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(Stroke. 1995;26:900-902.)
© 1995 American Heart Association, Inc.

Articles

Posterior Cerebral Artery Stenosis With Midbrain Infarction

Gary W. Duncan, MD Steven M. Weindling, MD

From the Division of Neurology, Meharry Medical College (G.W.D.), and the Rehabilitation Center (G.W.D.) and the Department of Medical Imaging, Columbia/HCA Centennial Medical Center, Nashville, Tenn.

Correspondence to Dr Duncan, Division of Neurology, Meharry Medical College, 1005 D.B. Todd Blvd, Nashville, TN 37208.

	Abstract

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Background Brain infarction secondary to stenosis of the posterior cerebral artery is uncommon. We report a patient with midbrain infarction and symptoms of both Benedikt's and pupil-sparing oculomotor palsy syndromes secondary to posterior cerebral artery stenosis.

Case Description A 51-year-old woman developed diplopia, left ptosis, and right hemiataxia and hyperactive tendon reflexes. Pupils were equal and reactive. Radiological examination revealed stenosis of the posterior cerebral artery and a left-sided midbrain infarct.

Conclusions Stenosis of the posterior cerebral artery may cause only midbrain infarction and may be responsible for Benedikt's and pupil-sparing oculomotor palsy syndromes.

Key Words: ataxia • brain stem infarction • oculomotor nerve • posterior cerebral artery • stenosis

	Introduction

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Symptoms from posterior cerebral artery (PCA) stenosis are uncommon and are usually secondary to ischemia of the distal territory of the vessel and include visual and sensory disturbances.¹ This report describes a patient with brain stem symptoms (Benedikt's syndrome and pupil-sparing oculomotor palsy syndrome) secondary to proximal PCA stenosis. We believe this report is of interest because it adds to previously described PCA stenosis symptomatology, and it provides a thorough neuroradiological evaluation of Benedikt's and pupil-sparing oculomotor palsy syndromes.

	Case Report

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A 51-year-old white woman with a history of hypertension and non–insulin-dependent diabetes mellitus presented to the emergency department with diplopia. Earlier that day, she had developed horizontal diplopia, numbness in the right side of the face, and a sensation of weakness in the right arm. Within 2 to 4 hours she had developed complete ptosis of the left eye.

On the day of onset, she was alert and oriented. Optic discs and visual fields were normal. Complete ptosis was present on the left. The right eye moved fully. The left eye deviated down and out and could not gaze up or to the right. The left pupil was 1 mm larger than the right pupil, and left pupillary light reaction was sluggish. Touch sensation was decreased on the right side of the face, but facial pain sensation was intact bilaterally. Facial movement, hearing, speech, and extremity strength were normal. Intention tremor was present in the right arm and leg, and gait was ataxic. Tendon reflexes were slightly hyperactive on the right, and the right plantar response was extensor. Vibratory, touch, and pain sensations were normal in both arms and legs.

One week later when examined by one of the authors (G.W.D.), the patient had pupil-sparing left oculomotor nerve palsy, right hemiataxia, slightly hyperactive tendon reflexes on the right, and flexor plantar responses.

Magnetic resonance imaging (MRI) of the brain was performed with a 1.5-T system (Signa; GE Medical Systems) on the 10th hospital day. Axial T₂-weighted (repetition time, 3600 milliseconds; echo time, 102 milliseconds) spin-echo images revealed a well-defined, hyperintense, left-sided midbrain lesion abruptly terminating at the midline most compatible with infarction (Fig 1A). The midbrain was spared on the 1.5-mm supra-adjacent axial MRI image at the uppermost superior colliculus level (Fig 1B). Brain stem structures involved on MRI included the left third cranial nerve nucleus and fascicles, medial longitudinal fasciculus, red nucleus, substantia nigra, and cerebral peduncle. MRI revealed no additional brain stem, cerebellar, or cerebral lesion. Towne projection of a left vertebral cerebral arteriogram demonstrated a high-grade distal left PCA peduncular segment stenosis (Fig 2) at the level of origin for small, penetrating brain stem branches.

View larger version (104K): [in this window] [in a new window]   Figure 1. A, Axial T2-weighted (repetition time, 3600 milliseconds; echo time, 102 milliseconds) 5-mm-thick image at the inferior colliculus level demonstrates left-sided, increased signal-intensity midbrain lesion (arrows) involving the cerebral peduncle, substantia nigra, red nucleus, medial longitudinal fasciculus, and region of the third cranial nerve nucleus and fascicles. B, Axial T2-weighted 5-mm-thick image just 1.5 mm superior to image 1A reveals midbrain sparing at the Edinger-Westphal nucleus level (arrow) corresponding to this patient's pupillary sparing.

View larger version (110K): [in this window] [in a new window]   Figure 2. Left vertebral cerebral arteriogram (Towne projection). Focal high-grade stenosis of the distal left posterior cerebral artery peduncular segment (arrow) is compared with the normal diameter of the proximal posterior cerebral artery (arrowhead).

	Discussion

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Ischemic infarction in the territory of the PCA is usually secondary to total occlusion of the vessel.² The clinical features vary and may include pure hemianopsia,² resemble middle cerebral artery occlusion,^{3 4} or be restricted to thalamic disturbances.⁵ Symptoms of PCA stenosis are uncommon. Pessin et al¹ reported the first series of patients with angiographically proven PCA stenosis. The major clinical features were transient ischemic attacks with contralateral visual symptoms and, in some patients, contralateral sensory symptoms. Only two of the six patients had permanent neurological deficits, and in both patients they were contralateral visual field disturbances.

Our patient is unique because only brain stem symptoms were present. Symptoms of medial temporal and occipital lobe ischemia were absent. Ipsilateral oculomotor nerve palsy and contralateral ataxia and corticospinal tract findings are consistent with Benedikt's syndrome.⁶ Previous reports of Benedikt's syndrome⁶ did not establish an arterial pathology. Our patient with signs of Benedikt's syndrome had clear midbrain infarction with involvement of red nucleus, cerebral peduncle, oculomotor fascicles, and lower oculomotor nucleus shown by MRI. Multiple small, peduncular arterial branches arise from the proximal PCA and immediately penetrate the ipsilateral cerebral peduncle to supply the corticospinal and corticobulbar tracts, substantia nigra, red nucleus, third and fourth cranial nerve nuclei, and other ipsilateral midbrain structures.⁷ Our patient's high-grade PCA peduncular segment stenosis visualized by vertebral arteriogram likely resulted in origin occlusion of several of these small, penetrating branches and subsequent midbrain infarction. MRI demonstrated midbrain sparing at the level of the upper superior colliculus and Edinger-Westphal nucleus, thus preserving pupillary parasympathetic innervation. While highly stenotic, the PCA remained patent with sparing of more distal brain territories.

Later in this patient's course, the pupillary function became normal, even though a complete external oculomotor nerve palsy persisted. Previous reports of pupil-sparing oculomotor nerve palsy^{8 9} have established that intra-axial midbrain infarction similar to that in this patient may have been responsible. This report establishes PCA stenosis as one type of arterial pathology responsible for the syndrome.

The clinical features of this patient provide additional symptoms to the syndrome of PCA stenosis, and their recognition may hasten the diagnosis of PCA stenosis and appropriate treatment.

Received January 9, 1995; revision received February 22, 1995; accepted February 22, 1995.

	References

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1. Pessin MS, Kwan ES, DeWitt LD, Hedges TR, Gale G, Caplan LR. Posterior cerebral artery stenosis. Ann Neurol. 1987;21:85-89. [Medline] [Order article via Infotrieve]
2. Pessin MS, Lathi ES, Cohen MB, Kwan ES, Hodges TR, Caplan LR. Clinical features and mechanisms of occipital infarction. Ann Neurol. 1987;21:290-299. [Medline] [Order article via Infotrieve]
3. Hommel M, Moreaud O, Besson G, Perret J. Site of arterial occlusion in the hemiplegic posterior cerebral artery syndrome. Neurology. 1991;41:604-605.
4. Chambers BR, Brooder RJ, Donnan GA. Proximal posterior cerebral artery occlusion simulating middle cerebral artery occlusion. Neurology. 1991;41:385-390. [Abstract/Free Full Text]
5. Caplan LR, DeWitt LD, Pessin MS, Gorelick PB, Adelman LS. Lateral thalamic infarcts. Arch Neurol. 1988;45:959-964. [Abstract]
6. Liu GT, Crenner AM, Logigian EL, Charness ME, Samuels MA. Midbrain syndromes of Benedikt, Claude, and Nothnagel: setting the record straight. Neurology. 1992;42:1820-1822. [Free Full Text]
7. Margolis MT, Newton TH, Hoyt WF. The posterior cerebral artery: gross and roentgenographic anatomy. In: Newton TH, Potts DG, eds. Radiology of the Skull and Brain, vol 2. St Louis, Mo: CV Mosby; 1974:1551-1578.
8. Nadeau SE, Trobe JD. Pupil sparing oculomotor palsy: a brief review. Ann Neurol. 1983;13:143-148. [Medline] [Order article via Infotrieve]
9. Breen LA, Hopf HC, Farris BK, Gutmann L. Pupil-sparing oculomotor nerve palsy due to midbrain infarction. Arch Neurol. 1991;48:105-106. [Abstract]

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