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Show Journal of Clillical Neuro-ophthalmology 13(3): 190-193, 1993. Do Thalamic Lesions Really Cause Vertical Gaze Palsies? R. Michael Siatkowski, M.D., Norman J. Schatz, M.D., Tony P. Sellitti, M.D., Steven L. Galetta, M.D., and Joel S. Glaser, M.D. © 1993 Raven Press, Ltd., New York Two patients with thalamic infarctions presented with vertical gaze palsies. Magnetic resonance imaging (MRI) demonstrated extension of the lesions into the upper midbrain. A common vascular supply to both areas, and the inability of computed tomography (CT) scans to adequately assess posterior fossa structures, necessitate MRI of the mesencephalon in the assessment of all patients with vertical gaze dysfunction. These cases shed further doubt regarding a specific role of the thalamus in control of vertical eye movements. Key Words: Thalamus-Vertical gaze palsy-Mesencephalon- MRI. From the Bascom Palmer Eye Institute (R.M.S., N.J.S., T.P.S., J.S.G.) and the University of Pennsylvania Hospital, Department of Neurology (S.L.G.), Philadelphia, Pennsylvania, U.S.A. Address correspondence and reprint requests to Dr. Joel S. Glaser, 900 NW 17th Street, Miami, FL 33136, U.S.A. 190 Vertical gaze abnormalities have been attributed solely to thalamic lesions (1-7). We present two patients in whom simultaneous thalamic and mesencephalic lesions resulted in vertical gaze palsy. In one patient, computed tomography (CT) revealed thalamic infarction only, but magnetic resonance imaging (MRI) subsequently disclosed an associated midbrain lesion. Since the thalamus and mesencephalon share a common blood supply (8), infarction of the latter might coexist in these patients. We agree with recent reports that in patients with thalamic infarction and vertical gaze palsy, there is coexistent midbrain pathology, which is responsible for the ocular motor disturbance. CASE STUDIES Case One A 33-year-old man was found in an unresponsive state; urine levels of cocaine and cannabinoids were elevated. CT revealed an area of hypodensity in the right thalamus felt to represent an acute infarction (Fig. 1), and a second left occipital infarct. Upon regaining consciousness, the patient complained of binocular vertical diplopia in all fields of gaze. Past medical history was significant for mitral valve prolapse and previous myocardial infarction. He admitted to a la-year history of cocaine abuse. Visual acuity was 20/20 in each eye and the pupils were 4 mm, round, and briskly reactive to light without an afferent defect. There were 2 mm of upper lid retraction present bilaterally. There was a total vertical gaze palsy of saccades and pursuit, with sparing of the vertical oculocephalic reflex. Horizontal eye movements were normal, but convergence and vertical optokinetic reflexes were THALAMIC LESIONS 191 FIG. 1. Axial view CT scan at mid-thalamic level. Arrow indicates lacunar infarct in right medial thalamus. abolished. Slit lamp and funduscopic examinations were normal. A gadolinium-enhanced MRI revealed abnormal signal intensity in both thalami, with extension into the subthalamic nuclei; the area of the right periaqueductal gray matter, red nucleus, and rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) were also involved. Encephalomalacia of the left occipital lobe was present (Fig. 2). Serum HIV titers were positive, the RPR was reactive at 1:16, and the FTA-Abs was positive. A tentative diagnosis of AIDS with syphilitic meningovasculitis was made. The patient refused further workup and treatment. Case Two A 67-year-old woman with a history of steroiddependent rheumatoid arthritis and congestive heart failure was admitted for increasing chest pain. Coronary angiography disclosed normal hemodynamic studies, but the right coronary artery was 99% stenosed. Four days later, successful right coronary angioplasty was performed. Immediately following angioplasty, the patient complained of binocular vertical diplopia and dysarthria. (A) (B) FIG. 2. Axial view T2-weighted MRI. (A) Right medial thalamic infarct (arrow). (B) At level of red nuclei, arrow shows mesencephalic extension of lesion, from aqueduct along medial raphe to interpeduncular space. 1Gill Neuro-opillhalmol, Vol. 13, No.3, 1993 192 R. M. SIATKOWSKI ET AL. Neuro-ophthalmological examination disclosed visual acuities of right eye 20/25 + 2, and left eye 20/70 + 1, due to cataract. Pupils were 2 mm, but briskly reactive to light and near, without an afferent defect. Visual fields were full to confrontation. There was a marked vertical gaze paresis of pursuit and saccades, with up and down gaze limited to 20% of normal. Vertical excursions were increased by either Bell's phenomenon or oculocephalic maneuvers. Horizontal eye movements were normal. Both fundi were normal, as was the remainder of the neurologic examination, except for a mild right-hand pronator drift. Gadolinium-enhanced magnetic resonance imaging performed 5 days later showed a 1.5-cm lesion involving the left thalamus and superior midbrain. A small area of abnormal signal intensity was also observed in the superior right thalamus (Fig. 3). These findings were felt to be consistent with new infarctions. Several days later, both the vertical gaze paresis and dysarthria had almost resolved. DISCUSSION The pathways for control of vertical gaze are imprecisely known, the relative roles of the thalamus and midbrain having recently been in dispute. The rostral mesencephalon is the proposed site of the vertical gaze center, particularly the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) (9-15). Buttner-Ennever et al. (14) have traced the contribution of the riMLF, noting that the medial aspect of the nucleus contains neurons involved in upgaze, while cells from the lateral portion are primarily responsible for downgaze. Conversely, others (15) have hypothesized that the medial parts of the riMLF are involved in downgaze. Clinically, however, lesions of the riMLF may disturb upgaze, downgaze, or both. Since fibers responsible for upgaze course posteriorly after leaving the riMLF, lesions involving the posterior commissure or periaqueductal gray area tend to produce isolated upgaze paresis or bidirectional palsies. Isolated downgaze paresis is a rare finding most often associated with bilateral lesions involving the riMLF or periaqueductal gray matter (9). Although there is no anatomic documentation for thalamic control of vertical gaze, isolated case reports have suggested that such evidence exists clinically (2-5). In a large series, Bogousslavsky (1) analyzed CT scans from 40 patients with thalamic infarcts and reported that paramedian infarctions of the thalamus are likely to cause abnormalities of vertical gaze. Again using CT as the sole neuroimaging modality, Steinke et al. (6) recently noted associated horizontal and vertical gaze abnormalities in 62 patients with thalamic stroke. Yet Miller (16) has pointed out that, although a few isolated thalamic lesions have been shown to cause horizontal gaze disturbances, the vertical gaze system remains intact; he states "most ocular motor dis- IAl (8) FIG. 3.. T2-:-veighted MRI. (A) AXi~1 section shows left medial thalamic infarct (arrow). (B) Coronal section shows the lesion involVing the rostral midbrain (large arrow), and small right superior thalamic infarct (small arrow). I Olll Nruro-ophthalmol, Vol. 13, No.3, 1993 THALAMIC LESIONS 193 turbances associated with paramedian thalamic infarction are, in fact, caused by damage to adjacent brainstem structures and not by damage to the thalamus itself." This confusion may be resolved when one considers two points. First, the poor detail of CT imaging of the posterior fossa (17), as Steinke et al. (6) clearly point out. Furthermore, Hommel and Bogousslavsky (9) reported 11 patients with a variety of vertical gaze abnormalities, but in five of the cases in which both CT and MRI were performed, MRI demonstrated additional thalamic and/or midbrain lesions not evident by CT alone. Second, is the common arterial supply to the thalamus and mesencephalon. The paramedian thalamosubthalamic artery arises near the midline from either the proximal portion of the posterior cerebral artery, or the terminal basilar. It supplies the dorsomedial thalamus directly, and its branches supply the rostral midbrain and subthalamus (8). Vessels subserving the thalamus act as end-arteries as they approach the diencephalon, and obstruction of a limited afferent segment may produce a relatively large area of infarction, including those regions of the rostral midbrain that control vertical gaze (8). Thus, paramedian thalamic infarcts often occur in conjunction with mesencephalic infarcts (especially those involving the riMLF and posterior commissure), and present clinically with vertical gaze abnormalities. Inferolateral and posterior thalamic lesions are not associated with ocular motility disturbances, for the blood supply to these areas is not shared with the midbrain (8). In case one, the initial CT failed to indicate the midbrain lesions, subsequently detected by MRI. In case two, MRI clearly showed both thalamic and mesencephalic infarctions. Although the major portion of the lesion involved the thalamus, clear extension into the superior midbrain was evident. We believe that the mesencephalic infarcts, and not the thalamic lesions, were responsible for the vertical gaze abnormalities in our two patients. The dorsal periaqueductal gray region is the site for interconnections between the two sides of the riMLF (18), and a lesion in this region could produce combined upgaze and downgaze palsies. Furthermore, in a recent series of eleven patients with paramedian thalamopeduncular infarction, concomitant mesencephalic infarction was documented by MRI in every patient who manifested a supranuclear vertical gaze deficit (7). All patients in this group had involvement of the mesencephalic reticular formation; lesions tended to be more caudal in the midbrain when upgaze was more impaired than downgaze. Our report confirms the importance of highresolution visualization of the midbrain when evaluating patients with vertical gaze dysfunction, and that CT is never adequate for this determination. MRI should be regarded as the current best technique for imaging the posterior fossa and neural tissues implicated in the control of vertical eye movements. Patients with vertical gaze palsies, especially those with demonstrable thalamic lesions, should be investigated carefully for associated mesencephalic disease. REFERENCES 1. Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes, etiology, and prognosis. Neurology 1988;38: 837-48. 2. Ghidoni E, Pattacini F, GaJimberti D, Aguzzoli L. Lacunar thalamic infarcts and amnesia. Eur Neurol1989;Suppl 2:13-5. 3. Lazzarino LG, Nicolai A. Aphonia as the only speech disturbance from bilateral paramedian thalamic infarction. Clin Neurol Neurosurg 1988;90:265-7. 4. Fensore C, Lazzarino LG, Nappo A, Nicolai A. 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