Christopher R. Showalter, Darren A. Rivett, Mark A. Jones Bob was a 52-year-old crop farmer. He was happily married and the father of two teenage children. Bob routinely worked 12- to 14-hour days on his 1800 acres, operating various pieces of equipment and machinery, which primarily involved prolonged sitting while operating the equipment. The sitting was interspersed with attaching and detaching heavy implements from the machines and occasional lifting of loads as heavy as 125 lb. His lifestyle was essentially sedentary for long hours, and he did not play any sports or perform any regular exercise. Bob was referred to our clinic at the insistence of his friend, a previous patient of the clinic, and began the first session by stating, ‘I’m here to see if anything can be done about my back problem’. He said he felt our consultation would ‘probably not help much’, as his regular chiropractor was unable to help with the pain. It was put to Bob that there was no harm in obtaining a second opinion, and he agreed to continue. He explained that he had been having low back pain (LBP) and some numbness in the right leg for 12 weeks. Bob described his pain as 6/10 (on a numerical pain rating scale) throughout the day on most days, which increased to 8/10 at night. His pain was worse in the morning (8–9/10). He reported ‘deep, sharp, biting’ pain and a ‘tight pulling’ in the right lower back and pointed to the area of L4–L5 on the right. He also reported numbness in the right anterior thigh and the lateral and posterior calf, as well as a feeling of weakness or ‘giving way’ in his right leg (Fig. 28.1). Bob generally retired to bed around 10.00 pm after taking 750 mg of acetaminophen (nonopioid analgesic), 15 mg of oxycodone (opioid analgesic) and 5 mg of prednisone (steroidal anti-inflammatory) that had been prescribed by his primary care physician 2 days earlier. He usually preferred to sleep on his back, but in recent months he had found he could only get comfortable lying on his left side. He usually awoke at approximately 2.00 am with 8/10 pain and took more acetaminophen and oxycodone. Bob reported he could not find a comfortable position in bed to get back to sleep, so he tried to sleep in a reclining chair to avoid waking his wife. He slept fitfully and finally awoke in the morning around 6.00 am with 8–9/10 pain and feeling stiff, like his ‘back is rusty’. He continued the drug regime three more times throughout the day, including before bed, as the pain became more intense. Bob was concerned with the amount and type of medications he felt he was ‘forced to take to remain working’. He was particularly concerned at the prospect of becoming addicted to oxycodone. Bob reported that his LBP was at its worst (8–9/10) in the morning upon waking. He reported that he was able to reduce the morning pain with a hot shower, medications and ‘getting moving’ soon afterward. The LBP varied throughout the day, although it was generally a 6/10, and became worse with prolonged postures of inactivity, including sitting in tractors or cultivator machinery for more than 30 minutes or standing for more than 15 minutes. Once elevated, the pain took approximately 1 hour to settle back to baseline levels, provided he discontinued static sitting and standing postures and ‘kept his back moving’ with slow gentle walking. Bob took his medications as prescribed but often self-prescribed an additional 750 mg of acetaminophen two to three times a day when his pain was elevated. He felt the need to keep moving and get his lower back ‘lubricated’ to feel better. As a consequence of his pain behavior, Bob had modified his workday schedule to involve sitting for no more than 30 minutes and standing for no more than 15 minutes. These activities were broken up with periods of slowly walking short distances, for approximately 2–3 minutes. This eased his pain to 4/10, but the relief was short-lived. This schedule was significantly affecting his productivity at work. Bob reported that the factors that aggravated his condition included sitting, bending backward and standing. His pain could occasionally be relieved by bending forward while sitting or walking for short periods. Although these movements might reduce his pain slightly, they provided only short-term relief. Bob had received chiropractic treatment monthly for approximately 18 years. He generally had visited the chiropractor once per month but sometimes more depending on how his back was feeling. The treatment had routinely comprised thrust manipulation to his lumbar, thoracic and cervical spinal areas. He had not been instructed in any post-treatment care or home exercise program. He felt that the chiropractor gave him some relief that lasted for 2–3 days, but he wondered why his back never seemed to get better to the point that he was pain-free. Bob stated that he had a ‘bad manipulation’ in the lumbar spine approximately 4 years ago, resulting in significant LBP and 2 weeks of total bed rest. He felt his back ‘has never felt the same since’. He changed chiropractors at that time and continued with monthly treatment. Twelve weeks prior, Bob started to experience increased intensity of LBP and the onset of numbness in his right leg. There was no event to precipitate these changes. Bob sought chiropractic treatment two to three times per week for 8 weeks with two different chiropractors. Bob had discontinued these chiropractic treatments for the 4 weeks prior to his consultation for physical therapy and had seen his primary care physician 2 days earlier because the pain had become ‘unbearable’ and the numbness seemed to be getting worse. The physician ordered medications and magnetic resonance imaging (MRI) of the lumbar spine. Bob took 20 mg of prednisone four times daily (QID), 750 mg of acetaminophen QID, and 15 mg of oxycodone QID for his LBP. Bob took no other medications and had no general health problems or red flags. He denied any symptoms of spinal cord compression or cauda equina syndromes. No prior imagery of the spine was available. An MRI scan had been ordered but not performed due to the cost involved. Bob completed a number of self-report forms, with the following results at baseline prior to treatment: Bob was examined in a pair of shorts. In standing with feet shoulder-width apart, decreased lumbar lordosis and bilateral paravertebral muscle wasting were observed. A slight shift to the left (contralateral to the right-sided pain) was observed in standing. Shoulder height, scapular position, arm position, gluteal folds, popliteal creases and Achilles tendon alignment were all within normal limits (WNL). The right upper limb showed slightly more muscle hypertrophy than the left (Bob was right-handed). Muscle development was WNL in both lower limbs. Resting pain prior to examination was 6/10. Testing was performed in supine without pillows. The left leg was WNL. On the affected (right) limb, deep tendon reflexes (DTRs) were 1+ at the patellar ligament (indicating potential L4 involvement) and WNL at the Achilles (S1). Sensation testing was performed with eyes closed, and the patient reported when he could feel sensation. Sensation loss was reported as a percentage of normal compared to the other limb. Light touch sensation was tested using cotton swabs, and deficits were found in the anterolateral thigh at 60% sensation, lateral tibia at 60% sensation and the lower calf displaying 80% sensation. These deficits in a dermatomal pattern were suggestive of involvement of the L4 and L5 nerve roots, respectively. Resisted movement was used to test motor function, and resisted knee extension was 4/5 implicating L3 and L4. No atrophy, increased resting tone, or pathological reflexes were observed in either limb, and Babinski signs and clonus were negative bilaterally, ruling out upper-motor-neuron involvement. The patient was properly instructed to immediately report any feelings, sensations, symptoms and, particularly, LBP that he experienced during any test movements. He was instructed to not proceed with any movement beyond the initial onset of his pain (P1). Resting pain was 6/10. Prior to testing active physiological movements, (R) glide correction of the (L) shift deformity was performed in standing. Glide correction involves gently gliding the shoulders to the right while pulling the pelvis to the left, while avoiding any lateral flexion, and evaluating symptom response. Glide correction in neutral flexion/extension immediately increased his LBP from a 6/10 to 7/10, and his lumbar paraspinal musculature began to spasm. Glide correction in slight extension immediately increased pain from 6/10 to 8/10, with increased spasm. Glide correction in slight lumbar flexion did not affect his pain levels or cause spasm, and he moved more freely and smoothly. The shift was slightly improved upon return to standing (Fig. 28.2).
Acute Exacerbation of Chronic Low Back Pain With Right-Leg Numbness in a Crop Farmer
Subjective Examination
Area, Nature and Type of Pain
Pain Behavior and Irritability
Aggravating and Easing Factors
Past and Present History
Medication and Special Questions
Imaging
Self-Report Questionnaires
Physical Examination
Observation
Neurological Examination
Active Physiological Movements
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Acute Exacerbation of Chronic Low Back Pain With Right-Leg Numbness in a Crop Farmer
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Fig. 28.1 Body chart depicting symptoms.
Fig. 28.2 Right side-glide correction of the left lateral shift deformity.
