An 82-year-old woman presented with low back pain for many years that had started insidiously and had lead to increasing functional limitations. She reported 7–8/10 sharp/burning daily pain that she experienced bilaterally, below the waist, and was worsened by standing, lifting, walking, and bending. There were no red flags. She had undergone numerous treatments without benefit including acupuncture, chiropractic, traction, physical therapy, aqua therapy, multiple epidural corticosteroid injections, and inpatient pain rehabilitation. She took prn naproxen for pain relief. Musculoskeletal examination revealed mild kyphoscoliosis, tenderness to palpation of both sacroiliac regions, and bilateral piriformis taut bands and trigger points. Neurological examination revealed symmetrical reflexes, 5/5 strength throughout, shortened stride length, and an anxious affect. The initial working diagnoses were (1) sacroiliac joint syndrome, (2) myofascial pain, and (3) anxiety for which physical therapy, sacroiliac joint injections, and gabapentin were prescribed.

One month later, she had experienced no pain reduction or functional improvement. A more detailed history uncovered the development over the past year of change in her voice (softening), handwriting (smaller), posture (increased forward flexion), and facial expression (less animated). A more detailed physical examination uncovered mild cogwheeling of her right arm. A neurology consultation was obtained to address the possibility of Parkinson’s disease. The consultant felt that there were “no full-blown Parkinsonian signs or symptoms,” but the presence of her masked facies, diminished blink, minimal asymmetrical cogwheeling, Myerson’s sign, and tendency to retropulse prompted a trial of levodopa/carbidopa 25/100 bid.

One month later, the patient reported average 4/10 pain (∼50 % reduction from baseline), improved posture, and balance as well as walking capacity and flexibility.

Discussion: The synthesis of this case is presented in Fig. 19.1. The treatment targets for this patient were her Parkinson’s disease and her myofascial pain. Her pain signature was comprised primarily of decreased physical function. Her impaired gait was also the primary comorbidity of concern. This placed her at heightened risk of falls. Had opioids been prescribed, the practitioner would have had to be especially vigilant for worsening mobility. Prior to prescribing such medications, the patient would have had to be educated about the risk of falls and hip fracture.

This case highlights the fact that PD is not infrequently associated with pain. Forty to fifty percent of patients with PD have pain that is not explained by other obviously painful disorders [80, 81]. Fifteen percent have pain as their presenting symptom (e.g., unilateral shoulder pain) [82]. Twenty-five percent have pain that precedes motor symptoms [83]. Patients may report muscle cramps or tightness, typically in the neck, paraspinal, or calf muscles; painful dystonias; joint pain; neuropathic pain; or less commonly, generalized pain [84]. Oral and genital pain syndromes that are similar to symptoms occurring in patients with tardive dystonia and akathisia from neuroleptics also have been described in patients with PD [85, 86]. The underlying pathogenesis of pain in PD can be central, peripheral, or mixed. Sensory thresholds to experimentally delivered painful stimuli are reduced in PD [87]. Unlike peripherally generated pain, such as that experienced by our patient, central PD pain that is associated with abnormal nociceptive input processing is not affected by dopamine administration [88].

Perhaps most importantly, this case illustrates that successful treatment of the older adult with low back pain requires identifying the proper treatment targets (Parkinson’s disease [PD]) rather than simply treating the weak link (axial spondylosis). Had this patient elected to go forward with spinal surgery, the likely outcome, as compared with the actual outcome, is depicted in Fig. 19.2. In this figure, the “existing approach” represents common practice and the “proposed approach” is what we recommend.

An 82-year-old woman presented with low back pain and right leg pain for two years with documented central canal stenosis on MRI. She had worked full time in a dress shop and was forced to retire 2 years ago because the company was downsizing. She said that her pain started at that time and had gotten progressively more severe. Her pain was made worse by prolonged standing or walking, and she was having increasing difficulty performing heavy housework. Her pain was made better with rest and heat application. She denied fever, chills, weight loss, and change in her bowels or bladder function. She reported poor balance and multiple near falls at home. She lived alone. She was becoming increasingly fearful of leaving her home. Medications at the time of presentation, all of which had been prescribed to treat her pain and pain-associated anxiety, included gabapentin, oxycodone CR, celecoxib, tramadol/acetaminophen, olanzapine, escitalopram, and lorazepam. Physical examination revealed poor balance, dementia (memory problems and very impaired clock-drawing test) [89], kyphoscoliosis, and tenderness of the right sacroiliac joint/lumbar paraspinal musculature/tensor fasciae latae/iliotibial band. Because of extreme guarding behavior, strength testing was invalid.

Because of polypharmacy, high falls risk, and social isolation, the patient was admitted to a nursing home for detoxification. All of her medications were discontinued with the exception of regularly scheduled acetaminophen and prn tramadol. She reported minimal pain and her balance improved markedly. It was recommended that her family strongly consider placing her in an assisted living facility. They chose to seek other opinions from pain practitioners. Immediately following discharge, the patient’s pain complaints escalated and multiple other pain regimens were attempted including a morphine pump trial, all of which failed. She was eventually placed in an assisted living facility where she did well.

Discussion: The synthesis of this case is presented in Fig. 19.3. As noted earlier in this chapter, to prescribe effective treatment, the practitioner must differentiate the weak link from the treatment target(s). In this case, chronic pain was the weak link and fear/social isolation the treatment targets. Her pain signature consisted of pain perseveration and significant utilization of health care resources. The main potentially treatment-limiting comorbidities were her dementia and balance frailty.

One of the first discussions that we have with patients in chronic pain revolves around treatment expectations. Specifically, patients with chronic pain need to understand that it is realistic to expect partial but not complete pain relief. Treatment of the older adult with dementia is complicated by the fact that information provided in treatment counseling sessions may not be remembered and ongoing reinforcement may be necessary. Such reinforcement is often successful when the patient has an involved and supportive caregiver (and one who does not catastrophize about the patient’s pain) and health care providers who are willing to communicate a consistent message. In this patient’s case, inconsistent messages were delivered (i.e., although it was clear that the patient’s fear and social isolation in the setting of dementia were primarily responsible for her suffering, the patient’s family insisted that her pain was responsible and more aggressive pain treatment was sought).

While many patients with dementia can report pain reliably [90, 91], the meaning of these reports must be ascertained in order to prescribe effective treatment. Is the patient’s pain reporting a manifestation of perseveration (that occurs not uncommonly in patients with dementia)? Or, is the patient’s pain reporting a more general signal of distress? Or, is the patient’s pain reporting an indication of pain-related suffering? If there is pain-related suffering, then pain-specific treatment must be implemented. In the case of our patient, her pain reporting appeared to be a manifestation of both perseveration and a more general signal of distress (i.e., anxiety surrounding social isolation and dementia). Thus, while treatment did involve analgesics, providing a supportive environment was the primary therapeutic element.

This case highlights the need to screen for dementia at the time of the initial history and physical examination. One of the most efficient and effective screening tools is the Mini-Cog, described in Table 19.2 [92, 93]. It takes no more than 2–3 min to perform. If this testing uncovers the possibility of dementia, the patient should be referred to a geriatrician for further evaluation. Older adults with and without dementia often have mobility difficulty and a risk of falling; thus, a balance screen should also be included as part of the baseline assessment. A modified postural stress test [94] can readily be done in the office and is described in Table 19.2 and shown in Fig. 19.4. If this test reveals poor balance, a referral to physical therapy should precede any intervention that could further impair balance (e.g., opioid prescription).

An 85-year-old man with advanced Alzheimer’s disease presented, along with his wife of 60 years and their daughter, for treatment recommendations to address “persistent reporting of pain” in his lower back. His primary care provider was concerned because the patient’s pain ratings had not changed despite numerous analgesic prescriptions. Most recently, he had been prescribed fentanyl that had been titrated to a dosage of 100 mcg/72 h and resulted in hospitalization because the patient became semicomatose. When the dosage was decreased to 50 mcg/72 h, his mental status returned to baseline and he continued to report pain so a pain clinic consult was requested.

At the time of the evaluation, he was sitting in a wheelchair, appeared very comfortable, smiled throughout most of the interview, and had no pain complaints. His history was unreliable because of advanced dementia. His wife reported that the patient had low back pain for many years. She was asked, “Do you think your husband is suffering from his pain, or is he just talking about it?” Without hesitation, she replied, “Oh…he’s just talking about it.” Together, we decided that the most appropriate treatment would include tapering him off the fentanyl and have him participate in a local day care program for socialization and distraction. His family was educated about the fact that patients with chronic low back pain cannot be made pain-free and that the main goal of treatment is preservation and/or improvement in function to the extent possible. She understood and fully supported the plan.

Discussion: The synthesis of this case is presented in Fig. 19.5 and reinforces the complexities of pain evaluation and management in older adults with dementia. In this patient, chronic pain was the weak link and pain perseveration the treatment target. Pain perseveration was also the major component of his pain signature. The main potentially treatment-limiting comorbidity was his dementia (i.e., increased risk of falls and/or delirium with opioids). As opposed to the patient in Case 2 whose pain reporting reflected pain perseveration as a general signal of distress, this patient’s pain reporting was a simple representation of pain perseveration that was treated with distraction. Often, this type of perseveration behavior in older adults with dementia is more a problem for the caregiver (i.e., it is stressful to observe the perceived suffering of a loved one, contributing to caregiver burden) than for the patient, and treatment strategies should keep this in mind.

This case also highlights the importance of patient-centered or patient/caregiver-centered decision making. In busy office practices, it may be difficult to take the extra time required to engage in these discussions. Not doing so, however, may lead to unnecessary morbidity, as was the case with this patient.

A 67-year-old man presented with low back and left leg pain for 10 months. He had injured his back nearly 50 years earlier associated with heavy lifting. He was treated conservatively and his pain abated within 1–2 months. Ten months ago, he experienced the insidious onset of sharp/burning pain in his left lower back with occasional radiation to the left leg (lateral aspect) that was getting progressively more severe. He reported occasional weakness and numbness of the left leg and progressively more restricted walking tolerance. At the time of presentation, he ambulated with a walking stick and could go one-half block before he had to stop because of pain. He reported multiple falls because his leg “gave way.” His pain was worsened by lying prone and trying to straighten his leg while lying supine. It was made better by lying on his side and assuming a fetal position. He denied fever, chills, or change in his bowels/bladder.

A lumbar MRI performed 2 months following the onset of his pain revealed diffuse lumbar spondylosis and moderate central canal stenosis. Treatment had included (1) physical therapy for lumbar spinal stenosis that resulted in no improvement in his pain or function; (2) tramadol that was ineffective; (3) gabapentin that caused nausea, vomiting, and a 15-lb weight loss; and (4) hydrocodone/acetaminophen that was associated with moderate pain relief. Spinal surgery was recommended, but he declined. His only significant medical comorbidity was hypertension.

Notable on physical examination was blood pressure 178/96, ¾ in. leg length discrepancy, mild scoliosis, mild left piriformis tenderness, and an antalgic gait with favoring of the left leg. His gait was slow but steady when performed with his walking stick. Examination of the left hip revealed <15° painful internal rotation. Right hip exam was normal. Neurological exam revealed symmetrical lower extremity reflexes and 5/5 strength throughout with the exception of the left hip flexors and left quadriceps that were 4/5. When the patient was lying supine and asked to raise his left leg, he did so by picking it up with his hands. Hip x-rays revealed marked joint space narrowing of the superior and inferior aspects on the left and no abnormalities on the right. Based on these findings, he was instructed to continue regularly scheduled hydrocodone/acetaminophen and he was referred to physical therapy specifically directed toward the left hip. If these strategies are ineffective, he will be referred for intra-articular hip injection. If he is refractory to all noninvasive and minimally invasive treatments, he will be referred for consideration of a total hip replacement.

Discussion: The synthesis of this case is shown in Fig. 19.6. The treatment target was his hip osteoarthritis. His pain signature consisted of severe self-reported pain and difficulty walking. His significant comorbidities included hypertension and difficulty walking/falls. Because his symptoms were initially attributed to the lumbar spine, he underwent an unnecessary lumbar MRI and was prescribed medications that resulted in significant adverse events, physical therapy that was ineffective, and a referral for spinal surgery that would likely not have relieved the “pain generator.”

This case is presented to highlight the important contribution of hip osteoarthritis to low back pain. The hip-spine syndrome was first described in 1983 and refers to symptoms that exist in the setting of concurrent degenerative pathology in the hip and spine [95]. Three types of hip-spine syndrome were postulated: (1) simple when history and physical examination clearly indicate whether the hip or the spine is the primary source of pain; (2) complex, when both the hip and the spine are responsible for pain; these cases are said to require ancillary investigations such as nerve root infiltration and intra-articular blocks of the hip joint to disentangle the primary source of pain; and (3) secondary, when altered hip function (e.g., flexion deformity with advanced OA) directly changes spinal biomechanics that cause low back pain. The contribution of hip OA to CLBP also is supported by more recent data. Specifically, total hip replacement surgery for patients with severe hip pain and advanced OA on x-ray reduces low back pain and improves overall spine function [96]. In patients with low back pain, diminished hip range of motion predicts poor outcomes following spinal manipulation [97] and after lumbar percutaneous electrical nerve stimulation (unpublished data). Preliminary data suggest that patients with self-reported hip OA respond less favorably to decompressive laminectomy for the treatment of lumbar spinal stenosis (LSS) than those without hip OA [98].

It is likely that many older adults have hip-spine syndrome that is both complex and secondary in which both the hip and spine are pain generators, but altered hip function causes abnormal spinal biomechanics and low back pain, that is, altered hip function adds insult to injury. Although severe hip flexion deformity may be absent, we hypothesize that underlying lumbar spondylosis makes the lower back vulnerable and, therefore, more modest alterations in hip function may be needed to cause low back pain. So, the lumbar spine is the weak link and the hip is the treatment target. Well-controlled studies are needed to test this hypothesis. Until definitive answers are available, practitioners must approach the older adult with low back and/or leg pain using a broad perspective to avoid unnecessary “diagnostics” and misguided/potentially harmful treatments. Table 19.3 highlights key history and physical examination differences between pain generated by lumbosacral degeneration and that associated with hip OA. It should be noted that hip x-rays alone cannot be used to make a diagnosis of clinically meaningful hip OA. Fewer than 50 % of patients with radiographic evidence of hip OA report pain [11]. A definitive diagnosis of hip OA should be based on a combination of clinical examination and x-ray findings [99, 100]. Thus, careful examination of the hip should be a routine part of evaluating all older adults who present with low back and/or leg pain.

Figure 19.7 depicts an integrative stepped-care approach for the treatment of nociceptive pain. Topical preparations, cognitive behavioral therapy, interdisciplinary pain treatment, and complementary and alternative modalities (CAM) may be used at any step, either alone or in combination. The individual steps shown in Fig. 19.7 are arranged from treatments associated with relatively low risk (step 1) to those associated with high risk (step 7).

At the foundation of treatment are education, weight loss, exercise, and other physical therapy approaches (including assistive devices). Sometimes, these approaches are alone sufficient to accomplish desired outcomes. For the older adult with fibromyalgia who is capable of participating in aerobic exercise, no further treatment may be needed. For the patient with kyphosis related to vertebral compression fractures and associated lumbar strain, a four-wheeled walker often is very effective for reducing pain and improving mobility. Education should be targeted at ensuring realistic treatment expectations (i.e., pain reduction but not elimination and improved function despite the persistence of pain) and quelling any pain-associated fears (e.g., becoming crippled and/or losing independence because of pain, having cancer associated with pain).

To avoid risks associated with systemic medication, injections should be considered for the older adult with pain in one or two joints, for example, knee osteoarthritis (OA). Trigger point injections can be an effective adjunct for treating myofascial pain syndromes [101]. There is no strong evidence to guide the prescription of spinal injections for older adults with chronic low back pain (CLBP). In general, injection therapies should be viewed as a tool to enhance compliance with rehabilitation efforts, which represent the mainstay of nociceptive pain treatment. For older adults with diabetes mellitus, patients should be instructed to monitor their blood sugar carefully following corticosteroid injections.

Systemic pharmacologic treatment of mild to moderate nociceptive pain should start with regularly scheduled acetaminophen because of its relatively safe side effect profile and few drug-drug or drug-disease interactions. Acetaminophen exerts its analgesic effect by weak, reversible, nonspecific cyclooxygenase inhibition, and, therefore, prostaglandin synthesis. It has no anti-inflammatory or antiplatelet effect and uncommonly causes gastrointestinal (GI) bleeding or nephrotoxicity [65]. An overdose of 10 g can cause liver failure and death. Hepatic injury can occur with lower doses when the patient drinks alcohol heavily or is taking hepatic enzyme inducing medications (e.g., rifampin, carbamazepine, phenytoin, phenobarbital). Preexisting liver disease, malnourishment, fasting, or dehydration can also increase the risk of liver injury. Table 19.4 provides dosing guidelines, pharmacokinetics, key drug-drug and drug-disease interactions, and important adverse effects associated with acetaminophen and other medications used for nociceptive pain. To avoid breakthrough pain, it is important to dose analgesics around the clock [102].