CLINICAL CONSIDERATIONS


Skull fractures may cause a unilateral lesion of the branchiomotor fibers to the muscles of mastication, which will result in a flaccid paralysisor paresiswith subsequent muscle atrophyof the ipsilateral muscles of mastication. This becomes apparent upon muscle palpation when the patient is asked to clench his jaw. When depressing the lower jaw it deviatestowardsthe affected side (weak side) primarily due to the unopposed action of the lateral pterygoid muscle of the unaffected side. This impairs chewing on the lesion side due to muscle paralysis. Damage to the fibers innervating the tensor tympani muscle results in hyperacusis(acute sense of hearing) and impaired hearing on the ipsilateral side
. Damage to the GSA fibers of the mandibular division will result in loss of sensation from the areas supplied by the branches of this division. Although the trigeminal nerve has an extensive distribution in the head, there is minimal overlapping of the areas innervated by its three divisions, especially in the central region of the face. Lesions in the peripheral branches of the trigeminal nerve can be located by testing for sensory deficits in the areas that are innervated by each of the three trigeminal divisions. If a lesion is located distal to the joining of the autonomic fibers that hitchhike with the trigeminal branches to the lacrimal gland or the salivary glands, then both sensory and autonomic innervation are interrupted. Infection of the trigeminal ganglion by herpes zoster virus (known as shingles) causes a significant amount of pain as well as damage to the sensory

f ibers of the three trigeminal divisions (the ophthalmic division is most commonly infected). This results in loss of sensation on the affected side. Damage to the sensory fibers innervating the cornea (via the ophthalmic division) results in a loss of the corneal reflex when the ipsilateral eye is stimulated (afferent limb damage of the corneal reflex). Trigeminal neuralgia (trigeminal nerve pain, tic douloureux) A common clinical concern regarding the trigeminal nerve is trigeminal neuralgia. This condition results from idiopathic etiology (unknown cause) and is manifested as intense, sudden onset, and recurrent unilateral pain in the distribution of one of the three divisions of the trigeminal nerve, most commonly the maxillary division. There may be a trigger zone in the distribution of the affected trigeminal division, and if it is stimulated it may trigger an attack that usually lasts for less than a minute. This condition may be treated pharmacologically or surgically. Surgical treatment includes sectioning of the affected trigeminal division as it emerges from the trigeminal ganglion or producing a lesion in the trigeminal ganglion. Although these procedures may alleviate the excruciating pain experienced by patients, they also abolish tactile sensation from the affected area. Sectioning of the descending spinal trigeminal tract proximal to its termination in the subnucleus caudalis selectively obliterates the afferents relaying nociception but spares the fibers relaying tactile sensation from the orofacial region

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