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An association between the flat back and postpolio syndromes: A report of three cases
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An Association Between the Flat Back and Postpolio Syndromes: A Report of Three Cases David Ring, MD, Alexander R. Vaccaro, MD, Gaetano Scuderi, MD, Greg Klein, BA, Daniel Green, MD, Steven R. Garfin, MD ABSTRACT. Ring D, Vaccaro AR, Scuderi G, Klein G, Green D, Garfin SR. An association between the flat back and postpolio syndromes: a report of three cases. Arch Phys Med Rehabil 1997;78:324-6. The cases of three patients with a history of paralytic poliomyelitis in childhood who developed the flat back syndrome before or after spinal fusion for degenerative disease as adults were reviewed. The flat back syndrome, a combination of an inability to stand erect because of forward flexion of the trunk and pain in the low back and/or legs, typically occurs in the setting of decreased lumbar lordosis as a result of distraction instrumentation of the spine for scoliosis, vertebral fracture, or degenerative disease. Focus was placed on determining the factors responsible for the development and/or persistence of the flat back syndrome in these patients despite maintenance of, or partial operative restoration of, lumbar lordosis. Considering the essential role that the trunk extensor musculature plays in maintaining upright posture, it may be that a new onset of weakness (postpolio syndrome) in this musculature represents a major contributing factor to the flat back syndrome in these patients. Spine surgeons considering operative procedures in patients with a remote history of paralytic poliomyelitis should be aware of the possible increased risk of the flat back syndrome in this population of patients.
© 1997 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilit'ation OME PATIENTS with decreased lumbar lordosis after spinal fusion or as a result of degenerative disease of the spine develop an abnormal posture and gait (trunk, knees, and hips flexed, and the neck extended), as well as pain in the neck, back, and/or legs.~4 This debilitating constellation of symptoms and signs is known as the flat back syndrome. A number of factors have been associated with increased risk of developing a flat back syndrome in the setting of a loss of lumbar lordosis: fixed thoracic hyperkyphosis, thoracolumbar kyphosis, pseudarthrosis, extension of fusion to the sacrum, and hip flexion contractures.4 Weakness of the paraspinal and hip extensor muscles has also been considered as a potential contributing factor to the flat back syndromeY We recently treated three patients who had paralytic poliomyelitis as children and subsequently developed the flat back syndrome either before or after attempted spinal fusion for lumbar
S
From the Departmentof Orthopedic Surgery,Universityof Californiaat San Diego Schoolof Medicine,San Diego, CA. Submittedfor publicationFebruary1, 1996.Acceptedin revisedformMay 26, 1996. No commercialparty havinga direct or indirectinterestin the subjectmatter of thisarticlehas or willconfera benefituponthe authorsor uponanyorganization with whichthe authors are associated. Reprintrequests to DavidRing,MD, 11 HancockStreet, Suite4, Boston,MA 02114. © 1997by the AmericanCongressof RehabilitationMedicineandthe Americml Academy"of PhysicalMedicineand Rehabilitation
0003-9993/97/7803-387253.00/0
Arch Phys Med Rehabi! Vo! 78, March 1997
degenerative disease. Weak paraspinal and hip extensor musculature, as the result either of prior poliomyelitis or the development of a postpolio syndrome, is believed to be a major contributing factor in the development of a flat back syndrome in these patients.
CASE REPORTS Patient 1 A 64-year-old woman presented with complaints of increasing lower back pain and difficulty maintaining an upright posture. She noted increased trunk flexion as the day progressed, necessitating a cane for ambulation. The patient stated that when ambulating in the house she bent forward "90 degrees" to relieve the pain. She suffered acute paralytic polio as a child. Her only obvious residual deficits were a decreased left Achilles deep tendon reflex and mild plantar flexion weakness on that side. She presented to our clinic with a 40 ° right thoracic kyphoscoliotic curve, and a 25 ° left lumbar curve, both mobile on bending films. On physical examination, she was found to be a healthy appearing woman who stood in a forward flexed position. Her hips and knees were flexed and her cervical spine was extended. The paraspinal musculature was tender diffusely over her lumbar spine, and there was no midline bony tenderness. She could flex forward to touch her toes, but exhibited limited trunk extension (approximately 10°). Her deep tendon reflexes and motor and sensory examinations were normal except for the deficits noted above. Radiographs demonstrated a lumbar lordosis of 18°. Because of significant pain and disability, as well as truncal imbalance, the patient underwent a recommended two-stage anterior and posterior fusion of the lumbar spine in an attempt to restore her lumbar lordosis. The first stage consisted of anterior release, discectomy, and fusion from the second to the fifth lumbar vertebrae. The second stage consisted of posterior segmental fixation with Texas Scottish Rite Hospital (TSRH) instrumentation of the second through the fifth lumbar vertebrae with iliac crest autograft fusion. The patient was discharged 10 days later in a thoraco-lumbar-sacral orthosis with a thigh cuff extension on the left. Radiographs demonstrated partial restoration of her lumbar lordosis to 32°. She was able to stand upright when in the brace; however, without it she noted fatigue, pain, and increasing flexion identical to but less severe than that noted preoperatively. After healing of the spine fusion, her physical examination remained unchanged except for a slight improvement in posture. The patient underwent supervised Med-X a lumbar extension muscle training therapy to increase paraspinal and hip extensor muscle strength. The Med-X is a machine that isolates the trunk flexor and extensor musculature and provides a measure of strength relative to normal for age and prior examinations in the same patient. Over a treatment period of 8 months, our patient doubled her trunk flexion strength (from 37 to 75 foot-pounds of torque, approaching 100% of normal for her age) but achieved minimal improvement in extension strength (improving from 15 to 20 foot-pounds of torque, approximately 25% of normal for age).
FLAT BACK/POSTPOLIO SYNDROMES, Ring
Patient 2
A 56-year-old man presented with complaints of back and right leg pain and difficulty maintaining an upright posture. He had suffered polio as a child, with the only obvious residual deficit being mild quadriceps weakness bilaterally. He had undergone lumbar 4-5 intervertebral discectomy 10 years earlier. The physical examination on presentation to us revealed a fiat back standing posture (both knees flexed slightly, trunk flexed forward, neck extended), mild to moderate diffuse lumbar paraspinal muscle tenderness to palpation, restricted extension of the spine, and no focal neurologic findings other than the mild bilateral quadriceps weakness related to previous polio. Imaging studies, including plain radiographs and computed tomography (CT), demonstrated degenerative changes in the lumbar spine with diminished lumbar lordosis and central and foraminal stenosis. At this time, his low back and right leg pain was ascribed to spinal and foraminal stenosis and the presence of lumbar spinal instability was considered. He therefore underwent laminectomy with bilateral foraminotomies from the first lumbar to the first sacral vertebrae and fusion with TSRH internal fixation and iliac crest autograft. The need to restore lumbar lordosis was also recognized, and his preoperative and postoperative lumbar lordoses were 15° and 33 °, respectively. Since the surgery, the forward flexion of his trunk has become worse and he requires bilateral crutch support to maintain an upright posture and manage his low back pain. He complains of persistent back pain and, more recently, bilateral, burning leg pain down the lateral aspect of both thighs. His posture becomes progressively stooped throughout the day. In compensation for the forward flexion of his thoracolumbar spine, his knees are flexed and his cervical and upper thoracic spine extended slightly. He continues to have paraspinal muscle tenderness to palpation and his neurologic examination remains nonfocal. Med-X muscle training was also utilized in this patient. Over a treatment period of 6 mouths, he improved from 40 to 60 foot-pounds of trunk flexion torque and remained at 30 foot-pounds of trunk extension torque (25% and 17% of normal for age, respectively). Patient 3
An obese 57-year-old man presented with persistent complaints of lower back pain and inability to stand erect after multiple back surgeries. The patient reported a history of acute paralytic poliomyelitis as a child, but did not have any permanent weakness or residual focal neurologic findings. His first spine surgery was a lumbar 3-5 laminectomy for spinal stenosis. Postoperatively, he began to note a stooped forward posture. His leg pain was relieved by the laminectomy, but his back pain increased. Over the next 3 to 4 years the patient underwent numerous surgeries for persistent back pain including Tg-L4 fusion with instrumentation, anterior and posterior refusion for nonunion, and a final surgery for removal of instrumentation. His lumbar lordosis was maintained between approximately 30 ° to 40 ° after each surgery. Following these operations, he continued to complain of inability to stand upright and low back pain. His forward flexed posture had worsened and he flexed his knees and extended his cervical and upper thoracic spine in order to maintain his head in an upright position. He began to use a cane to ambulate. Physical examination found lumbar paraspinal muscle tenderness to palpation, limited spine range of motion with extension to neutral at best, and no focal neurologic findings. This patient also began Med-X strength training. Over a treatment period of 6 months, his trunk flexion torque improved from 110 to 140 foot-pounds of torque, approaching 60% of normal for his age. However, he achieved minimal
325
improvement in extension strength (from 50 to 60 foot-pounds of torque, approximately 28% of normal for age). DISCUSSION These three patients all developed or maintained a fiat back syndrome despite at least partial restoration of lumbar lordosis. While each had at least one other contributing factor (Patient 1 had a kyphoscoliotic deformity, patient 2 had a fusion including the sacrum, and patient 3 had nearly complete lumbar fusion and hip flexion contractures), it seems likely that trunk extensor weakness as a result of damage to motor units at the time of acute poliomyelitis and/or new-onset weakness due to delayed motor unit damage (the postpolio syndrome) is an important etiologic factor in the flat back syndrome in these patients. In an early description of the •t-back syndrome, it was suggested that residual weakness from paralytic poliomyelitis may contribute to the development of the syndrome in some patients. 3 Subsequent reports suggested that loss of lumbar lordosis may cause fatigue of spinal and hip extensor musculature secondary to increased demands and that the back pain symptoms in this syndrome may be of a muscular origin. 4'5 The important role of the paraspinal and hip extensor musculature in the maintenance of upright posture has been well described. In the average healthy human subject the line of gravity of the trunk falls ventral to the center of the fourth lumbar vertebra (and thus to the transverse axis of motion of the spine) when standing. 6 Thus, a continuous paraspinal muscle contraction is required to maintain an upright posture due to the forward-bending moment to which the motion segments of the spine are subjected. Continuous EMG activity has been demonstrated in the erector spinae muscles of standing normal human subjects] The potential contributing factors that have been previously described all cause either a ventral shift of the line of gravity of the trunk (loss of lumbar lordosis, thoracolumbar kyphosis, fixed thoracic kyphosis, psuedarthrosis) or interference with compensatory mechanisms for minimizing the forward-bending moment on the spine (hip flexion contractures, fusion to the sacrum). 4 These factors cause an increase in the force required by the trunk extensor musculature to maintain an upright posture. This suggests two possible roles for paraspinal extensor muscle weakness as a contributing factor in the etiology of the flat-back syndrome: (1) weakness in these muscles may contribute to an inability to maintain an upright posture in the face of increasing demands; (2) increased demands on the paraspinal extensor musculature may result in pain of muscular origin due to overuse injury. Operative restoration of lumbar lordosis is intended to result in a shift posteriorly of the center of gravity of the body, thereby facilitating the maintenance of an upright posture and limiting the demands on the trunk extensor musculature. 3'4 However, in our three cases, improvement in lumbar lordosis failed to improve posture or provide pain relief. The occurrence of new weakness and pain following a period of stable functioning in a patient who suffered paralytic poliomyelitis many years earlier has been termed the postpolio syndrome. 8'9 Although the precise pathophysiologic mechanisms remain uncertain, it is clear that the motor units of postpolio patients have been damaged and reorganized in such a manner that their physiologic reserve (ability to adapt to insult and injury) is decreased. Increased demands, new damage, or deconditioning may lead to the development of a new onset weakness and pain (postpolio syndrome) in these patients. Our three patients all suffered paralytic poliomyelitis as children, with minimal residual weakness. Considering that weakness of the trunk extensor musculature appears to have played
Arch Phys Med Rehabil Vol 78, March 1997
326
FLAT BACK/POSTPOLIO SYNDROMES, Ring
an important role in the development of the flat back syndrome in these patients, the possibility arises that this represents newonset weakness caused by postpolio motor unit alterations. In patient 1, the kyphoscoliotic deformity and apparent loss of lumbar lordosis due to degenerative disease may have caused excessive demands on her poliomyelitis-damaged trunk extensor motor units leading to new-onset weakness and pain. Operative spinal fusion may have worsened the condition because of both perioperative deconditioning and intraoperative damage to motor units with limited ability to recover due to decreased physiologic reserve. Thus, the patient's posture and pain were not improved despite at least partial restoration of her lumbar lordosis. Patients 2 and 3 developed the flat back syndrome after numerous spinal surgeries, again despite operative improvement in lumbar lordosis. It is likely that new-onset weakness due to increased demands and muscle overuse damage and/or operative damage to fragile motor units resulted in the development of the postpolio and flat back syndromes in these patients. The postpolio motor unit has an abnormal structure and a decreased physiologic reserve which may limit its ability adapt to and recover from increased demands, deconditioning, and operative damage. In summary, these three patients illustrate a possible association between the postpolio and flat back syndromes. Postpolio patients appear to be at risk for the fiat back syndrome because of alterations in the skeletal muscle motor units following acute paralytic poliomyelitis that either decrease their physiological reserve for responding to increased demands or injury, or make them more fragile and susceptible to degeneration, or both. Noting the important role of the paraspinal and hip extensor musculature in maintaining upright posture, the increased demands placed on these muscles by factors known to contribute
Arch Phys Med Rehabil Vo178, March 1997
to the flat back syndrome, and the existence of new-onset and progressive weakness in poliomyelitis-damaged muscles from which excessive work is demanded, we postulate that postpolio weakness of the paraspinal musculature may be associated with an increased risk of developing a flat-back syndrome. Spine surgeons considering operative procedures in patients with a remote history of acute paralytic poliomyelitis should be aware of these factors and of the possible risk of precipitating the postpolio and flat back syndromes in these patients.
References 1. Benner B, Ehni G. Degenerative lumbar scoliosis. Spine 1979;4: 548-52. 2. Epstein JA, Epstein BS, Jones MD. Symptomatic lumbar scoliosis with degenerative changes in the elderly. Spine 1979;4:542-7. 3. Grobler LJ, Moe JH, Winter RB, Bradford DS, Lonstein JE. Loss of lumbar lordosis following surgical correction of thoracolumbar deformities: its recognition, treatment, and prevention. Orthop Trans 1978;2:239. 4. La Grone MO. Loss of lumbar lordosis: a complication of spinal fusion for scoliosis. Orthop Clin North Am 1988;19:383-93. 5. Swank SM, Mauri TM, Brown JC. The lumbar lordosis below Harrington instrumentation for scoliosis. Spine 1990;15:181-6. 6. Asmussen E, Klausen K. Form and function of the erect human spine. Clin Orthop 1962;25:55. 7. Morris J, Benner G, Lucas D. An electromyographic study of the intrinsic muscles of the back in man. J Anat 1962;196:509-12. 8. Munsat T, editor. Post-polio syndrome. Boston: Butterworth-Heinemann, 1991. 9. Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller I. Epidemiology of the post-polio syndrome. Am J Epidemiol 1992;136:76986. Supplier a. MedX Corporation, 1401 Northeast 77th Street, Ocala, FL 34479.
An Association Between the Flat Back and Postpolio Syndromes: A Report of Three Cases David Ring, MD, Alexander R. Vaccaro, MD, Gaetano Scuderi, MD, Greg Klein, BA, Daniel Green, MD, Steven R. Garfin, MD ABSTRACT. Ring D, Vaccaro AR, Scuderi G, Klein G, Green D, Garfin SR. An association between the flat back and postpolio syndromes: a report of three cases. Arch Phys Med Rehabil 1997;78:324-6. The cases of three patients with a history of paralytic poliomyelitis in childhood who developed the flat back syndrome before or after spinal fusion for degenerative disease as adults were reviewed. The flat back syndrome, a combination of an inability to stand erect because of forward flexion of the trunk and pain in the low back and/or legs, typically occurs in the setting of decreased lumbar lordosis as a result of distraction instrumentation of the spine for scoliosis, vertebral fracture, or degenerative disease. Focus was placed on determining the factors responsible for the development and/or persistence of the flat back syndrome in these patients despite maintenance of, or partial operative restoration of, lumbar lordosis. Considering the essential role that the trunk extensor musculature plays in maintaining upright posture, it may be that a new onset of weakness (postpolio syndrome) in this musculature represents a major contributing factor to the flat back syndrome in these patients. Spine surgeons considering operative procedures in patients with a remote history of paralytic poliomyelitis should be aware of the possible increased risk of the flat back syndrome in this population of patients.
© 1997 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilit'ation OME PATIENTS with decreased lumbar lordosis after spinal fusion or as a result of degenerative disease of the spine develop an abnormal posture and gait (trunk, knees, and hips flexed, and the neck extended), as well as pain in the neck, back, and/or legs.~4 This debilitating constellation of symptoms and signs is known as the flat back syndrome. A number of factors have been associated with increased risk of developing a flat back syndrome in the setting of a loss of lumbar lordosis: fixed thoracic hyperkyphosis, thoracolumbar kyphosis, pseudarthrosis, extension of fusion to the sacrum, and hip flexion contractures.4 Weakness of the paraspinal and hip extensor muscles has also been considered as a potential contributing factor to the flat back syndromeY We recently treated three patients who had paralytic poliomyelitis as children and subsequently developed the flat back syndrome either before or after attempted spinal fusion for lumbar
S
From the Departmentof Orthopedic Surgery,Universityof Californiaat San Diego Schoolof Medicine,San Diego, CA. Submittedfor publicationFebruary1, 1996.Acceptedin revisedformMay 26, 1996. No commercialparty havinga direct or indirectinterestin the subjectmatter of thisarticlehas or willconfera benefituponthe authorsor uponanyorganization with whichthe authors are associated. Reprintrequests to DavidRing,MD, 11 HancockStreet, Suite4, Boston,MA 02114. © 1997by the AmericanCongressof RehabilitationMedicineandthe Americml Academy"of PhysicalMedicineand Rehabilitation
0003-9993/97/7803-387253.00/0
Arch Phys Med Rehabi! Vo! 78, March 1997
degenerative disease. Weak paraspinal and hip extensor musculature, as the result either of prior poliomyelitis or the development of a postpolio syndrome, is believed to be a major contributing factor in the development of a flat back syndrome in these patients.
CASE REPORTS Patient 1 A 64-year-old woman presented with complaints of increasing lower back pain and difficulty maintaining an upright posture. She noted increased trunk flexion as the day progressed, necessitating a cane for ambulation. The patient stated that when ambulating in the house she bent forward "90 degrees" to relieve the pain. She suffered acute paralytic polio as a child. Her only obvious residual deficits were a decreased left Achilles deep tendon reflex and mild plantar flexion weakness on that side. She presented to our clinic with a 40 ° right thoracic kyphoscoliotic curve, and a 25 ° left lumbar curve, both mobile on bending films. On physical examination, she was found to be a healthy appearing woman who stood in a forward flexed position. Her hips and knees were flexed and her cervical spine was extended. The paraspinal musculature was tender diffusely over her lumbar spine, and there was no midline bony tenderness. She could flex forward to touch her toes, but exhibited limited trunk extension (approximately 10°). Her deep tendon reflexes and motor and sensory examinations were normal except for the deficits noted above. Radiographs demonstrated a lumbar lordosis of 18°. Because of significant pain and disability, as well as truncal imbalance, the patient underwent a recommended two-stage anterior and posterior fusion of the lumbar spine in an attempt to restore her lumbar lordosis. The first stage consisted of anterior release, discectomy, and fusion from the second to the fifth lumbar vertebrae. The second stage consisted of posterior segmental fixation with Texas Scottish Rite Hospital (TSRH) instrumentation of the second through the fifth lumbar vertebrae with iliac crest autograft fusion. The patient was discharged 10 days later in a thoraco-lumbar-sacral orthosis with a thigh cuff extension on the left. Radiographs demonstrated partial restoration of her lumbar lordosis to 32°. She was able to stand upright when in the brace; however, without it she noted fatigue, pain, and increasing flexion identical to but less severe than that noted preoperatively. After healing of the spine fusion, her physical examination remained unchanged except for a slight improvement in posture. The patient underwent supervised Med-X a lumbar extension muscle training therapy to increase paraspinal and hip extensor muscle strength. The Med-X is a machine that isolates the trunk flexor and extensor musculature and provides a measure of strength relative to normal for age and prior examinations in the same patient. Over a treatment period of 8 months, our patient doubled her trunk flexion strength (from 37 to 75 foot-pounds of torque, approaching 100% of normal for her age) but achieved minimal improvement in extension strength (improving from 15 to 20 foot-pounds of torque, approximately 25% of normal for age).
FLAT BACK/POSTPOLIO SYNDROMES, Ring
Patient 2
A 56-year-old man presented with complaints of back and right leg pain and difficulty maintaining an upright posture. He had suffered polio as a child, with the only obvious residual deficit being mild quadriceps weakness bilaterally. He had undergone lumbar 4-5 intervertebral discectomy 10 years earlier. The physical examination on presentation to us revealed a fiat back standing posture (both knees flexed slightly, trunk flexed forward, neck extended), mild to moderate diffuse lumbar paraspinal muscle tenderness to palpation, restricted extension of the spine, and no focal neurologic findings other than the mild bilateral quadriceps weakness related to previous polio. Imaging studies, including plain radiographs and computed tomography (CT), demonstrated degenerative changes in the lumbar spine with diminished lumbar lordosis and central and foraminal stenosis. At this time, his low back and right leg pain was ascribed to spinal and foraminal stenosis and the presence of lumbar spinal instability was considered. He therefore underwent laminectomy with bilateral foraminotomies from the first lumbar to the first sacral vertebrae and fusion with TSRH internal fixation and iliac crest autograft. The need to restore lumbar lordosis was also recognized, and his preoperative and postoperative lumbar lordoses were 15° and 33 °, respectively. Since the surgery, the forward flexion of his trunk has become worse and he requires bilateral crutch support to maintain an upright posture and manage his low back pain. He complains of persistent back pain and, more recently, bilateral, burning leg pain down the lateral aspect of both thighs. His posture becomes progressively stooped throughout the day. In compensation for the forward flexion of his thoracolumbar spine, his knees are flexed and his cervical and upper thoracic spine extended slightly. He continues to have paraspinal muscle tenderness to palpation and his neurologic examination remains nonfocal. Med-X muscle training was also utilized in this patient. Over a treatment period of 6 mouths, he improved from 40 to 60 foot-pounds of trunk flexion torque and remained at 30 foot-pounds of trunk extension torque (25% and 17% of normal for age, respectively). Patient 3
An obese 57-year-old man presented with persistent complaints of lower back pain and inability to stand erect after multiple back surgeries. The patient reported a history of acute paralytic poliomyelitis as a child, but did not have any permanent weakness or residual focal neurologic findings. His first spine surgery was a lumbar 3-5 laminectomy for spinal stenosis. Postoperatively, he began to note a stooped forward posture. His leg pain was relieved by the laminectomy, but his back pain increased. Over the next 3 to 4 years the patient underwent numerous surgeries for persistent back pain including Tg-L4 fusion with instrumentation, anterior and posterior refusion for nonunion, and a final surgery for removal of instrumentation. His lumbar lordosis was maintained between approximately 30 ° to 40 ° after each surgery. Following these operations, he continued to complain of inability to stand upright and low back pain. His forward flexed posture had worsened and he flexed his knees and extended his cervical and upper thoracic spine in order to maintain his head in an upright position. He began to use a cane to ambulate. Physical examination found lumbar paraspinal muscle tenderness to palpation, limited spine range of motion with extension to neutral at best, and no focal neurologic findings. This patient also began Med-X strength training. Over a treatment period of 6 months, his trunk flexion torque improved from 110 to 140 foot-pounds of torque, approaching 60% of normal for his age. However, he achieved minimal
325
improvement in extension strength (from 50 to 60 foot-pounds of torque, approximately 28% of normal for age). DISCUSSION These three patients all developed or maintained a fiat back syndrome despite at least partial restoration of lumbar lordosis. While each had at least one other contributing factor (Patient 1 had a kyphoscoliotic deformity, patient 2 had a fusion including the sacrum, and patient 3 had nearly complete lumbar fusion and hip flexion contractures), it seems likely that trunk extensor weakness as a result of damage to motor units at the time of acute poliomyelitis and/or new-onset weakness due to delayed motor unit damage (the postpolio syndrome) is an important etiologic factor in the flat back syndrome in these patients. In an early description of the •t-back syndrome, it was suggested that residual weakness from paralytic poliomyelitis may contribute to the development of the syndrome in some patients. 3 Subsequent reports suggested that loss of lumbar lordosis may cause fatigue of spinal and hip extensor musculature secondary to increased demands and that the back pain symptoms in this syndrome may be of a muscular origin. 4'5 The important role of the paraspinal and hip extensor musculature in the maintenance of upright posture has been well described. In the average healthy human subject the line of gravity of the trunk falls ventral to the center of the fourth lumbar vertebra (and thus to the transverse axis of motion of the spine) when standing. 6 Thus, a continuous paraspinal muscle contraction is required to maintain an upright posture due to the forward-bending moment to which the motion segments of the spine are subjected. Continuous EMG activity has been demonstrated in the erector spinae muscles of standing normal human subjects] The potential contributing factors that have been previously described all cause either a ventral shift of the line of gravity of the trunk (loss of lumbar lordosis, thoracolumbar kyphosis, fixed thoracic kyphosis, psuedarthrosis) or interference with compensatory mechanisms for minimizing the forward-bending moment on the spine (hip flexion contractures, fusion to the sacrum). 4 These factors cause an increase in the force required by the trunk extensor musculature to maintain an upright posture. This suggests two possible roles for paraspinal extensor muscle weakness as a contributing factor in the etiology of the flat-back syndrome: (1) weakness in these muscles may contribute to an inability to maintain an upright posture in the face of increasing demands; (2) increased demands on the paraspinal extensor musculature may result in pain of muscular origin due to overuse injury. Operative restoration of lumbar lordosis is intended to result in a shift posteriorly of the center of gravity of the body, thereby facilitating the maintenance of an upright posture and limiting the demands on the trunk extensor musculature. 3'4 However, in our three cases, improvement in lumbar lordosis failed to improve posture or provide pain relief. The occurrence of new weakness and pain following a period of stable functioning in a patient who suffered paralytic poliomyelitis many years earlier has been termed the postpolio syndrome. 8'9 Although the precise pathophysiologic mechanisms remain uncertain, it is clear that the motor units of postpolio patients have been damaged and reorganized in such a manner that their physiologic reserve (ability to adapt to insult and injury) is decreased. Increased demands, new damage, or deconditioning may lead to the development of a new onset weakness and pain (postpolio syndrome) in these patients. Our three patients all suffered paralytic poliomyelitis as children, with minimal residual weakness. Considering that weakness of the trunk extensor musculature appears to have played
Arch Phys Med Rehabil Vol 78, March 1997
326
FLAT BACK/POSTPOLIO SYNDROMES, Ring
an important role in the development of the flat back syndrome in these patients, the possibility arises that this represents newonset weakness caused by postpolio motor unit alterations. In patient 1, the kyphoscoliotic deformity and apparent loss of lumbar lordosis due to degenerative disease may have caused excessive demands on her poliomyelitis-damaged trunk extensor motor units leading to new-onset weakness and pain. Operative spinal fusion may have worsened the condition because of both perioperative deconditioning and intraoperative damage to motor units with limited ability to recover due to decreased physiologic reserve. Thus, the patient's posture and pain were not improved despite at least partial restoration of her lumbar lordosis. Patients 2 and 3 developed the flat back syndrome after numerous spinal surgeries, again despite operative improvement in lumbar lordosis. It is likely that new-onset weakness due to increased demands and muscle overuse damage and/or operative damage to fragile motor units resulted in the development of the postpolio and flat back syndromes in these patients. The postpolio motor unit has an abnormal structure and a decreased physiologic reserve which may limit its ability adapt to and recover from increased demands, deconditioning, and operative damage. In summary, these three patients illustrate a possible association between the postpolio and flat back syndromes. Postpolio patients appear to be at risk for the fiat back syndrome because of alterations in the skeletal muscle motor units following acute paralytic poliomyelitis that either decrease their physiological reserve for responding to increased demands or injury, or make them more fragile and susceptible to degeneration, or both. Noting the important role of the paraspinal and hip extensor musculature in maintaining upright posture, the increased demands placed on these muscles by factors known to contribute
Arch Phys Med Rehabil Vo178, March 1997
to the flat back syndrome, and the existence of new-onset and progressive weakness in poliomyelitis-damaged muscles from which excessive work is demanded, we postulate that postpolio weakness of the paraspinal musculature may be associated with an increased risk of developing a flat-back syndrome. Spine surgeons considering operative procedures in patients with a remote history of acute paralytic poliomyelitis should be aware of these factors and of the possible risk of precipitating the postpolio and flat back syndromes in these patients.
References 1. Benner B, Ehni G. Degenerative lumbar scoliosis. Spine 1979;4: 548-52. 2. Epstein JA, Epstein BS, Jones MD. Symptomatic lumbar scoliosis with degenerative changes in the elderly. Spine 1979;4:542-7. 3. Grobler LJ, Moe JH, Winter RB, Bradford DS, Lonstein JE. Loss of lumbar lordosis following surgical correction of thoracolumbar deformities: its recognition, treatment, and prevention. Orthop Trans 1978;2:239. 4. La Grone MO. Loss of lumbar lordosis: a complication of spinal fusion for scoliosis. Orthop Clin North Am 1988;19:383-93. 5. Swank SM, Mauri TM, Brown JC. The lumbar lordosis below Harrington instrumentation for scoliosis. Spine 1990;15:181-6. 6. Asmussen E, Klausen K. Form and function of the erect human spine. Clin Orthop 1962;25:55. 7. Morris J, Benner G, Lucas D. An electromyographic study of the intrinsic muscles of the back in man. J Anat 1962;196:509-12. 8. Munsat T, editor. Post-polio syndrome. Boston: Butterworth-Heinemann, 1991. 9. Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller I. Epidemiology of the post-polio syndrome. Am J Epidemiol 1992;136:76986. Supplier a. MedX Corporation, 1401 Northeast 77th Street, Ocala, FL 34479.