Furthermore, the thalamic inferolateral arteries and the pulvinarian inferolateral arteries supply most of the ventral lateral nucleus, the pulvinar, and the ventral posterior nucleus. The paramedian artery supplies the dorsomedial portion of the thalamus as well as the paramedian section of the midbrain. These areas can alternatively be supplied by the paramedian artery in individuals lacking the thalamotuberal artery. The thalamus has vascular support provided by several arterial branches, such as the thalamotuberal artery supplying the posterior section of the hypothalamus, anterior thalamic nuclei, ventral section of the internal medullary lamina, ventral pole of the medial dorsal nucleus, and the rostral ventrolateral nucleus. Locations of thalamic lesions and subsequent ocular motility deficitĬompromised vascular supply to any of these areas can cause important ocular deficits. Pseudo-abducens palsy (thalamic esotropia) Inhibitory descending pathways for convergence, caudal territory Loss of voluntary motor actions and arousal Ventral lateral and ventral anterior nuclei Ventrolateral neurons, paralaminar regions of the mediodorsal and ventroanterior nuclei Paramedian area, medial rectus sub-nucleus Specific ocular motility issues that can be caused from damage to pathways located in various sections of the thalamus are summarized in Table 1. This includes the vestibulo-ocular pathway, connections to the frontal eye fields, and pathways to the posterior parietal cortex responsible for visual processing. The thalamus is one of the principal relay stations for pathways linking cortical regions to the brainstem. Risk factors for acute thalamic lesions include the common vasculopathic risk factors, such as hypertension, diabetes, and a history of smoking. While vascular accidents, either hemorrhagic or ischemic, are the most common etiologies causing acute thalamic lesions, other reported etiologies include migraine, metabolic (e.g., thiamine deficiency), inflammatory (e.g., cerebral lupus), infectious (e.g., bacterial abscesses, cerebral syphilitic gumma), traumatic, neoplastic (e.g., tumors or cysts) and iatrogenic (e.g., deep brain stimulation). Deficits can result from various etiologies and can result in ocular motility difficulties presenting most commonly as vertical gaze palsies, but can also include skew deviation, convergence problems, third cranial nerve palsy, nystagmus, pupil and lid abnormalities, or deficits in saccades or smooth pursuits. Thalamic lesions are associated with possible neuro-ophthalmologic deficits that are important to distinguish from those caused by lesions in the midbrain or other locations.
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