Bilaterally Persistent Horizontal Gaze Palsy and Facial Palsy. Caused by Pontine Infarction. Ufuk Utku, MD, Yahya C¸ elik, MD, and Kemal Balci, MD. Tegmental ...
Case Report
Bilaterally Persistent Horizontal Gaze Palsy and Facial Palsy Caused by Pontine Infarction Ufuk Utku,
MD,
Yahya C ¸ elik,
MD,
and Kemal Balci,
MD
Tegmental pontine infarctions make up only a small portion of all isolated pontine infarcts. These lesions cause isolated cranial nerve palsies, neuro-ophthalmologic signs, and sensory deficits. Clinical and anatomic correlation of these lesions has been made simple with the use of cranial magnetic resonance imaging (MRI). In this article, we report on a 43-year-old hypertensive woman with bilateral horizontal gaze palsy and peripheral facial paralysis but no limb weakness. Pontine paramedian tegmental infarct was visible on cranial MRI. Key Words: Tegmental pons—Stroke—Horizontal gaze palsy—Cranial MRI. Copyright © 2001 by National Stroke Association
A 43-year-old woman was admitted to the Trakya University Hospital because of sudden dizziness and headache. She had suffered from hypertension for the previous 3 months. On neurologic examination, the patient was alert, cooperative, and oriented to her surroundings. She had bilateral horizontal lateral gaze palsy in all types of eye movement and vestibulo-ocular reflex was absent, but vertical eye movements were intact. Her pupils were equal, reactive to light, and near. The patient also had bilateral peripheral seventh nerve palsy, the motion of her soft palate was decreased bilaterally, and she had difficulty in swallowing. There was no limb weakness or ataxia, and muscle strength reflexes were bilaterally increased; plantar reflexes were flexor. No abnormalities were visible on a cranial computed tomography (CT) scan taken after hospitalization. We initially thought that the disorder was multiple cranial neuropathy, but we abandoned this diagnosis because the pa-
From the Department of Neurology, Trakya University Medical Faculty, Edirne, Turkey. Received March 12, 2001; accepted October 10, 2001. Address reprint requests to Yahya C ¸ elik, MD, Department of Neurology, Trakya University Medical Faculty, 22030 Edirne, Turkey. Copyright © 2001 by National Stroke Association 1052-3057/01/1005-0008$35.00/0 doi:10.1053/jscd.2001.30405
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tient’s gaze palsy findings were specific for pontine lesion, and her electromyographic and cerebrospinal fluid test results were normal. On the fifth day of hospitalization, flair and T2weighted cranial MRI showed an ischemic lesion that expanded ventrally in the paramedian tegmental region at the midpontine level (Fig 1). There was no contrast medium enhancement. No abnormalities were visible in Doppler images of the bilateral carotid and vertebral arteries. However, cranial MR angiography showed left vertebral artery hypoplasia, and the basilar artery was patent. Results of the electrocardiogram and transesophageal echocardiogram were normal. The patient exhibited no risk factors for a hypercoagulable state such as a history of oral contraceptive use or protein C, protein S, or antithrombin (AT) III deficiency; no other risk factors for stroke were found. We began antiaggregant (aspirin 300 mg/day) and antihypertensive therapy. After 1 month of treatment, no change in the patient’s condition was noted on neurologic examination.
Discussion Tegmental pontine infarctions make up only a small portion of all isolated pontine infarcts1,2 and can cause isolated cranial nerve palsies, neuro-ophthalmologic signs, and sensory deficits.3-6 Clinical and anatomic cor-
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concluded that basilar artery branch occlusion was the cause of our patient’s stroke mechanism because MR angiography showed that the basilar artery was patent, and there was no cardioembolic source. The relationship between vertebrobasilar hypoplasia and brain stem infarcts has been documented in the literature, and it is possible that vertebral artery hypoplasia predisposes to posterior circulation ischemia, but the role of this condition in stroke is still not understood.12 A similar case of bilateral peripheral facial palsy and horizontal gaze palsy that mimics peripheral lesions has not been reported in the literature.
References
Figure 1. T2-weighted cranial MRI showing an ischemic lesion in the paramedian tegmental region at the midpontine level.
relation of tegmental pontine infarctions has been made simple with the use of cranial magnetic resonance imaging (MRI).3,4,7,8 Our patient’s lesion was visible on cranial MRI and was restricted to the bilateral paramedian area of the midpontine tegmentum involving the paramedian pontine reticular formation. The site of infarction was presumably located in a portion of the seventh cranial nerve nucleus and/or fascicle and sixth cranial nerve nuclei because pure paramedian pontine reticular formation (PPRF) lesions do not result in the loss of the vestibulo-ocular reflex.9 We hypothesized that the lesion may have affected corticospinal tractus because muscle strength reflexes were increased bilaterally, but there was no limb weakness. The patient’s difficulty swallowing can be explained by the ventral expansion of the lesion and bilateral corticobulbar tract involvement. These infarcts are larger than lacunar infarcts, and they expand the pontine surface as a result of basilar artery branch occlusion.10,11 Lacunar infarcts are typically smaller than 1.5 cm in diameter, and they do not expand the pontine surface.1,2 Basilar artery branch disease may be caused by the occlusion of arterial branch ostia or an arterial branch itself by atherothrombotic plaque.11 In these cases, hypertension is a major risk factor, as seen in our patient.2 We
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