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Show Journal of Clinical Neuro- ophthalmology 9( 1): 47- 49, 1989. Mesencephalic Hemorrhage and Unilateral Pupillary Deficit Ashfaq Shuaib, M. D., Gaspar Israelian, M. D., F. R. C. P., and Mary Anne Lee M. D., F. R. C. P. © 1989 Raven Press, Ltd., New York An isolated dilated and fixed pupil in the absence of other neurological dysfunction usually suggests ciliary ganglion dysfunction or direct pharmacological blockade of the parasympathetic fibers to the pupil. A unilateral dilated pupil as a manifestation of a mesencephalic hemorrhage has not, to our knowledge, previously been reported. We now describe a 35- year- old woman who had a headache and a dilated and nonreactive right pupil. A cranial computed tomography scan showed a small hemorrhage in the midbrain, and a cerebral angiogram was normal. Mesencephalic hemorrhage should be considered in the differential diagnosis of an isolated dilated pupil. Key Words: Hemorrhage- Midbrain- Dilated pupilNeuro- ophthalmology. From the Foothills Hospital, Calgary, Alberta, Canada. Address correspondence and reprint requests to Dr. A. Shuaib, Duke VA Center for Cerebrovascular Research, Building 16, Room # 29, Veterans Administration Hospital, 508 Fulton St., Durham, NC 27705, U. S. A. Dr. Shuaib is a clinical felIow of the Medical Research Council of Canada and the Alberta Heritage Foundation for Medical Research. 47 A dilated and nonreactive pupil in the absence of other neurological symptoms is likely to be related to ciliary ganglion involvement or direct pharmacological blockade. These can easily be diagnosed by pharmacological testing ( 1). Ciliary ganglion damage results in very characteristic signs that include poor pupillary reaction to light, accommodative paresis, and cholinergic hypersensitivity of the denervated muscles ( 2). Accidental or surreptitious instillation of drugs that cause pupillary dilatation is seen most commonly in persons in a medical setting. One percent pilocarpine should constrict any pupil that is dilated due to damage to the third nerve but will not overcome a pharmacological blockade. An isolated and fixed pupil as the sole manifestation of an extra- axial third- nerve palsy is uncommon. Sunderland and Hughes have proposed that lesions compressing the extra- axial oculomotor nerve from above and medially can result in isolated pupillary dilatation ( 3). Aneurysms or neoplasms produce a fixed and dilated pupil by such a mechanism. This is, however, virtually always associated with other signs of oculomotor nerve dysfunction ( 1). Extraocular weakness in the absence of pupillary involvement is suggestive of a vascular cause, especially if the weakness is complete and the pupillary responses are normal ( 4). This rule, however, does not always hold true. In a recent report, Lustbader and Miller ( 5) described a patient with a basilar artery aneurysm who had a painless third- nerve palsy and complete sparing of the pupil. Other conditions that may cause a dilated pupil by extra- axial third- nerve involvement include tuberculous and syphilitic basilar meningitis ( 6,7). Finally, pupil dilatation can also result from lesions that involve the dorsal midbrain. Such conditions include tumors, inflammation, and hemor- 48 A. SHUAIB ET AL. rhage ( 1,8- 13). Again, because of the close proximity of other structures, there are almost alw~ ys other associated neurological features, such as mvolvement of the motor or sensory tracts, cerebellar outflow tracts, or other cranial nerves. In this communication, we describe a patient with a mesencephalic hemorrhage who initially appeared with an isolated fixed and dilated pupIl and a headache. To our knowledge, such a mamfestation has never been previously reported with mesencephalic hemorrhage. CASE REPORT A 35- year- old woman was referred to our neurology service for evaluation of the recent onset of a headache and associated pupillary disturbance. The headache had developed suddenly, lasted for 24 h and then gradually resolved. Two days later, however, the headache recurred and was now associated with blurred vision. The patient had no diplopia or other neurological symptoms. There was no history of any neurological or ophthalmological problems. She was taking no medications and denied using recreational drugs. On examination, the patient was in no distress, alert, cooperative, and attentive. The general physical examination results were normal. Neurological examination revealed no abnormalities. Specifically, the motor and sensory examination results were normal, and tendon reflexes were 2+ in the upper and lower extremities. Visual acuity and fundoscopic examination results were normal. The right pupil was 8 mm, and the left pupil was 3 mm. The right pupil showed no response to direct or consensual light. Under the slit lamp, no pupillary movements were observed. The pupillary sphincter was intact, and there was no evidence of trauma. Extraocular movements were full in all directions, and attempted accommodation showed no decrease in the right pupillary size. Pharmacological tests for pupillary hypersensitivity were not done. A serologic study for syphilis was also not done. Because of the history of headache, a computed tomography ( CT) scan of the head was done that showed a small right- sided hemorrhage in the midbrain close to the cerebral peduncle ( Fig. 1). A cerebral angiogram was normal. A review of her photographs established that the pupils had been equal prior to the midbrain hemorrhage. A few days after admission, she noticed double vision on looking toward the right. Clinical examination failed to show any extraocular movement deficits. A Hess screen showed some minimal dysfunction of the right inferior and medial rectus \ " I Y, N". 1, 1989 FIG. 1. Unenhanced computed tomographic scan showing right- sided mesencephalic hemorrhage ( arrowheads), muscles. A CT scan repeated seven days after admission showed the hemorrhage to be resolving. The pupil had returned to normal within 1 month of the hemorrhage. In 30 months of follow- up observation, she has remained well and has had no new problems. The cause of the hemorrhage in our case could not be determined. This is in keeping with the majority of recent descriptions of cases similar to ours in which angiography failed to reveal an arterialvenous malformation ( AVM) or an aneurysm. Cryptic AVMs have only rarely been found in such small hematomas ( 11). DISCUSSION Spontaneous nontraumatic mesencephalic hemorrhage was until recently considered extremely uncommon, with only three reports published to our knowledge prior to the report of Durward et al ( 13). In recent years, however, a number of reports on the subject would suggest this is not too uncommon ( 8- 13). In most publications to date, neuro- ophthalmological involvement has been prominent. In Weisberg's description of six patients ( 8), all had impaired upward gaze, and two had downward HEMORRHAGE AND PUPILLARY DEFICIT 49 ocular deviation. The pupils were unequal and poorly reactive to light in all cases. All three patients described by Sand et al. ( 9) had eye movement involvement. The first patient had Parinaud's syndrome; the second patient had a vertical gaze palsy, skew deviation, and bilateral Horner's syndrome; and the third had bilateral fourth- nerve palsies and a unilateral Horner's syndrome. In the report of Shuaib and Murphy, both patients showed prominent third- nerve dysfunction and minimal associated symptoms ( 10). Finally, the patient described by Stern and Bernick had bilateral ptosis and left inferior rectus weakness ( 11). Our patient with isolated pupil dilation on initial appearance further extends the interesting spectrum of neuro- ophthalmological findings seen with small mesencephalic hemorrhages. The diverse neuro- ophthalmological abnormalities can be explained by the location of the hematomas. Partial or complete third- nerve palsy results from involvement of the third- nerve nucleus or fascicle. Nuclear involvement results in bilateral superior rectus and levator palpebrae superioris dysfunction because the innervation to these muscles is mainly crossed. Such lesions can be separated from fascicular damage where motor deficits are restricted to one eye only. Lesions at the inferior collicular level tend to have trochlear nerve involvement and result in inferior oblique dysfunction ( 1). Hematomas in the superior collicular and posterior commissure region result in Parinaud's syndrome. In our case, initially only the pupillary parasympathetic fibers were affected, and the CT scan showed a lesion in the area of the oculomotor fascicular region. Later, diplopia secondary to inferior and medial rectus dysfunction suggested involvement of further fascicular fibers, possibly secondary to edema. REFERENCES 1. Miller NR. Walsh and Hoyt's clinical neuro- ophthalmology. Vol. 2. Baltimore: Williams & Wilkins Co, 1985: 652- 784. 2. Thompson HS. Adie's syndrome: some new observations. Trans Am Ophthalmol Soc 1977; 75: 587~ 25. 3. Sunderland S, Hughes ESR. The pupillo- constrictor pathway and the nerves to the ocular muscles in man. Brain 1946; 69: 301- 9. 4. Trobe JD. Third nerve palsy and the pupil. Arch Ophthalmol 1988; 106: 601- 2. 5. Lustbader JM, Miller NR. Painless, pupil- sparing but otherwise complete oculomotor nerve palsy caused by a basilar artery aneurysm. Arch OphthalmoI1988; 106: 583- 4. 6. Sandyk R. Pupillary signs in tuberculous meningitis. 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