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Orthopaedic Manifestations of Familial Dysautonomia A Review of One Hundred and Thirty-six Patients*
Elhanan Bar-On, M.D.†; Yizhar Floman, M.D.‡; Shaul Sagiv, M.D.§; Kalman Katz, M.D.†; Rivka D. Pollak, M.D.#; Channa Maayan, M.D.#
View Disclosures and Other Information
Investigation performed at Hadassah Medical Center, Jerusalem, and Schneider Children's Medical Center of Israel, Rabin Medical Center, Petach-Tivka, Israel
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.
†Pediatric Orthopedic Unit, Schneider Children's Medical Center of Israel, 14 Kaplan Street, Petach-Tivka 49202, Israel. E-mail address for E. Bar-On: elbar@barak-online.net.
‡Israel Spine Center, Assuta Hospital, 62 Jabotinsky Street, Tel Aviv 62748, Israel.
§Department of Orthopedics, Kaplan Medical Center, P.O. Box 1, Rehovot 76100, Israel.
#Department of Medicine (R. D. P.) and Israel Center for Familial Dysautonomia (C. M.), Hadassah University Hospital, Mount Scopus, Jerusalem 91240, Israel.

The Journal of Bone & Joint Surgery.  2000; 82:1563-1563 
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Abstract

Background: Familial dysautonomia is a hereditary multisystemic disease primarily affecting people of Ashkenazi Jewish descent. Musculoskeletal problems are related to gait disorders, spinal deformities, foot deformities, fractures, and arthropathies.

Methods: The charts and radiographs of 136 patients who ranged in age from three months to forty-six years (mean, sixteen years) were reviewed. Sixty-four patients were available for follow-up examination.

Results: Spinal deformity was the most common orthopaedic problem and was diagnosed in seventy-eight patients starting at the age of four years, with a prevalence of 86 percent (forty-eight of fifty-six) by the age of fifteen years. Forty-one (53 percent) of the seventy-eight patients had scoliosis only, thirty-four (44 percent) had kyphoscoliosis, and three (4 percent) had kyphosis only. Bracing was accompanied by emotional, pulmonary, and skin problems, leading to a high rate of noncompliance and progression of the curve.

Twenty-four patients had an operation at a mean age of thirteen years (range, five to eighteen years): twenty patients had posterior spinal arthrodesis, and four had combined anterior and posterior arthrodesis. Fifteen patients had a total of nineteen complications, of which seven were systemic and twelve were related to the spinal fixation. Eight patients had revision surgery. At the time of the surgery, scoliosis was corrected from a mean of 55 degrees to a mean of 35 degrees and kyphosis was corrected from a mean of 69 degrees to a mean of 61 degrees.

After a mean duration of follow-up of sixty-five months, scoliosis measured 49 degrees (range, 18 to 62 degrees) and kyphosis measured 67 degrees (range, 30 to 115 degrees). Postoperative progression of the deformity was caused by failure of the instrumentation or progression in unfused segments. Walking was delayed in 72 percent (ninety-four) of the 130 patients who were of walking age. All sixty-four of the patients who were examined had an ataxic gait. Foot deformities were found in sixteen patients, six of whom were treated surgically. Two patients had Charcot joints. Fifty-five patients sustained at least one fracture before skeletal maturity, with a mean of 1.5 fractures per patient. All but one of the fractures was treated nonoperatively, and fracture-healing was often accompanied by profuse callus formation.

Conclusions: Spinal deformity is common in patients with familial dysautonomia. Bracing is of questionable benefit, and surgical intervention should be considered once curve progression is well documented. Arthrodesis should be extended as far proximally as possible to prevent junctional kyphosis. Swelling and warmth in a limb should raise suspicion of an undiagnosed fracture.

Figures in this Article
    Familial dysautonomia, also known as Riley-Day syndrome8,18 or hereditary sensory and autonomic neuropathy Type III9, is a multisystemic disease with numerous musculoskeletal manifestations. Inheritance is autosomal recessive, and, with one exception13, all reported cases3 have been in patients of Ashkenazi Jewish descent. The prevalence in this population has been found to be twenty-seven per 100,000 individuals15.
    The gene responsible has been mapped to chromosome 9q31-q33, and DNA markers now enable prenatal diagnosis and carrier identification7. The pathological processes of the disease include a decrease in peripheral unmyelinated and small myelinated neuronal fibers as well as a paucity of neurons in the spinal cord and in sensory and autonomic ganglia17. In addition, the metabolism of catecholamine is impaired. It is unclear which of these factors is the primary defect, and the exact pathogenesis of the disease has yet to be clarified5,9.
    The diagnostic criteria include Ashkenazi Jewish heritage, diminished tear production, lack of axon flare after intradermal injection of histamines, lack of lingual fungiform papillae, and decreased deep-tendon reflexes. Clinical features include diminished pain sensation, unexplained fevers, hypertension, and postural hypotension caused by defective control mechanisms for temperature and blood pressure. Patients have oropharyngeal incoordination and abnormal gastroesophageal motility, causing feeding difficulties, vomiting, and recurrent aspiration pneumonia, which in turn lead to chronic lung disease. Developmental milestones and maturation are delayed, and there is an increased prevalence of convulsions, especially at an older age2,8,9. Musculoskeletal problems are related to gait disorders, foot deformities, arthropathies, fractures, and spinal deformities1,10-12,16,19,20,24.
    The purpose of our study was to examine these orthopaedic problems with regard to age at onset, clinical consequences, and results of treatment.
     
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    +Fig. 1: Radiograph, made fifteen years and nine months postoperatively, showing progression of the scoliotic curve distal to the site of the arthrodesis in a thirty-year-old woman. The progression is causing decompensation.
     
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    +Fig. 2: Radiograph, made two years postoperatively, showing cervicothoracic kyphosis proximal to the site of the arthrodesis in a thirteen-year-old girl.
     
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    +Fig. 3: Radiograph, made one year and eight months postoperatively, showing pullout of the hook at the proximal end of the instrumentation in a fifteen-year-old girl.
     
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    +Fig. 4: Radiograph, made two years and ten months postoperatively, showing pullout of the screw at the distal end of the instrumentation with disengagement of the transverse crosslink in an eighteen-year-old man.
     
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    +Fig. 5:Radiograph showing severe genu valgum with early Charcot arthropathy of the left knee in a twenty-five-year-old man. The patient was treated with a distal femoral osteotomy.
     
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    +Fig. 6:Radiograph showing bilateral slipped capital femoral epiphysis in a five-year-old boy. The painless hip was treated nonoperatively, and the painful hip was treated with screw fixation.
     
    Anchor for JumpAnchor for JumpTable I:  Distribution of Fractures
    LocationNo. of Fractures
    Radius and/or ulna28
    Tibia and/or fibula16
    Hand14
    Humerus  8
    Femur  7
    Clavicle  6
    Foot  6
    Patella  1
    Mandible  1
      Total87
    The Israel Center for Familial Dysautonomia at Hadassah University Hospital in Mount Scopus and Hebrew University in Jerusalem, Israel, is a national referral center for patients with familial dysautonomia. One hundred and thirty-six patients who were registered in the center formed the base of our study. The charts and radiographs of all of the patients were reviewed. Of ninety living patients, sixty-four were available for examination by the senior author (E. B.-O.) at the time of the study.
    We recorded data regarding milestones in motor development, gait disturbances, spine and limb deformities, arthropathies, fractures, and musculoskeletal infections or decubitus ulcers, as well as any additional problems that may affect musculoskeletal function.
    The records of 136 patients (sixty-five males and seventy-one females) were reviewed. The mean age of the patients at the time of the review was sixteen years (range, three months to forty-six years). Fifty-six patients (41 percent) were in the first decade of life, forty-one (30 percent) were in the second decade, and thirty-nine (29 percent) were in the third or fourth decade. At the time of the review, forty-six patients had died. The mean age at the time of death was nineteen years (range, three months to forty-four years). Fourteen (30 percent) of these forty-six patients died in the first decade of life; ten (22 percent), in the second decade; and twenty-two (48 percent), in the third or fourth decade.
    The most common causes of death were acute aspiration (thirteen patients; 28 percent) and chronic pneumonia (ten patients; 22 percent). Additional causes included sudden death during sleep (eight patients; 17 percent), trauma from either a fall or a motor-vehicle accident (two patients; 4 percent), and various other causes such as drug overdose or surgical complications (four patients; 9 percent). The cause of death was not clear for the remaining nine patients (20 percent).
    The most common orthopaedic problems were gait abnormalities, spinal deformities, foot deformities, fractures, and Charcot arthropathy.

    Gait Abnormalities

    Independent walking was started at a mean age of twenty-seven months (range, fourteen to eighty-four months). It was delayed beyond the normal age of eighteen months in 72 percent (ninety-four) of the 130 patients who were of walking age. All sixty-four patients who were examined had an ataxic gait, although the degree of ataxia was highly variable. Despite these gait disturbances, all of these patients retained the ability to walk and none required assistive devices.

    Foot Deformities

    Foot deformities were found in sixteen (12 percent) of the 136 patients. Nine patients had an equinovarus or cavovarus deformity, five had a planovalgus deformity, and two had polydactyly.
    An equinovarus or cavovarus deformity developed during childhood in eight patients; the remaining patient who had such a deformity had a congenital clubfoot. No associated spasticity was found in any patient. Three of the nine patients had operative treatment. The patient with a congenital clubfoot had a posteromedial release at the age of five months. He needed a re-release at the age of two years, but, at the time of the review, correction had been maintained through the age of thirteen years. The other two patients had surgery for a progressive deformity. One patient had a plantar and posterior release at the age of nine years. She required a relengthening of the Achilles tendon one year later, but, at the time of the review, correction had been maintained through the age of fifteen years. The other patient had a posterior release at the age of thirteen years and wore an ankle-foot orthosis until his death at the age of twenty-nine years. In the remaining six patients, the deformity was adequately managed with shoe modifications and did not interfere with walking.
    Although all five patients who had a planovalgus deformity had bothersome pressure points on the medial side of the foot, four of the patients were adequately treated with shoe modifications. The fifth patient had a bilateral distal tibiofibular derotation osteotomy. She subsequently had multiple decubitus ulcers and osteomyelitis of the os calcis, which were treated with d衲idement.
    Both of the patients with polydactyly were treated operatively.

    Spinal Deformity

    Spinal deformity was found in seventy-eight patients. Thirty-six of these patients were male and forty-two were female, for a male:female ratio of 1:1.2. Spinal deformity was diagnosed at a mean age of eight years (range, four to sixteen years), and baseline radiographs were made once the deformity was noted clinically. The prevalence of spinal deformity was 48 percent (thirty-eight of eighty) by the age of ten years, 86 percent (forty-eight of fifty-six) by the age of fifteen years, and 85 percent (thirty-three of thirty-nine) by the age of twenty years or more.
    Forty-one patients (53 percent) had scoliosis only, thirty-four (44 percent) had kyphoscoliosis, and three (4 percent) had kyphosis without scoliosis. The curve pattern of the scoliosis in the seventy-five patients with a coronal deformity was highly variable. Forty-nine patients (65 percent) had a single thoracic or thoracolumbar curve; twenty-eight of these curves were to the right and twenty-one were to the left. Twenty-six patients (35 percent) had a double curve; fourteen had a right thoracic or thoracolumbar curve and a left lumbar curve, and twelve had a left thoracic or thoracolumbar curve and a right lumbar curve. Thoracic hyperkyphosis was found in 65 percent (seventeen) of the twenty-six patients with a double curve but in only 33 percent (sixteen) of the forty-nine patients with a single curve.

    Nonoperative Treatment

    Twenty-three patients were treated with a cast or brace. A cast was used for one patient who was treated early, a Milwaukee brace was used for sixteen patients, and an underarm thoracolumbar spinal orthosis was used for eight patients (two of whom had initially been treated with a Milwaukee brace). Bracing was initiated at a mean age of ten years and was continued for a mean of three years. The mean curve was 34 degrees (range, 23 to 51 degrees) at the start of bracing and 56 degrees (range, 28 to 79 degrees) at the end of bracing. Bracing was accompanied by multiple pulmonary problems and pressure sores, causing discontinuation of treatment in four patients. These problems, as well as the emotional lability associated with familial dysautonomia, resulted in extremely poor compliance with the bracing. Three patients were lost to follow-up during brace treatment, and seventeen patients showed marked progression of the deformity. In only three patients was bracing continued successfully to maturity, with documented arrest of curve progression.

    Operative Treatment

    Twenty-four patients were treated operatively. In general, surgery was considered when the deformity reached 40 degrees of scoliosis and/or 65 degrees of kyphosis. However, the exact indication was dependent on the age and size of the patient, with attempts being made to postpone arthrodesis until adolescence. The decision was influenced by a number of other factors, including the patient's general, pulmonary, and nutritional status as well as parental consent.
    The mean age at the time of surgery was thirteen years (range, five to eighteen years). Fourteen patients had a single thoracic or thoracolumbar curve: eight curves were to the right and six were to the left. Ten patients had a double major curve: seven had a right thoracic and left lumbar curve, and three had a left thoracic and right lumbar curve. Seventeen patients had a kyphotic curve of more than 50 degrees,and in three patients the sagittal deformity was the primary indication for surgery.
    Twenty patients had a posterior spinal arthrodesis with use of Harrington instrumentation (thirteen patients), Harrington-Luque instrumentation (one patient), or Cotrel-Dubousset instrumentation (six patients). Four other patients, who had a kyphotic deformity of 87 to 110 degrees, underwent combined one-stage anterior and posterior arthrodesis with Cotrel-Dubousset instrumentation. Harrington or Harrington-Luque instrumentation was used until 1991; since then, Cotrel-Dubousset has been the instrumentation of choice.
    In the group as a whole, scoliosis was corrected from a mean of 55 degrees (range, 20 to 90 degrees) to a mean of 35 degrees (range, 20 to 50 degrees), which represented a mean correction of 36 percent. In the group of twenty-one patients in whom the primary indication for surgery was progressive coronal deformity, the mean scoliotic curve measured 60 degrees (range, 38 to 90 degrees) preoperatively and 37 degrees (range, 20 to 50 degrees) immediately postoperatively, constituting a mean correction of 38 percent (range, 19 to 68 percent). When these patients were divided into those with and without kyphosis, we found no differences between the two groups regarding the magnitude of the preoperative coronal curve or the amount of correction obtained at the time of the operation.
    In the group as a whole, kyphosis was corrected from a mean of 69 degrees (range, 43 to 110 degrees) to a mean of 61 degrees (range 30 to 100 degrees), which represented a mean correction of 12 percent (range, -29 to 48 percent). In the group of three patients in whom the sagittal deformity was the primary indication for surgery, the mean kyphotic curve measured 80 degrees preoperatively and 71 degrees postoperatively; specifically, the curve decreased from 63 to 44 degrees in one patient, from 87 to 85 degrees in another, and from 90 to 85 degrees in the third.
    At the time of the latest examination, performed at a mean of sixty-five months (range, twelve to 192 months) postoperatively, the mean scoliosis measured 49 degrees (range, 18 to 62 degrees) and the mean kyphosis measured 67 degrees (range, 39 to 115 degrees). Compared with the preoperative values, this constituted a mean correction of 18 percent (range, -25 to 50 percent) for scoliosis and 3 percent (range, -64 to 50 percent) for kyphosis. Progression at the site of the arthrodesis did not occur unless the instrumentation had failed. Progression of scoliosis occurred both distal (Fig. 1) and proximal to the site of the arthrodesis, whereas progression of kyphosis occurred only proximal to the site of the arthrodesis (Fig. 2).

    Complications and Reoperations

    There were a total of nineteen complications in fifteen patients. Early complications included severe postoperative hypovolemia in two patients, one of whom died and one of whom was resuscitated. Four patients had pneumonia. One case progressed to generalized sepsis and necessitated a prolonged period of intensive care in the hospital. One patient had upper gastrointestinal bleeding.
    Twelve complications, in nine patients, were related to the hardware used in the spinal fixation. The complications included hook disengagement at either end of the instrumentation in six patients (three of whom had been treated with Harrington instrumentation and three of whom had been treated with Cotrel-Dubousset instrumentation) (Fig. 3), hardware breakage in two patients who had been treated with Harrington instrumentation, screw pullout in one patient who had been treated with Cotrel-Dubousset instrumentation (Fig. 4), and screw misplacement in one patient who had been treated with Cotrel-Dubousset instrumentation. These complications generally occurred in the early postoperative period, and there were no proven cases of pseudarthrosis. One patient had a deep infection with Proteus mirabilis, and one had skin irritation over the hardware. In addition, four patients had decompensation in the coronal plane. Two of them had revision surgery, at six and sixteen years after the initial arthrodesis.
    Eight (33 percent) of the twenty-four patients who had been treated surgically needed at least one additional procedure. A total of ten revision operations were performed.

    Fractures

    A total of eighty-seven fractures occurred in fifty-five patients (40 percent). Twenty-seven patients had one fracture, thirteen had two, and nine had three or more. Eighty-three of the eighty-seven fractures occurred before skeletal maturity. The anatomical distribution of the fractures is shown in Table I. Because of decreased pain sensation, fractures were often diagnosed late, after parents noted local swelling and warmth. This was especially true of fractures of the hand and foot. One fracture of the proximal aspect of the femur was treated with internal fixation. All other fractures were treated nonoperatively. Fracture-healing often occurred with profuse callus formation. There were no cases of delayed union or nonunion.

    Charcot Joints

    Evidence of Charcot arthropathy (joint effusion, instability, and arthritic changes) was found in two patients. One of the patients had bilateral ankle involvement, which was treated with observation only, and the other patient had severe genu valgum (Fig. 5), which was treated with a distal femoral osteotomy.

    Additional Musculoskeletal Problems

    Three patients had an obstetrical brachial plexus palsy, two were being followed for asymptomatic acetabular dysplasia, one had mild spastic hemiplegia due to neonatal asphyxia, one had Perthes disease and was treated with a varus derotation osteotomy, and one had bilateral slipped capital femoral epiphysis at the age of five years. This last patient had received prolonged corticosteroid treatment for severe pulmonary problems. One of the hips in this patient was painless and was treated nonoperatively; the contralateral hip was painful and was treated operatively with screw fixation (Fig. 6). Although a pseudarthrosis developed on the side that had been treated nonoperatively, the patient regained the ability to walk and the pain on the contralateral side reversed after screw fixation.
    There are two known major concentrations of patients with familial dysautonomia: one is in North America, and the other is in Israel. In 1971, Yoslow et al.24 reviewed the orthopaedic problems in a group of sixty-five patients at New York University Medical Center. Rubery et al.20 recently reported their experience with surgical treatment of spinal deformity in twenty-two patients from the same center. The treatment of spinal deformity in some of the patients followed in the Jerusalem center was reviewed in 1984 by Robin19 and more recently by Kaplan et al.12.
    Because of the rarity of familial dysautonomia, several reports regarding the musculoskeletal aspects of the disease have included small numbers of patients or have grouped them with patients who had various other neuromuscular disorders that predominantly affect sensory pathways or motor function1,10,11. However, the problems found in patients with familial dysautonomia differ importantly from those found in patients with other neuromuscular conditions2. In addition, patients with familial dysautonomia have a variety of medical problems that have a direct effect on orthopaedic management. Although the deformities seen in these patients seem to be of neurogenic origin, the neurological defect that is associated with the disease affects the afferent pathways and the agonist-antagonist muscle balance is normal and without spasticity. The gait disturbance is mainly due to ataxia, probably resulting from defective proprioception with the additional factors of unbalanced spinal deformity and generalized weakness. Although the onset of gait was delayed in most of our patients, they retained independent walking ability throughout life. Muscle balance around the foot and ankle is normal, and the reason for the increased prevalence of foot deformities in patients with the disease remains unclear.
    Joint problems were rare in our study. Only two (1.5 percent) of the 136 patients had acetabular dysplasia compared with eleven (17 percent) of the sixty-five patients in the study by Yoslow et al.24. However, because pelvic radiographs were not made routinely in the present study and because the dysplasia in both patients was asymptomatic and discovered incidentally, we cannot comment on the true prevalence of hip dysplasia in our series.
    One of our patients had Perthes disease, and two had Charcot joints. Our findings may be comparable with those of Mitnick et al.16. Nine of their 180 patients had avascular necrosis, and three of the nine had necrosis of the hip. Distinguishing between Charcot joints and avascular necrosis in peripheral joints may be difficult. Slipped capital femoral epiphysis has not been previously described in association with familial dysautonomia, to our knowledge. It may have occurred in one of our patients because of prolonged steroid treatment.
    The prevalence of fractures in patients with familial dysautonomia is not known. Yoslow et al.24 reported that nineteen (29 percent) of sixty-five patients with familial dysautonomia had sustained a total of twenty-eight fractures and stated that this prevalence was higher than would be expected in a normal population. However, in a large epidemiological survey of fractures in normal children, Landin14 found a prevalence of 42 percent in boys and 27 percent in girls in the general population of patients who were sixteen years old or less. In the present study, 40 percent (fifty-five) of the 136 patients (including 43 percent [twenty-eight] of the sixty-five male patients and 38 percent [twenty-seven] of the seventy-one female patients) sustained a fracture before skeletal maturity, a rate similar to the normal value found by Landin. Our findings, however, only include diagnosed fractures, many of which were detected late, and we presume that there were additional fractures that healed unnoticed.
    In addition, the number of fractures per patient was found to be substantially higher than in the normal population. Whereas Landin found 8682 fractures in 7961 children, for a mean of 1.1 fractures per child sustaining a fracture, we found a total of eighty-three fractures sustained before skeletal maturity in fifty-five children, for a mean of 1.5 fractures per child. When one considers that patients with familial dysautonomia are less involved in outdoor activities than healthy children are, we agree with Yoslow et al. that there is an increased prevalence of fractures in patients with familial dysautonomia. The reason for this is unclear, but it may be due to a reduction in the protective effect of pain sensation as a result of the sensory neuropathy. In our patients, fracture-healing appeared to be normal and was accompanied by profuse callus production. We did not encounter any cases of delayed healing or nonunion of fractures.
    Of special interest is the pathophysiology of the spinal deformity in patients with familial dysautonomia. The atypical curve patterns and their natural history are similar to those found in patients with various other neuromuscular conditions. However, patients with familial dysautonomia do not have the muscle weakness, imbalance, and lack of coordination that often are associated with these conditions. The reason for the development of the spinal deformities may be the disturbance in the afferent sensory pathways, and, indeed, an association between altered proprioceptive and vibratory sensation and idiopathic scoliosis has been reported22,23. The severity of the spinal deformity in patients with familial dysautonomia manifests not only in a high prevalence but also in early and severe progression. As the disease itself causes obstructive changes in pulmonary function, the effects of severe spinal deformity can be extremely harmful, adding a restrictive component, particularly as patients survive into adulthood with better medical management. In our series, bracing was not found to be effective for preventing or delaying curve progression, and its negative side effects - both cutaneous and pulmonary - were considerable. We believe that surgical intervention should not be postponed once notable curve progression is documented. Earlier intervention may increase the amount of correction that can be achieved. In the present study, the rate of complications was high (79 percent; nineteen of twenty-four), with one-third (eight) of the twenty-four patients having a total of ten additional surgical procedures; however, it compares favorably with the rates reported in other series. Albanese and Bobechko1 reported complications in all sixteen of their patients. Rubery et al.20 reported that fifteen (68 percent) of their twenty-two patients had a major complication and that a total of twenty-nine reoperations were performed to treat complications.
    The postoperative loss of correction during the follow-up period is of concern and probably has several causes. There was a high rate of fixation failure, resulting from both hardware breakage and hook and screw pullout. The deforming force is great, as evidenced by the severe preoperative progression. Many patients have poor bone quality, and increased early motion postoperatively (resulting from a lack of guarding created by the sensory changes) also may play a part in weakening the fixation (Fig. 3 and Fig. 4). An additional cause of loss of correction was continued progression of the deformity proximal and distal to the site of the arthrodesis, especially in the sagittal plane. The development of severe kyphosis proximal to the site of the arthrodesis has also been observed by other authors1,20. We therefore agree with Rubery et al.20 that the arthrodesis should be extended as far proximally as possible. Although curve progression can also occur distally and although extending the arthrodesis distally might prevent such progression, we believe that lumbar motion segments should be preserved whenever possible because most patients with familial dysautonomia are usually fully able to walk.
    The problem of instrumentation failure may be partially solved by improved constructs combining hooks, wires, and pedicle screws. However, we believe that the possibility of instrumentation failure should be anticipated and that parents should be counseled accordingly. Although the postoperative loss of correction is of concern, deformity in the arthrodesed segments did not progress beyond preoperative values unless the instrumentation failed. Considering the natural history of severe progressive deformity in untreated patients6, we believe that preventing this progression is a reasonable operative goal that can be achieved with posterior spinal arthrodesis in most patients. The complication rate, although high, is decreasing because of improved medical, surgical, and anesthetic management3,4,21. The small number of patients treated with combined anterior and posterior arthrodesis does not allow us to draw clear conclusions regarding the efficacy of this approach.
    Albanese, S. A., and Bobechko, W. P.: Spine deformity in familial dysautonomia (Riley-Day syndrome). J. Pediat. Orthop.,7: 179-183, 1987.7179  1987 
     
    Axelrod, F. B., and Pearson, J.: Congenital sensory neuropathies. Diagnostic distinction from familial dysautonomia. Am. J. Dis. Child.,138: 947-954, 1984.138947  1984  [PubMed]
     
    Axelrod, F. B.; Donenfeld, R. F.; Danziger, F.; and Turndorf, H.: Anesthesia in familial dysautonomia. Anesthesiology,68: 631-635, 1988.68631  1988  [PubMed]
     
    Axelrod, F. B.; Gouge, T. H.; Ginsburg, H. B.; Bangaru, B. S.; and Hazzi, C.: Fundoplication and gastrostomy in familial dysautonomia. J. Pediat.,118: 388-394, 1991.118388  1991  [PubMed]
     
    Axelrod, F. B.: Familial dysautonomia: a 47-year perspective. How technology confirms clinical acumen. J. Pediat.,132(3 part 2): 2-S5, 1998.132(3 part 2)2  1998 
     
    Bar-On, E.; Harari, M.; Floman, Y.; Bar-Ziv, J.; and Maayan, C.: Compression of the esophagus by the spine and the aorta in untreated scoliosis. Arch. Orthop. and Trauma Surg.,117: 405-407, 1998.117405  1998 
     
    Blumenfeld, A.; Slaugenhaupt, S. A.; Axelrod, F. B.; Lucente, D. E.; Mayaan, C.; Liebert, C. B.; Ozelius, L. J.; Trofatter, J. A.; Haines, J. L.; Breakefield, X. O.; and Gusella, J. F.: Localization of the gene for familial dysautonomia on chromosome 9 and definition of DNA markers for genetic diagnosis. Nature Genet.,4: 160-164, 1993.4160  1993  [PubMed]
     
    Dancis, J.: Familial dysautonomia (Riley-Day syndrome). In Autonomic Failure, pp. 615-639. Edited by R. Bannister. New York, Oxford University Press, 1983. 
     
    Dyck, P. J.: Neuronal atrophy and degeneration predominantly affecting peripheral sensory and autonomic neurons. In Peripheral Neuropathy, edited by P. J. Dyck, P. K. Thomas, G. W. Griffin, P. A. Low, and J. F. Podulso. Ed. 3, pp. 1065-1093. Philadelphia, W. B. Saunders, 1993. 
     
    Guidera, K. S.; Multhopp, H.; Ganey, T.; and Ogden, J. A.: Orthopaedic manifestations in congenitally insensate patients. J. Pediat. Orthop.,10: 514-521, 1990.10514  1990 
     
    Hensinger, R. N., and MacEwen, G. D.: Spinal deformity associated with heritable neurological conditions: spinal muscular atrophy, Friedrich's ataxia, familial dysautonomia, and Charcot-Marie-Tooth disease. J. Bone and Joint Surg.,58-A: 13-24, Jan 1976.58-A13  1976 
     
    Kaplan, L.; Margulies, J. Y.; Kadari, A.; Floman, Y.; and Robin, G. C.: Aspects of spinal deformity in familial dysautonomia (Riley-Day syndrome). European Spine J.,6: 33-38, 1997.633  1997 
     
    Klebanoff, M. A., and Neff, J. M.: Familial dysautonomia associated with recurrent osteomyelitis in a non-Jewish girl. J. Pediat.,,96: 75-77, 1980.9675  1980 
     
    Landin, L. A.: Fracture patterns in children. Analysis of 8,682 fractures with special reference to incidence, etiology and secular changes in a Swedish urban population 1950-1979. Acta Orthop. Scandinavica,Supplementum : 202, 1983.Supplementum 202  1983 
     
    Maayan, C.; Kaplan, E.; Shachar, S.; Peleg, O.; and Godfrey, S.: Incidence of familial dysautonomia in Israel 1977-1981. Clin. Genet.,32: 106-108, 1987.32106  1987  [PubMed]
     
    Mitnick, J. S.; Axelrod, F. B.; Genieser, N. B.; and Becker, M.: Aseptic necrosis in familial dysautonomia. Radiology,142: 89-91, 1982.14289  1982  [PubMed]
     
    Pearson, J., and Pytel, B. A.: Quantitative studies of sympathetic ganglia and spinal cord intermedio-lateral gray columns in familial dysautonomia. J. Neurol. Sci.,,39: 47-59, 1978.3947  1978 
     
    Riley, C. M.; Day, R. L.; Greeley, D. M.; and Langford, W. S.: Central autonomic dysfunction with defective lacrimation: a report of 5 cases. Pediatrics,3: 468-477, 1949.3468  1949  [PubMed]
     
    Robin, G. C.: Scoliosis in familial dysautonomia. Bull. Hosp. Joint Dis.,44: 16-26, 1984.4416  1984 
     
    Rubery, P. T.; Spielman, J. H.; Hester, P.; Axelrod, E.; Burke, S. W.; and Levine, D. B.: Scoliosis in familial dysautonomia. Operative treatment. J. Bone and Joint Surg.,77-A: 1362-1369, Sept 1995.77-A1362  1995 
     
    Udassin, R.; Seror, D.; Vinograd, I.; Zamir, O.; Godfrey, S.; and Nissan, S.: Nissen fundoplication in the treatment of children with familial dysautonomia. Am. J. Surg.,164: 332-336, 1992.164332  1992  [PubMed]
     
    Wyatt, M. P.; Barrack, R. L.; Mubarak, S. J.; Whitecloud, T. S.; and Burke, S. W.: Vibratory response in idiopathic scoliosis. J. Bone and Joint Surg.,68-B(5): 714-718, 1986.68-B(5)714  1986 
     
    Yekutiel, M.; Robin, G. C.; and Yarom, R.: Proprioceptive function in children with adolescent idiopathic scoliosis. Spine,6: 560-566, 1981.6560  1981  [PubMed]
     
    Yoslow, W.; Becker, M. J.; Bartels, J.; and Thompson, W. A. L.: Orthopaedic defects in familial dysautonomia. A review of sixty-five cases. J. Bone and Joint Surg.,,53-A: 1541-1550, Dec 1971.53-A1541  1971 
     

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    Anchor for JumpAnchor for Jump
    +Fig. 1: Radiograph, made fifteen years and nine months postoperatively, showing progression of the scoliotic curve distal to the site of the arthrodesis in a thirty-year-old woman. The progression is causing decompensation.
    Anchor for JumpAnchor for Jump
    +Fig. 2: Radiograph, made two years postoperatively, showing cervicothoracic kyphosis proximal to the site of the arthrodesis in a thirteen-year-old girl.
    Anchor for JumpAnchor for Jump
    +Fig. 3: Radiograph, made one year and eight months postoperatively, showing pullout of the hook at the proximal end of the instrumentation in a fifteen-year-old girl.
    Anchor for JumpAnchor for Jump
    +Fig. 4: Radiograph, made two years and ten months postoperatively, showing pullout of the screw at the distal end of the instrumentation with disengagement of the transverse crosslink in an eighteen-year-old man.
    Anchor for JumpAnchor for Jump
    +Fig. 5:Radiograph showing severe genu valgum with early Charcot arthropathy of the left knee in a twenty-five-year-old man. The patient was treated with a distal femoral osteotomy.
    Anchor for JumpAnchor for Jump
    +Fig. 6:Radiograph showing bilateral slipped capital femoral epiphysis in a five-year-old boy. The painless hip was treated nonoperatively, and the painful hip was treated with screw fixation.
    Anchor for JumpAnchor for JumpTable I:  Distribution of Fractures
    LocationNo. of Fractures
    Radius and/or ulna28
    Tibia and/or fibula16
    Hand14
    Humerus  8
    Femur  7
    Clavicle  6
    Foot  6
    Patella  1
    Mandible  1
      Total87
    Albanese, S. A., and Bobechko, W. P.: Spine deformity in familial dysautonomia (Riley-Day syndrome). J. Pediat. Orthop.,7: 179-183, 1987.7179  1987 
     
    Axelrod, F. B., and Pearson, J.: Congenital sensory neuropathies. Diagnostic distinction from familial dysautonomia. Am. J. Dis. Child.,138: 947-954, 1984.138947  1984  [PubMed]
     
    Axelrod, F. B.; Donenfeld, R. F.; Danziger, F.; and Turndorf, H.: Anesthesia in familial dysautonomia. Anesthesiology,68: 631-635, 1988.68631  1988  [PubMed]
     
    Axelrod, F. B.; Gouge, T. H.; Ginsburg, H. B.; Bangaru, B. S.; and Hazzi, C.: Fundoplication and gastrostomy in familial dysautonomia. J. Pediat.,118: 388-394, 1991.118388  1991  [PubMed]
     
    Axelrod, F. B.: Familial dysautonomia: a 47-year perspective. How technology confirms clinical acumen. J. Pediat.,132(3 part 2): 2-S5, 1998.132(3 part 2)2  1998 
     
    Bar-On, E.; Harari, M.; Floman, Y.; Bar-Ziv, J.; and Maayan, C.: Compression of the esophagus by the spine and the aorta in untreated scoliosis. Arch. Orthop. and Trauma Surg.,117: 405-407, 1998.117405  1998 
     
    Blumenfeld, A.; Slaugenhaupt, S. A.; Axelrod, F. B.; Lucente, D. E.; Mayaan, C.; Liebert, C. B.; Ozelius, L. J.; Trofatter, J. A.; Haines, J. L.; Breakefield, X. O.; and Gusella, J. F.: Localization of the gene for familial dysautonomia on chromosome 9 and definition of DNA markers for genetic diagnosis. Nature Genet.,4: 160-164, 1993.4160  1993  [PubMed]
     
    Dancis, J.: Familial dysautonomia (Riley-Day syndrome). In Autonomic Failure, pp. 615-639. Edited by R. Bannister. New York, Oxford University Press, 1983. 
     
    Dyck, P. J.: Neuronal atrophy and degeneration predominantly affecting peripheral sensory and autonomic neurons. In Peripheral Neuropathy, edited by P. J. Dyck, P. K. Thomas, G. W. Griffin, P. A. Low, and J. F. Podulso. Ed. 3, pp. 1065-1093. Philadelphia, W. B. Saunders, 1993. 
     
    Guidera, K. S.; Multhopp, H.; Ganey, T.; and Ogden, J. A.: Orthopaedic manifestations in congenitally insensate patients. J. Pediat. Orthop.,10: 514-521, 1990.10514  1990 
     
    Hensinger, R. N., and MacEwen, G. D.: Spinal deformity associated with heritable neurological conditions: spinal muscular atrophy, Friedrich's ataxia, familial dysautonomia, and Charcot-Marie-Tooth disease. J. Bone and Joint Surg.,58-A: 13-24, Jan 1976.58-A13  1976 
     
    Kaplan, L.; Margulies, J. Y.; Kadari, A.; Floman, Y.; and Robin, G. C.: Aspects of spinal deformity in familial dysautonomia (Riley-Day syndrome). European Spine J.,6: 33-38, 1997.633  1997 
     
    Klebanoff, M. A., and Neff, J. M.: Familial dysautonomia associated with recurrent osteomyelitis in a non-Jewish girl. J. Pediat.,,96: 75-77, 1980.9675  1980 
     
    Landin, L. A.: Fracture patterns in children. Analysis of 8,682 fractures with special reference to incidence, etiology and secular changes in a Swedish urban population 1950-1979. Acta Orthop. Scandinavica,Supplementum : 202, 1983.Supplementum 202  1983 
     
    Maayan, C.; Kaplan, E.; Shachar, S.; Peleg, O.; and Godfrey, S.: Incidence of familial dysautonomia in Israel 1977-1981. Clin. Genet.,32: 106-108, 1987.32106  1987  [PubMed]
     
    Mitnick, J. S.; Axelrod, F. B.; Genieser, N. B.; and Becker, M.: Aseptic necrosis in familial dysautonomia. Radiology,142: 89-91, 1982.14289  1982  [PubMed]
     
    Pearson, J., and Pytel, B. A.: Quantitative studies of sympathetic ganglia and spinal cord intermedio-lateral gray columns in familial dysautonomia. J. Neurol. Sci.,,39: 47-59, 1978.3947  1978 
     
    Riley, C. M.; Day, R. L.; Greeley, D. M.; and Langford, W. S.: Central autonomic dysfunction with defective lacrimation: a report of 5 cases. Pediatrics,3: 468-477, 1949.3468  1949  [PubMed]
     
    Robin, G. C.: Scoliosis in familial dysautonomia. Bull. Hosp. Joint Dis.,44: 16-26, 1984.4416  1984 
     
    Rubery, P. T.; Spielman, J. H.; Hester, P.; Axelrod, E.; Burke, S. W.; and Levine, D. B.: Scoliosis in familial dysautonomia. Operative treatment. J. Bone and Joint Surg.,77-A: 1362-1369, Sept 1995.77-A1362  1995 
     
    Udassin, R.; Seror, D.; Vinograd, I.; Zamir, O.; Godfrey, S.; and Nissan, S.: Nissen fundoplication in the treatment of children with familial dysautonomia. Am. J. Surg.,164: 332-336, 1992.164332  1992  [PubMed]
     
    Wyatt, M. P.; Barrack, R. L.; Mubarak, S. J.; Whitecloud, T. S.; and Burke, S. W.: Vibratory response in idiopathic scoliosis. J. Bone and Joint Surg.,68-B(5): 714-718, 1986.68-B(5)714  1986 
     
    Yekutiel, M.; Robin, G. C.; and Yarom, R.: Proprioceptive function in children with adolescent idiopathic scoliosis. Spine,6: 560-566, 1981.6560  1981  [PubMed]
     
    Yoslow, W.; Becker, M. J.; Bartels, J.; and Thompson, W. A. L.: Orthopaedic defects in familial dysautonomia. A review of sixty-five cases. J. Bone and Joint Surg.,,53-A: 1541-1550, Dec 1971.53-A1541  1971 
     
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