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User:A E Francis/Cases

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Spinal stenosis edit

Case 1: Undiagnosed cervical stenosis edit

The patient was a 46-year-old man referred to physical therapy for the treatment of low back pain that was present for the previous 10 months. Neurologic findings were significant, with upper and lower extremity hyperreflexia bilaterally and positive Romberg, Lhermitte, and Hoffman signs. Due to the strong suspicion of spinal cord involvement, the physical therapist contacted the referring physician and recommended expedited cervical spine magnetic resonance imaging, which revealed severe central canal stenosis at C3-4 and C5-6, secondary to spondylotic changes, and altered spinal cord intensity consistent with myelomalacia (permanent damage to the cervical spinal cord). Despite a neurosurgeon's recommendations, the patient denied surgical intervention. It is recommended that physical therapists utilize screening questions regarding changes in sensation, strength, gait, and bowel and bladder function during the patient interview. A positive response to any of these questions should prompt the completion of a thorough neurological examination, including assessment and interpretation of pathological reflexes.[1]

Case 2: Athlete with stingers edit

An 18-year-old male high school student showed great promise to obtain a college scholarship because of his sporting ability. During his senior year, while playing linebacker for the school football team, he experienced a vicious hit to the head. He immediately noticed marked pain in his right arm, followed by numbness. He continued to play, but the pain became so great that he was pulled in the second half. After two weeks, his pain had subsided to the point he could again play. It did not recur. When he attended college the next year, the stingers returned and were worse. He was referred to a spinal surgeon who ordered an MRI of the cervical spine. He was noted to have a small canal between C4 and C7. It was recommended that he not pursue a career in football, and that he should not continue to play college ball.[2]

Case 3: Thoracic disc, college student edit

An 18-year-old male college student experienced the onset of paralysis while shooting pool in a local bar. He was 6 foot 3 inches tall and weighed 320 pounds. He was attending college on a football scholarship. The nurse-practitioner at the university was not sure what was wrong with him. He could not walk and was moved about in a wheelchair. He went back to his apartment where he stayed for three days. After that, he was referred to a neurosurgeon. An MRI showed a blockage of the mid-thoracic canal. The diagnosis was not obvious, but it appeared to possibly be a spinal tumor. He was taken to surgery where the spinal canal was opened and a large amount of swelling was found. Biopsy was sent for frozen section, which the pathologist reported was most likely a glioblastoma or astrocytoma. The wound was closed. Paralysis was complete below T6 by this time. The patient was referred to a cancer center. There, two weeks after the onset of paralysis, a second MRI was performed. Now the diagnosis of herniated thoracic disc was made. He was taken to surgery a second time where a disc was removed one level above the first surgery. The patient remained paralyzed below the level of T6 permanently.[3][4][5][6][7]

Case 4: Thoracic disc, lawyer edit

A 38 year old lawyer had been experiencing mid-thoracic pain and some numbness in the legs for several months. At first she thought it was due to stress and long hours. It became worse. Her family physician thought it might be due to diabetes mellitus, however work-up for this showed no such disease. She tried to ignore the problem. She was not obese, although she was about 20 pounds overweight. She decided her symptoms were due to this condition, so she joined a gym in an effort to lose weight. Her symptoms worsened. She awoke one morning completely numb in the legs. Her physician referred her to a spinal surgeon who diagnosed a herniated thoracic disc at T6 after an MRI of the thoracic spine. He recommended a discectomy with associated fusion. She decided to wait to see if her symptoms would get better, which they did. Two months later, during a jury trial, she experienced complete numbness in the legs, perineum and completely lost bladder function. At this time, she was rushed into surgery where the offending disc was removed and a fusion with metal rods was completed. She completely regained neurologic function within two weeks.[8][9][10][11][12]

Case 5: Stenosis in spondylolisthesis edit

A 47-year-old salesman drove a car for more than 200 miles a day in the course of making his sales calls. He began to notice a sensation that he thought was related to lack of blood in his legs around 10 AM several days a week. After six months of increasing symptoms, he was referred to a spinal surgeon who diagnosed a Grade II spondylolisthesis at L5 S1. His symptoms had reached the point that he could no longer work. He underwent a decompressive laminectomy, reduction of the spondylolisthesis with a fusion and metal fixation. After six months, he was able to resume his activities as a salesman. After two years, he was no longer able to take long car trips, and found a job in an office. He filed a worker’s compensation claim, and after a long litigation, his spondylolisthesis was adjudged to have been caused or aggravated by his employment. The insurance carrier argued that the condition of spinal stenosis and spondylolisthesis were preexisting conditions, hence not compensable. The judge determined the company must “take the claimant worker as he is found.”[13][14][15]

Case 6: Stenosis in ankylosing spondylitis edit

A 32-year-old teacher with ankylosing spondylitis developed intermittent pain and numbness in the legs after she delivered a child. At first, she ignored the problem, thinking it was a side effect of an epidural anesthetic administered during childbirth. The problem continued to worsen over the next year. A spinal surgeon examined her and found from the old medical records that she was positive for HLA-B27 antigen. During the previous year, she had a flare up of her condition with a sed rate of 80 mm/hour and an elevated C-reactive protein titer. Rheumatoid factor (RF) and anti-nuclear antibody (ANA) were negative. Blood sugar was normal, and there was no evidence of diabetes mellitus. She had been placed on anti tumor necrosis factor-alpha (anti-TNF-alpha) therapy of infliximab and etanercept about six months earlier, with a general decrease in symptoms. Recently, the problems with her legs had recurred. An x-ray of the pelvis demonstrated fused sacro-iliac joint (SI joints). Exam showed a diffuse patchy loss of sensation in the legs and perineum. There was not a radicular pattern in the loss. She kept rubbing her legs during the exam, stating there was not enough blood getting to them. Good peripheral pulses were noted with Doppler exam. MRI of the lumbar spine demonstrated marked stenosis of L2-3 and L5-S1. She underwent a successful decompressive laminectomy with resolution of her symptoms.[16][17][18][19][20][21][22]

Case 7: Depression edit

A 37-year-old male with a history of several major depressive episodes, requiring hospitalization for suicide attempts, had long standing complaints of back and leg pain. He had seen several spinal surgeons, who had diagnosed spinal stenosis, but none had recommended surgical intervention. He became obsessed that if he had surgery, he would become cured of his problems. Finally, a surgeon performed a decompressive laminectomy with fusion consisting of bone graft and metal implants. Instead of relieving his symptoms, the surgery did not help him and he only became worse. He experienced another major depressive disorder in the post operative course. His depression became all-consuming and he died from an overdose of narcotics six months after the surgery.[23]

Case 8: Multiple surgeries edit

A 34-year-old female was involved in a motor vehicle accident with resultant low back and leg pain. She was diagnosed with lumbar stenosis by MRI. After nine months of expectant therapy, she did not improve. She underwent a decompressive laminectomy with excellent results for about two years. After that, her symptoms of leg and back pain returned. At three years after her first surgery, she underwent a second surgery to remove the scar tissue that had formed over the previous laminectomy area, and fusion. The second surgery was complicated by an undetected tear of the dural. This required a third surgery to repair the leak. By the time she was dismissed from the hospital from the second and third surgeries, she was taking morphine sulfate 80 mg. per day. She had recurrence of her symptoms at one month post op and remained significantly impaired and unable to resume employment.[24][25][26]

Case 9: Stenosis and vascular disease edit

A 72-year-old man had noticed he was unable to play nine holes of golf without developing severe pain in the legs. After about a year, he was unable to play, even if he rode in a golf cart. On exam, he was noted to have markedly advanced atherosclerotic vascular disease in his legs as well as a severe L4-5 stenosis of the lumbar spine. It was decided to perform a decompressive laminectomy. He had some improvement in his symptoms for about six months. Then his pain in the legs returned. At this time it was determined that his vascular situation had worsened. He underwent a vascular bypass on the left leg. This was successful in relieving his symptoms for about three years, although he continued to experience some element of pain in the right leg. This case demonstrates a situation in which both stenosis and peripheral vascular disease occurred concurrently in the same patient.

Case 10: Anterior interbody fusion edit

40 year old Japanese business man had severe pain and numbness in the legs. He was diagnosed with spinal stenosis of the lumbar spine. After he failed conservative therapy, an anterior spinal fusion was carried out at L4-5 and L5-S1 combined with a decompression. He was kept at strict bed rest for three weeks, then allowed slow progression of ambulation. At two years post op, he reported his symptoms were 95% improved. He continued to pursue his business career.[27][28][29]

Case 11: Steroid epidural injection edit

42 year old with spinal stenosis was injured on the job. He was lifting boxes while sorting inventory at a store. The boxes weighed about 30 pounds each. He experienced low back pain which then became a diffuse numbness in the legs. It persisted for two months. He was referred to a spinal surgeon who diagnosed multilevel stenosis between L2 and S1. He was given a series of steroid epidural injections over a three month period. These provided relief for about six months, but then his symptoms returned, when it was decided he should undergo an extensive decompression from L2 to S1.[30]

Case 12: Steroid injection in failed back syndrome edit

38 year old male truck driver was injured when his truck inadvertently drove over a large pot hole which was about two feet deep. He experienced a jarring sensation in his back. This progressed to generalized leg pain. He was diagnosed with a stenotic segment at L3-4. After six months he underwent a surgical decompression. This relieved his symptoms for about six months. He returned to truck driving, when his symptoms returned. He underwent another surgical procedure with removal of scar from the previous laminectomy and posterior fusion with metal placement. He was never able to return to work, and developed a chronic pain syndrome with consumption of large amounts of prescribed narcotics on a daily basis. At three years post op, he was diagnosed with arachnoiditis of the lumbar spine. He was given a series of steroid epidural injections, but without any lasting benefit. Finally, he had a third surgery for placement of a spinal cord stimulator. This reduced his perception of pain by about 25%, but he continued with the same consumption of narcotics as before surgery. He was now diagnosed as a failed back syndrome.[31][32][33]

Case 13: Post op infection edit

A 41-year-old welder fell approximately eight feet onto a concrete surface at a construction site where he was working. He landed on his back and buttocks. He immediately experienced low back pain and leg pain. He ignored it for the rest of the day. He tried to continue working, but over the next two weeks, his pain in the back became worse, and his legs began to go numb for several hours at a time. He filed a comp claim and was sent to the company doctor who referred him to a spinal surgeon. There, he was diagnosed with L2-3, L3-4 and L4-5 spinal stenosis. It was felt this had been a previously undiagnosed and asymptomatic condition which had been aggravated by the fall. Since his symptoms were not improving after a few months, a decompressive laminectomy was advised. He underwent the surgery. On the fourth post-op day, he spiked a fever of 102 degrees F. His white count was 13,500. He appeared in some distress. His sed rate was 110 mm/hour. His wound in the lumbar spine was red and draining pus. It had a foul, fecal odor to it. A diagnosis of wound infection was made, and he was returned to surgery where the wound was opened, drained and irrigated. Cultures grew methicillin sensitive staphylococcus aureus and streptopeptcoccus. Two more surgeries were necessary, along with a two month course of intravenous antibiotics. He was cured of the infection after two months. He continued to have sharp and unrelenting pain in his back and radiating into his legs. Severely impaired from his pain, at two years he was still unemployed and maintained on the oral narcotics morphine sulphate, 80 mg. per day supplemented with OxyContin and Percocet for breakthrough pain. He was now diagnosed as a failed back syndrome.[34][35][36][37][38][39][40][41]

  1. ^ Lee, L., and Elliott, R. L. J. Orthop Sports Phys Ther. 2008;38(12):798-98
  2. ^ Castro, F. P., et al., The American Journal of Sports Medicine 25:603-08, 1997
  3. ^ Arce, C. A., et al., Neurol. Clin. 1985; 3:383
  4. ^ Alvarez, O., et al.,J. Comput, Assist. Tomogr., 1988; 12:649
  5. ^ Benson, M. K., Byrnes, D. P., J. Bone Joint Surg. 57 B: 471, 1975
  6. ^ Otani, K., et al., Spine 1988; 13: 1262
  7. ^ Wood, K. B., et al., J. Bone Joint Surg., 77 A; 1631, 1995
  8. ^ Arce, C. A., et al., Neurol. Clin. 1985; 3:383
  9. ^ Alvarez, O., et al.,J. Comput, Assist. Tomogr., 1988; 12:649
  10. ^ Benson, M. K., Byrnes, D. P., J. Bone Joint Surg. 57 B: 471, 1975
  11. ^ Otani, K., et al., Spine 1988; 13: 1262
  12. ^ Wood, K. B., et al., J. Bone Joint Surg., 77 A; 1631, 1995
  13. ^ Colonial Ins. Co. V, Industrial Accident Comm., (1946), 29 Cal. 2d 79, 172 P.2d 884,887
  14. ^ C. Finbeiner, Inc. v. Flowers (1971) 251 Ark. 241, 471, S. W. 2d 772
  15. ^ Ingalls Shipbuilding Corp. v. Cahela (1948) 251 Ala. 163, 36 So.2d 531
  16. ^ Gorman, J. D., et al., N. Engl. J. Med. 346:1439:2002
  17. ^ Braun, J., et al., Lancet 359:1187, 2002
  18. ^ Brandt, J., et al., J. Rheumatol. 29:118, 2002
  19. ^ Bowness, P, Rheumatology (Oxford) 41:857, 2002
  20. ^ Brown, M. A., Curr. Opin. Rheumatol. 14:354, 2002
  21. ^ Dougados, M., et al., Arthritis Rhem. 34:1218, 1991
  22. ^ Gladman, D. D., Curr. Opin. Rheumatol. 14:361, 2002
  23. ^ Sinikallio, S., et al. Eur. Spine J. 2007 July; 16(7): 905-12
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  32. ^ Banwart, J. C., et al., Spine 1995; 20:1055-60
  33. ^ Colterjohn, N. R., and Bednar, D. A., J. Bone Joint Surg. [Am] 1997; 79:756-59
  34. ^ Sponseller, P. D., et al., Spine 25:2461-66, 2000
  35. ^ Weinstein, M. A., et al., J. Spinal Disord. 13:422-26, 2000
  36. ^ Massie, J. B., et al., Clin. Orthop. Rel. Res. 284:99-108, 1992
  37. ^ Rechtine, G. R., et al., J. Ortho. Trauma 15:566-69, 2001
  38. ^ Eck, K. R., et al., Spine 26::E182-E91, 201
  39. ^ Capen, D. A., et al., Orthop. Clin. North. Am. 27:83-86, 1996
  40. ^ Hee, H. T., et al., J. Spinal Disord. 14:533-40, 2001
  41. ^ Aydinli, U., et al., Acta Orthop. Belg. 65:182-87, 1999
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