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Show PHOTO ESSAY Isolated Bilateral Internuclear Ophthalmoplegia After Ischemic Stroke Daniel Ciampi de Andrade, MD, Leandro T. Lucato, MD, PhD, Fdbio I. Yamamoto, MD, Paulo E. Marchiori, MD, PhD, Milberto Scaff, MD, PhD, and Adriana B. Conforto, MD, PhD FIG. 1. A. T2 MRI shows high signal in the midbrain tegmentum, in the region of the medial longitudinal fasciculus bilaterally { arrows). B. Diffusion imaging shows high signal in the same region { arrow). C. Apparent diffusion coefficient ( ADC) map shows low signal in the same region { arrow), confirming stroke as the likely cause of the bilateral INO. Abstract: A 63- year- old man suddenly developed an isolated bilateral internuclear ophthalmoplegia ( INO). High- resolution brain MRI showed signal abnormalities consistent with acute ischemic stroke limited to the infra- aqueductal region of the midbrain bilaterally. This case offers graphic evidence that stroke can be responsible for an isolated bilateral INO. (/ Neuro- Ophthalmol 2007; 27: 125- 126) A63- year- old white man suddenly noticed blurred vision after waking up. He reported vertical diplopia that improved after closing either eye. He did not complain of oscillopsia and had neither headache nor other symptoms. He had arterial hypertension, ischemic heart disease, and a record of heavy smoking. Neurologic examination revealed exodeviation of both eyes in primary gaze position. He had bilateral adduction weakness on side gaze associated with bilateral Department of Neurology ( DCdeA, FIY, PEM, MS, ABC), University of Sao Paulo, Sao Paulo, Brazil; and Department of Radiology ( LTL), Department of Neurology, University of Sao Paulo, Sao Paulo, Brazil. Address correspondence to Daniel Ciampi de Andrade, MD, Av Dr Eneas de Carvalho 155, 5° andar sala 5084, CEP 05403- 900, Sao Paulo- SP, Brazil; E- mail: ciampi@ terra. com. br abduction nystagmus. Convergence was unimpaired. Volitional vertical gaze tested by smooth pursuit was normal. Both upward and downward vestibulo- ocular reflexes showed reduced gain, with eye velocity lagging behind head velocity. Pupillary function and palpebral elevation were normal. The neurologic examination was otherwise intact. A diagnosis of isolated bilateral internuclear ophthalmoplegia ( INO) was made. A brain CT scan showed no acute lesions. MRI revealed findings consistent with an ischemic stroke involving the medial longitudinal fasciculus ( MLF) bilaterally in the midbrain, seen on a thin- section ( 3 mm) T2 sequence ( Fig. 1A). The lesion was hyperintense on diffusion imaging ( Fig. IB) and hypointense on the apparent diffusion coefficient ( ADC) map ( Fig. 1C). A region of interest encompassing the abnormality on T2 and diffusion imaging was chosen to obtain the ADC value of the lesion. ADC values were also obtained from equal-sized regions of interest in the normal contralateral white matter. The ADC ratio was calculated as ADC of the lesion/ ADC of the contralateral normal white matter. The ADC of the lesion was 0.71 X lfr3 mm7s; the diffusion coefficient of the normal white matter was 0.86 X 10~ 3 mm2/ s. An ADC ratio was estimated to be 0.82, demonstrating restriction to the diffusion of water molecules in the lesion, corroborating the hypothesis of a recent ischemic lesion. J Neuro- Ophthalmol, Vol. 27, No. 2, 2007 125 J Neuro- Ophthalmol, Vol. 27, No. 2, 2007 de Andrade et al Magnetic resonance angiography ( MRA) ( not shown) disclosed occlusion of the left internal carotid artery, an ulcerated plaque in the right internal carotid artery, and significant stenosis of the left vertebral artery. Digital subtraction angiography confirmed these findings. Cerebrospinal fluid analysis and echocardiography were normal. After extensive investigation, the most likely stroke etiology was penetrating arterial branch disease. A dose of 300 mg/ day aspirin was prescribed. The ocular motility findings improved over the following days. The most common cause of bilateral INO is demyeli-nization ( 1,2), and bilateral INO has been most commonly associated with multiple sclerosis ( MS) ( 40.9% of 22 cases) ( 3). However, ischemic stroke in the anteromedial midbrain territory is an alternative cause, especially in patients with vascular risk factors. In one series ( 3), stroke was the second most common cause of INO ( 27.2%). There is an interesting relationship between age and the etiology of INO. In a group of patients with bilateral INO caused by MS, eight of nine patients were younger than 45 years, whereas in the group of patients with INO caused by stroke, five of six patients were 45 years or older ( 3). Despite the higher frequency of vascular disease in older patients, age alone does not suffice to differentiate between ischemic and demyelinating disease as the cause of INO. MRI, MRA, cardiovascular investigation, and cerebrospinal fluid analysis with evaluation of oligoclonal bands should aid clinical judgment. Bilateral INO can be caused by occlusion of a single perforating paramedian tegmental pontine artery branch of the basilar artery ( 4). However, some patients presenting initially with bilateral INO progress to more extensive brain stem infarcts. Therefore, making the correct etiologic diagnosis is a mandatory step in the initial management of these patients ( 5- 7). In this case, MRI thin- section brain stem slices allowed the characterization of lesions not previously identifiable on a regular MRI scan. This method also confirmed the fact that the infarct zone was confined to the MLF bilaterally and did not extend to nearby structures of the midbrain. The diffusion imaging sequence and the ADC map signal patterns confirmed the likely cause to be stroke. Locally restricted ischemic lesions may have an earlier resolution of diplopia ( 7). Likewise, isolated INO caused by brain stem stroke has been reported to improve faster than INO associated with mild neurologic deficits ( 8). REFERENCES 1. Frohman EM, Zhang H, Kramer PD, et al. MRI characteristics of the MLF in MS patients with chronic internuclear ophthalmoparesis. Neurology 2001; 57: 762- 8. 2. Leigh RJ, Zee DS. The Neurology of Eye Movements, 4th ed. New York: Oxford University Press; 2006: 620- 7. 3. Bolanos I, Lozano D, Cantii C. Internuclear ophthalmoplegia: causes and long- term follow- up in 65 patients. Acta Neurol Scand 2004; 110: 161- 5. 4. Fisher CM. Neuroanatomic evidence to explain why bilateral internuclear ophthalmoplegia may result from occlusion of a unilateral pontine branch artery. JNeuroophthalmol 2004; 24: 39^ U. 5. Keane JR. Internuclear ophthalmoplegia: unusual causes in 114 of 410 patients. Arch Neurol 2005; 62: 714- 7. 6. Spengos K, Wohrle JC, Tsivgoulis G, et al. Bilateral paramedian midbrain infarct: an uncommon variant of the " top of the basilar" syndrome. J Neurol Neurosurg Psychiatry 2005; 76: 742- 3. 7. Eggenberger E, Golnik K, Lee A, et al. Prognosis of ischemic internuclear ophthalmoplegia. Ophthalmology 2002; 109: 1676- 8. 8. Kim JS. Internuclear ophthalmoplegia as an isolated or predominant symptom of brainstem infarction. Neurology 2004; 62: 1491- 6. 126 © 2007 Lippincott Williams & Wilkins |
