MUSCLE IMBALANCE IN THE AETIOLOGY OF IDIOPATHIC CLUB FOOT AN ELECTROMYOGRAPHIC

STUDY

z. FELDBRIN, A. N. GILAI, E. EZRA, 0. KHERMOSH, U. KRAMER, S. WIENTROUB From Dana Children ‘s Hospital, Tel-Aviv Medical Centre and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

We performed electrophysiological studies on both legs of 52 children, aged from 3 months to 15 years, with idiopathic club foot. In only nine (17%) was no abnormality found. Isolated peroneal nerve damage was seen in 14 (27%). Abnormality of both peroneal and posterior tibial nerves was found in five (10%). Four patients (8%) had evidence of isolated spinal-cord

dysfunction,

whereas

combined

spinal-cord

and

peripheral-nerve lesions were seen in 14 (27%). Six patients (11 %) had variable neurogenic

electrophysiological patterns. In 13 patients in whom the studies were repeated neither progression nor improvement of the electrophysiological parameters was observed. Pathological electrophysiological findings were found in 66% of conservatively-treated patients. In the 43 patients treated surgically, all 16 with fair and poor results

had

pathological

electrophysiological

findings

and 12 required further operations. Multiplicity

of the pathological

findings was related

to the severity of the deformity of the foot; normal studies represent a good prognostic sign. Electrophysiological studies are useful in idiopathic club foot with residual deformities after conservative or operative treatment. Our findings support the theory

that muscle imbalance is an aetiological factor in idiopathic club foot. J Bone Joint Surg [Br] l995:77-B:596-601.

Received 8 June 1994; Accepted 14 September 1994

Calf atrophy with a decrease in foot size and tibial length is found in all children with congenital talipes equinovarus, but its prevalence varies in the many reported series (Turco 1979; Laaveg and Ponseti 1980; Thompson, Richardson and Westin 1982; DePuy and Drennan 1989; Levin et al 1989; Magone et at 1989). Reduction in the length and girth of the leg muscles has been observed (Wiley 1959; Schlicht 1963; Settle 1963; Reimann 1967; Waisbrod 1973) but it is not clear whether this is a primary or a secondary defect. Wasting of the calf is already seen in the fetal period (Wiley 1959; Irani and Sherman 1963; Laaveg and Ponseti 1980). It becomes more prominent with age (Laaveg and Ponseti 1980) and may gradually improve in some cases (Turco 1979) but it is not influenced by the age at surgical correction (DePuy and Drennan 1989). These findings may reflect changes of neural origin, and suggest a neuromuscular defect as the cause of the deform ity. It is believed that minor changes in innervation cause an increase in muscle fibrosis leading to shortening of the posteromedial muscles (Handelsman, Youngleson and Malkin 1965; Isaacs et al 1977; Handelsman and Badala mente 1981). There are conflicting reports of EMG studies in congeni tat club foot (Tonnis

1969; Abbruzzese

et at 1972; Pereui

and Surace 1976; Costa, Gualtieri and Mertini 1978; Koc zocik-Przedpelska and Marciniak 1979; Bill and Versfeld 1982). The findings have included neurogernc and myo pathic alterations which suggested neural damage or prim ary muscular

abnormalities.

The diagnosis

of idiopathic

club foot may include a heterogeneous group of conditions with myopathic or neurogenic disorders as the underlining cause.

z. Feldbrin,MD, OrthopaedicSurgeon E. Ezra, MD, Orthopaedic Surgeon 0. Khermosh, MD, Senior Lecturer in Orthopaedics S. Wientroub, MD, Professor and Head Department of Pediatric Orthopaedics U. Kramer, MD, Pediatric Neurologist Department of Pediatric Neurology Dana Children's Hospital, Tel-Aviv Medical Centre, 6 Weizmann Street, Tel-Aviv 64239, Israel. A. N. Gilai, PhD, Head of Department of Clinical Neurophysiology, Alyn Children's Hospital, Jerusalem 91090, Israel. Correspondence should be sent to Professor S Wientroub. 101995 British Editorial Society of Bone and Joint Surgery 0301-620X/95/4973 $2.00 596

We have performed detailed electrophysiological inves tigations to try to define the neuromuscular status of the leg in this group of patients. PATIENTS AND METHODS We performed EMG studies on 57 children with congenital club foot; of these, five were excluded from the study, three girls with microcephaly, spinal muscular atrophy and con genital autosomal dominant sensory motor neuropathy, and two boys with Charcot-Marie-Tooth disease and congenital tibial dysplasia. The remaining 52 children (37 boys and 15 THE JOURNALOF BONE AND JOINTSURGERY

MUSCLE IMBALANCE IN ThE AETIOLOGY OF IDIOPAThIC CLUB FOOT

girls) had idiopathic club foot. Both feet were affected in 22; in 14 the right foot only was involved and in 16 the left (Table I). Both legs were always investigated. In 39 chit then EMG was performed once, but to exclude the possibil ity of the progression of the electrophysiological findings 12 were studied twice and one child was assessed three times.

patientsTreatmentConservativeSurgicalPrimarySecondaryTotalPatients Table L Detailsof the

Unilateral 22Number Bilateral6

316

330

168

of feet12481474

The age when studied varied from three months to 15 years. Sixteen studies were performed in the first year of life, 30 between the ages of one and five years, 16 between five and ten years, and four between ten and 15 years. Nine children were treated conservatively with a combi nation of intensive physiotherapy and casting; of these, six had unilateral and three bilateral involvement. Once clinical and radiological correction had been achieved it was main Wined by our special orthosis (Wientroub and Khermosh 1991) which was worn initially for 24 hours every day and then gradually left off during the day, but continued as a night splint for at least one year. Forty-three

children

had surgery;

32 were operated

on in

our hospital and 11 were referred to our clinic after the recurrence of one or more components of the deformity. In the 32 children, 48 feet had a primary procedure which included posteromedial release according to Turco (Turco 1979; Otremski et at 1987) in 22. In nine feet complete posterotateral and medial release through the Cincinnati incision was performed, while 16 feet had posterior capsu lotomies and lengthening of tendo Achillis. One patient who had been treated conservatively and maintained cor rection for several years subsequently had a plantar strip ping and transfer of the tibialis anterior tendon to the dorsum of the foot. Twelve additional secondary surgical procedures were performed. This group was a heterogeneous one, and the operations were tailored to suit the residual deformities. Four feet were treated by complete posteromedial release according to Turco (1979) which was similar to the primary operation; in three feet transfer of the tibiatis anterior tendon and plantar stripping were undertaken. Shortening of the lateral column and calcaneocuboid joint resection, plantar stripping, metatarsal osteotomies, subtalar extra articular

arthrodesis

and posteromediat

release on a patient

who had a posterior release as a primary procedure, were each performed once. MRI of the lumbar and sacrat spine was carried out in 11 children. In one child, two MRI VOL. 77-B, No. 4, JULY 1995

597

studies were done. Three electrophysiological techniques were used to measure the neuromuscular status of the legs: Electromyography. This was used to estimate the number of functional motor units, their firing rate and their recruit ment during maximal voluntary effort. The quantitative estimate for these parameters was derived by using the turns-amplitude (T and A) method (Gitai 1989). Values were recorded from the tibiatis anterior, the extensor haltu cis longus, the peronei and the gastrocnemius muscles and were used to distinguish normal children from those with myopathy or neurogenic disorders. Nerve-conduction tests (NCT). We used NCTs to evalu ate the functional integrity of the axon fibres, Schwann cells, myelin, and the neuromuscular junction in the posterior tibial and peroneal nerves. The conduction and amplitude of the compound muscle action potentials were used to distinguish between conditions with axonal degeneration and segmental demyelination . F-responses of the tibial and peroneal nerves were used to assess the integrity of the proximal and lumbosacrat regions of the nerves. The spinal monosynaptic reflex (H-reflex). This was used to estimate the excitability level of the spinal motorneurone pool of the triceps surae and soteus motor units. Values of H-reflex latency and amplitude are sensitive to changes in the functional level of spinal motorneurones (Trontelj 1973). We performed all the studies using the Viking EP System (Nicolet, Madison, Wisconsin). The nerve conduction and reflex studies were carried out using surface electrodes and for EMG concentric needle electrodes of type 13L50 (Dan tec; Denmark) were used. The posterior tibial nerve was examined by stimulation with a short square pulse (0.05 msec) delivered at the ankle or the popliteal fossa. Surface electrodes were attached to the abductor hallucis muscle and the amplitude, conduction time and conduction velocity were measured. The peroneal nerve was examined using the same technique but with stimulation above and below the fibular head. Recordings were taken from the extensor digitorum brevis. The Fresponses of all nerves were analysed by averaging the absolute amplitudes of ten consecutive responses and the latency difference between the muscle responses (M) and the F-wave (in msec) of these responses. H-reflex studies were performed by stimulating the pos tenor tibial nerve at the popliteal fossa with current pulses of short duration and low intensity. The recording was taken using surface electrodes placed on the tower part of the triceps surae. Normal values for EMG T and A, the amplitude of the compound muscle action potential, conduction time and conduction velocity had previously been established from a large group of age-matched healthy subjects with no known history of systemic or neurological disease (Liveson and Dong 1992) and were confirmed in our laboratory.

@

z. FELDBRIN,A.N.GILAI, E.EZRA,

598

AL

Table II. Electrophysiological findings and clinical correlation. Numbers in parentheses indicate conservatively-treated patients Total Type of abnormality None (normal)

Percentage UnilateralBilateralNumber5(2)4(1)9(3)7(1)2(1)9(2)—II3(1).3(1)1—14(1)59(1)459 17

Isolated peroneal nerve

17

Peroneal and post-tibial nerve

2

Isolated spinal cord

6

2

Denervation EMG pattern Neurogenic (NCT + EMG)

17

Spinal and peripheral nerve (NCT + H-reflex)

17

Spinal and peripheral axonal lesions (EMG + H-reflex)

1

-

I

Central

5(1)

2

7(1)

and peripheral

2 14

involvement (all parameters)

Asymmetry

-

Number of patients

30 (6)

RESULTS Only nine patients, four out of the 22 with bilateral club foot and five of the 30 with unilateral involvement, had results for EMG, NCT and H-reflex studies which were completely within the normal range for both legs (Table

II). Nine patients, seven with unilateral involvement, had evidence of isolated peroneal nerve damage. None had isolated involvement of the posterior tibial nerve. In 34, 19 with unilateral and 15 with bilateral club foot, peroneal nerve dysfunction was combined with one or more electro physiological changes. In one patient with bilateral involve ment, the posterior tibial nerve was also affected. Abnormality of etectrophysiological function of the tibialis anterior and of the peroneal muscles was present in five patients (3 with unilateral and 2 with bilateral involvement) who also had dysfunction of the peroneal nerve. Damage to both the peroneal and posterior tibial nerves with abnormal EMG findings was recorded in four patients, three in the bilateral group. Pathological EMG values in the presence of normal NCr and H-reflex studies were seen only in one patient with unilateral club foot. The muscle stretch reflex of the triceps surae provides a measure of motorneurone excitability in neurological con ditions suggesting spinal affection. Recording of the stretch reflex after direct electrical stimulation of the 1A afferent fibres of the tibial nerve allows accurate evaluation of Hreflex parameters. The level of excitability of the L5/Sl lumbar spinal motorneurone pool of the triceps surae motor units was abnormal in three patients with unilateral involvement without any other evidence of electrophysio logical disturbance and one other patient with unilateral club foot had an abnormal EMG combined with disturb ance of the spinal monosynaptic

reflex. None of the bilat

emily affected children had this type of lesion. In nine

3(1)

3(1)

52 (9)

22 (3)

6

100

patients recordings of the H-reflex showed abnormality in amplitude, conduction or both (four with unilateral and five with bilateral involvement) with damage to the peroneal and posterior tibial nerves. Disturbance of all three para meters (EMG, NCT and the H-reflex) was seen in five unilateral and two bilateral patients. In three with bilateral disease, our studies showed marked asymmetry between the legs. Asymmetry was present when the values of con duction velocity, the amplitude of the compound muscle action potential and the number of active motor units (as recorded by needle EMO) in one limb differed by 1.7 to 2.2 SD units

from

the contralateral

side

(Table

II).

To determine if the neuromuscular abnormalities were progressing 13 children had further studies with at least one year between the examinations. Two, one with unilateral and one with bilateral club foot, had two further studies which were normal. There were no Signs of significant improvement or deterioration in these patients. Twelve MRI studies of the lumbar spine were performed in 11 patients who had electrophysiological evidence of a neurogenic lesion with absence of activity of the peroneal muscles on clinical examination. These were normal regardless of the existence or absence of spina bifida on plain radiographs of the spine. In the nine children treated conservatively the studies were completely normal in only three, two with bilateral and one with unilateral involvement. Two patients, one unilateral and one bilateral, had isolated peroneal neuro pathy and one other, with unilateral involvement, had pathological H-reflex recordings suggestive of neurogenic abnormality. Combined lesions were detected in two addi tional unilateral cases. In one, a peroneal nerve lesion was associated with EMG abnormalities while the other had, in addition, a spinal monosynaptic H-reflex dysfunction. One bilaterally affected child had asymmetry in the recorded values. THE JOURNAL OF BONE AND JOINT SURGERY

MUSCLE IMBALANCE IN THE AETIOLOGY OF IDIOPAThIC CLUB FOOT

In the surgically-treated group of 32 children (48 alTec ted feet) there was a direct correlation between the electro physiological findings and the clinical severity of the involvement and final outcome. When asymmetry was detected the changes were always more pronounced in the more severely affected foot. In 11 patients differences in recordings between the two sides were confirmed clinically. In three bilateral cases, only one foot was operated upon. In three others, severe electrophysiologicat abnormality was detected in the feet on which the secondary surgical procedures had been done. In five patients with asymmetrical findings three had been operated on bilaterally and two unilaterally. All the patients (12 feet) who had had additional surgical procedures for partial or complete recurrence had abnormal findings. Nine patients had a residual forefoot adduction

deformity; in seven it was unilateral and in two bilateral. All have been treated surgically. There were no specific electrophysiologicat patterns in this group. Three had a peroneal nerve lesion and five had abnormality of the Hreflex.

In 16 feet etectrophysiological evaluation showed patho logical values in at least three different parameters reflect ing neurogenic and spinal involvement. Fourteen had had complete posteromedial or posteromedial-lateral release and two posterior release only. In this group, seven already had had additional surgery. In six, complete recurrence of the deformity had been treated by extensive soft-tissue and bony procedures. The other feet in this group were rated as fair or poor due to overcorrection or supination and fore foot adduction. DISCUSSION Only 17 of the 52 patients had normal findings. The group included patients with one or both feet involved, and who had been treated conservatively or by operation. Abnor malities involving the peripheral nerves and/or the spinal cord were seen in 83% of the remaining 35 patients, and the findings were consistent throughout repeated studies, sug gesting that there is a neurological pathology which does not vary with age. MRI performed on a selected group of patients did not show abnormal pathology in the lumbar spine, suggesting that our definition of spinal dysraphism should be confined to ultrastructural and functional changes rather than macro scopic abnormality. The distribution of the abnormal elec trophysiological findings in this group of patients excludes the possibility of secondary changes occurring because of methods of conservative treatment or as a result of the operations. There have been several etectrophysiological studies on the muscles of the leg and foot in congenital club foot. The findings have varied from normal to those showing neuro genic and myopathic alteration. Peretti and Surace (1976) reported EMG changes in numerous muscles of the leg and VOL. 77-B, No. 4, JULY 1995

599

foot in all patients examined, irrespective of age or whether conservative or operative treatment had been undertaken. There was reduced recruitment of motor-unit potentials and decreased duration and shape. Abbruzzese et al (1972) found spontaneous denervation activity in one subject. Motor-unit potential duration was increased in seven, decreased in six, and normal in eight. Koczocik-Przedpet ska and Marciniak (1979) described myopathic and neuro genic changes in 40% of EMGs performed, and Trontelj and Pavlovcic (1992) reported an altered calf tendon reflex in club foot. Tonnis (1969), however, performed EMG and histological studies on different muscles of the lower leg in children with club foot, and found no evidence to suggest neural damage or primary muscular disease. Histological studies performed on formatin-fixed tissue were also neg ative. Bill and Versfeld (1982) found no abnormalities indicating a neurogenic or myopathic disorder and no changes in terminal latencies or maximum motor conduc tion velocities in muscle studies. Attenborough (1972) showed no obvious differences in duration, amplitude and phasicity between the action poten tials obtained from the peroneat muscles, tibialis anterior and gastrocnemius on the affected side and those from the same muscles in the normal leg. In two cases there was evidence of weakness of the peroneat muscles and perhaps of the tibialis anterior. This absence of differences suggests that the lesion is peripheral rather than in the brain or spinal cord, affecting the lateral popliteal nerve or the muscles supplied by it. There appears to be dysfunction with, perhaps, a delay in maturation of nerve or muscles, since there is no sign of actual disease. It is possible that talipes equinovarus is due to a muscle imbalance. A contracture of one of the flexors (e.g., soleus) is also possible, but the

primary abnormality may be relative weakness of the per onei and possibly the anterior tibial group of muscles, with

secondary tightness of the flexors and invertors. In patients who had been treated surgically, the patterns of EMG activity for the medial gastrocnemius and tibialis anterior muscles and the stride characteristics during gait were measured and compared with normal values. The duration of activity of the medial gastrocnemius was sig mficantly greater than normal whereas that of the tibialis anterior, the stride length, and the single-limb support times were not different. No correlation was found between the results of the gait analysis and the quality of the surgical result (Otis and Bohne 1986). Histochemicat examination of muscle tissue in club foot by Henkel, Woods and Arnold (197 1) showed no sig mficant abnormalities, although there was some suggestion that the muscle fibres in the affected calf were smaller in diameter. A subsequent histochemical study by Isaacs et at (1977) showed that hypotrophy, predominance of type-i fibres, and loss of direction and grouping of the fibres were common in patients with club foot. They also demonstrated electron-microscopic changes in the muscle and suggested that club foot may have a neurological basis.

600

z. FELDBRIN,A.N.GILAI, E.EZRA, @[email protected].

Ippolito and Ponseti (1980) found that the proportion of muscle fibres to connective tissue was lowest in the triceps surae, tibialis posterior, and flexor digitorum communis. No appreciable differences were noted in the size of the per oneal muscles. Both the deep and the superficial fasciae were thicker in the affected leg. In the lower part of the right leg, bundles of connective-tissue fibres from the deep fascia penetrated the muscles. Gray and Katz (1981) found the structure of the muscle in club foot to be normal; there was no evidence of atrophy, denervation, degeneration, grouping of the fibre types or loss of fibre direction. This is in contrast to the changes described in older children by Isaacs et al (1977). Evidence of neurogenic disease was seen in most instances and was more obvious in the older patients. The pattern of abnor mality was similar in all muscle groups. Immobilisation, stretching or relaxation of the muscles did not account for the anomalies observed. This study of the extrinsic muscles in talipes equinovarus indicates a dominant neurogenic factor in causation (Isaacs et al 1977). Other investigators, using routine histochemical meth ods, disagree with Isaacs (Flinchum 1953; Wiley 1959; Irani and Sherman 1963; Settle 1963; Henkel et al 1971; Kaplan 1972). Gray and Katz (1981) found these features only in children with an associated clinical syndrome. Their observations agree closely with the disproportion of type-l fibres previously reported by Isaacs et al (1977) and with their observation that this abnormality is more common in older children and may be iatrogenic or secondary to the deformity. The relatively low frequency of this phenomen on in the younger age groups suggests that it may not be an aetiological factor in club foot. This indicates that wasting of the calf muscle is due to a reduction in the number of fibres rather than their size which may be due to a defective neural influence on the development of the limb (Gray and Katz 1981). Scher, Handelsman and Isaacs (1977), in a study of extrinsic muscles of the foot in young baboons in which one leg was splinted in a position of catcaneovalgus for 8, 17 and 25 weeks, respectively, found no histochemical or electron-microscopic abnormalities in the posteromedial or peroneal muscles of either the splinted or the control legs. These observations in animals with muscles closely resem bling those of man, suggest that preoperative stretching and immobilisation are not the cause of the changes reported here. Histological studies of the lower lumbar segments of the spinal cord of 14 human fetuses, each having a unilateral club-foot deformity, have shown that the neural canal of those of 16 to 24 weeks' gestation, was still not closed on the dorsal aspect at and distal to the L5 level (Swart 1993). Other evidence of immaturity at the L5/Sl level included the persistence of a rich capillary plexus at the unclosed dorsal aspect, the continuing shedding of sensory neuro blasts, the presence of full-bodied neuroepithelial cells, compared with the ventral (motor) aspect and the presence

of inflammatory lymphoid and plasma cells within the cord at the L5/Sl level. There was a marked reduction in the number of motorneurones on the side of the deformity, and most on this side were in the process of destruction, with clear evidence of advanced chromatolysis. There was evid ence of destructive changes involving the anterior motor neurones of the muscles of the calf and foot at the L5/Si segment level. A viral infection involving the fetus during the late developmental phase of intrauterine existence has

been suggested to explain these findings. Currently, the evidence is in favour of abnormal innerva tion as the prime factor in the development of this peripher al deformity. A minor degree of muscle imbalance may produce a disproportionate deformity, particularly if it develops at an early intrauterine stage. Most of our patients with idiopathic club foot had abnormal electrophysiological studies. The severity of the abnormality in the foot is reflected in multiple pathological findings. A normal elec trophysiological study is a good prognostic factor. We recommend detailed analysis only in patients with severe deformity. It provides information to the surgeon and the parents about the expected results, and indicates the need for a more extensive operation in these cases rather than a limited procedure which may prove inadequate. In our experience patients with isolated or combined peroneal nerve abnormality benefit from transfer of the tibialis anter ior tendon to the dorsum of the foot. This operation will help to improve the muscle imbalance and to prevent progressive supination and adduction of the foot. 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.

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