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229. Lesoin, F., Petit, H., Destee, A. et al. Spinal dysraphia and elongated spinal 252. Richardson, J. & Bedder, M. Transient anterior spinal cord syndrome with
cord in adults. Surg. Neurol. 1984; 21: 119“24. continuous postoperative epidural analgesia. Anesthesiology 1990; 72:
230. Kirollos, R. W. & Van Hille, P. T. Evaluation of surgery for the tethered cord 764“6.
syndrome using a new grading system. Br. J. Neurosurg. 1996; 10: 253“60. 253. Dunn, D. W. & Ellison, J. Anterior spinal artery syndrome during the post-
231. Gupta, S. K., Khosla, V. K., Sharma, B. S. et al. Tethered cord syndrome in partum period. Arch. Neurol. 1981; 38: 263.
adults. Surg. Neurol. 1999; 52: 362“70. 254. Kozody, R., Palahniuk, R. J., Wade, J. G. et al. The effect of subarachnoid
232. Huttmann, S., Krauss, J., Collmann, H. et al. Surgical management of epinephrine and phenylephrine on spinal cord blood flow. Can. Anaesth.
tethered spinal cord in adults: report of 54 cases. J. Neurosurg. 2001; 95: Soc. J. 1984; 31: 503“8.
173“8. 255. Porter, S. S., Albin, M. S., Watson, W. A. et al. Spinal cord and cerebral
233. van Leeuwen, R., Notermans, N. C. & Vandertop, W. P. Surgery in adults blood flow responses to subarachnoid injection of local anesthetics with
with tethered cord syndrome: outcome study with independent clinical and without epinephrine. Acta Anaesthesiol. Scand. 1985; 29: 330“8.
review. J. Neurosurg. 2001; 94: 205“9. 256. Urquhart-Hay, D. Paraplegia following epidural analgesia. Anaesthesia
234. Giles, L. G. Review of tethered cord syndrome with a radiological and 1969; 24: 461“70.
anatomical study: case report. Surg. Radiol. Anat. 1991; 13: 339“43. 257. Dohi, S., Takeshima, R. & Naito, H. Spinal cord blood flow during spinal
235. Lapsiwala, S. B. & Iskandar, B. J. The tethered cord syndrome in adults with anesthesia in dogs: the effects of tetracaine, epinephrine, acute blood loss,
spina bifida occulta. Neurol. Res. 2004; 26: 735“40. and hypercapnia. Anesth. Analg. 1987; 66: 599“606.
236. Heinz, E. R., Rosenbaum, A. E., Scarff, T. B. et al. Tethered spinal cord 258. Ackerman, W. E., Juneja, M. M. & Knapp, R. K. Maternal paraparesis after
following meningomyelocele repair. Radiology 1979; 131: 153“60. epidural anesthesia and cesarean section. South. Med. J. 1990; 83: 695“7.




214
PERIPHERAL NEUROPATHY
11
Felicity Reynolds




Introduction
Table 11.1 Classification of neuropathies
Peripheral neuropathy takes many forms and may occur as a
HEREDITARY/GENETIC NEUROPATHIES
primary condition or as a component of many diseases with
 Charcot-Marie-Tooth disease
Hereditary sensory motor
multisystem manifestations. There are manifold etiologies:
neuropathies (HSMN) (types I and II)
genetic, inflammatory, traumatic/compressive, metabolic, vas-
 the X-linked form of HSMN
culitic, neoplastic, dietary, toxic/drug-induced. They may be clas-
 Dejerine-Sottas disease (type III)
sified as mononeuropathy, plexopathy, multifocal neuropathy
 Refsum disease (type IV)
(mononeuropathy multiplex), or polyneuropathy. They may
Hereditary neuropathy with liability to pressure palsy
affect primarily the cell body and/or the axon (neuropathy, axono-
 Riley-Day syndrome
Familial dysautonomia
pathy), or the myelin sheath (demyelinating neuropathy/neura-
 Congenital deficiency of
praxia).1 As these categories are confused and confusing, and of
dopamine b-hydroxylase
little use to the anesthesiologist, a simple etiological classification
 (Shy-Drager syndrome)
is used here (Table 11.1).
Neurofibromatosis types 1 and 2
Neuropathies may affect sensory, motor, or autonomic nerves,
or a combination. Longer neurons are usually the most suscept- INFLAMMATORY DEMYELATING POLYNEUROPATHIES
ible, so a predominantly distal distribution is common. Signs and Guillain-Barr´ syndrome
e
symptoms may include muscle weakness and wasting, peripheral Chronic inflammatory demyelinating polyneuropathy
in onset, usually affecting the lower limbs first, with loss of tendon
TRAUMATIC/COMPRESSIVE MONONEUROPATHIES
reflexes and sometimes with fasciculation, glove and stocking
AND PLEXOPATHIES
sensory loss, paresthesias, spontaneous pain, and autonomic
Cranial nerve lesions (V, VI, VII, VIII)
dysfunction.1
Upper limb neuropathies
Pregnancy may exacerbate some neuropathies, while preg-
 Brachial plexus palsy
nancy or parturition may be a direct or indirect cause of a variety
 Radial nerve palsy
of mononeuropathies and plexopathies,2 many of which may be
 Carpal tunnel syndrome
incorrectly attributed to neuraxial anesthesia.3 Some peripheral
neuropathies may alter drug sensitivity or impair respiration, and
Lower limb neuropathies (obstetric palsies)
therefore present special challenges to the anesthesiologist.
 Lumbosacral plexus palsy
Pregnancy can also cause physical deterioration in restrictive
 Femoral, obturator, sciatic,
respiratory disease, particularly if associated with scoliosis; it is
lateral femoral cutaneous
important to remember that relief does not follow immediately
(meralgia paresthetica),
after delivery, so the puerperium can be a dangerous time.4,5
peroneal nerve palsies

NEUROPATHIES SECONDARY TO OTHER CONDITIONS
Hereditary/genetic neuropathies
 Diabetes
Charcot-Marie-Tooth disease, also called peroneal  Porphyria
muscular atrophy or hereditary sensorimotor  Infection: leprosy, HIV, diphtheria
neuropathy (HSMN) types I & II  Vasculitis
 Sarcoidosis
This is an autosomal dominant genetic disease, but it can occur
 Poisoning with heavy metals (lead, thallium, arsenic, mercury) and
by mutation, so there may be no family history. It presents in
solvents
childhood with difficulty walking, sometimes accompanied by
 Deficiency states
pes cavus. There is weakness and wasting of the lower legs, foot
 Drug-induced neuropathies
drop, steppage gait, and reduced tendon reflexes, with later invol-
vement of the hands and trunk, and variable distal sensory loss. These conditions are listed in the order in which they appear in
The condition is slowly progressive. Type I is a diffuse demyeli- the text
nating neuropathy presenting in the first decade. It is caused by a
segmental duplication on chromosome 17p, which includes the


Obstetric Anesthesia and Uncommon Disorders, eds. David R. Gambling, M. Joanne Douglas and Robert S. F. McKay. Published by Cambridge University Press.
# Cambridge University Press 2008.
3 Nervous system disorders


Dejerine-Sottas disease (HSMN type III)
gene for peripheral myelin protein. As with any cause of paralysis
that may involve the trunk muscles during growth, there may be
This condition is similar to CMT disease, but usually recessive. It
scoliosis and stunting, with impaired respiratory function. Type II
is slowly progressive with childhood onset, and may be charac-
is an axonal neuropathy; it presents later in life and is less severe.1
terized by enlargement of peripheral nerve trunks. There are no
The condition, particularly the more severe type I, may be
reported cases of pregnancy in mainstream literature, but a case
exacerbated in pregnancy.6 The gravid uterus splints the dia-
was described in 1990 of a woman with this condition who had
phragm, so forced vital capacity (FVC) may fall and progressive
a > 908 scoliosis.5 Her FVC fell during pregnancy from 950 to
respiratory compromise is well documented.7,8 Paradoxically,
400 ml at term and she suffered increasing respiratory failure
however, a paralyzed abdominal wall may diminish respiratory
with cor pulmonale. She was delivered by C/S at 33 weeks under
embarrassment in pregnancy, as the abdomen and uterus can
GA and required noninvasive mechanical ventilation postpartum.
expand more easily, thereby reducing diaphragmatic splinting.
This suggests that considerations for these patients should be
Nevertheless, small stature is associated with premature labor.5
similar to those with CMT disease.
In a woman with severe Charcot-Marie-Tooth (CMT) disease
type I, weighing 24 kg and with a 308 scoliosis and an FVC of
500 ml, requirement for mechanical ventilation increased during Refsum disease (HSMN type IV)
pregnancy from nocturnal only up to 22 hours a day, until she
This is a rare autosomal recessive condition characterized not only
went into spontaneous labor at 30 weeks™ gestation.7 After cesar-
by a mixed motor and sensory neuropathy, usually distal, but also
ean section (C/S) under general anesthesia (GA) she was weaned
by ataxia, anosmia, pigmentary retinal degeneration, abnormal
gradually from daytime artificial ventilation without problems. If
pupils, deafness, cardiomyopathy, and ichthyosis.1 It presents in
these needs are not anticipated, the sequence of events may be
late childhood or early adult life, usually with night blindness, and
stormy. For example, a less severely disabled 100-kg parturient
is slowly progressive or relapsing. Peripheral nerves may become
with CMT disease (presumably type II) who was not initially
hypertrophic. It is due to an inability to metabolize dietary phyta-
respirator-dependent, was also delivered by C/S under GA, but
mic acid. It affects males and females equally.15
underwent numerous extubations and reintubations postpartum
Mainstream literature contains no references to anesthesia or
for 26 days until she was finally weaned.8 There are many stories
pregnancy in association with Refsum disease, but logically,
like this, some ending in disaster.4 Orotracheal intubation is not
anesthetic considerations must take account of possible impair-
suitable for weaning partially respirator-dependent patients, but
ment of cardiac function as well as respiratory insufficiency and
neither is tracheostomy mandatory; a noninvasive form of venti-
peripheral neuropathy.
lation such as a nasal mask, a mouthpiece, or, in the old days, an
iron lung, can be tolerated without sedation and can therefore
allow gradual or partial weaning, which is essential.5,9
Hereditary neuropathy with liability to pressure
For those severely affected with CMT disease type I, difficulty
palsies (HNPP)
sleeping, increasing need to draw breath while speaking, and an
FVC falling below one liter, may indicate the need for increased This is an autosomal dominant disorder with variable penetrance
respiratory assistance during pregnancy. that can present at any age. The cause is a deletion of the distal
There is no evidence of any sensitivity to malignant hyperther- segment of chromosome 17p, which contains the gene for peri-
pheral myelin protein,16 the gene that is duplicated in CMT
mia triggers, or abnormal sensitivity to succinylcholine in those
with CMT disease,10 but small scoliotic and paralyzed patients disease. The condition should therefore occur with the same
tolerate sedatives, respiratory depressants, and neuromuscular frequency as CMT disease, but it must often go undiagnosed.
blocking (NMB) drugs poorly, and may die without respiratory There are recurrent focal peripheral nerve palsies particularly in
support postoperatively.4,5,10 Those who are orthopneic may areas that are susceptible to compression or stretch, such as the
equally be unable to tolerate the wedged supine position for brachial plexus, the median nerve in the carpal tunnel, and the
awake C/S.11 Though continuous spinal anesthesia has been peroneal nerve.1 Such nerve injuries lead to areas of local demye-
used,11 it may not be without problems, and GA with noninvasive lination and cause episodes of numbness or weakness of varying
duration.16 Sausage-shaped swelling of myelin sheaths may be
respiratory support postpartum may be the best option for those
with respiratory difficulties.7 Patients who are already paralyzed evident. The condition may exacerbate neuropathies associated
require little extra muscle relaxation and less postoperative analge- with pregnancy and delivery, such as lumbosacral plexus,
sia than normal.12 It is essential to take account of body weight femoral, lateral femoral cutaneous, obturator or peroneal nerve
palsies, more often than is appreciated.17 Dense local anesthetic
when estimating drug doses for GA and regional anesthesia.
Although access to the epidural space may be difficult if severe (LA) blockade should be avoided as it may mask a compression
scoliosis is present, there is no apparent reason why less severely neuropathy. If a patient known to have this condition presents
during pregnancy, Lepski and Alderson16 suggest the following
affected individuals should not be given epidural analgesia and
undergo vaginal delivery.5,13 management principles:
 consult with a neurologist and anesthesiologist in the antenatal
The x-linked form of HSMN is a rare sex-linked dominant
disorder, similar to type 1, but female carriers are asymptomatic period
or only mildly affected.14  assess neurological status antepartum


216
Chapter 11


 avoid prolonged immobilization in labor catecholamines there is supersensitivity to exogenous transmitter
 avoid instrumental delivery substances, but insensitivity to indirect acting vasopressors such
 avoid dense epidural blockade as ephedrine. There are many important anesthetic considera-
 consider operative delivery if a pressure palsy develops in labor. tions for labor and delivery in those suffering from dysautono-
Then if C/S is selected, The HNPP website (www.hnpp.org) gives mia, which are addressed below. Among childhood sufferers,
the following advice to the ˜˜surgical team™™: ketamine has been reported to yield the least hemodynamic
disturbance,22 but epidural anesthesia has also been used
 Position arms out to sides. An angle of less than 908 will help to
successfully.23
alleviate stretch on the brachial plexus.
 Move arms (supinate/pronate) every 15 minutes under general Dysautonomia is more commonly encountered as a complica-
anesthesia. tion of diabetes than as a genetic condition (see later). The Shy-
 Pad arms and legs/feet in stirrups. As a general rule: PAD Drager syndrome as a cause of autonomic dysfunction does not
EVERYTHING. The need to pad arms and legs is dependent normally affect women of childbearing age.
upon the individual patient (frequency and severity of palsies).
Anesthetic considerations for parturients
One inch foam or similar type material is usually sufficient.
with dysautonomia
 If possible avoid leaning against the patient, especially against
the arms and legs. A woman with dysautonomia is at greatly increased risk in preg-
 Tape endotracheal tube more centrally so that the tube is fully nancy and parturition as she may have been suffering from
supported by the tape and not at all by the mouth. Tape other repeated vomiting, she may have blunted respiratory responses,
tubing in a similar manner as appropriate. Consider position- inability to compensate for intravascular volume depletion, and
ing while awake. denervation supersensitivity. There may also be reduced respira-
In order not to mask any developing neuropathy, anything but the tory reserve (see Charcot-Marie-Tooth disease).
mildest block for postoperative pain should be avoided. During labor, and of course for C/S, histamine H2-receptor
blockers (e.g. ranitidine) and prokinetics (metoclopramide) are
advocated for aspiration prophylaxis. Early recognition and treat-
Familial dysautonomia
ment of fluid depletion can reduce hemodynamic instability.
One type of familial dysautonomia, Riley-Day syndrome, is a rare Inadequate analgesia may precipitate an autonomic crisis, while
autosomal recessive genetic disorder found in Ashkenazi Jews, in norepinephrine deficiency and an unpredictable response to
which deficient norepinephrine stores impair the development of vasopressors may complicate spinal or epidural anesthesia. One
the autonomic and sensory nervous systems. It is characterized by alternative is to use intrathecal opioids, with appropriate respira-
autonomic instability (abnormal sweating, loss of vasomotor con- tory monitoring, for first stage pain relief, and pudendal or saddle
trol, labile blood pressure) and sensory involvement (impaired taste block if necessary for second stage analgesia.
with absence of fungiform papillae, diminished pain and tempera- Cesarean section has been conducted successfully under cau-
ture sensation, hyporeflexia) unexplained fever, vomiting attacks, tiously titrated epidural anesthesia, combined spinal“epidural
(CSE) anesthesia using a low dose of bupivacaine with fentanyl20
impaired respiratory reflexes with frequent episodes of aspiration
pneumonia, blunted responses to hypoxia and hypercarbia,18 dry and also local anesthesia.24 For GA, doses of induction agents and
eyes and corneal anesthesia with ulceration. The symptoms are inflation pressures should be kept to a minimum to avoid circu-
present from birth; short stature and scoliosis may become evident latory disturbance. Fluid lost must be scrupulously replaced,
during growth.1 Viable pregnancies with normal offspring have irrespective of the anesthetic technique. Direct arterial pressure
been described in women with Riley-Day syndrome.19 monitoring and postoperative ventilation should be considered.
A rare type of dysautonomia is caused by congenital deficiency Small titrated doses of direct-acting cardiovascular drugs such as
of dopamine b-hydroxylase, the enzyme that catalyzes the conver- phenylephrine (vasoconstrictor), isoproterenol (to increase heart
sion of dopamine to norepinephrine. Neonates with dopamine rate), and esmolol (to decrease heart rate), rather than indirect
b-hydroxylase deficiency have hypothermia, hypotension, and acting agents, may be used to treat either sympathetic excess or
hypoglycemia.20 Survivors have postural hypotension, as in the deficiency. Sodium nitroprusside does not alter uterine blood
Riley-Day syndrome, but other features vary: nocturia, hypoprolac- flow or vascular resistance, but because of the possibility of fetal
tinemia, ptosis, hypermobile joints, high-arched palate, nasal stuffi- cyanide toxicity its use should be brief.
ness and occasionally abnormal behavior, sluggish reflexes, Modest narcotic analgesia, augmented by LA infiltration, may
hypotonia, and raised blood urea.21 Hypotension may be so severe provide effective postoperative pain relief, as these patients have
as to provoke seizures.20 There are reports of pregnancy in this a reduced analgesic requirement.
condition, unlike the Riley-Day syndrome, and the course of preg-
nancy may be complicated. The condition has been treated success-
Neurofibromatosis types 1 and 2 (NF1 and 2):
fully with dihydrophenylserine, which is converted by dopa
see Chapter 8 for further details
decarboxylase to norepinephrine.21
Familial dysautonomia may be diagnosed by detecting a These conditions affect both central and peripheral nervous sys-
plasma norepinephrine/dopamine ratio of much less than tems. Both are autosomal dominant, but are caused by mutation
one.20 Because of chronic exposure to low levels of in about 50% of cases. Nevertheless they are genetically distinct.



217
3 Nervous system disorders


Both are characterized by a tendency to form tumors associated The presence of a gravid uterus increases the need for ventila-
with nervous tissue and other organs.25 Skin and peripheral nerve tory assistance and exacerbates circulatory instability. Guillain-
lesions are more common in NF1 (von Recklinghausen disease) Barr´ syndrome is associated with an increased relapse rate and
e
high maternal morbidity in pregnancy and the puerperium.33,34,35
and lesions in the central nervous system (CNS) in NF2 (also
known as acoustic neurofibromatosis). The classical caf´ -au-lait
e The outlook for the fetus is believed to be good, however, pro-
spots, together with freckling, are the hallmarks of NF1, while in vided maternal physiology is well managed.
NF2 acoustic neuromas are present in > 90% and skin plaques are
Management
common. The types and distribution of nervous system tumors
and other organ involvement in the two conditions are described It has been suggested that pregnancy does not alter the manage-
thoroughly by Huson26 and by Hirsch et al.25 Spinal deformities ment of GBS,36 and that GBS does not alter the process of preg-
may be present in both conditions. NF1 has a prevalence of in the nancy and labor, though these patients certainly require
region of 1:5000 and is about 40 times commoner than NF2.26 particular attention. It is vital to be on the lookout for, and treat
They are usually diagnosed in young adult life. promptly, both respiratory weakness and swallowing difficulty.
Pregnancy can stimulate tumor growth in both diseases. The Forced vital capacity should be monitored, since it is desirable to
most important anesthetic consideration is whether lesions in the treat respiratory weakness before the blood gases are seriously
spinal canal will interfere with neuraxial anesthesia, and whether disturbed. While noninvasive respiratory support has obvious
neuraxial anesthesia will cause bleeding. While GA is often con- advantages, the presence of bulbar weakness may necessitate
sidered preferable for this reason,27 the decision may be balanced tracheostomy in order to prevent aspiration pneumonitis, to pro-
if there is tumor involvement in the airway itself. Modern imaging vide safe mechanical ventilation and tracheobronchial suction.
within the CNS can allow accurate tumor localization, and judi- Circulatory support, attention to electrolyte balance and throm-
boprophylaxis are also needed.36 Severe cases, including those in
cious use of regional techniques has been described in selected
cases.28,29 Restrictive respiratory impairment, if present, requires pregnancy, may be treated with plasma exchange and immuno-
globulins, which attenuate the disease; steroids are useless.37,38
particular attention (see Charcot-Marie-Tooth disease).
Massive or repeated treatment with plasmapheresis or immuno-
globulin is sometimes needed during pregnancy.35,39 Where
Inflammatory demyelating polyneuropathies there is dysautonomia, plasmapheresis should be preceded by
fluid loading.
´
Guillain-Barre syndrome (acute inflammatory
polyneuropathy)
Anesthetic considerations in parturition
Since the widespread use of poliomyelitis vaccination, Guillain- Regional analgesia may be desirable in order to avoid exaggerated
hemodynamic responses during labor.40 Epidural40,41,42,43 and
Barr´ syndrome (GBS) has become the commonest cause of acute
e
paralysis, with an annual incidence of 0.6“2.4 cases per 100 000.30 CSE35 techniques have been used successfully for both pain relief
It is probably a collection of diseases, either axonal or demyeli- in labor and anesthesia for C/S. Sensitivity to regional blockade
nating,31 that may be idiopathic or triggered by various infections with LA is usually increased,36,41 while hypotension and brady-
such as Campylobacter jejuni, Cytomegalovirus, Epstein-Barr cardia may be excessive. Small gradually titrated doses of low-
virus, Mycoplasma, hepatitis B, human immunodeficiency virus dose LA/opioid combinations are therefore advisable, with small
doses of a direct-acting vasopressor if needed.36 Responses to the
(HIV), Chlamydia or even an upper respiratory tract infection or
surgery.1,32 It affects both sexes and all ages, but with peak inci- latter drugs are erratic. If regional anesthesia is to be used for C/S,
dences in young adults and the elderly, while pregnancy may it is important to be on the lookout for respiratory compromise.
predispose to it. General anesthesia presents a problem in the parturient with
The condition develops over a few days to a few weeks, during GBS, since succinylcholine may cause dangerous hyperkalemia,
even in the recovery phase of the disease.36 Autonomic instability
which time the patient™s condition may deteriorate rapidly. The
first symptom is usually severe upper and lower back pain, fol- may provoke major hypotension from the induction agent.
lowed by progressive symmetrical weakness starting in the legs Sensitivity to all NMB agents is increased, while respiratory
depressant drugs are also best avoided.41 Bulbar weakness neces-
and progressing to the trunk and sometimes the cranial nerves,
with facial and bulbar weakness. There may be some sensory loss, sitates thorough antacid prophylaxis in order to mitigate the
but more commonly paresthesia of similar distribution. danger of aspiration during both induction and recovery from
Dysautonomia is common, usually short lived, and may be man- anesthesia.
ifest by sinus tachycardia or bradycardia, facial flushing, profuse
or absent sweating, labile blood pressure, ileus and urinary reten-
Chronic inflammatory demyelinating
tion. The cerebrospinal fluid protein is raised in the acute phase
polyneuropathy
of the disease. The patient usually recovers within weeks or
months. In 10“40% of cases there may be residual muscle weak- Occasionally a condition that appears similar to GBS turns out to
be chronic or relapsing, with widespread demyelination,1 and is
ness. Most mortality is due to autonomic instability, though
respiratory and bulbar failure may contribute; the mortality rate known as chronic inflammatory demyelinating polyneuropathy.
therefore varies depending on the quality of care. The frequency of both onset and relapse, and of exacerbations of



218
Chapter 11


the condition, is increased in pregnancy.44 Relapse may occur further pregnancy. This was followed by ectopic pregnancy,
which provoked a further attack.57 How unlucky can you get?
during the latter half of pregnancy, sometimes postpartum and
occasionally with the use of oral contraceptives. It may be treated Radial nerve palsy. The radial nerve is vulnerable in the spiral
with plasmapheresis or immunoglobulin, but, unlike GBS, the groove at the midhumeral region. Radial neuropathy, resulting in
chronic condition also responds to corticosteroids. upper arm weakness and commonly known as Saturday night
The fetus and neonate are not affected by the disease itself. palsy, has been described following prolonged use of a birthing
bar.58 Women should be instructed to rest the forearms rather
Obstetric and anesthetic management are similar to that for GBS.
than the upper arms on the bar.
Carpal tunnel syndrome resulting from compression of the
Traumatic/compressive mononeuropathies
median nerve beneath the flexor retinaculum at the wrist is a
and plexopathies
familiar problem during pregnancy.46 Numbness, tingling, and
Most mononeuropathies and plexopathies that arise in preg- burning sensations in the hand may radiate up the arm and are
nancy or parturition have a physical origin, but some, such as worse at night, often causing severe sleep disturbance. There may
brachial plexus palsy, may have an inflammatory element. also be thenar wasting. The symptoms may be relieved by shaking
the hand or otherwise keeping it moving. Although it usually
resolves postpartum, it may arise de novo at this time (lactational
Cranial nerve lesions
carpal tunnel syndrome) and resolve only after weaning.
Idiopathic facial (VII) nerve palsy is about three times more
common in pregnancy than in the nonpregnant population,45
Obstetric palsies
with most cases arising in the third trimester. It is probable that
pregnancy increases the likelihood of compression of the nerve In the past, when labor might continue for several days, and C/S,
within the facial canal. It appears to be associated with pre- like anesthesia, was rare, obstetric palsies were well recognized.
eclampsia, diabetes, migraine, and other cranial nerve palsies in Several surveys in the years between 1935 and 1965 reported
incidences around 1 in 2000 deliveries.59,60,61,62 The classical syn-
pregnancy. On the affected side the sufferer is unable to wrinkle
the brow, raise the eyebrow, close the eye, purse the lips, whistle, drome, once termed traumatic neuritis of the puerperium, arose
or smile.46 There may also be dribbling and dysphagia; involve- from pressure of the baby™s head on the lumbosacral trunk as it
crossed the pelvic brim.46,63 The treatment was held to be bed
ment of the chorda tympani branch may cause partial loss of taste
in the tongue and altered lacrimal and salivary secretion.47 rest, so the end result could be death from pulmonary embolus.46
Permanent dysfunction is unusual: recovery within the first The current incidence of postpartum neuropathy is difficult to
three months postpartum is the norm. Treatment with predni- determine as many surveys are too small to detect what has

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