(Radiographics. 2002;22:257-268.)
© RSNA, 2002
Progressive Bone and Joint Abnormalities of the Spine and Lower Extremities in Cerebral Palsy1
David S. Morrell, MD,
J. Michael Pearson, MD and
Donald D. Sauser, MD
1 From the Department of Radiology, Oregon Health Sciences University, Mail Code L340, 3181 SW Sam Jackson Park Rd, Portland, OR 97201. Recipient of a Certificate of Merit award for an education exhibit at the 2000 RSNA scientific assembly. Received March 15, 2001; revision requested May 29 and received July 13; accepted July 13. Address correspondence to J.M.P. (e-mail: pearsonm@ohsu.edu).
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Abstract
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Bone and joint changes in cerebral palsy result from muscle spasticity and contracture. The spine and the joints of the lower extremity are most commonly affected. Scoliosis may progress rapidly and may continue after skeletal maturity. Increased thoracic kyphosis and lumbar lordosis, spondylolisthesis, spondylolysis, and pelvic obliquity may accompany the scoliosis. Progressive hip flexion and adduction lead to windswept deformity, increased femoral anteversion, apparent coxa valga, subluxation, deformity of the femoral head, hip dislocation, and formation of a pseudoacetabulum. In the knee, flexion contracture, patella alta, and patellar fragmentation are the most commonly seen abnormalities. Recurvatum deformity can also develop in the knee secondary to contracture of the rectus femoris muscle. Progressive equinovalgus and equinovarus of the foot and ankle are associated with rocker-bottom deformity and subluxation of the talonavicular joint. Early recognition of progressive deformity in patients with cerebral palsy allows timely treatment and prevention of irreversible change.
© RSNA, 2002
Index Terms: Cerebral palsy, 30.829, 40.829 • Foot, abnormalities, 46.829 • Hip, abnormalities, 442.829 • Knee, abnormalities, 45.829 • Spine, curvature, 30.86
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LEARNING OBJECTIVES FOR TEST 2
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After reading this article and taking the test, the reader will be able to:
- Describe the pathophysiology of musculoskeletal changes in cerebral palsy.
- Recognize the radiographic findings of cerebral palsy in the spine and lower extremities.
- Discuss the progression of musculoskeletal changes and the objectives of treatment in cerebral palsy.
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Introduction
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Cerebral palsy is a central nervous system disorder with motor impairment and a frequency of 1–5 per 1,000 live births (1). Spastic diplegia is the most common form of cerebral palsy and predominately affects the lower extremities (2).
Premature delivery and low birth weight are closely associated with cerebral palsy. Other risk factors include intrauterine asphyxia, congenital infection, placental infarction, and occlusion of a cerebral artery or vein (3,4). These perinatal insults cause cerebral infarction and periventricular leukomalacia. Loss of supraspinal inhibition on spinal stretch reflexes results in increased reflex activity. This leads to spasticity, motor weakness, impaired sensory perception, and muscle and joint contractures (3). Spasticity typically develops between 6 and 18 months of age and alters the previously normal skeletal anatomy (5). The most commonly affected muscles are the paraspinal muscles, hip flexors, hip adductors, hamstrings, gastrocnemius, and soleus.
In this article, we illustrate the progressive radiographic manifestations of cerebral palsy in the thoracolumbar spine, hip, knee, and foot. Descriptions and illustrations of the characteristic bone and joint findings accompany discussions of pathophysiology and treatment.
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Thoracolumbar Spine
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The prevalence of scoliosis in patients with spastic cerebral palsy ranges from 15% to 61% (6,7). Males are more commonly affected (8). This is in contrast to idiopathic scoliosis, which has an 8:1 female predominance (9). Curves are typically less than 40° but can range from 10° to 146° (8).
The incidence of scoliosis increases with age and decreased ambulation. Most scoliotic curves progress from postural to fixed deformities. Progression of scoliosis is greatest during the growth spurt and may continue after skeletal maturity, especially when associated with pelvic obliquity (10). One study noted curve progression of 0.8° per year when the largest curve was less than or equal to 50° at skeletal maturity and curve progression of 1.4° per year when the largest curve was greater than 50° at skeletal maturity (7). Thoracolumbar curves tend to have the most progression (Fig 1). Increased thoracic kyphosis and lumbar lordosis may also occur.
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Figure 1a. Progressive thoracolumbar scoliosis. Sequential anteroposterior radiographs show minimal thoracolumbar scoliosis at 8 years of age with a 15° curve (a), progression of the curve to 30° at 11 years of age (b), more severe deformity with the curve measuring 48° at 13 years of age (c), and progression to 70° at 14 years of age (d).
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Figure 1b. Progressive thoracolumbar scoliosis. Sequential anteroposterior radiographs show minimal thoracolumbar scoliosis at 8 years of age with a 15° curve (a), progression of the curve to 30° at 11 years of age (b), more severe deformity with the curve measuring 48° at 13 years of age (c), and progression to 70° at 14 years of age (d).
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Figure 1c. Progressive thoracolumbar scoliosis. Sequential anteroposterior radiographs show minimal thoracolumbar scoliosis at 8 years of age with a 15° curve (a), progression of the curve to 30° at 11 years of age (b), more severe deformity with the curve measuring 48° at 13 years of age (c), and progression to 70° at 14 years of age (d).
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Figure 1d. Progressive thoracolumbar scoliosis. Sequential anteroposterior radiographs show minimal thoracolumbar scoliosis at 8 years of age with a 15° curve (a), progression of the curve to 30° at 11 years of age (b), more severe deformity with the curve measuring 48° at 13 years of age (c), and progression to 70° at 14 years of age (d).
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Increased lumbar lordosis results in greater compression and shearing forces, leading to spondylolisthesis (Fig 2). The prevalence of spondylolysis of L5 increases from 21% to 29% when lordosis is greater than 50°. Facet arthropathy at L5-S1 occurs in 67% of cases. The prevalence of low back pain increases with increasing lumbar lordosis; low back pain is reported in up to 75% of patients when lordosis is greater than 70° (11). Associated abnormalities include pelvic obliquity (68%), hip contractures (79%), and femoral head subluxation (59%) (9).
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Figure 2. Increased lumbar lordosis with pars defects. Lateral radiograph shows increased lumbar lordosis with L4 and L5 pars defects (arrows) and associated grade 1 spondylolisthesis.
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Treatment is primarily aimed at improving sitting balance and halting curve progression. Severe deformities may be prevented by external bracing if scoliosis is detected early (8). Anterior release or fusion combined with posterior fusion may be necessary (10). Additional measures include correction of increased kyphosis, pelvic obliquity, hip flexion deformity, and hip dislocation (10,12).
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Hip
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Hip subluxation and dislocation are the second most common deformities in patients with spastic cerebral palsy, with a reported prevalence of up to 28% (13,14). The spastic adductors and iliopsoas muscles overpower the weaker hip abductors and extensors (15). This may result in scissor gait (bilateral adduction hip contracture) or windswept deformity. Windswept deformity (adduction contracture of one hip and abduction contracture of the other hip) occurs in up to 23% of patients (9) (Fig 3). Impaired ambulation and sitting balance, greater trochanteric decubiti, and pain may also be present (14,16).
Femoral anteversion, defined as the angle the femoral neck makes to a transverse plane through the femoral condyles when the femur is viewed on end, is increased in spastic cerebral palsy (17). Various indirect methods have been applied in the past, requiring complex biplane radiography and application of trigonometric calculation to arrive at the true anteversion angle (18). This approach has been replaced by direct computed tomographic (CT) measurement of the femoral anteversion angle (19) (Fig 4). Femoral anteversion is normally 30°–50° in infants and diminishes throughout childhood (20). Persistent increased femoral anteversion in cerebral palsy patients is related to delayed weight bearing and muscle imbalance (15). The normal anteversion angle in adults ranges from 8° to 15°, whereas in spastic cerebral palsy the anteversion angle averages 55° in ambulatory patients and 57° in nonambulatory patients (21).
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Figure 4a. Increased femoral anteversion. CT scans show determination of femoral anteversion, which is defined as the angle between a line through the axis of the femoral head (a) and the femoral neck (b) and a plane through the femoral condyles (c). Note the marked increased femoral anteversion of 55° (normal range, 8°-15°).
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Figure 4b. Increased femoral anteversion. CT scans show determination of femoral anteversion, which is defined as the angle between a line through the axis of the femoral head (a) and the femoral neck (b) and a plane through the femoral condyles (c). Note the marked increased femoral anteversion of 55° (normal range, 8°-15°).
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Figure 4c. Increased femoral anteversion. CT scans show determination of femoral anteversion, which is defined as the angle between a line through the axis of the femoral head (a) and the femoral neck (b) and a plane through the femoral condyles (c). Note the marked increased femoral anteversion of 55° (normal range, 8°-15°).
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The femoral neck-shaft angle, measured on a true anteroposterior radiograph, is defined as the angle between the midaxis of the femoral shaft and a line along the midaxis of the femoral head and neck (22). The term coxa valga, or increase in femoral neck-shaft angle, as typically used is not strictly accurate (21). This is because the femoral neck-shaft angle defined from an anteroposterior radiograph neglects the projectional effects that femoral anteversion and rotation have on this measurement. An increase in the anteversion angle results in projectional foreshortening of the femoral neck on the anteroposterior radiograph, creating the false impression of a markedly increased neck-shaft angle (17,21) (Fig 5). It is for this reason that we refer to the apparent neck-shaft angle on the anteroposterior radiograph, recognizing these geometric distortions of the true angle between the femoral neck and shaft. Most authors referring to coxa valga in cerebral palsy are, in fact, describing this apparent coxa valga, or apparent increased neck-shaft angle based on the anteroposterior radiograph alone. The average apparent neck-shaft angle in patients with spastic cerebral palsy is 147°–154° (normal, 125°–130°) (21,23). The spastic flexors and adductors act to force the femoral head in a superolateral direction. The increased femoral anteversion accentuates the forces displacing the femoral heads (15).
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Figure 5a. Apparent coxa valga. (a) Anteroposterior radiograph of a cerebral palsy patient with increased femoral anteversion shows foreshortening of the femoral neck and gives the false impression of a markedly increased neck-shaft angle. (b) Comparison anteroposterior radiograph of a normal hip shows a normal apparent neck-shaft angle.
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Figure 5b. Apparent coxa valga. (a) Anteroposterior radiograph of a cerebral palsy patient with increased femoral anteversion shows foreshortening of the femoral neck and gives the false impression of a markedly increased neck-shaft angle. (b) Comparison anteroposterior radiograph of a normal hip shows a normal apparent neck-shaft angle.
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Subluxation occurs superolaterally (Fig 6) and may progress to dislocation at a mean age of 7 years (14) (Fig 7). Chronic subluxation and dislocation result in acetabular dysplasia and secondary degenerative joint disease (24). As subluxation progresses, medial or lateral flattening of the femoral head may occur. A triangular shape may be seen if both are present (17) (Fig 8). Dislocation may result in development of pseudoacetabulum along the lateral margin of the ilium (Fig 9). Pseudoacetabulum has been reported in 3.8% of patients with spastic cerebral palsy (23).
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Figure 7a. Progressive subluxation with acetabular dysplasia. Sequential anteroposterior radiographs show minimal lateral subluxation of the left femoral head at 3 years of age (a) with progression of superolateral subluxation of the left femoral head and secondary acetabular dysplasia at 6 years of age (b).
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Figure 7b. Progressive subluxation with acetabular dysplasia. Sequential anteroposterior radiographs show minimal lateral subluxation of the left femoral head at 3 years of age (a) with progression of superolateral subluxation of the left femoral head and secondary acetabular dysplasia at 6 years of age (b).
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Figure 8a. Femoral head flattening. (a) Anteroposterior radiograph shows bilateral subluxation and medial flattening of the femoral heads. (b) Anteroposterior radiograph shows triangular deformity and subluxation of the femoral head.
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Figure 8b. Femoral head flattening. (a) Anteroposterior radiograph shows bilateral subluxation and medial flattening of the femoral heads. (b) Anteroposterior radiograph shows triangular deformity and subluxation of the femoral head.
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Figure 9a. Dislocation and pseudoacetabulum. Anteroposterior radiographs of the right (a) and left (b) hips show bilateral dislocation of the femoral heads, medial and lateral flattening of the femoral heads, acetabular dysplasia, and pseudoacetabula.
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Figure 9b. Dislocation and pseudoacetabulum. Anteroposterior radiographs of the right (a) and left (b) hips show bilateral dislocation of the femoral heads, medial and lateral flattening of the femoral heads, acetabular dysplasia, and pseudoacetabula.
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Treatment is aimed at preventing adduction and flexion deformity and progression to subluxation or dislocation (14). Nonsurgical management involves stretching the spastic agonist muscles and strengthening the weaker antagonist muscles. Abduction splinting may also be used (15). Surgical therapy includes tenotomy and neurectomy. Varus derotation osteotomy may also be performed to correct apparent coxa valga and femoral anteversion (5,14) (Fig 10).
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Figure 10a. Varus osteotomy. (a) Anteroposterior radiograph shows an increased apparent femoral neck-shaft angle with subluxation. (b) Anteroposterior radiograph obtained after varus derotation osteotomy shows correction of the apparent coxa valga and reduction of the subluxation.
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Figure 10b. Varus osteotomy. (a) Anteroposterior radiograph shows an increased apparent femoral neck-shaft angle with subluxation. (b) Anteroposterior radiograph obtained after varus derotation osteotomy shows correction of the apparent coxa valga and reduction of the subluxation.
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Knee
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Knee flexion deformity (crouch knee) is the most common knee abnormality in spastic cerebral palsy (Fig 11). This deformity is associated with hip and ankle flexion contractures and is due to spasticity of the hamstrings (25). As flexion progresses, more force is placed on the quadriceps muscles, leading to overstretching of the quadriceps muscle fibers and the infrapatellar tendon, causing patella alta, patellar fragmentation, chondromalacia, joint instability, muscle weakness, and pain (26).
Patella alta is found in 58%–72% of patients with spastic cerebral palsy (27,28). Patella alta is measured by determining the ratio of the patellar tendon length (measured from the inferior pole of the patella to the tibial tuberosity) to the greatest diagonal length of the patella (normal range, 0.8–1.2) (29,30). Increased diagonal length and fragmentation may complicate the patellar measurement in cerebral palsy. Patella alta alters the patellofemoral and tibiofemoral joint mechanics, leading to weakness in terminal extension and late patellofemoral degenerative joint disease (28,31).
Fragmentation of the lower pole of the patella may occur in as many as 28% of patients with spastic cerebral palsy as knee flexion contracture progresses (32) (Fig 12). Increased stress and repeated minor trauma disturb ossification of the cartilaginous patella and can cause a stress fracture. Associated abnormalities include an elongated or crescent-shaped patella, chondromalacia, and tibial tubercle changes resembling Osgood-Schlatter disease. At radiography, fragmentation appears similar to Sinding-Larsen-Johansson disease, although patella alta and kneeflexion deformity are characteristic of spastic cerebral palsy (27,32).
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Figure 12a. Progression of patella alta and patellar fragmentation. Sequential lateral radiographs show early patella alta at 12 years of age (Insall-Salvati ratio [A/B] = 4.3/2.8 = 1.5, normal value < 1.2) (a); patella alta with early patellar fragmentation at 13 years of age (b); and progressive fragmentation of the inferior patellar pole and patella alta at 19 years of age (c). In (c), note that a distal femoral extension osteotomy has been performed to help correct the knee flexion deformity.
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Figure 12b. Progression of patella alta and patellar fragmentation. Sequential lateral radiographs show early patella alta at 12 years of age (Insall-Salvati ratio [A/B] = 4.3/2.8 = 1.5, normal value < 1.2) (a); patella alta with early patellar fragmentation at 13 years of age (b); and progressive fragmentation of the inferior patellar pole and patella alta at 19 years of age (c). In (c), note that a distal femoral extension osteotomy has been performed to help correct the knee flexion deformity.
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Figure 12c. Progression of patella alta and patellar fragmentation. Sequential lateral radiographs show early patella alta at 12 years of age (Insall-Salvati ratio [A/B] = 4.3/2.8 = 1.5, normal value < 1.2) (a); patella alta with early patellar fragmentation at 13 years of age (b); and progressive fragmentation of the inferior patellar pole and patella alta at 19 years of age (c). In (c), note that a distal femoral extension osteotomy has been performed to help correct the knee flexion deformity.
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Genu recurvatum (knee hyperextension in gait) may occur due to progression of rectus femoris contracture in association with gastrocnemius weakness, increased lumbar lordosis, and hip flexion deformity (25) (Fig 13). Genu valgus and genu varus can occur as a secondary process due to abnormalities at other joints, including excess femoral anteversion and valgus instability of the subtalar joint (31).
Treatment of knee flexion deformity is aimed at halting progression. Hamstring lengthening and adductor myotomy are usually combined with a quadriceps strengthening program (26). Distal rectus femoris transfer to the iliotibial band or semitendinosus tendon may be required (33). A distal femoral extension osteotomy can also help correct knee flexion deformity.
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Foot
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Equinus deformity (plantar-flexed calcaneus) is the most common musculoskeletal abnormality in patients with spastic cerebral palsy (15). A fixed or spastic contracture of the gastrocnemius and soleus causes the characteristic tiptoe or toe-heel gait with an inability to keep the heel in the shoe. Equinus is commonly associated with knee flexion and valgus or varus deformity of the hindfoot and forefoot (34).
Equinovalgus results from spasticity of the gastrocnemius, soleus, and peroneus brevis. Transient deformity typically becomes a fixed deformity with time as a result of muscle shortening. As the contracture worsens, the calcaneus becomes displaced posterolaterally and everts, allowing the talus to drop into a vertical position, causing a rocker-bottom deformity (34) (Fig 14). Joint abnormalities may develop, including talonavicular subluxation and severe chondromalacia at the talocalcaneal, talonavicular, and metatarsophalangeal joints (35). Unrelenting progression is typical, without spontaneous improvement (36).
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Figure 14a. Equinovalgus and rocker-bottom deformity. (a) Lateral radiograph shows equinus deformity (plantar-flexed calcaneus) and hindfoot valgus (increased talocalcaneal angle), which result in rocker-bottom deformity. (b) Anteroposterior radiograph shows hindfoot valgus, with the talus directed medial to the base of the first metatarsal.
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Figure 14b. Equinovalgus and rocker-bottom deformity. (a) Lateral radiograph shows equinus deformity (plantar-flexed calcaneus) and hindfoot valgus (increased talocalcaneal angle), which result in rocker-bottom deformity. (b) Anteroposterior radiograph shows hindfoot valgus, with the talus directed medial to the base of the first metatarsal.
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Equinovarus is less common than equinovalgus and is twice as common in males, with a reported prevalence of up to 20% in patients with spastic cerebral palsy (37). Increased parallelism of the talus and calcaneus (decreased talocalcaneal angle) is seen on both lateral and anteroposterior radiographs in hindfoot varus (Fig 15). Adduction and inversion deformities of the hindfoot and forefoot are often present along with equinus.
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Figure 15a. Equinovarus. Lateral (a) and anteroposterior (b) radiographs show hindfoot equinus and hindfoot varus, which is characterized by increased parallelism of the talus and calcaneus (ie, decreased talocalcaneal angle).
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Figure 15b. Equinovarus. Lateral (a) and anteroposterior (b) radiographs show hindfoot equinus and hindfoot varus, which is characterized by increased parallelism of the talus and calcaneus (ie, decreased talocalcaneal angle).
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The goal of treatment is to prevent and correct deformities to increase function. Physical therapy and braces attempt to stretch shortened muscles (34,38). Surgical therapy involves proximal release or elongation of the distal tendon or permanent muscle weakening by neurectomy or tendon transfer. The most common operation is Achilles tendon lengthening (39).
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Conclusions
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Cerebral palsy is a central nervous system disorder characterized by muscle spasticity and contracture. Progressive bone and joint radiographic findings are seen in the spine and lower extremities. Scoliosis and flexion deformities of the hips, knees, and feet occur. Early recognition of progressive deformity allows timely treatment and prevention of irreversible change.
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E. G Fowler, T. H. Kolobe, D. L Damiano, D. E Thorpe, D. W Morgan, J. E Brunstrom, W. J Coster, R. C Henderson, K. H Pitetti, J. H Rimmer, et al.
Promotion of Physical Fitness and Prevention of Secondary Conditions for Children With Cerebral Palsy: Section on Pediatrics Research Summit Proceedings
Physical Therapy,
November 1, 2007;
87(11):
1495 - 1510.
[Abstract]
[Full Text]
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G. de Lissovoy, L. S. Matza, H. Green, M. Werner, and T. Edgar
Cost-effectiveness of Intrathecal Baclofen Therapy for the Treatment of Severe Spasticity Associated With Cerebral Palsy
J Child Neurol,
January 1, 2007;
22(1):
49 - 59.
[Abstract]
[PDF]
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J.M. Rodda, H.K. Graham, G.R. Nattrass, M.P. Galea, R. Baker, and R. Wolfe
Correction of Severe Crouch Gait in Patients with Spastic Diplegia with Use of Multilevel Orthopaedic Surgery
J. Bone Joint Surg. Am.,
December 1, 2006;
88(12):
2653 - 2664.
[Abstract]
[Full Text]
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Abstract
LEARNING OBJECTIVES FOR TEST...
