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The initiation and progression of ischemic and hemorrhagic stroke are the result of a complex cascade of processes that determine both the extent of the lesion and long-term outcome. Several of these processes, including peripheral inflammation, neuroinflammation, and neuroplasticity are influenced by the activity of the afferent as well as efferent pathways of the vagus nerve. It was shown that vagus nerve stimulation significantly reduces the extent of stroke-induced lesion of brain parenchyma. However, the mechanisms of beneficial effect of increased vagal activity on pathological processes related to stroke remains largely unclear. The aim of this article is to describe the role of afferent and efferent vagal pathways in the mechanisms that influence the initiation of stroke as well as its detrimental effects.
Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. email@example.com
This article was published in the following journal.
Name: Autonomic neuroscience : basic & clinical
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The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx).
The inferior (caudal) ganglion of the vagus (10th cranial) nerve. The unipolar nodose ganglion cells are sensory cells with central projections to the medulla and peripheral processes traveling in various branches of the vagus nerve.
The 12th cranial nerve. The hypoglossal nerve originates in the hypoglossal nucleus of the medulla and supplies motor innervation to all of the muscles of the tongue except the palatoglossus (which is supplied by the vagus). This nerve also contains proprioceptive afferents from the tongue muscles.
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Neurology - Central Nervous System (CNS)
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