Eight consecutive patients with CT scan evidence of a bilateral infarct in the territory of the paramedian thalamic artery are reported. In seven cases the infarct also extended to the territory of the polar artery. The main symptoms were: disorder of vigilance which cleared in a few days, and hypersomnolence which lasted longer and in two patients was still present a year later; amnesia, detectable clinically in four patients and only with tests in two patients, which persisted in one patient for three years; changes of mood and bulimia present in five and four patients respectively; and vertical gaze paresis in five patients. Only one patient died, and in the remainder the symptoms tended to subside, but none of the patients who could be followed-up for a year returned to normal behaviour. Clinical and CT scan correlations pointed to the mammillo-thalamic tract as the structure whose damage was responsible for the memory disorders.

https://jnnp.bmj.com/content/jnnp/50/7/900.full.pdf

Bilateral paramedian thalamic artery infarcts: report of eight cases.

Background In healthy subjects, the act of walking and turning is accomplished by a sequential horizontal reorientation of gaze, head, and body toward the direction of the turn. Subjects with stroke, however, have difficulty altering their walking direction and present with loss of balance when performing a head turn or whole body rotation.Objective. To study, in a pilot case study, the spatial and temporal coordination of gaze and posture during preplanned turns executed while walking in severely disabled and mildly disabled subjects with stroke as compared to a healthy control walking at slow speed.Methods. Horizontal plane orientations of gaze, head, thorax, pelvis, and feet as well as the body’s center of mass (CoM) trajectory were analyzed as subjects were walking straight or executing a 90-deg turn.Results. Subjects with stroke revealed altered orientation and sequencing of gaze body segments. These alterations were more pronounced in the most severely disabled subject with stroke, especially when t...

https://journals.sagepub.com/doi/pdf/10.1177/1545968306290822

Stroke Affects the Coordination of Gaze and Posture During Preplanned Turns While Walking

Infarction in the territory of the anterior choroidal artery (AchA) has been the subject of several recent reports. To the classical clinical syndrome of hemimotor, hemisensory, and visual field deficit has been added hemiataxia acute pseudobulbar mutism, pure motor and pure sensory syndromes and disorders of higher cortical function. The definition of anatomic and clinical correlates to AchA stroke is aided by CT-MRI findings and reveals an unexpected superior extension of infarct to include the periventricular caudate nucleus and inferior corona radiata. Prognosis depends upon unilaterally, bilateral strokes having often a fatal outcome. Etiology and treatment may be intimately related to hypertension.

A new view of anterior choroidal artery territory infarction.

Purpose of reviewAll functional classes of eye movements require exquisite coordination between cortical, basal ganglia and brainstem centers involved in ocular motor control. Vertebrobasilar stroke may produce a wide spectum of isolated or combined eye-movement disorders. The intent of this article

Vertebro-basilar syndromes causing oculo-motor disorders

We present two cases with acute onset of vertical gaze palsy, mainly consisting of impaired downgaze and apraxia of downward head movements, together with neuropsychological deficits (hypersomnia, impaired attention and disorders of memory and affective control). CT and MRI revealed bilateral post-ischaemic lesions in the dorsomedial thalamus and the mesodiencephalic junction, dorsomedial to the red nucleus, thus being restricted to the territory of the posterior thalamosubthalamic paramedian artery, which includes the region of the rostral interstitial nucleus of the medial longitudinal fascicle as the main premotor nucleus for the generation of vertical saccades. In our patients, oculographic examination with electro-oculography and magnetic search coil recording showed severe impairment of downward more than upward saccades and only minor deficits of vertical pursuit and the vestibulo-ocular reflex. Visual functions were normal, with one exception: a psychophysical test of motion perception revealed a significant deficit in the detection of vertical movements. This could be due to a central adaptive mechanism which, in order to minimize oscillopsia, might elevate thresholds for vertical motion perception in cases of vertical gaze palsy. As an alternative explanation, lesions within the midbrain tegmentum could have damaged subcortical visual pathways involved in motion perception.

Impairment of vertical motion detection and downgaze palsy due to rostral midbrain infarction.

Ocular and head movements in infarctions of the thalamic region

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Ocular and head movements in infarctions of the thalamic region