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Show Journal of Neuro- Ophthalmology 20( 3): 154- 155, 2000. © 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Isolated Inferior Rectus Palsy as a Result of Paramedian Thalamopeduncular Infarction Irsel Tezer, MD, Cigdem F. Dogulu, MD, and Tulay Kansu, MD The authors present the cases of two patients with isolated inferior rectus muscle paresis presumed to be caused by paramedian thalamopeduncular infarction that involved supranuclear descending pathways, just before the inferior rectus subnucleus in one patient, and just before subnucleus or fascicular fibers in the other patient. Both patients had no other associated neurologic dysfunction. The lesions that cause isolated inferior rectus palsy in these patients are documented by magnetic resonance findings. Although vascular ischemic lesions as the cause of isolated inferior rectus palsy were reported previously, to the authors' knowledge, it has not been demonstrated radiologically, Key Words: Isolated inferior rectus palsy- Paramedian thalamopeduncular infarction. A number of reports describe various forms of partial oculomotor paresis, but isolated inferior rectus paresis is a relatively uncommon entity. Reported causes include trauma, diabetes mellitus, thyroid disease, vascular disease, multiple sclerosis, myasthenia gravis, migraine, and carcinoma metastasis, and congenital and idiopathic causes ( 1,2). Although it was previously stated that strategically placed small ischemic lesions may cause paralysis of isolated muscles of oculomotor complex that may result from supranuclear damage, including selective " prenuclear," partial nuclear, or fascicular damage, this has not been documented with neuro- imaging findings in isolated inferior rectus palsy ( 3- 5). CASE REPORTS Case 1 A 51- year- old previously healthy man presented with sudden onset of vertical diplopia. He denied any fluctuation of his symptom and had no other neurologic or ophthalmologic symptoms. There was no history of head trauma, thyroid disease, migraine, multiple sclerosis, hy- Manuscript received March 6, 2000; accepted May 8, 2000. From the Institute of Neurological Sciences and Psychiatry, Department of Neurology, Neuro- Ophthalmology Unit, Hacettepe University, Ankara, Turkey. Address correspondence and reprint requests to Irsel Tezer, MD, Hacettepe University Hospitals, Department of Neurology, Ankara 06100, Turkey. pertension, or diabetes mellitus, but he was a heavy smoker. Findings from a neuro- ophthalmologic examination were normal, except for a moderate reduction of depression OS, particularly in abduction. His left inferior rectus palsy was documented by results of Maddox Rod and Hess screen tests. Results of 5- hour glucose tolerance test, whole blood count, sedimentation rate, and thyroid function tests were normal, and blood lipid levels, including cholesterol, triglycerid, and low- density lipoprotein cholesterol were high. Results of intravenous infusion of edrophonium ( 10 mg) and forced duction tests were negative. Magnetic resonance imaging showed increased signal intensity on the left paramedian thalamopeduncular region on T2- weighted images, without contrast enhancement, that was compatible with an infarction ( Fig 1A). Results of carotid- vertebral doppler ultrasonography and echocardiography were normal. The patient was administered 300 mg/ day acetylsalicylic acid, which is an antihyper-lipidemic agent, and it was recommended that he quit smoking. The patient's symptoms resolved in 3 weeks. The stroke mechanism was presumed to be a result of atheromatous disease of the left thalamo- subthalamic artery. Case 2 A 48- year- old woman with hypertension presented with sudden onset of vertical diplopia with no other neurologic symptoms. The diplopia was present during the previous 5 days. Findings from the neuro- ophthalmologic examination were compatible with right isolated inferior rectus palsy that was also documented by results of Maddox Rod and Hess screen tests. Blood pressure was 180/ 100 mm Hg, and findings from the rest of the examination were normal. There was no history of head trauma. Results of intravenous edrophonium HC1 and forced duction tests were negative, and results of thyroid function tests were normal. Cranial magnetic resonance imaging demonstrated infarction in the right paramedian thalamopeduncular region ( Fig. IB). A stroke because of atheromatous disease of the right paramedian mesencephalic artery was thought to be responsible from her inferior rectus palsy. Results of laboratory tests for cerebrovascular disease risk factors were all normal, except for high serum lipid levels. The patient was administered acetylsalicylic acid 300 mg daily, in addition to adminis- 154 ISOLATED INFERIOR RECTUS PALSY 155 FIG. 1. T2- weighted magnetic resonance scans in the coronal plane show increased signal intensity in the left paramedian thala-mopeduncular region that was presumed to involve supranuclear descending pathways just before the inferior rectus subnucleus in case 1 ( A) and a right paramedian thalam-opeduncular infarction at the level of inferior rectus subnucleus or fascicular fibers in case 2 ( B). tration of antihypertensive treatment. Her symptom disappeared in 3 weeks. DISCUSSION The paramedian thalamopeduncular region is supplied by the superior mesencephalic and posterior thalamo-subthalamic arteries ( 6). Paramedian mesencephalic arteries originate from the proximal portion of the basilar communicating artery to supply the cerebral peduncle, ied nucleus, and medial portions of the substantia nigra and the fascicles of the third cranial nerve. The thalamic-subthalamic arteries originate from the basilar communicating artery segment of the posterior cerebral artery. Medial thalamic infarcts in the territories of the thalamic-subthalamic arteries usually involve the subthalamus, the rostral interstitial nucleus of the medial longitudinal fasciculus ( riMLF), the nucleus parafascicularis, and the medial part of the centromedian nucleus ( 7,8). A distinctive feature of paramedian thalamopeduncular infarction is third- nerve dysfunction that may be because of nuclear, infranuclear, or supranuclear damage. These structures are compactly located in a volume of a few cubic centimeters ( 6). In the first case, the unilateral paramedian infarct seen with magnetic resonance imaging was compatible with the ipsilateral riMLF region that was just rostral to the third nerve nucleus on the left. The patient's left isolated inferior rectus palsy may be explained by damage to the descending pathways for downgaze from the riMLF that selectively affected prenuclear fibers innervating the ipsilateral inferior rectus. Magnetic resonance imaging in the second case showed a more inferiorly placed unilateral paramedian infarct that affected the right midbrain. At this level, the patient's right isolated inferior rectus palsy was probably caused by damage to the subnucleus or fascicles of the ipsilateral inferior rectus. Paramedian thalamopeduncular infarcts generally result in widespread disturbances in neurologic function, such as altered consciousness and pyramidal and cerebellar dysfunction, in addition to impaired ocular motility ( 6). We report the cases of two patients with strategically located unilateral paramedian infarction that led to isolated inferior rectus palsy by highly selective prenuclear damage in one patient and nuclear or fascicular injury in the other patient, which was demonstrated with magnetic resonance imaging scans. REFERENCES 1. Putaseri TJ, Sedwick LA, Margo CE. Isolated inferior rectus muscle palsy from a solitary metastasis to the oculomotor nucleus. Arch Ophthalmol 1987; 105: 675- 7. 2. Chou TM, Demer JL. Isolated inferior rectus palsy caused by a metastasis to the oculomotor nucleus. Am J Ophthalmol 1998; 737- 40. 3. Castro O, Johnson LN, Mamourian AC. Isolated inferior oblique paresis from brain- stem infarction. Arch Neurol 1990; 47: 235- 7. 4. Roper- Hall G, Burde RM. Inferior rectus palsies as a manifestation of atypical Illrd cranial nerve disease. Am Orthopt J 1975; 25: 122- 30. 5. Ksiazek SM, Slamovits TL, Rosen CE, et al. Fascicular arrangement in partial oculomotor paresis. 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