Anesth Analg 2005;100:547-548
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000144776.51550.47
OBSTETRIC ANESTHESIA
Inherited Neuropathy Can Cause Postpartum Foot Drop
Gary Peters, MRCP, and
Nigel P. Hinds, MRCP
Department of Neurology, Walton Centre for Neurology and Neurosurgery, Fazakerley, Liverpool, UK
Address correspondence and reprint requests to Gary Peters, MRCP, Department of Neurology, Walton Centre for Neurology and Neurosurgery, Lower Lane, Fazakerley, Liverpool, UK L9 7LJ. Address e-mail to gary.peters@ thewaltoncentre.nhs.uk.
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Abstract
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Postpartum neurological complications occur in up to 1% of deliveries. Often prior anesthetic procedures are blamed, with medicolegal implications. We describe a young woman who presented with postpartum foot drop diagnosed as an iatrogenic L5 root lesion after uncomplicated epidural anesthesia. After neurological assessment some 5 mo later she tested positive for the common hereditary neuropathy with liability to pressure palsies mutation that was a likely contributing factor in the development of her postpartum neuropathy. Anesthesiologists should consider hereditary neuropathies in the differential diagnosis of postpartum or postsurgical neurological deficits if there is a suggestive clinical history.
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Introduction
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The incidence of neurological complications arising in the peripartum period may be as frequent as 0.92% (1). Epidural or spinal analgesia/anesthesia is commonly performed during delivery and can cause inadvertent spinal cord or nerve root injury as a result of direct trauma, hematoma, or infection (2). Early (3) and more recent (4–6) reports have concluded that postpartum foot drop can also be a result of compression of the lumbosacral trunk by the fetal head at the pelvic brim in short women or result from proximal sciatic or peroneal nerve injuries. Postpartum neurological injuries often resolve spontaneously, and neurological assessment may not be necessary. The available literature seems to have overlooked an obvious contributory factor present in a recent case seen at our unit, and it seems likely that anesthetic procedures may be unnecessarily blamed for a proportion of neurological deficits with potential medicolegal implications.
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Case Report
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A 28-yr-old woman presented 5 mo after undergoing a transverse cesarean section delivery under epidural anesthesia for failure of descent during stage two of her first delivery. There were no acute complications after this procedure but in the immediate postpartum period she noticed a right foot drop causing her to trip and lateral right foot numbness. A diagnosis of iatrogenic L5 root injury after epidural anesthesia was made by the attending anesthesiologist after neurological examination. She was referred to the neurology clinic, but after a few weeks she began to improve and had fully recovered when first seen in clinic 5 mo later. A history obtained in the clinic revealed that 8 yr previously her left leg was similarly affected, and she also reported paresthesia in the ulnar fingers of her left hand. There was no family history of neurological disease and a full neurological examination at the present visit was normal.
Nerve conduction studies of the right leg revealed pathologically small sural and peroneal sensory potentials. The right radial sensory potential was also reduced and all right arm motor conduction velocities were slightly reduced (median conduction velocity was 41 m/s and ulnar conduction velocity was 46 m/s; normal upper limb motor conduction velocity, >49 m/s). Right ulnar motor conduction was moderately reduced around the elbow. An electromyelogram (EMG) of the right gastrocnemius and both tibialis anterior muscles was normal.
The combination of a suggestive clinical history and electrophysiological evidence of a sensory neuropathy with mild slowing of motor conduction across the elbow led to genetic testing for the presence of a deletion at 17p11.2 by STS dosage polymerase chain reaction, which detected the common 1.5 megabase deletion in the peripheral myelin protein-22 gene (PMP22) associated with hereditary neuropathy with liability to pressure palsies (HNPP).
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Discussion
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Although our patient was not examined neurologically and did not undergo neurophysiological testing at the time of her maximal neurological deficit, it seems highly probable that she had a postpartum foot drop caused by an intrapartum lumbosacral plexopathy or high sciatic neuropathy resulting from fetal head compression causing segmental demyelination. Our patient did not describe direct external compression on the peroneal nerve, from inappropriate leg positioning in stirrups, or from hand pressure during prolonged pushing with knee hyperflexion.
De Jong (7,8) originally described HNPP in a Dutch coal miner and in 4 relatives from 3 generations. A single epidemiological study has estimated the prevalence of HNPP to be 16 per 100,000 population (9). It is an autosomal dominant condition with variable penetrance that can present at any age, although most patients develop symptoms during the second or third decade (10). HNPP typically presents as painless focal neuropathies at common entrapment sites after minor trauma or compression. Some patients develop a chronic sensorimotor neuropathy and rarer manifestations include painless brachial plexus palsy and central nervous system demyelination (10,11). The neurological deficits typically resolve over days to months, although recovery can be delayed or incomplete. The family history may be unrevealing and there is no specific treatment. Most patients have a 1.5 megabase deletion of the PMP22 gene, although up to 25% of patients have other PMP22 mutations (11). Studies using PMP22 transgenic animals suggest that PMP22 deficiency leads to the formation of unstable neuronal mature myelin, which predisposes to demyelination (12). Diagnosing HNPP in the peripartum period has important implications for mother and baby as unnecessary investigations can be avoided.
Hereditary Neuralgic Amyotrophy (HNA) is another inherited neuropathy that can cause transient episodes of painful brachial plexopathy after infections or childbirth. HNA may be associated with dysmorphic features such as epicanthic folds and hypotelorism but no confirmatory genetic test is routinely available (12).
A history suggestive of recurrent entrapment neuropathies, particularly after minor trauma or compression, should prompt anesthesiologists to consider hereditary neuropathies in the differential diagnosis of postpartum neurological complications and to seek neurological advice if necessary.
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Footnotes
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August 27, 2004.
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References
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Abstract
Introduction
