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Show Joumal of Clillical NCllro- ophtilalnwlogy 11( 1): 58- 61, 1991 © 1991 Raven Press, Ltd., New York Magnetic Resonance Findings in a Patient with Internuclear Ophthalmoplegia NeuroradioIogicaI- CIinicaI Correlation Julia A. Alexander, M. D., Mauricio Castillo, M. D., and James c. Hoffman, Jr., M. D. A 49- year- old female presented with symptoms compatible with internuclear ophthalmoplegia. Magnetic resonance using T2- weighted images showed an eccentric area of high signal intensity in the mid pons corresponding to the right medial longitudinal fasciculus, Magnetic resonance is the method of choice when internuclear ophthalmoplegia is suspected. The findings should be differentiated from the normal central hyperintensity called the " pseudo MLF hyperintensity." Key Words: Internuclear ophthalmoplegia- Medial longitudinal fasciculus- Magnetic resonance imaging. From the Department of Radiology, Emory University, Atlanta, Georgia, U. S. A. Address correspondence and reprint requests to Dr. J. C. Hoffman at Department of Radiology, Emory University, 1364 Clifton Road, N. E., Atlanta, GA 30322, U. S. A. 58 Magnetic resonance imaging ( MRI) is the modality of choice for evaluation of brain stern and cranial nerve lesions. The following case demonstrates the utility of MRl in the clinical evaluation of a patient with a lesion involving the medial longitudinal fasciculus, CASE HISTORY A 48- year- old diabetic black woman presented with a one- week history of dizziness. Pertinent physical examination showed inability to adduct the right eye and nystagmus of the left eye upon horizontal leftward gaze. The remainder of the physical evaluation was unremarkable. Routine laboratories and CSF analysis were normal. The presumed clinical diagnosis was a lesion involving the right median longitudinal fasciculus ( MLF). Noncontrast computed tomography of the brain showed an old lacunar infarct involving the left lentiform nuclei. Since this finding did not explain the patient's problem, a non- enhanced MRl study of the brain was obtained. Tl- weighted images showed the old lacunar infarct, but were otherwise negative. T2- weighted images showed an illdefined area of high signal intensity located eccentrically to the right in the midbrain ( Fig. lA and B). This abnormality was located in the dorsal pons immediately anterior to the periaqueductal gray matter and extended the length of both the inferior and superior colliculi. Although the abnormality was seen on the proton density images, it was less obvious as compared to the T2- weighted images. Unfortunately, further follow- up was unobtainable, because the patient did not return for continued evaluation. / MR FINDINGS IN PATIENT WITH INO 59 FIG. 1. A: Axial T2- weighted image ( 2200/ 90/ 256 x 256/ 1 [ TRITE, matrix/ NEX]) at the level of the high dorsal midbrain shows an ill- defined area of increased signal intensity ( arrow) located eccentrically to the right. This corresponds to the anatomic location of the right medial longitudinal fasciculus. B: Coronal T2- weighted image through the midbrain again shows an ill defined area of increased signal intensity on the right ( arrow) in the region of the MLF. This finding is nonspecific and may be secondary to a demyelinating process or an infarction. Also seen is a small punctate area of high signal intensity in the region of the left basal ganglia corresponding to a prior lacunar infarction. DISCUSSION Internuclear ophthalmoplegia ( INa) is a gaze disturbance secondary to a lesion involving the MLF. This results in ipsilateral adduction impairment and nystagmus of the contralateral eye, especially upon lateral horizontal gaze ( 1). The abducens nuclei are located in the dorsal low pons at the level of the floor of the fourth ventricle. These nuclei contain two types ofaxons, those that innervate the lateral recti muscles, and those that project to the contralateral oculomotor nuclei via the MLF. These latter axons innervate the medial recti ( 2). At the level of the sixth cranial nerve nuclei, the fasciculi decussate and then travel upward in a paramedian location anterior to the periaqueductal gray matter to join the opposite third cranial nerve nuclei. The nuclei for the ocu-lomotor nerves are located in the dorsal midbrain at the level of the upper pole of the superior colliculi. These anatomic correlations clearly indicate how a lesion involving one MLF will result in paralysis of the ipsilateral medial rectus and, therefore, in impaired adduction of that eye. The various etiologies for INO include vascular infarction, multiple sclerosis, trauma, infection and neoplasias ( 3). Of these, the former two are believed to be responsible for the majority of cases of INa. Traditionally it was thought that bilateral INO was secondary to multiple sclerosis while unilateral INO was most likely due to infarction ( 4). However, in a recent report, multiple sclerosis was found to be responsible for one- third of the cases with unilateral INO ( 3). Radiologic evaluation of patients with INO is optimally performed with MRl; Computed tomogra- JClin NMiro- ophthalmol, Vol. 11. No. 1, 1991 FIG. 2. Axial T2- weighted image through the cerebral peduncles show the slight hyperintensity of the periaqueductal gray matter ( small arrows). Anterior to this, a small linear area of increased intensity is noted in the midline, representing the " pseudoMLF hyperintensity" ( white arrow) and should not be confused with a true lesion. The origin of this finding is uncertain, but it may represent a normal signal from the region of the median raphe. Curved arrows point to the superior colliculi. The thin long arrow corresponds to the aqueduct of Sylvius. FIG. 3. Superior colliculi ( A); oculomotor nucleus ( B); MLF ( C); abducens nucleus ( 0); vestibular nucleus ( E). I Clill Neuro- ophlhalmol. Vol. II. No. I. 1991 phy is unable to discretely identify different structures within the pons and midbrain, and evaluation of these regions is frequently hampered by artifacts ( 5). The reported MRI findings in INO consist of areas of high signal intensity seen on T2- weighted images in the region of the MLF ( 3). In that same series, these findings were present in 9 out of 10 patients with INa ( 3). Although that paper describes a case in which the lesion enhanced following gadolinium- DTPA administration, in our experience both acute infarctions and active multiple sclerosis plaques may enhance. Therefore, enhancement is a nonspecific finding, and it is better to seek the etiology of INa using clinical and laboratory evaluations. A possible pitfall seen in MR axial images is the presence of the so- called " pseudo- MLF hyperintensity" described by Atlas et a1. ( 3). This term refers to the presence of a small, strictly midline linear hyperintensity anterior to the aqueduct of Sylvius on T2- weighted images ( Fig. 2). This finding, of uncertain origin, is present in all normal individuals. In our experience, this normal finding is easily recognized and is difficult to mistake for true lesions, which are usually more nodular and less well- defined. Specifically, in our patient the etiology of INa was thought to be secondary to infarction. As MR FINDINGS IN PATIENT WITH INO 61 shown in our case, MRI is the best diagnostic modality to evaluate the relevant neuroanatomy of the MLF and the cranial nerve nuclei. REFERENCES 1. Rowland LP. Merritt's textbook of neurology. 7th ed. Philadelphia: Lea & Febiger, 1984: 785. 2. Asbury AK, McKhann CM, McDonald WI. Diseases of the nervous system: clinical neurobiology. 1st ed. Philadelphia: Ardmore Medical Books, 1986: 508. 3. Atlas SW, Crossman RI, Savino PJ, et al. Internuclear ophthalmoplegia: MR- anatomic correlation. A/ NR 1987; 8: 243- 7. 4. Kupfer C, Cogan DC. Unilateral internuclear ophthalmoplegia: a clinicopathological case report. Arch Ophthalmol 1966; 75: 484- 9. 5. Han JS, Bonstelle CT, Kaufman B, et al. Magnetic resonance imaging in the evaluation of the brainstem. Radiology 1984; 150: 70S- 12. 1Clin Neuro-< Jphthalmol. Vol. 11, No. 1. 1991 |
