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Show Journal ofNeuro- Ophthalmology 20( 2): 127- 129, 2000. © 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Unilateral Thalamic Infarction and Vertical Gaze Palsy: Cause or Coincidence? Maaike M. van der Graaff, MD, Jan A. L. Vanneste, MD, PhD, Gareth ap A. G. Davies, MRCP, FRCR Although vertical gaze palsy ( VGP) is commonly associated with lesions of the rostral mesencephalon, there is some evidence that VGP may also be caused by a unilateral thalamic lesion. The case of a 68- year- old man with persistent upward gaze palsy after a unilateral thalamic infarction, demonstrated on computed tomography and magnetic resonance imaging scans, is presented. Subsequent high- resolution magnetic resonance scanning, however, showed involvement of the rostral mesencephalon as well. The authors suggest that in previous patients with VGP ascribed to a unilateral thalamic infarction, a coexisting mesencephalic involvement may have been missed because of inappropriate imaging techniques. Strong evidence of unilateral thalamic infarction as a cause of VGP is still lacking. Key Words: Thalamic infarction- Vertical gaze palsy. Post mortem studies in animals and men have shown a correlation between vertical gaze palsy ( VGP) and lesions of the mesencephalic rostral interstitial nucleus of the medial longitudinal fasciculus ( riMLF), the interstitial nucleus of Cajal, the posterior commissure, and the periaqueductal gray region ( 1). In unilateral lesions of the riMLF causing VGP, upward gaze is usually more affected than downward gaze ( 1). In more recent years, it has been suggested from computed tomography ( CT) and magnetic resonance imaging ( MRI) studies that VGP may also be caused by a unilateral dorsomedial thalamic lesion ( 2- 5). We recently saw a patient with VGP that initially was erroneously attributed to a unilateral thalamic lesion. CASE REPORT A 68- year- old man arrived at the emergency department with upward and downward gaze palsy, diplopia, dysarthria, and gait ataxia. A week later, several symp- Manuscript received June 10, 1999; accepted February 1, 2000. From the Departments of Neurology ( MMVDG, JALV) and Radiology ( GAGD), St. Lucas Andreas Hospital, Amsterdam, the Netherlands. Address correspondence to Maaike M. van der Graaff, MD, Department of Neurology, St. Lucas Andreas Hospital, PO Box 9243, 1006 AE, Amsterdam, the Netherlands. toms had resolved, but upward gaze palsy and vertical diplopia remained. A neuro- ophthalmologic examination revealed normal visual acuity, fields, and fundi. The pupils were equal and reacted normally to light and near-stimuli. There was no ptosis. There was no eye deviation in primary position. Horizontal saccades were normal. Horizontal smooth pursuit was unremarkable, except for a slight in- and- downward deviation OS when gazing to the right. This deviation became more evident in the upper right field of gaze, suggesting a paresis of the left inferior oblique muscle, causing vertical diplopia. Vertical saccades, measured in an electrooculography- direct current 1 week after the onset of symptoms with 20° visually guided saccades, were slow and hypometric. Velocity of upward saccade was 66°/ sec OD and 72°/ sec OS. Velocity of downward saccade was 138°/ sec OD and 102°/ sec OS. Latency was not measured. Downward smooth pursuit was normal, but upward smooth pursuit was incomplete. Both the VGP and the paresis of the left inferior oblique muscle could be overcome by the doll's eye maneuver. The Bell phenomenon was intact ( i. e., forced eyelid closure induced reflectory upward deviation OU). A CT scan of the brain showed a right dorsomedial thalamic infarction. A subsequent MRI scan showed the same ischemic thalamic lesion ( Fig. 1A) without associated mesencephalic involvement ( Fig. IB). Because the left inferior oblique muscle paresis strongly suggested additional involvement of the rostral mesencephalon, a second MRI scan with 3- mm slices to maximize resolution was performed; only then did it become apparent that the lower border of the infarction encroached upon the diencephalic- mesencephalic junction, therefore probably including the riMLF ( Figs. 2A and 2B). Further clinical course was uneventful. Two years later, an upward gaze paresis is still present. DISCUSSION Our patient had a mainly upward VGP that was of a supranuclear origin, as demonstrated by the doll's eye maneuver and intact Bell phenomenon. In addition, he had vertical diplopia in the upper right field of gaze, and the left eye was hypotropic. Because the lesion was at the 127 M. M. VAN DER GRAAFF ET AL. FIG. 1. Magnetic resonance imaging showing right dorsomedial thalamic infarction ( A: T2- weighted) and no apparent mesencephalic involvement ( B: proton density). right side of the rostral mesencephalon, we could not explain the vertical diplopia by a nuclear or infranuclear paresis of the left inferior oblique muscle. We presume that the patient's minimal vertical misalignment was of a supranuclear origin, as well. Brandt and Dieterich ( 6) found that skew deviation because of a rostral brainstem lesion always presented with the hypometric eye contralateral to the lesion, as was found in our patient. Before the era of sophisticated neuroimaging techniques, the attribution of neurologic signs to specific brain lesions was based on pathologic studies. Since the introduction of CT and MRI, many publications have tried to correlate particular signs or syndromes with the lesions seen on CT or MRI images. This was also true for VGP, for which some reports suggested a causal relation with a unilateral thalamic lesion ( 2- 5). This was also the case in our patient, whose CT and MRI scans suggested a unilateral thalamic infarction as the cause of the VGP. High- resolution MRI, however, showed that the rostral mesencephalon was also involved. A review of the ad hoc literature could not disclose a post mortem- proven unilateral thalamic infarction as the cause of VGP. Publications ascribing VGP to a unilateral thalamic infarction lack pathologic evidence ( 2- 5). In articles with post mortem data, a coexisting lesion of the rostral mesencephalon, therefore including the riMLF, was always demonstrated ( 7- 9). This may be explained by the fact that the paramedian thalamus and the rostral mesencephalon often have a common blood supply, namely the paramedian thalamic artery, which usually / • HEM . FIG. 2. T2- weighted MRI showing involvement of the rostral mesencephalon on axial ( A) and sagittal ( B) images ( arrows). J Neuro- Ophthalmol, Vol. 20. No. 2, 2000 UNILATERAL THALAMIC INFARCTION AND VERTICAL GAZE PALSY 129 arises from the PI segment of the posterior cerebral artery, either individually or by a common trunk with the superior paramedian mesencephalic artery ( 9). Basic research has failed to show a specific role of the thalamus in controlling vertical eye movements. Stanton et al. ( 10,11) used anterograde tracers in macaque monkeys to visualize frontal eye field efferents. They did not find a direct pathway from the frontal eye field or thalamus to the riMLF, indicating that there is no direct input from the frontal eye field or thalamus to the riMLF. They presumed that the riMLF probably receives its input from the pontine reticular formation and the cerebellum. Schlag and Schlag- Rey ( 12,13) investigated the role of the thalamus in gaze control with single- unit micro-electrode recordings. Based on their findings, they presumed that the thalamus possibly played a role in initiating eye movements, but this role seemed nonspecific. They found no preponderance for vertical gaze. The findings in our own patient, similar case reports, and basic research confirm the doubts of Siatkowski et al. ( 14) regarding the role of thalamic lesions in VGP. They stated that neuroimaging may be inadequate to exclude a coexisting lesion of the rostral mesencephalon. In view of the evidence so far available, unilateral thalamic lesions alone seem unlikely to cause VGP. REFERENCES 1. Buttner- Ennever JA, Buttner U, Cohen B, Baumgartner G. Vertical gaze paralysis and the rostral interstitial nucleus of the medial longitudinal fasciculus. Brain 1982; 105: 125^ t9. 2. Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes, etiology, and prognosis. 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Unit activity related to visual events, targeting, and fixation. J Neurophysiol 1984; 51: 1175- 95. 14. Siatkowski RM, Schatz NJ, Sellitti TP, Galetta SL, Glaser JS. Do thalamic lesions really cause vertical gaze palsies? J Clin Neu-roophthalmol 1993; 13: 190- 3. J Neuro- Ophthalmol, Vol. 20, No. 2, 2000 |
