Pearls & Oy-sters: Ocular motor abnormalities in bilateral paramedian thalamic stroke

Abstract

Pearls & Oy-sters: Ocular motor abnormalities in bilateral paramedian thalamic stroke PEARLS• The thalamus is supplied by 4 bilateral arterial systems: 3 derived from the vertebrobasilar system and 1 derived from the posterior communicating artery (PCA), each supplying the ipsilateral thalamus.• Top of the basilar syndrome caused by occlusion of the rostral portion of the basilar artery can present with an array of visual, oculomotor, and behavioral abnormalities as a result of ischemia to midbrain, thalami, and temporal and occipital lobes. OY-STERS• The artery of Percheron (AOP) is an anatomical variant arising from a single PCA and supplies the bilateral medial thalamus.• Bilateral paramedian thalamic strokes due to AOP occlusion are characterized by altered mental status, vertical gaze palsy, and memory impairment, and are similar in presentation to top of the basilar syndrome. The absence of posterior cortical visual disturbances favors AOP occlusion.CASE 1 A 67-year-old right-handed man with hypertension was admitted to a rural hospital with sudden onset of confusion, double vision, and bilateral drooping of the eyelids. He had difficulty walking and altered behavior. He was afebrile and rest of his clinical examination had normal results. He was admitted to the intensive care unit and managed as a suspected krait bite (due to its high prevalence in the area), although there was no history of a snakebite. Forty-eight hours later, the patient was fully oriented. His eye signs were persistent and he was referred to our institution for further evaluation. Neurologic examination of the eyes (figure 1) revealed bilateral asymmetric ptosis and skew eye deviation (vertical misalignment of the eyes where the eyes move upward, but in opposite directions) with an exotropia (divergent squint). Adduction of the eyes was impaired bilaterally. There was no nystagmus. Vertical saccadic and pursuit eye movements were minimal. On oculocephalic maneuvers, the eye movements were restored. Pupillary examination, convergence, and the rest of the cranial nerves were normal. The rest of the cerebellar, motor, and sensory systems were normal. His brain MRI, which was done 1 week after the onset of symptoms, revealed bilateral thalamic T1 low signal intensities and T2 high signal intensities with minimal gadolinium enhancement suggestive of bilateral thalamic infarctions. Diffusion-weighted imaging demonstrated restricted diffusion in the same region. There was no concurrent midbrain lesion. Magnetic resonance angiogram and venogram had normal results. A diagnosis of bilateral thalamic infarction due to occlusion of the AOP was made. A source of cardiothromboembolism was not elicited. The patient was managed with antiplatelets. Lid crutches were prescribed for his ptosis.CASE 2 A 47-year-old woman presented with 3 days history of acute onset of dizziness, transient loss of consciousness, and binocular diplopia with difficulty in walking unassisted. She was confused and amnesic after she regained consciousness in the hospital. Her ...

Association between functional network connectivity, retina structure and microvasculature, and visual performance in patients after thalamic stroke: An exploratory multi‐modality study

“…Reduced vision is one clinical manifestation after thalamic stroke (Gooneratne et al., 2015 ; Schaller‐Paule et al., 2021 ; Ye et al., 2022a , 2022b). Our previous report showed that visual loss in thalamic stroke patients is associated with retinal neurodegeneration (Ye et al., 2022b ).…”