Anesth Analg 2006;102:1865-1866
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000217117.77826.dd
REGIONAL ANESTHESIA
Divergence Paresis Without Positional Headache: An Unusual Presentation of Cerebrospinal Fluid Hypovolemia After Spinal Anesthesia
Motomi Arai, MD, PhD,
Satoko Matsushima, MD, and
Hiroshi Terada, MD
Departments of Neurology and Ophthalmology, Seirei Mikatahara General Hospital; Choseido Terada Clinic, Hamamatsu, Japan.
Address correspondence and reprint requests to Motomi Arai, MD, Department of Neurology, Seirei Mikatahara General Hospital, Mikatahara-cho 3453, Hamamatsu, Shizuoka 433-8558, Japan. Address e-mail to arai-m{at}sis.seirei.or.jp.
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Abstract
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We report a rare complication of spinal anesthesia—divergence paresis—which is characterized by an acquired horizontal diplopia at distance without evidence for abducens palsy. A 64-yr-old man underwent prostatectomy under spinal anesthesia with 2.5 mL of dibucaine hydrochloride 0.3% injected through a 20-gauge cutting-tip spinal needle. Seventeen days after the operation, the patient noticed horizontal diplopia for distant objects. Although cranial magnetic resonance imaging demonstrated diffuse pachymeningeal gadolinium enhancement and subdural effusion, characteristic findings of cerebrospinal fluid hypovolemia, the patient had no positional headache. Gadolinium-enhanced magnetic resonance imaging may be useful when a patient develops neurologic symptoms after dural puncture.
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Introduction
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Dural puncture sometimes causes persistent loss of cerebrospinal fluid (CSF) through a dural tear, resulting in CSF hypovolemia. The classic syndrome of CSF hypovolemia consists of positional headache, low CSF pressure, and diffuse pachymeningeal gadolinium enhancement (DPGE) on cranial magnetic resonance imaging (MRI) (1). However, CSF hypovolemia does not always cause positional headache (2) and may be associated with tinnitus (3) or arm pain (4) occurring in the upright position.
We report a rare complication of spinal anesthesia—divergence paresis—which is characterized by an acquired esotropia at distance and full abduction bilaterally (5,6). Although cranial MRI demonstrated DPGE and subdural effusion, characteristic findings of CSF hypovolemia (7–9), the patient had no positional headache.
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Case Report
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A 64-yr-old previously healthy man underwent prostatectomy for benign prostatic hypertrophy under spinal anesthesia (Day 1). A 20-gauge cutting-tip spinal needle was positioned with a single attempt at the L3-4 interspace via a midline approach, and 2.5 mL of dibucaine hydrochloride 0.3% was injected intrathecally. Postoperatively, the patient received IV infusion of antibiotics for epididymitis and was kept in an upright position only for a short time because of fever and fatigue. He was discharged on Day 17. On Day 26, the patient was referred to our clinic with a 10-day history of horizontal diplopia for distant objects. He was not aware of diplopia on waking in the morning. He denied any head trauma, positional headache, tinnitus, or vertigo.
On examination, his pupils were equal, measuring 3 mm in diameter, and reacted promptly to light. The patient noticed horizontal diplopia for objects beyond 2 m. Separation of the two images did not markedly change as the object was moved at a constant distance from the patient. However, diplopia completely disappeared when the object was within 1 m. Ductions and versions were normal in all directions. Nystagmus was absent. Both distant and near visual acuity were normal in each eye. The Hess-Lancaster red-green test, a test for ocular alignment, showed an esotropia, but no muscle overaction or underaction. The patient had 8 prism diopters of esotropia at distance. The remainder of the neurologic examination was unremarkable. A diagnosis of divergence paresis was made. Cranial MRI demonstrated a narrow prepontine cistern, bilateral subdural effusion, and DPGE (Fig. 1). There was no enhancement of cortical sulci and leptomeninges surrounding the brainstem. The subdural effusion was thin and had no mass effect on the brain. Without specific treatment, divergence paresis had resolved by Day 46.
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Figure 1. Gadolinium-enhanced coronal magnetic resonance image of the brain showing bilateral subdural effusion (arrows) and diffuse pachymeningeal gadolinium enhancement (arrow heads).
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Discussion
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DPGE and subdural effusion are characteristic MRI features of CSF hypovolemia (7–9). DPGE is considered to represent a compensatory vasodilatation of the dura (7,8). The lack of leptomeningeal enhancement in our patient excludes meningeal carcinomatosis and meningitis (7,9). Although hypertrophic pachymeningitis or granulomatous diseases are difficult to differentiate from CSF hypovolemia based only on MRI findings (9), spontaneous recovery argues for CSF hypovolemia in the current case.
Conditions causing diplopia at distance include convergence spasm, bilateral abducens palsies, and divergence paresis (5,6). Convergence spasm was excluded because near-distance esotropia, miotic pupils, and myopia were absent. Abducens palsy in patients with CSF hypovolemia, with or without a history of dural puncture (8,10–12), is considered to be caused by traction of the nerves by a sagging brain (1). Because abduction was normal and esotropia remained unchanged in the lateral gaze in our patient, it was unlikely that he had bilateral abducens palsies. Divergence paresis is characterized by the abrupt onset of an acquired esotropia with diplopia at distance and fusion at a near fixation point of 1 m or less, although abduction is normal. The esotropia remains unchanged in the lateral gaze (5,6). Thus, the eye movement disorder of our patient was consistent with divergence paresis.
Divergence paresis has been reported with a number of neurologic diseases causing intracranial hypertension, mass lesion in the midbrain (5,6,13), and ingestion of diazepam (14). After the operation, however, our patient did not take diazepam. Divergence paresis associated with CSF hypovolemia has not been described before. He developed diplopia 17 days after lumbar puncture when he could maintain an upright position in the daytime. Symptom of postdural puncture headache may have been present earlier but was resolved. It is impossible to know because he did not maintain a sitting position long enough before day 17. Thus, downward deviation of the brain at that time might have caused distortion of the brainstem, resulting in dysfunction of the divergence neurons in the brainstem reticular formation (15,16).
Postdural puncture CSF hypovolemia results in a variety of complications, which are usually heralded by, or associated with, positional headache. Our case suggests that some patients develop neurologic complications without complaining of positional headache. Therefore, gadolinium-enhanced MRI may be useful when a patient develops neurologic symptoms after dural puncture.
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Footnotes
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Accepted for publication February 8, 2006.
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Abstract
Introduction
