Injuries to the lumbosacral plexus during labor and delivery have been reported in the literature for years, but have lacked electrophysiologictesting to substantiate the location of the nerve injury. We report 2 cases with comprehensive electrophysiologictesting which localizes the site of this obstetrical paralysis to the lumbosacral trunk (L4-5) and S-1 root where they join and pass over the pelvic rim. The paralysis may be mild or severe. Small maternal size, a large fetus, midforceps rotation, and fetal malposition may place the mother at risk for this nerve injury. 0 1992 John Wiley & Sons, Inc. Key words: obstetric paralysis lumbosacral plexus injury birth trauma nerve injury MUSCLE & NERVE
15:937-940 1992
OBSTETRICAL LUMBOSACRAL PLEXUS INJURY T.E. FEASBY, S.R. BURTON, and A.F. HAHN
Maternal obstetrical paralysis has been recognized as a clinical entity, at least since the independent clinical descriptions of von Basedow’ and Beatty2 in 1938. Since then, further case reports have been documented, but little has been added to the clinical d e ~ c r i p t i o n . ~ Pain in one leg has been described as the earliest symptom, occurring in the sciatic nerve territory and sometimes increased by uterine contractions. Paresthesias become evident, usually over the lateral aspect of the calf and over the dorsum of the foot. The paralysis has usually been discovered when the patient attempts walking, and foot drop with weakness of ankle inversion, dorsiflexion, and eversion has been seen. Several different mechanisms have been postulated for postpartum nerve p a l ~ i e s . ~ ~ ’ ~ ~ CASE 1
A 35-year-old primagravida was admitted at 41 weeks of gestation to a tertiary care obstetric unit following 12 hours of induced labor. She labored as a right occiput transverse lie. The second stage of labor was prolonged at over 3 hours. Forceps were applied and the fetus was rotated to an ocFrom the Department of Clinical Neurological Sciences, University of Western Ontario, Victoria Hospital, London, Ontario, Canada. Address reprint requests to Dr. T.E. Feasby, Department of Clinical Neurosciences, University of Calgary, Foothills Hospital, 1403 29th Street NW, Calgary, Alberta, T2N 2T9 Canada. Accepted for publication January 7, 1992. CCC 0148-639W92/080937-04 $04.00 0 1992 John Wiley & Sons, Inc.
Obstetrical Lumbosacral Plexus Injury
ciput anterior position and then delivered with further manipulation. Neonatal weight was 8 lbs 1 oz. T h e mother was 5 ft 1 in tall and weighed 110 lbs prior to her pregnancy. During the labor, she experienced considerable pain in her left lower abdomen and left thigh. Additional epidural anesthesia was necessary to control this pain during the labor. Following delivery, the left leg pain persisted and radiated down the lateral aspect of the left leg and into the foot. Cramps occurred in the left calf. A burning sensation occurred in the foot and she had shooting pains into the first and third toes. Back pain was absent. She noted weakness in her left leg and a left foot drop. Examination at 7 weeks postinjury showed atrophy of the left hamstrings, tibialis anterior, and extensor digitorum brevis muscles. Mild weakness was present in the left hip extensors and left hamstrings. She had an almost complete foot drop with marked weakness of both foot inversion and eversion. She was barely able to fan her left toes. Diminished pin prick sensation was noted over the lateral calf. Knee and ankle reflexes were present and symmetrical in the legs. Electrophysiologic studies (Table 1) showed considerable denervation in the L-4, L-5, S-1 innervated muscles of the leg with sparing of the paraspinal muscles. T h e compound muscle action potential of the left extensor digitorum brevis muscle was decreased (Table 2). The amplitude of the sensory nerve action potential from the left sural nerve was significantly less than the right (Table 2). Examination at 16 weeks postpartum docu-
MUSCLE & NERVE
August 1992
937
Table 1. Electromyography in case 1 (7 weeks postpartum). Spontaneous activity ~~
Muscle
FIB
PSW
Motor units
4+
4+ 4+ 2+ 0 0 0 4+ 4+ 0 0 0 0
Decreased recruitment Decreased recruitment Decreased recruitment Normal Normal Normal Decreased recruitment Decreased recruitment Normal Normal Normal Normal
~~
Lt. tibialis anterior Lt. tibialis posterior Lt. soleus Lt. gastrocnemius Lt. adductor longus Lt. vastus lateralis Lt. biceps femoris (longhead) Lt. gluteus medius Lt. gluteus maximus Lt. L-4 paraspinals Lt. L-5 paraspinals Lt. S-1 paraspinals
4+
2+ 0 0 0 4+ 4+ 0 0 0 0
2+, Moderate spontaneous activity, 4 + , severe spontaneous activity, N B , fibrillation potentials, PSW, positive sharp waves
mented significant improvement. Her leg pain was nearly gone, the shooting pains were much less frequent, and she felt stronger. There was still mild wasting of the hamstrings and tibialis anterior muscles. Mild weakness was now present in the ankle dorsiflexors, invertors, and evertors. Repeat electrophysiologic studies demonstrated reduced spontaneous activity (grade 1 to 2) in the tibialis anterior and the tibialis posterior compared to the examination at 7 weeks. There was no spontaneous activity in the gluteus medius and biceps femoris muscles. Polyphasic units, indicative of reinnervation, were seen in the biceps femoris muscle. CASE 2
A 25-year-old woman delivered her second child at 40 weeks gestation. The second stage of labor lasted 10 hours, with the fetus in a left occiput transverse lie. Epidural anesthesia was used but
forceps were not. The infant weighed 8 Ibs 9 oz and the mother was 5 ft 1 in tall and weighted 100 Ibs before her pregnancy. There was no leg pain during labor. After delivery she complained of weakness of her right leg and numbness over the lateral side of her right lower leg and the dorsum of the foot. Examination on the second postpartum day showed mild weakness of right hip flexion, extension, and abduction with marked weakness of ankle dorsiflexion, eversion and inversion, and extension of the toes, and mild weakness of plantar flexion of the ankle and toes. Pin prick sensation was reduced over the lateral side of the right lower leg and the dorsum of the foot. The knee jerks and left ankle jerk were 2+ and the right ankle jerk was absent. Reexamination at 10 days postpartum showed significant improvement. Strength at the hip was normal, and there was mild weakness of knee flexion. Her foot drop had improved slightly. The
Table 2. Nerve conduction studies in case 1 (7 weeks postpartum), Left Velocity
Ampitude (mv)
Velocity (m/s)
Amplitude (mv)
Ankle to ext. dig. brevis Fib. head to ext. dig. brevis Pop. fossa to ext. dig. brev. Ankle to abd. hallucis Pop. fossa to abd. hallucis
34.8 49.7
52.6 54.3
44.8
0.95 0.95 0.94 21.44 15.52
47.7
7.54 7.39 7.28 28.08 20.92
Post. lower leg to lat. mal.
40.4
0.016
38.7
0.030
Stimulus to recording site Motor nerve Deep peroneal
Tibia1 Sensory nerve Sural
938
Right
Obstetrical Lumbosacral Plexus Injury
-
MUSCLE & NERVE
August 1992
sensory exam was normal and her right ankle jerk was present but depressed. Her neurologic examination was normal at 4 months. EMG examination at 10 days postpartum showed only a decreased recruitment pattern in the weak muscles, but no signs of denervation. DISCUSSION
In our first case, the clinically affected nerves and muscles correlated well with the electrophysiologic abnormalities. Muscles from the L-4, L-5, and S-1 segments were denervated in a sciatic nerve distribution in both the peroneal and tibia1 components, with involvement of the gluteus medius and sparing of the gluteus maximus. In addition, there was a reduced sural (S-1) nerve amplitude on the left compared to the right by a factor of 50%. This pattern of denervation places the injury in the region of the lumbosacral trunk and includes the S-1 root, either just before or just after it joins the trunk (Fig. 1). T o explain why the superior gluteal nerve (gluteus medius) was affected while the inferior gluteal nerve (gluteus maximus) was unaffected, one may propose that a fascicular pattern of damage occurs, affecting some components of a nerve and sparing others.’ The nerve lesion probably results from direct
FIGURE 1. Diagram of the lumbosacral plexus showing the presumed site of the compressive nerve lesion (circle).
Obstetrical Lurnbosacral Plexus Injury
pressure by the descending fetal head compressing the lumbosacral trunk and the S-1 root as it joins the trunk against the rim of the pelvis during the rotation and descent of the second state of labor. The foot drop is almost always unilateral and, generally, on the same side as the infant’s brow during the descent. In our first case, the infant’s brow was on the left as was the foot drop and, in the second case, both were on the right. The typical syndrome occurs in a short primagravida (5 ft, 152 cm) carrying a relatively large baby (8.25 lbs, 3.75 kg) with prolonged labor, malpresentation, and midforceps rotation after a transverse arrest.3 There are no studies of the incidence of obstetrical paralysis. Whittakerg suggested that as many as 1/2000 deliveries may be complicated by this palsy after he reviewed the known cases in Toronto over a 5-year period. Most cases, as in our second example, probably, have only mild symptoms, which may be dismissed by the patient and physician and which resolve completely. More severe nerve damage with prolonged disability, as in our first case, may be unusual. It is important to distinguish this obstetrical paralytic syndrome from compression of the peroneal nerve where it crosses the fibular head. This also causes numbness along the lateral calf and a foot drop, and it can be seen during labor as a result of compression by legholders. Some of the reported examples of obstetrical paralysis may be due to peroneal nerve compression, but the lack of electrophysiological assessment in most reports makes this judgment difficult.9 O’Connell‘ observed lumbar intervertebral disc herniations causing various L4-5, S- 1 radiculopathies, some occurring during labor and delivery. He observed the increased propensity for disc herniations during pregnancy and, therefore, the need to consider this cause of foot drop in the differential diagnosis. Disc herniations usually are associated with back pain, a symptom absent in our cases. Another possible cause of obstetrical paralysis is damage to lumbosacral roots from an epidural anesthetic catheter. This is extremely rare and would be unlikely to cause damage to multiple roots. Advice for subsequent pregnancies is speculative. If the infant is deemed not too large and a trial of labor is progressing well, then vaginal delivery might be attempted. Midforceps rotations probably should be avoided and Cesarean section employed if malpresentation or arrest of labor occurs.
MUSCLE & NERVE
August 1992
939
REFERENCES 1. von Basedow KA: Uber Neuralgia pueperarum cruralis.
Wochenschrift fur die gesammte Heilkunde 1983;6:636-639. 2. Beatty T E : Paralysis after delivery. Irish J Med Sci 1838;12:304- 306. 3. Brown JT, MacDougall A: Traumatic maternal birth palsy. J Obstet Gynecol Brit Emp 1957;64:431-435. 4. Donaldson JO: Neurology of Prengnacy (2nd ed). London, Saunders, 1989.
940
Obstetrical Lurnbosacral Plexus Injury
5. Kane RE: Neurologic deficits following epidural or spinal anesthesia. Anesth Analg 1981;60:150- 161. 6. OConnell JEA: Material obstetrical paralysis. Surg Gynecol Obstet 1944;79:374-382. 7. Stewart JD: Focal Peripheral Neuropathies. New York, Elsevier, 1987. 8. Tillman AJB: Traumatic neuritis in the puerperium. A m J Obstet Gynecol 1935;29:660-666. 9. Whittaker WG: Injuries of the sacral plexus in obstetrics. Can Med Assoc J 1958;79:622-626.
MUSCLE & NERVE
August 1992
15:937-940 1992
OBSTETRICAL LUMBOSACRAL PLEXUS INJURY T.E. FEASBY, S.R. BURTON, and A.F. HAHN
Maternal obstetrical paralysis has been recognized as a clinical entity, at least since the independent clinical descriptions of von Basedow’ and Beatty2 in 1938. Since then, further case reports have been documented, but little has been added to the clinical d e ~ c r i p t i o n . ~ Pain in one leg has been described as the earliest symptom, occurring in the sciatic nerve territory and sometimes increased by uterine contractions. Paresthesias become evident, usually over the lateral aspect of the calf and over the dorsum of the foot. The paralysis has usually been discovered when the patient attempts walking, and foot drop with weakness of ankle inversion, dorsiflexion, and eversion has been seen. Several different mechanisms have been postulated for postpartum nerve p a l ~ i e s . ~ ~ ’ ~ ~ CASE 1
A 35-year-old primagravida was admitted at 41 weeks of gestation to a tertiary care obstetric unit following 12 hours of induced labor. She labored as a right occiput transverse lie. The second stage of labor was prolonged at over 3 hours. Forceps were applied and the fetus was rotated to an ocFrom the Department of Clinical Neurological Sciences, University of Western Ontario, Victoria Hospital, London, Ontario, Canada. Address reprint requests to Dr. T.E. Feasby, Department of Clinical Neurosciences, University of Calgary, Foothills Hospital, 1403 29th Street NW, Calgary, Alberta, T2N 2T9 Canada. Accepted for publication January 7, 1992. CCC 0148-639W92/080937-04 $04.00 0 1992 John Wiley & Sons, Inc.
Obstetrical Lumbosacral Plexus Injury
ciput anterior position and then delivered with further manipulation. Neonatal weight was 8 lbs 1 oz. T h e mother was 5 ft 1 in tall and weighed 110 lbs prior to her pregnancy. During the labor, she experienced considerable pain in her left lower abdomen and left thigh. Additional epidural anesthesia was necessary to control this pain during the labor. Following delivery, the left leg pain persisted and radiated down the lateral aspect of the left leg and into the foot. Cramps occurred in the left calf. A burning sensation occurred in the foot and she had shooting pains into the first and third toes. Back pain was absent. She noted weakness in her left leg and a left foot drop. Examination at 7 weeks postinjury showed atrophy of the left hamstrings, tibialis anterior, and extensor digitorum brevis muscles. Mild weakness was present in the left hip extensors and left hamstrings. She had an almost complete foot drop with marked weakness of both foot inversion and eversion. She was barely able to fan her left toes. Diminished pin prick sensation was noted over the lateral calf. Knee and ankle reflexes were present and symmetrical in the legs. Electrophysiologic studies (Table 1) showed considerable denervation in the L-4, L-5, S-1 innervated muscles of the leg with sparing of the paraspinal muscles. T h e compound muscle action potential of the left extensor digitorum brevis muscle was decreased (Table 2). The amplitude of the sensory nerve action potential from the left sural nerve was significantly less than the right (Table 2). Examination at 16 weeks postpartum docu-
MUSCLE & NERVE
August 1992
937
Table 1. Electromyography in case 1 (7 weeks postpartum). Spontaneous activity ~~
Muscle
FIB
PSW
Motor units
4+
4+ 4+ 2+ 0 0 0 4+ 4+ 0 0 0 0
Decreased recruitment Decreased recruitment Decreased recruitment Normal Normal Normal Decreased recruitment Decreased recruitment Normal Normal Normal Normal
~~
Lt. tibialis anterior Lt. tibialis posterior Lt. soleus Lt. gastrocnemius Lt. adductor longus Lt. vastus lateralis Lt. biceps femoris (longhead) Lt. gluteus medius Lt. gluteus maximus Lt. L-4 paraspinals Lt. L-5 paraspinals Lt. S-1 paraspinals
4+
2+ 0 0 0 4+ 4+ 0 0 0 0
2+, Moderate spontaneous activity, 4 + , severe spontaneous activity, N B , fibrillation potentials, PSW, positive sharp waves
mented significant improvement. Her leg pain was nearly gone, the shooting pains were much less frequent, and she felt stronger. There was still mild wasting of the hamstrings and tibialis anterior muscles. Mild weakness was now present in the ankle dorsiflexors, invertors, and evertors. Repeat electrophysiologic studies demonstrated reduced spontaneous activity (grade 1 to 2) in the tibialis anterior and the tibialis posterior compared to the examination at 7 weeks. There was no spontaneous activity in the gluteus medius and biceps femoris muscles. Polyphasic units, indicative of reinnervation, were seen in the biceps femoris muscle. CASE 2
A 25-year-old woman delivered her second child at 40 weeks gestation. The second stage of labor lasted 10 hours, with the fetus in a left occiput transverse lie. Epidural anesthesia was used but
forceps were not. The infant weighed 8 Ibs 9 oz and the mother was 5 ft 1 in tall and weighted 100 Ibs before her pregnancy. There was no leg pain during labor. After delivery she complained of weakness of her right leg and numbness over the lateral side of her right lower leg and the dorsum of the foot. Examination on the second postpartum day showed mild weakness of right hip flexion, extension, and abduction with marked weakness of ankle dorsiflexion, eversion and inversion, and extension of the toes, and mild weakness of plantar flexion of the ankle and toes. Pin prick sensation was reduced over the lateral side of the right lower leg and the dorsum of the foot. The knee jerks and left ankle jerk were 2+ and the right ankle jerk was absent. Reexamination at 10 days postpartum showed significant improvement. Strength at the hip was normal, and there was mild weakness of knee flexion. Her foot drop had improved slightly. The
Table 2. Nerve conduction studies in case 1 (7 weeks postpartum), Left Velocity
Ampitude (mv)
Velocity (m/s)
Amplitude (mv)
Ankle to ext. dig. brevis Fib. head to ext. dig. brevis Pop. fossa to ext. dig. brev. Ankle to abd. hallucis Pop. fossa to abd. hallucis
34.8 49.7
52.6 54.3
44.8
0.95 0.95 0.94 21.44 15.52
47.7
7.54 7.39 7.28 28.08 20.92
Post. lower leg to lat. mal.
40.4
0.016
38.7
0.030
Stimulus to recording site Motor nerve Deep peroneal
Tibia1 Sensory nerve Sural
938
Right
Obstetrical Lumbosacral Plexus Injury
-
MUSCLE & NERVE
August 1992
sensory exam was normal and her right ankle jerk was present but depressed. Her neurologic examination was normal at 4 months. EMG examination at 10 days postpartum showed only a decreased recruitment pattern in the weak muscles, but no signs of denervation. DISCUSSION
In our first case, the clinically affected nerves and muscles correlated well with the electrophysiologic abnormalities. Muscles from the L-4, L-5, and S-1 segments were denervated in a sciatic nerve distribution in both the peroneal and tibia1 components, with involvement of the gluteus medius and sparing of the gluteus maximus. In addition, there was a reduced sural (S-1) nerve amplitude on the left compared to the right by a factor of 50%. This pattern of denervation places the injury in the region of the lumbosacral trunk and includes the S-1 root, either just before or just after it joins the trunk (Fig. 1). T o explain why the superior gluteal nerve (gluteus medius) was affected while the inferior gluteal nerve (gluteus maximus) was unaffected, one may propose that a fascicular pattern of damage occurs, affecting some components of a nerve and sparing others.’ The nerve lesion probably results from direct
FIGURE 1. Diagram of the lumbosacral plexus showing the presumed site of the compressive nerve lesion (circle).
Obstetrical Lurnbosacral Plexus Injury
pressure by the descending fetal head compressing the lumbosacral trunk and the S-1 root as it joins the trunk against the rim of the pelvis during the rotation and descent of the second state of labor. The foot drop is almost always unilateral and, generally, on the same side as the infant’s brow during the descent. In our first case, the infant’s brow was on the left as was the foot drop and, in the second case, both were on the right. The typical syndrome occurs in a short primagravida (5 ft, 152 cm) carrying a relatively large baby (8.25 lbs, 3.75 kg) with prolonged labor, malpresentation, and midforceps rotation after a transverse arrest.3 There are no studies of the incidence of obstetrical paralysis. Whittakerg suggested that as many as 1/2000 deliveries may be complicated by this palsy after he reviewed the known cases in Toronto over a 5-year period. Most cases, as in our second example, probably, have only mild symptoms, which may be dismissed by the patient and physician and which resolve completely. More severe nerve damage with prolonged disability, as in our first case, may be unusual. It is important to distinguish this obstetrical paralytic syndrome from compression of the peroneal nerve where it crosses the fibular head. This also causes numbness along the lateral calf and a foot drop, and it can be seen during labor as a result of compression by legholders. Some of the reported examples of obstetrical paralysis may be due to peroneal nerve compression, but the lack of electrophysiological assessment in most reports makes this judgment difficult.9 O’Connell‘ observed lumbar intervertebral disc herniations causing various L4-5, S- 1 radiculopathies, some occurring during labor and delivery. He observed the increased propensity for disc herniations during pregnancy and, therefore, the need to consider this cause of foot drop in the differential diagnosis. Disc herniations usually are associated with back pain, a symptom absent in our cases. Another possible cause of obstetrical paralysis is damage to lumbosacral roots from an epidural anesthetic catheter. This is extremely rare and would be unlikely to cause damage to multiple roots. Advice for subsequent pregnancies is speculative. If the infant is deemed not too large and a trial of labor is progressing well, then vaginal delivery might be attempted. Midforceps rotations probably should be avoided and Cesarean section employed if malpresentation or arrest of labor occurs.
MUSCLE & NERVE
August 1992
939
REFERENCES 1. von Basedow KA: Uber Neuralgia pueperarum cruralis.
Wochenschrift fur die gesammte Heilkunde 1983;6:636-639. 2. Beatty T E : Paralysis after delivery. Irish J Med Sci 1838;12:304- 306. 3. Brown JT, MacDougall A: Traumatic maternal birth palsy. J Obstet Gynecol Brit Emp 1957;64:431-435. 4. Donaldson JO: Neurology of Prengnacy (2nd ed). London, Saunders, 1989.
940
Obstetrical Lurnbosacral Plexus Injury
5. Kane RE: Neurologic deficits following epidural or spinal anesthesia. Anesth Analg 1981;60:150- 161. 6. OConnell JEA: Material obstetrical paralysis. Surg Gynecol Obstet 1944;79:374-382. 7. Stewart JD: Focal Peripheral Neuropathies. New York, Elsevier, 1987. 8. Tillman AJB: Traumatic neuritis in the puerperium. A m J Obstet Gynecol 1935;29:660-666. 9. Whittaker WG: Injuries of the sacral plexus in obstetrics. Can Med Assoc J 1958;79:622-626.
MUSCLE & NERVE
August 1992
