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Peroneal nerve palsy: the role of early electromyography
doi: 10.1053/ejpn.2000.0312 available online at http://www.idealibrary.com on European Journal of Paediatric Neurology 2000; 4: 239±242
CASE STUDY
Peroneal nerve palsy: the role of early electromyography È GE, È KSEL YILMAZ,1 A EMRE O YU
2
Æ PIRMENCI, SERPIL YILMAZ-DEG
1
AYSU SAY1
1
Paediatric Neurology Unit, Zeynep Kamil Children's and Maternity Hospital; 2Department of Neurology, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey
Footdrop is rare in the newborn period. In this report, the clinical and electrophysiological features of a newborn whose peroneal neuropathy was detected in the delivery room is presented. Her first electrophysiological examination, at the 13th hour of life, revealed a peroneal nerve lesion. All findings elicited in this and subsequent examinations suggested an antenatal onset. Clinical recovery began within weeks of the birth and she was able to walk, with no residual neurological abnormality, by her first birthday. Early electrophysiological examination of a newborn with peripheral neuropathy may provide valuable information about the time of onset and pathophysiological features of the nerve lesion. In spite of the early electromyogram findings revealing severe nerve injury, a good prognosis is possible in newborns with peroneal neuropathy. Keywords: Peroneal palsy. EMG footdrop. Neonatal neuropathy.
Introduction Neonatal footdrop due to peroneal neuropathy is a rare condition, and there are few reports clarifying its aetiology and electrophysiological findings.1±5 The pathophysiology and early electrophysiological findings are not yet clear, particularly in cases without any obvious factor causing peroneal nerve injury. We are reporting the clinical and electrophysiological findings obtained 13 hours after birth in a baby with a peroneal neuropathy of possibly intrauterine onset.
Case report FE was the first child of a healthy 23-year-old woman. After an uneventful pregnancy, she was born at term by spontaneous vaginal delivery with
breech presentation. The duration of labour was normal. There was neither any other obstetric complication, nor obvious birth trauma. Apgar scores at 1, 5, and 20 minutes were 8, 9 and 10 respectively. Her birthweight was 3900 g. At the first routine paediatric examination in the delivery room, asymmetric posture of the feet was noticed (Fig. 1). Neurological examination revealed a left footdrop, with inability to dorsiflex the left foot and toes in response to painful stimuli. Eversion of the left foot was also impaired. Pinprick stimulation applied to various points of the lower extremities also did not seem to indicate any sensory abnormality. All deep tendon reflexes were normal, and there were no other abnormal neurological and physical findings. Additionally, there were no skin changes, which can indicate a previous compression on a body part or a compartment syndrome. The first electrophysiological study was performed 13 hours after birth. In motor nerve
Received 23.2.2000. Revised 1.5.2000. Accepted 24.5.2000. Correspondence: Dr YuÈkel Yilmaz, Acibadem Tekin Sk. Turan Ap. No: 18/14, KadikoÈy-Istanbul-Turkey. e-mail: [email protected]
1090±3798/00/04/0239+4 $35.00
& 2000 European Paediatric Neurology Society
240
Case study: Y Yilmaz et al.
Fig. 2. Needle EMG examination-performed at the 13th hour of life-showing (+++) fibrillations and positive waves in the left hallucis longus muscle with no muscle unit potential activity. Fig. 1.
Left footdrop noticed at birth.
conduction studies compound muscle action potentials could not be recorded with the surface electrodes placed over left extensor digitorum brevis and tibialis anterior muscles by stimulation of the peroneal nerve at the ankle and fibular head. Stimulation at the left fibular head was repeated without eliciting any recordable muscle response while a concentric needle-recording electrode was inserted into the tibialis anterior muscle. The left tibial nerve motor conduction was normal with a 4.3 mV compound muscle action potential amplitude, 2.6 ms distal and 4.3 ms popliteal fossa±ankle latency. In needle electromyography (EMG), (+++) fibrillations and positive waves were present in the left extensor hallucis longus muscle with no motor unit potential activity (Fig. 2). There were neither pathological spontaneous activity nor motor unit potentials in the left tibialis anterior muscle. Needle EMG of the left medial gastrocnemius, quadriceps femoris, and gluteus medius muscles were normal. On the 13th day, she was able to dorsiflex her left foot nearly 90 degrees. Dorsal flexion of the toes was more limited. The second electrophysiological examination was performed at 21 days of age. Sensory nerve conduction studies were performed for the first time in this examination which revealed normal orthodromic left medial plantar (3 mV amplitude and 2.3 ms onset latency with ring electrode stimulation of the big toe and recording at ankle level) and unrecordable superficial peroneal nerve sensory action potentials. The left tibial motor nerve conduction study was normal, as it was in the first examination. In the peroneal motor nerve conduction examination, no compound muscle action potential was detected by the surface recording electrodes placed over the left exterior digitorum brevis muscle. In needle EMG, (+) (+++) fibrillations and positive waves with long
duration polyphasic motor unit potentials with reduced interference were observed in the left tibialis anterior, peroneus longus, and extensor hallucis longus muscles. The left medial gastrocnemius and short head of the biceps femoris were bioelectrically normal. The girl was followed up as an outpatient with physical therapy consisting of tactile stimulation. When she was examined at the age of 2 months, there was no evidence of footdrop. She was able to walk independently, with no muscle weakness in the left lower extremity, by her first birthday.
Discussion The peroneal nerve is one of the two branches of the sciatic nerve which innervates the muscles that are responsible for dorsiflexion of the toes and dorsiflexion and eversion of the foot.6 Although mononeuropathies are uncommon in childhood, peroneal neuropathy is one of the most frequently encountered mononeuropathy syndromes.1 However, this neuropathy is extremely rare in the newborn, with only a few reported cases in the literature.1±5 Neonatal peroneal neuropathy sometimes has a clear postnatal onset and a demonstrable cause, such as footboard compression, compartment syndromes secondary to intravenous fluid infiltration, or umbilical arterial injection of vasoconstricting agents or hypertonic solutions.3±5 Some babies, however, are found to have footdrop shortly after birth. These patients are usually born at term to primiparous mothers after a complicated labour and delivery (such as breech presentation) or prolonged delivery leading to cesarean section. The presence of footdrop is sometimes associated
Case study: Peroneal palsy in the newborn with birth trauma.2,7 Cutaneous signs of trauma indicating the site of the nerve compression are sometimes found in these newborns. The traditional belief that all of these types of peripheral mononeuropathies and neonatal brachial plexopathies can be attributed to the birth trauma has been revised in recent years. This is due to the accumulating electrophysiological evidence indicating their prenatal onset in some patients.1,4,6 Uterine contraction rings, amniotic bands, or prolonged extended posture of a limb are implicated as antenatal causes of nerve trauma. As is to be expected, the possibility of an antenatal cause for neonatal mononeuropathies has great medicolegal importance ± especially for obstetricians. In the case of our patient, unilateral peroneal neuropathy was noticed in the first hours of life. Breech presentation is often associated with this type of neonatal mononeuropathy, and may have played a role in the pathogenesis of our patient's nerve lesion. On the other hand, there was no sign indicating the presence and/or site of the nerve compression or traction in the clinical examination. Her peroneal nerve lesion was localized electrophysiologically to a point between the popliteal fossa and the innervation point of the tibialis anterior muscle, most plausibly to the fibular head segment. The peroneal nerve is considered to be more vulnerable to compression or traction at this segment, where it is quite superficial and relatively fixed. Craig and Clark7 emphasized that prolonged extension of the limb in a baby during breech presentation can cause a lesion at this point, due to the traction of the nerve. Electrophysiological examination performed at the 13th hour of life showed that there was a severe lesion in the peroneal nerve which possibly produced a total axonal loss as shown by the absence of compound muscle action potentials in response to nerve stimulation, and of voluntarily activated motor unit potentials and the presence of pathological spontaneous activity in the distal anterior crural muscle. The second examination provided additional information allowing the localization of the nerve injury, and showed motor unit potentials probably produced by the reinnervation of the tibialis anterior muscle. These observations demonstrated that sufficient time had elapsed between the occurrence of the nerve injury and the first electrophysiological examination to produce the motor conduction changes and pathological spontaneous activity. There is some controversy regarding the interval between the nerve trauma and the appearance of these changes in newborn babies.4 The traditional 10- to 14-day
241 period which is necessary for positive waves and fibrillations to appear in adults is thought to be shorter in newborns.4 However, even in the newborn period, 13 hours after nerve injury is too early for the emergence of the pathological spontaneous activity and of the nerve conduction changes reflecting Wallerian degeneration, because nearly all human and experimental data indicate that at least several days are necessary before the appearance of these electrophysiological changes after nerve injury in the newborn period. Therefore our findings most reasonably suggest that peroneal nerve injury in the present case must have taken place before birth. The earliest reported electrophysiological examination which showed these denervational changes in human neonatal neuropathy was performed by Jones et al at 18.5 hours after birth and was meticulously discussed.4 Thus, our EMG examination was the earliest one reported up to now. Neonatal peroneal neuropathies are reported to have very good prognoses with complete resolution of the weakness in weeks or months in almost all cases. This fact may account for the reported rarity of this condition. There is evidence that the rapid restoration of function in most patients results in cases of mild nerve injury being overlooked.7 Our patient also made an excellent recovery which began within weeks after birth and was functionally complete in a few months. The paradox of this clinical course with the initial electrophysiological findings suggesting the presence of a total axonal loss lesion seems to be confusing at first sight. In a newborn, it appears that the very short distances between the lesion site and the muscles make a very quick reinnervation possible, as we observed in the needle EMG of the tibialis anterior muscle on day 21. It is conceivable that some other currently unknown attributes of the newborn neuromuscular system can also promote this rapid reinnervation process. In conclusion, an electrophysiological examination, which must be performed as early as possible in a neonatal mononeuropathy, can provide information about the onset and pathophysiological features of the nerve lesion. However, early electrophysiological findings indicating severe nerve lesion may not necessarily indicate a poor prognosis.
References 1 Jones R, Felice KJ, Gross PT. Pediatric peroneal mononeuropathy: a clinical and electromyographic study. Muscle Nerve 1993; 16: 1167±1173.
242 2 3 4
Crumrine PK, Koenigsberger R, Chutorian AM. Footdrop in the neonate with neurological and electrophysiological data. J Pediatr 1975; 86: 779±780. Fischer A, Strasburger J. Footdrop in the neonate secondary to use of footboards. J Pediatr 1982; 101: 1003±1004. Jones HR, Herbison GJ, Jacobs SR, et al. Intrauterine onset of a mononeuropathy: peroneal neuropathy in a newborn with electromyographic findings at age one day compatible with prenatal onset. Muscle Nerve 19: 88±91.
Case study: Y Yilmaz et al. 5
Kreusser KL, Volpe JJ. Peroneal palsy produced by intravenous fluid infiltration in a newborn. Dev Med Child Neurol 1984; 26: 509±527.
6
Jones HR. Mononeuropathies. In: Jones HR, Bolton CF, Harper CM (eds) Pediatric Clinical Electromyography. Philadelphia: Lippincott±Raven Publishers, 1996: 173±175.
7
Craig WS, Clark MP. Of peripheral nerve palsies in the newly born. J Obstet Gyn Br Empire 1958; 65: 229± 237.
CASE STUDY
Peroneal nerve palsy: the role of early electromyography È GE, È KSEL YILMAZ,1 A EMRE O YU
2
Æ PIRMENCI, SERPIL YILMAZ-DEG
1
AYSU SAY1
1
Paediatric Neurology Unit, Zeynep Kamil Children's and Maternity Hospital; 2Department of Neurology, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey
Footdrop is rare in the newborn period. In this report, the clinical and electrophysiological features of a newborn whose peroneal neuropathy was detected in the delivery room is presented. Her first electrophysiological examination, at the 13th hour of life, revealed a peroneal nerve lesion. All findings elicited in this and subsequent examinations suggested an antenatal onset. Clinical recovery began within weeks of the birth and she was able to walk, with no residual neurological abnormality, by her first birthday. Early electrophysiological examination of a newborn with peripheral neuropathy may provide valuable information about the time of onset and pathophysiological features of the nerve lesion. In spite of the early electromyogram findings revealing severe nerve injury, a good prognosis is possible in newborns with peroneal neuropathy. Keywords: Peroneal palsy. EMG footdrop. Neonatal neuropathy.
Introduction Neonatal footdrop due to peroneal neuropathy is a rare condition, and there are few reports clarifying its aetiology and electrophysiological findings.1±5 The pathophysiology and early electrophysiological findings are not yet clear, particularly in cases without any obvious factor causing peroneal nerve injury. We are reporting the clinical and electrophysiological findings obtained 13 hours after birth in a baby with a peroneal neuropathy of possibly intrauterine onset.
Case report FE was the first child of a healthy 23-year-old woman. After an uneventful pregnancy, she was born at term by spontaneous vaginal delivery with
breech presentation. The duration of labour was normal. There was neither any other obstetric complication, nor obvious birth trauma. Apgar scores at 1, 5, and 20 minutes were 8, 9 and 10 respectively. Her birthweight was 3900 g. At the first routine paediatric examination in the delivery room, asymmetric posture of the feet was noticed (Fig. 1). Neurological examination revealed a left footdrop, with inability to dorsiflex the left foot and toes in response to painful stimuli. Eversion of the left foot was also impaired. Pinprick stimulation applied to various points of the lower extremities also did not seem to indicate any sensory abnormality. All deep tendon reflexes were normal, and there were no other abnormal neurological and physical findings. Additionally, there were no skin changes, which can indicate a previous compression on a body part or a compartment syndrome. The first electrophysiological study was performed 13 hours after birth. In motor nerve
Received 23.2.2000. Revised 1.5.2000. Accepted 24.5.2000. Correspondence: Dr YuÈkel Yilmaz, Acibadem Tekin Sk. Turan Ap. No: 18/14, KadikoÈy-Istanbul-Turkey. e-mail: [email protected]
1090±3798/00/04/0239+4 $35.00
& 2000 European Paediatric Neurology Society
240
Case study: Y Yilmaz et al.
Fig. 2. Needle EMG examination-performed at the 13th hour of life-showing (+++) fibrillations and positive waves in the left hallucis longus muscle with no muscle unit potential activity. Fig. 1.
Left footdrop noticed at birth.
conduction studies compound muscle action potentials could not be recorded with the surface electrodes placed over left extensor digitorum brevis and tibialis anterior muscles by stimulation of the peroneal nerve at the ankle and fibular head. Stimulation at the left fibular head was repeated without eliciting any recordable muscle response while a concentric needle-recording electrode was inserted into the tibialis anterior muscle. The left tibial nerve motor conduction was normal with a 4.3 mV compound muscle action potential amplitude, 2.6 ms distal and 4.3 ms popliteal fossa±ankle latency. In needle electromyography (EMG), (+++) fibrillations and positive waves were present in the left extensor hallucis longus muscle with no motor unit potential activity (Fig. 2). There were neither pathological spontaneous activity nor motor unit potentials in the left tibialis anterior muscle. Needle EMG of the left medial gastrocnemius, quadriceps femoris, and gluteus medius muscles were normal. On the 13th day, she was able to dorsiflex her left foot nearly 90 degrees. Dorsal flexion of the toes was more limited. The second electrophysiological examination was performed at 21 days of age. Sensory nerve conduction studies were performed for the first time in this examination which revealed normal orthodromic left medial plantar (3 mV amplitude and 2.3 ms onset latency with ring electrode stimulation of the big toe and recording at ankle level) and unrecordable superficial peroneal nerve sensory action potentials. The left tibial motor nerve conduction study was normal, as it was in the first examination. In the peroneal motor nerve conduction examination, no compound muscle action potential was detected by the surface recording electrodes placed over the left exterior digitorum brevis muscle. In needle EMG, (+) (+++) fibrillations and positive waves with long
duration polyphasic motor unit potentials with reduced interference were observed in the left tibialis anterior, peroneus longus, and extensor hallucis longus muscles. The left medial gastrocnemius and short head of the biceps femoris were bioelectrically normal. The girl was followed up as an outpatient with physical therapy consisting of tactile stimulation. When she was examined at the age of 2 months, there was no evidence of footdrop. She was able to walk independently, with no muscle weakness in the left lower extremity, by her first birthday.
Discussion The peroneal nerve is one of the two branches of the sciatic nerve which innervates the muscles that are responsible for dorsiflexion of the toes and dorsiflexion and eversion of the foot.6 Although mononeuropathies are uncommon in childhood, peroneal neuropathy is one of the most frequently encountered mononeuropathy syndromes.1 However, this neuropathy is extremely rare in the newborn, with only a few reported cases in the literature.1±5 Neonatal peroneal neuropathy sometimes has a clear postnatal onset and a demonstrable cause, such as footboard compression, compartment syndromes secondary to intravenous fluid infiltration, or umbilical arterial injection of vasoconstricting agents or hypertonic solutions.3±5 Some babies, however, are found to have footdrop shortly after birth. These patients are usually born at term to primiparous mothers after a complicated labour and delivery (such as breech presentation) or prolonged delivery leading to cesarean section. The presence of footdrop is sometimes associated
Case study: Peroneal palsy in the newborn with birth trauma.2,7 Cutaneous signs of trauma indicating the site of the nerve compression are sometimes found in these newborns. The traditional belief that all of these types of peripheral mononeuropathies and neonatal brachial plexopathies can be attributed to the birth trauma has been revised in recent years. This is due to the accumulating electrophysiological evidence indicating their prenatal onset in some patients.1,4,6 Uterine contraction rings, amniotic bands, or prolonged extended posture of a limb are implicated as antenatal causes of nerve trauma. As is to be expected, the possibility of an antenatal cause for neonatal mononeuropathies has great medicolegal importance ± especially for obstetricians. In the case of our patient, unilateral peroneal neuropathy was noticed in the first hours of life. Breech presentation is often associated with this type of neonatal mononeuropathy, and may have played a role in the pathogenesis of our patient's nerve lesion. On the other hand, there was no sign indicating the presence and/or site of the nerve compression or traction in the clinical examination. Her peroneal nerve lesion was localized electrophysiologically to a point between the popliteal fossa and the innervation point of the tibialis anterior muscle, most plausibly to the fibular head segment. The peroneal nerve is considered to be more vulnerable to compression or traction at this segment, where it is quite superficial and relatively fixed. Craig and Clark7 emphasized that prolonged extension of the limb in a baby during breech presentation can cause a lesion at this point, due to the traction of the nerve. Electrophysiological examination performed at the 13th hour of life showed that there was a severe lesion in the peroneal nerve which possibly produced a total axonal loss as shown by the absence of compound muscle action potentials in response to nerve stimulation, and of voluntarily activated motor unit potentials and the presence of pathological spontaneous activity in the distal anterior crural muscle. The second examination provided additional information allowing the localization of the nerve injury, and showed motor unit potentials probably produced by the reinnervation of the tibialis anterior muscle. These observations demonstrated that sufficient time had elapsed between the occurrence of the nerve injury and the first electrophysiological examination to produce the motor conduction changes and pathological spontaneous activity. There is some controversy regarding the interval between the nerve trauma and the appearance of these changes in newborn babies.4 The traditional 10- to 14-day
241 period which is necessary for positive waves and fibrillations to appear in adults is thought to be shorter in newborns.4 However, even in the newborn period, 13 hours after nerve injury is too early for the emergence of the pathological spontaneous activity and of the nerve conduction changes reflecting Wallerian degeneration, because nearly all human and experimental data indicate that at least several days are necessary before the appearance of these electrophysiological changes after nerve injury in the newborn period. Therefore our findings most reasonably suggest that peroneal nerve injury in the present case must have taken place before birth. The earliest reported electrophysiological examination which showed these denervational changes in human neonatal neuropathy was performed by Jones et al at 18.5 hours after birth and was meticulously discussed.4 Thus, our EMG examination was the earliest one reported up to now. Neonatal peroneal neuropathies are reported to have very good prognoses with complete resolution of the weakness in weeks or months in almost all cases. This fact may account for the reported rarity of this condition. There is evidence that the rapid restoration of function in most patients results in cases of mild nerve injury being overlooked.7 Our patient also made an excellent recovery which began within weeks after birth and was functionally complete in a few months. The paradox of this clinical course with the initial electrophysiological findings suggesting the presence of a total axonal loss lesion seems to be confusing at first sight. In a newborn, it appears that the very short distances between the lesion site and the muscles make a very quick reinnervation possible, as we observed in the needle EMG of the tibialis anterior muscle on day 21. It is conceivable that some other currently unknown attributes of the newborn neuromuscular system can also promote this rapid reinnervation process. In conclusion, an electrophysiological examination, which must be performed as early as possible in a neonatal mononeuropathy, can provide information about the onset and pathophysiological features of the nerve lesion. However, early electrophysiological findings indicating severe nerve lesion may not necessarily indicate a poor prognosis.
References 1 Jones R, Felice KJ, Gross PT. Pediatric peroneal mononeuropathy: a clinical and electromyographic study. Muscle Nerve 1993; 16: 1167±1173.
242 2 3 4
Crumrine PK, Koenigsberger R, Chutorian AM. Footdrop in the neonate with neurological and electrophysiological data. J Pediatr 1975; 86: 779±780. Fischer A, Strasburger J. Footdrop in the neonate secondary to use of footboards. J Pediatr 1982; 101: 1003±1004. Jones HR, Herbison GJ, Jacobs SR, et al. Intrauterine onset of a mononeuropathy: peroneal neuropathy in a newborn with electromyographic findings at age one day compatible with prenatal onset. Muscle Nerve 19: 88±91.
Case study: Y Yilmaz et al. 5
Kreusser KL, Volpe JJ. Peroneal palsy produced by intravenous fluid infiltration in a newborn. Dev Med Child Neurol 1984; 26: 509±527.
6
Jones HR. Mononeuropathies. In: Jones HR, Bolton CF, Harper CM (eds) Pediatric Clinical Electromyography. Philadelphia: Lippincott±Raven Publishers, 1996: 173±175.
7
Craig WS, Clark MP. Of peripheral nerve palsies in the newly born. J Obstet Gyn Br Empire 1958; 65: 229± 237.