In the present review, we summarize the neuroanatomy, clinical syndromes, and diagnostic techniques of critical illness-associated brainstem dysfunction for the critical care setting. Detection of brainstem dysfunction is challenging but of utmost importance in comatose and deeply sedated patients both to guide therapy and to support outcome prediction. Of particular importance for characterizing brainstem dysfunction and identifying the underlying etiology are a detailed clinical examination, MRI, neurophysiologic tests such as brainstem auditory evoked potentials, and an analysis of the cerebrospinal fluid. The brainstem is prone to various primary and secondary insults, resulting in acute or chronic dysfunction. Brainstem dysfunction may lead to sensory and motor deficits, cranial nerve palsies, impairment of consciousness, dysautonomia, and respiratory failure. It controls the sleep-wake cycle and vital functions via the ascending reticular activating system and the autonomic nuclei, respectively. Gustatory input from the posterior 1/3 of the tongue and pharynx as well as somatosensory input from the outer ear, tympanic membrane and middle ear would be affected.The brainstem conveys sensory and motor inputs between the spinal cord and the brain, and contains nuclei of the cranial nerves. Sensory loss would also follow section of the glossopharyngeal nerve. Lesions would also result in the loss of the carotid sinus reflex because the glossopharyngeal nerve carries viscerosensory afferents innervating the carotid body and sinus. Section of the nerve would interfere with the afferent limb of the reflex arc. Lesions of the glossopharyngeal nerve would result in loss of the pharyngeal (gag) reflex because the glossopharyngeal nerve contains somatosensory afferents innervating the pharynx. Damage to the lower motor neurons results in the impairment of salivary production.Īt this level of the medulla (pontomedullary junction) the ambiguus nucleus is difficult to see. The postganglionic axons of the otic ganglion innervate the parotid gland. The axons of the inferior salivatory nucleus travel in the glossopharyngeal (IX) nerve as parasympathetic efferents and synapse in the otic ganglion. The inferior Salivatory nucleus is too small to be seen here, but is located superior to the solitary tract. Chemosensory fibers innervate taste buds in the posterior third of the tongue and the pharynx and end in the rostral (gustatory) component of the nucleus solitarius.Somatosensory fibers innervate the outer ear canal, eardrum, and middle ear and end in the spinal trigeminal nucleus.Viscerosensory fibers innervate the pharynx, soft palate, tonsils, and eustachian tube and end in the nucleus solitarius.Motor fibers of the nucleus ambiguus travel in the glossopharyngeal nerve to innervate the stylopharyngeus muscle.The parasympathetic (preganglionic) fibers from the inferior salivatory nucleus terminate in a parasympathetic (otic) ganglion located near the parotid gland. ![]() The components of the Glossopharyngeal Nerve include: Lab 9 (ƒ 10) - Cranial Nerve Nuclei and Brain Stem Circulation Cranial Nerve IX - Glossopharyngeal Nerve
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