A case of double depressor palsy followed by pursuit deficit due to sequential infarction in bilateral thalamus and right medial superior temporal area.

BACKGROUND: We present a unique case of a patient who suffered two rare events affecting the supranuclear control, first of the vertical and second of the horizontal eye movements. The first event involved bilateral thalamic infarcts that resulted in double depressor palsy. The second event occurred 1 year later and it involved supranuclear control of horizontal eye movements creating pursuit deficit. CASE PRESENTATION: A 47-year-old male presented with complaints of diplopia upon awakening. He had atrial fibrillation, mitral valve regurgitation, aortic valve regurgitation, and a history of spleen infarction 1 year ago. His right eye was hypertrophic and right eye downgaze was limited unilaterally of equal degree in adduction and abduction. The patient was diagnosed with double depressor palsy of the right eye. Magnetic resonance imaging (MRI) of the brain showed an old infarction of the left thalamus, and diffusion MRI showed acute infarction of the right thalamus. The patient's daily warfarin dose was 2 mg and it was increased to 5 mg with cilostazol 75 mg twice a day. Seven weeks later, the patient's ocular movement revealed near normal muscle action, and subjectively, the patient was diplopia free. At follow-up 12 months later, the patient revisited the hospital because of sudden onset of blurred vision on right gaze. He was observed to have smooth pursuit deficit to the right side, and orthophoric position of the eyes in primary gaze. MRI of the brain showed an acute infarction in the right medial superior temporal area. CONCLUSIONS: The patient experienced very rare abnormal eyeball movements twice. This case highlights the importance of evaluating vertical movement of the eyes and vascular supplies when patients present with depressor deficit and supports the theory of a supranuclear function in patients who present with pursuit deficit.

Weber's syndrome with vertical gaze palsy.

Weber's syndrome with vertical gaze palsy is rarely reported in literature. We present a case of a 47-year-old female who developed sudden onset of left exotropia, right sided hemiplegia and vertical gaze palsy. Magnetic resonance imaging (MRI) showed multiple infarcts involving both thalami and extending caudally into the midbrain. This case presents the diverse clinical picture following midbrain infarcts.

[A case of vertical gaze palsy associated with a unilateral infarct in the thalamo-mesencephalic junction on MR imaging].

We report a case of a 54-year-old man with sudden-onset double-vision. On admission, neurological examination showed upward and downward gaze palsy on voluntary and smooth pursuit movements, and vertical oculocephalic maneuver elicited a full upward and downward response. Bell's phenomenon, horizontal eye movements and convergence were not impaired. Based on these findings, supranuclear dissociated vertical gaze palsy was diagnosed. T1-weighted MR images revealed low intensity on the medial side of the right thalamo-mesencephalic junction, which impaired the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). T2-weighted MR images revealed a high-intensity area. The posterior commissure was spared. The clinical signs gradually improved, and the vertical gaze palsy almost disappeared one month after onset. Based on these findings, unilateral infarct in the thalamo-mesencephalic junction in the distribution of the right paramedian thalamic artery was diagnosed. Only two cases of upward and downward gaze palsy in association with unilateral upper midbrain lesion without posterior commissure have been previously reported. Since we did not perform a pathological examination, we cannot deny that there may have been some denervation of fibers at the posterior commissure. Cases of upward and downward gaze palsy in association with unilateral upper midbrain lesion without posterior commissure are rare, and it is very interesting that the lesion in our patients, like that seen in the two pathological reports, was right-sided.

[A case of transient vertical gaze palsy following right thalamic and midbrain infarction].

The authors report a 71-year-old male who suffered from vertical gaze palsy due to infarction localized on MRI in the right midbrain. Vertical gaze palsy was observed 1 hour after the onset of his stroke. Upgaze palsy was noted the following day. Four days later, the disturbances of ocular movement disappeared. T2 weighted MR imaging showed a high signal intensity lesion, which was localized in the right side of the thalamo-mesencephalic portion. However, since the vertical gaze palsy appeared only transiently for a short time in the initial stage and since the level of consciousness decreased during that time, it was suggested that there was a bilateral functional disorder caused by mild edema, etc., in the hyperacute stage, which was not demonstrated on MRI. This disorder had been overlooked either because the duration of the vertical gaze palsy due to the unilateral lesion was very short, i.e. improvement was seen 4 days after onset, or the lesion was not clearly delineated in a CT scan of the head. It appeared possible that this sign might not be very rare if careful observations are performed in the hyperacute stage of midbrain infarction.

[A case report of Weber's syndrome associated with supranuclear vertical gaze palsy caused by the ipsilateral thalamomesencephalic lesion].

We report a rare case showing Weber's syndrome associated with supranuclear vertical gaze palsy caused by the ipsilateral lesion of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), which is regarded as the supranuclear control center of vertical gaze. To date, no literature concerning Weber's syndrome associated with the ipsilateral riMLF lesion was documented. The patient was a 53-year-old female, who suddenly developed unconsciousness and left-sided weakness. Neurological findings on admission revealed right third nerve palsy, severe supranuclear vertical gaze palsy, almost complete convergence palsy, left hemiparesis and hyperreflexia with positive Babinski's sign on the left side. There was no sign of pupillary disturbance or no abnormality of the horizontal movements of the left eye. The vestibulo-ocular reflex of the left eye was preserved. There was no sensory disturbance. Cranial MRI had the advantages in demonstrating unilateral ischemic lesions at the cerebral peduncle and the thalamomesencephalic junction involving the unilateral riMLF on the right side. Recent reports have demonstrated that supranuclear vertical gaze palsy is caused by the unilateral riMLF lesion. We confirm that the unilateral riMLF lesion causes supranuclear vertical gaze palsy in our case and that cranial MRI has the advantages in demonstrating the specific lesion.