Dural puncture, or more precisely dural-arachnoid puncture, was first described by Quincke in 1891.1 It has been used for diagnostic evaluation of cerebrospinal fluid (CSF), therapeutic interventions to drain CSF, and as a means to inject drugs into the subarachnoid space. Adverse consequences of dural puncture include headache, ocular abnormalities, and auditory difficulties.2 Ocular abnormalities include double vision and deviated gaze from weakness or total paralysis of the lateral rectus muscle, attributed to palsy of cranial nerve (CN) VI (abducens nerve).1–17 Accompanying palsies of the third18 and fourth19 CN have also been reported, although more rarely.
One of the first patients of Quincke was a 21-month-old boy admitted with coma, pneumonia, and strabismus.1 Serial dural punctures were performed, and during the second dural puncture, 10 mL of CSF was intentionally removed. Bilateral abducens palsies developed the following day; low CSF pressure was recorded during the third dural puncture. This is the first documented case of CN VI palsy with intracranial hypotension after dural puncture.
The purpose of this focused review is to summarize the incidence, time course, presentation, pathophysiology, risk factors, prevention, and treatment of CN VI palsy after dural-arachnoid puncture. The literature search was conducted using PubMed, Ovid, and Google Scholar search engines; search criteria were limited to human subjects and English language. In addition, bibliographies of identified manuscripts were hand-searched for relevant literature. This review includes 1 prospective observational study, a systematic review of 95 cases published in 2004, several case series, and individual case reports from the anesthetic, neurologic, radiologic, and obstetric literature.
In 1956, Vandam and Dripps2 published their sentinel single-center, prospective, observational study of adverse events after spinal anesthesia in 9277 patients. Headache occurred in 1011 patients (11%) and ocular abnormalities in 34 patients (0.4%). In a retrospective audit of 2500 myelography cases, the incidence of CN VI palsy was 1:500.8 In another retrospective study of 11,600 diagnostic lumbar puncture procedures, there were 2 cases of abducens nerve palsy, 1 unilateral and 1 bilateral (incidence <1:5800).11 Although the risk of CN VI palsy after dural puncture appears consistently low in different studies, it is difficult to estimate the actual incidence from these results. Most reports are of individual cases3,5,6,10,12,13,19 and case series.7–9,11,14–18 Unreported sample population sizes and unknown denominators make it difficult to estimate the incidence. Using retrospective methods in the cited studies may have led to underestimation of true frequency. Adding to the difficulty are differences in study design (retrospective,20 observational,21 and reviews4,22), and within the cited studies, a spectrum of patient characteristics and procedural variables.
The incidence of CN VI injury is also likely underreported because of loss of follow-up. Patients are rarely questioned regarding symptoms of CN VI palsy, and discharge from the hospital after dural puncture may precede onset of symptoms. Patients presenting with ocular symptoms after dural puncture may be referred to neurologists or ophthalmologists rather than to the anesthesiologist who performed the procedure.
Headache almost always precedes the development of ocular changes.22 Abducens abnormalities occurred in 2.6% of patients with headache in the report by Vandam and Dripps.2 CN VI palsy remains a diagnosis of exclusion that requires consideration of other potential neurologic and ophthalmic abnormalities, even when associated with dural puncture.23 If the CN VI palsy is an isolated neurologic deficit that occurs within 3 weeks of dural puncture and is preceded by a spinal headache, it is likely a consequence of dural puncture.22
The diagnosis of CN VI palsy is based on clinical presentation. Patient complaints may include blurred or double vision, sensitivity to light, and trouble focusing or reading.2 Findings on physical examination range from minimal to impaired ocular abduction that may present as partial eye adduction when the patient looks straight ahead. Palsy is unilateral in 80% of cases.22 Magnetic resonance imaging may reveal signs of intracranial hypotension, including meningeal enhancement, subdural effusions, and downward brain displacement.18,24,25 These findings are consistent with intracranial hypotension, however, and are not specific to CN VI palsy.26
A systematic review of 95 case reports of extraocular muscle paralysis associated with dural puncture by Nishio et al.22 revealed that CN VI palsy typically presents 4 to 10 days after dural puncture although it may present as early as 1 day or as late as 3 weeks after the procedure. Diplopia may persist for weeks to months.22 The authors reported that 89% of patients had recovered within 8 months, and damage was permanent in 2 patients whose symptoms lasted longer than 8 months. The 2 patients underwent surgical correction at 12 months3 and at 18 months19 after onset of double vision, respectively. Because of the prolonged time course to recovery, Nishio et al. recommended conservative treatment for 8 months for an isolated CN VI palsy without other neurological symptoms and consideration of corrective surgery after that time. However, recovery has occurred as late as 21 months after dural puncture.12
The leading hypothesis for mechanism of injury is that the loss of CSF and resulting intracranial hypotension cause caudal displacement of the brain and brainstem which puts traction on CNs.26 The anatomic course of CN VI (a 90-degree bend over the petrous bone) makes it uniquely susceptible to traction stress during intracranial hypotension.12,27 The tortuous path of the nerve along with traction stress from caudal displacement of the pons and compression by the dura may explain preferential damage to the abducens nerve; palsies to CN VI make up 92% to 95% of cases of CN injury associated with intracranial hypotension.6,22,28
Stretch triggers neural vulnerability to ischemia and dysfunction. Even when the magnetic resonance images appear normal after intracranial hypotension has resolved, the ischemic injury to the nerve may result in lasting sequelae.22 Neural ischemia may result in focal segmental demyelination (neuropraxia) and/or axonal interruption. Electrical activity is often preserved immediately after the insult; nerve degeneration and impaired conductivity become apparent days later. The protracted time course for recovery reflects the degree of demyelination and the time needed for myelin regeneration; if axonal loss is present, the damage may be permanent.22
Because headache usually precedes diplopia, and both are related to intracranial hypotension, the 2 conditions may share common risk factors. Factors that increase the risk of postdural puncture (spinal) headache include younger age; several studies have documented a higher incidence of postdural puncture headache in patients between 20 and 30 years of age compared with those older than 50 years.2,29–32 A higher incidence of spinal headache in women is attributed to inclusion of obstetric patients having vaginal delivery.2,33 Vaginal delivery after unintentional dural puncture increases the risk of headache compared with cesarean delivery,34 and headache rate increases with prolonged pushing times.33 It is hypothesized that changes in intra-abdominal pressure during labor, which may affect CSF pressure, combined with dehydration during labor, rapid changes in blood volume after delivery, and inadequate postpartum fluid replacement explain this higher rate of spinal headache associated with vaginal delivery.2 However, even though females are at significantly higher risk for spinal headache than males,30–32 the systematic review by Nishio et al.22 revealed no significant sex predilection for CN VI palsy: males represented 55% of cases and females represented 45%.
PREVENTION AND TREATMENT
It is likely that measures that decrease the rate of postdural puncture headache may reduce the risk for developing CN VI palsy. Use of small-gauge and noncutting needles decreases the incidence of headache31,32 but does not eliminate the risk.10,32,35,36 In 1 report, a patient developed a postdural puncture headache and diplopia after administration of sequential combined spinal–epidural labor analgesia via a 25-gauge Sprotte spinal needle and a 16-gauge Tuohy epidural needle.10 The authors attributed the CN symptoms to the dural puncture with the 25-gauge needle; however, it seems equally likely that the patient may have suffered an unrecognized dural puncture with the large-bore epidural needle. An additional report from the French literature describes a case of headache and abducens palsy after spinal anesthesia administered via a 25-gauge pencil-point spinal needle.14
Although a therapeutic epidural blood patch provides partial or complete relief of headache in 61% to 95% of cases,37,38 it does not reliably reverse the CN VI palsy because neural demyelination has already occurred.5,6,9,12,14,16 Early epidural blood patch within 24 hours of ocular symptoms has been beneficial in restoring CSF pressure with partial resolution of diplopia.13 Yet, other case reports describe failure of CN VI palsy to respond to an epidural blood patch even when the patch is performed early.5,9 Because a CN VI palsy rarely develops before day 4 after a dural puncture (although it can occur as early as day 1 after dural puncture),22 or after resolution of a headache, some have suggested that conservative treatment for postdural puncture headache should be abandoned after 4 days in favor of an epidural blood patch to prevent the development of CN VI palsy.9 However, it is difficult to make generalizations from the small number of published case reports. To decrease the likelihood of spinal headache and CN VI palsy after dural puncture, we suggest the use of small-gauge, noncutting pencil-point spinal needles and a time limit for intracranial hypotension and traction stress on CN VI in the presence of a headache, especially when symptoms are severe. Early conversion from conservative therapy to an epidural blood patch when ocular changes manifest may decrease the morbidity of CN VI palsies.
Although the documented incidence of CN VI palsy after dural puncture is low, the condition may be underreported. It is important for anesthesiologists to use techniques that minimize the risk of developing a spinal headache after dural puncture, to inquire about diplopia, to recognize deviated gaze after dural puncture as a potential consequence of intracranial hypotension, and to educate patients about mild and severe ocular symptoms that may develop in the presence of a spinal headache. Early intervention with an epidural blood patch, especially when ocular symptoms are present, may decrease the morbidity of dural puncture complications.
Name: Jennifer E. Hofer, MD.
Contribution: This author helped write the manuscript and review the literature.
Attestation: Jennifer E. Hofer approved the final manuscript.
Name: Barbara M. Scavone, MD.
Contribution: This author helped write the manuscript and review the literature.
Attestation: Barbara M. Scavone approved the final manuscript.
This manuscript was handled by: Cynthia A. Wong, MD.
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