(Stroke. 1995;26:1467-1470.)
© 1995 American Heart Association, Inc.
Articles |
Vertical Gaze Palsies From Medial Thalamic Infarctions Without Midbrain Involvement
From the Stanford Stroke Center, Palo Alto, Calif.
Correspondence to Joni Clark, MD, Stanford Stroke Center, 701 Welch Rd, Suite 325, Palo Alto, CA 94304.
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Abstract |
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Background Although the supranuclear pathways for vertical gaze control are not well defined, lesions of the mesencephalic reticular formation including the nucleus of Darkschewitsch, the rostral interstitial medial longitudinal fasciculus, the interstitial nucleus of Cajal, and the posterior commissure are known to produce vertical gaze palsies. MRI studies have not previously reported isolated thalamic lesions as the cause of vertical gaze palsies.
Case Descriptions Three patients with acute paralysis of vertical gaze were imaged with MRI. Sagittal T1 and axial T1, T2, and proton-weighted images were obtained. All three patients had repeated scans performed from 3 days to 6 weeks after the original study. Two patients exhibited unilateral right thalamic infarcts (polar and paramedial territory), and one patient had a bilateral paramedian thalamic infarction. There was no evidence of midbrain involvement on any of the images.
Conclusions Vertical gaze palsies are known to be produced by lesions of the rostral interstitial medial longitudinal fasciculus. This MRI study reveals thalamic infarctions without associated midbrain infarctions in three patients with vertical gaze palsies. This may be explained by interruption of supranuclear inputs.
Key Words: eye abnormalities • magnetic resonance imaging • thalamus
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Introduction |
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Vertical gaze palsies are common manifestations of paramedian thalamic infarctions.1 2 3 4 These gaze palsies have been attributed to associated lesions of vertical eye movement control centers in the rostral midbrain rather than the thalamic injury. The frequent coexistence of both midbrain and paramedian thalamic infarction is related to their vascular supply; a single vessel arising near the top of the basilar may branch to supply both the paramedian region of the thalamus and the rostral medial mesencephalon.1 Alternatively, isolated medial thalamic or midbrain infarcts can occur in individuals in whom the paramedian peduncular arteries arise separately from the paramedian thalamic vessels (Fig 1
). In patients with infarcts of the
midbrain/thalamic junction, clinical features can be correlated with
lesion location with the use of MRI. A previous study described three
anatomic levels (upper midbrain, midbrain/thalamic junction, and
ventral thalamus) that can be clearly identified with
MRI.5 This study confirmed previous pathological series
that implicate associated lesions of the rostral midbrain or the
midbrain/thalamic junction as the cause of vertical gaze palsies in
patients with thalamic infarctions. To our knowledge, only one case has
been depicted by MRI of a patient with a vertical gaze palsy and a
paramedian thalamic infarction without an apparent lesion of the
midbrain.6 We report three cases of patients with
MRI-documented medial thalamic infarctions without midbrain involvement
who presented with vertical gaze palsies. MRI images were 5.0
mm thick with slice separation of 2.5 mm. MRI lesion localization was
made with the use of corresponding sections from the atlas of
Haines7 (Fig 2). These cases may have
implications regarding the supranuclear pathways that mediate vertical
gaze.
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Case 1 |
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An 86-year-old man experienced an acute onset of diplopia. He had no associated nausea, vomiting, vertigo, paresthesia, or weakness. He had severely limited upward and downward vertical gaze that could be overcome with the doll's head maneuver. Horizontal gaze was intact. Pupils were equal and reactive. MRI of the brain performed on the day of symptom onset revealed an acute infarction in the paramedial thalamus bilaterally. In addition, T2 signal hyperintensity was noted in the pons bilaterally and the right cerebellar hemisphere in the posterior inferior cerebellar artery distribution. No abnormality was present in the midbrain. MR angiography demonstrated patent vertebral and basilar arteries. Two months after onset the patient was able to look downward, but there was still significant restriction of upward gaze. A repeated MRI again revealed the paramedian thalamic infarction without midbrain involvement (Fig 3A
).
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Case 2 |
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A 47-year-old man with an unremarkable medical history experienced an acute onset of nausea, vertigo, confusion, and blurred vision. CT of the head was negative. On examination the patient was lethargic and had difficulty following simple commands. Speech was dysarthric. There was severe restriction of upward gaze. Horizontal eye movements were intact, and pupils were equal and reactive. A cerebral angiogram, performed within 2 hours of symptom onset, did not reveal evidence of basilar or vertebral artery stenosis or an embolus. The patient's clinical symptoms resolved within 4 hours. A transesophageal echocardiogram was significant for a small patent foramen ovale with a positive echo contrast study. His antithrombin III level was 71% on admission (normal, 80% to 120%) but was normal when repeated 1 week later. Protein C and S levels were normal. MRI of the brain obtained on the day of symptom onset was completely normal except for T2 hyperintensity in the right anterior/medial thalamus. A repeated MRI 2 months later clearly revealed an isolated right thalamic infarct (Fig 3B
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Case 3 |
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A 72-year-old man with a history of diabetes, hypertension, and a right cerebellar infarction experienced an acute onset of difficulty in swallowing, right facial weakness, diplopia, and slurred speech. These symptoms resolved within 2 hours but recurred the next morning. CT of the head revealed an old right posterior inferior cerebellar artery infarction. On examination the patient's speech was dysarthric, and he had a vertical gaze palsy involving both upward and downward gaze that could be overcome with the doll's head maneuver. Horizontal gaze was intact. He had a right lower motor neuron–type seventh nerve palsy, bilateral horizontal gaze-evoked nystagmus, and a decreased gag reflex. His gait was ataxic. MRI of the brain revealed a right paramedian thalamic infarction (Fig 3C
). There was also an old
right cerebellar infarction in the posterior inferior
cerebellar artery territory. A repeated MRI scan 3 days later revealed
the interval development of infarction in the right medulla at the
pontomedullary junction and in the right medullary pyramid. There was
also increased signal intensity in the left medulla. The right thalamic
lesion was still present, again with no evidence of
ischemia in the midbrain. Cerebral angiogram demonstrated
complete occlusion at the origin of the right vertebral artery with
reconstitution 2 cm distally. This vessel extended distally to the
vertebrobasilar junction, where there was a reocclusion. The left
vertebral artery was normal. |
Discussion |
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A prominent clinical finding in these three patients was an acute vertical gaze palsy. However, none of the patients had other clinical evidence of midbrain ischemia such as a third nerve palsy, and MRI did not reveal evidence of ischemia of the midbrain or the midbrain/thalamic junction despite repeated testing. Two of these patients had other ischemic lesions identified by MRI; however, these lesions were not in areas known to be involved with control of vertical gaze. Two of the patients had infarction of the paramedian thalamic territory, while in the other (case 2) the infarction appeared to be in the polar artery territory.
Previous reports have described vertical gaze palsies in patients with either unilateral or bilateral paramedian infarction. These patients typically present with upward and downward gaze palsies associated with confusion and a decreased level of consciousness.3 The gaze palsies have been attributed to coexisting lesions of the rostral midbrain. For example, Bogousslavsky et al3 described a case of a patient with an isolated thalamic infarct visible by CT who had an upward gaze palsy for voluntary saccades, smooth pursuit, and vestibulo-ocular movements. Necropsy revealed infarction of the intralaminar, dorsomedial, and ventral posterior nuclei of the thalamus. In addition, the posterior commissure, rostral interstitial medial longitudinal fasciculus, interstitial nucleus of Cajal, and nucleus of Darkschewitsch were involved. This case is in accordance with lesioning studies in animals and other autopsy studies of patients with ischemic vertical gaze palsies that suggest that midbrain damage is required to cause an acute disturbance of vertical gaze.8 9
The neural structures known to be involved in the mediation of vertical gaze lie in the mesencephalic reticular formation. These include the nucleus of Darkschewitsch, the interstitial nucleus of Cajal, and the posterior commissure. Isolated paralysis of downward gaze can also be produced by bilateral lesions of the rostral mesencephalic reticular formation, which includes the interstitial nucleus of the medial longitudinal fasciculus.8 The rostral interstitial medial longitudinal fasciculus contains burst neurons for vertical saccades, and in most pathological studies cases of upward and downward gaze paralysis have been attributed to bilateral infarction in the rostral interstitial medial longitudinal fasciculus.8 10 Paralysis of upward gaze can be produced with lesions of the posterior commissure. A combined upward and downward gaze paresis has been produced in primates by damaging the interstitial nucleus of Cajal and nucleus of Darkschewitsch in addition to the posterior commissure.8
In contrast to the supranuclear pathways for horizontal gaze, those involved in mediation of vertical gaze are not well understood. It has been shown, however, that pathways from the frontal and supplementary eye fields do traverse the medial thalamus in the monkey.11 The primate thalamus also has reciprocal inputs to the frontal and supplementary eye fields. This input arises from the internal medullary lamina. The central thalamus is traversed by frontocortical axons, which send collaterals to internal medullary lamina complex neurons. The internal medullary lamina complex also receives afferents from several brain stem populations and the superior colliculus, and it has reciprocal connections with the inferior parietal pole.11
Only a few cases with infarctions limited to the paramedian thalamus have been reported in autopsy series. Castaigne et al1 reported four cases of paramedian thalamic infarction that did not involve the subthalamic region or hypothalamus. Clinical descriptions were given for only two of the four cases, but vertical gaze palsies were not described. Some investigators have postulated that the vertical gaze disorder in paramedian thalamic infarctions may be secondary to interruption of supranuclear fibers as they traverse the medial thalamus en route to the pretectal and prerubral areas.2 12 Gentilini et al2 reported a CT study of five patients with vertical gaze palsies and isolated paramedian thalamic infarction. Two of the patients had additional marginal damage to the medial longitudinal fasciculus, whereas three had no apparent midbrain involvement. However, none of these cases were studied with MRI or confirmed pathologically.
Only one study has correlated oculomotor findings with MRI lesions in a series of patients with infarctions in the midbrain/thalamic junction.5 Patients were included if they had a third nerve palsy, supranuclear vertical gaze palsy, or both. Of 11 patients described in the study, 7 had vertical gaze palsies, and 4 of these had no evidence of a third nerve palsy. These 4 patients all had MRI-documented infarction of the mesencephalic reticular formation and posterior commissure. Three of the 4 had associated thalamic infarction. The authors attributed the vertical gaze palsy to the mesencephalic lesions. To our knowledge, only one previous case has been reported of a patient with an acute vertical gaze palsy and an isolated thalamic infarction on MRI.6 In this case, however, the rostral midbrain (the level of the red nucleus) was not visualized.
Our cases illustrate MRI lesions in the medial thalamus in three patients with vertical gaze palsies. The only previous MRI study evaluating vertical gaze palsies in patients reported associated lesions in the midbrain. In two of our cases the thalamic lesions were unilateral, and in one case there were bilateral lesions. The mechanism for complete vertical gaze paresis with unilateral lesions is uncertain; however, we can speculate that some of the frontocortical fibers may decussate in the medial thalamus. It is conceivable that brain stem lesions could have contributed to the gaze palsies in some of our cases; however, the clinical and imaging features are more suggestive of mesencephalic localization. Imaging studies in our patients did not reveal lesions in the midbrain despite reimaging in all cases. Reasons for this might include the fact that the lesion was too small to be detected by the thickness of our MRI slices and the lack of sagittal T2-weighted images. Another postulation is that the thalamic lesion may have produced the vertical gaze palsy by interrupting supranuclear inputs. This will need to be confirmed further with pathological and MRI studies.
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Acknowledgments |
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The authors thank Phyllis Grant for preparation of the manuscript.
Received December 5, 1994; revision received April 17, 1995; accepted May 3, 1995.
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References |
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