or surgical treatments.

Furthermore, the treatment of pain itself, may produce additional insults to normal neurologic function. Potential treatments for intractable perineal pain and incident pain include neurolytic anesthetic procedures and cordotomy. However, although they may be effective in relieving pain, potential complications of these procedures also include paralysis, bladder and bowel incontinence, and loss of sexual function. When informed of these potential complications, some patients elect suboptimal pain control. This is an even more im-

Pain Management/Payne

portant consideration in patients with prostate cancer because many live for several years (rather than months). The tumor may produce significant pain by local spread long before there is compromise of any vital organ function.

It is important to assess the effects of pain on the quality of life in multidimensional terms, and the devel- opment of valid and reliable measurement instruments for this purpose is an area of current intense re~earch.~' Of course, the loss of function, the fear of death, and the multitude of other psychosocial ramifications of cancer and pain are intertwined. The term "suffering" has been used in this context to describe the overall negative impact of cancer on the life of the patient,42 and while it must be recognized that pain is only one aspect of suffering, it is often a major one. Comprehen- sive management of the patient with cancer and pain requires that all factors associated with the quality of life of the patient as a whole be considered. If they are not, the optimal treatment of pain cannot be accomplished.

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Pain management in the patient with prostate cancer

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