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The principal clinically relevant functions of the trigeminal nerve are facial somatic sensation and innervation of the muscles of mastication. The trigeminal nerve also innervates one palate muscle (tensor veli palitini) and one inner ear muscle (tensor tympani).
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The trigeminal nerve supplies somatic sensation to the face, the inside of the mouth (although not taste), the sinuses, and most of the dura mater (including all supratentorial dura and the tentorium cerebelli; the rest of the posterior fossa dura mater is supplied by cranial nerve 10). The three divisions of the trigeminal nerve and the regions for which they supply sensation are:
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Ophthalmic division (V1): forehead, upper lid, upper half of cornea
Maxillary division (V2): cheek, lower lid, lower half of cornea, roof of mouth, upper gums/teeth/lip
Mandibular division (V3): lower gums/teeth/lip, lower jaw, anterior tongue
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The muscles of mastication innervated by CN 5 are:
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See Table 14–1 for a summary of the functions shared between CNs 5, 7, 9, and 10.
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Trigeminal Sensory Pathways
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The facial sensory pathways of the trigeminal nerve are analogous to those for the body: All sensory information travels back to a ganglion, and pain and temperature sensation travel separately from other modalities (Fig. 13–1). The sensory ganglion of CN 5 is called the gasserian ganglion, which resides in Meckel’s cave (mnemonic: ganglion for cranial nerve V resides in Meckel’s cave). The gasserian ganglion receives somatosensory input from the face and transmits that information to the brainstem at the level of the pons. Distal to the gasserian ganglion, the trigeminal nerve divides into three branches: ophthalmic (V1), maxillary (V2), and mandibular (V3). V1 and V2 pass through the cavernous sinus, whereas V3 does not pass though the cavernous sinus. V1 exits the skull through the superior orbital fissure, V2 through the foramen rotundum, and V3 through the foramen ovale.
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Proximal to the gasserian ganglion, the somatosensory information from CN 5 enters the brainstem at the level of the pons. Although the point of entry of CN 5 into the brainstem is at the level of the pons (as would be expected for the 5-6-7-8 schema described in Ch. 9), CN 5 has nuclei throughout the three levels of the brainstem. Light touch sensation from the face is transmitted primarily to the main sensory nucleus of 5 (also called the chief or principal sensory nucleus of 5) at the level of entry in the pons, and the output from this nucleus crosses to join the medial lemniscus (carrying sensory information from the body), which ascends to the thalamus. Facial sensation information projects to the ventral posterior medial (VPM) nucleus of the thalamus, and sensation from the limbs and trunk travels to the ventral posterior lateral (VPL) nucleus of the thalamus (see Ch. 4). VPM and VPL project to the somatosensory cortex in the postcentral gyrus.
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Pain and temperature sensation from the face descend to the medulla in the spinal tract of 5 (the facial analogue of the anterolateral tract) along with its associated spinal nucleus of 5. The spinal nucleus and tract of 5 extend as inferiorly as the upper cervical spine. The output of the spinal nucleus of 5 crosses to join the contralateral spinothalamic tract from the body and ascends to the ventral posterior medial (VPM) nucleus of the thalamus (pain and temperature sensation from the limbs and trunk travel to the VPL nucleus of the thalamus).
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Jaw proprioception information is relayed to the mesencephalic nucleus of 5 in the midbrain.
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Trigeminal Motor Pathways
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The motor nucleus of 5 is medial to the main sensory nucleus of 5 in the dorsal pons. Unlike the common symptom of facial weakness in both central and peripheral nervous system diseases (see “Upper and Lower Motor Neuron Facial Weakness” below), jaw weakness due to a lesion in the nervous system is uncommon. This is in part due to the fact that the trigeminal motor nuclei receive bilateral cortical input, so unilateral hemispheric lesions such as strokes do not typically cause unilateral jaw weakness.
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Brainstem Reflexes Involving the Trigeminal Nerve
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The trigeminal nerve is involved in two brainstem reflexes, the corneal reflex and the jaw jerk reflex.
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Corneal reflex—The corneal reflex is elicited by stimulating the cornea, which normally leads to reflex closure of the eyes. The trigeminal nerve is the afferent limb of the reflex (sensation from the cornea is carried by V1), and the facial nerve (CN 7) is the efferent limb responsible for closure of the eye (by contraction of the orbicularis oculi muscle). The reflex is bilateral, so stimulating one cornea normally leads to bilateral closure of both eyes.
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Jaw jerk reflex—The jaw jerk reflex is elicited by asking the patient to let the jaw gently hang open, and then tapping on the upper chin gently with a reflex hammer. This reflex is mediated by the mesencephalic nucleus of 5 (afferent) and the motor nucleus of 5 (efferent). If the jaw jerk reflex is markedly brisk, this demonstrates upper motor neuron (central nervous system) pathology above the level of the spinal cord (i.e., in the brainstem or brain). The jaw jerk reflex is often tested in patients with upper motor neuron signs in the extremities to evaluate for signs of pathology superior to the spinal cord (i.e., to determine if the corticobulbar tracts are affected in addition to corticospinal tracts).
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Disorders of the Trigeminal Nerve
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Loss of facial sensation can occur due to a lesion in:
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The trigeminal nerve in the face, skull base, or cavernous sinus
The trigeminal pathways in the dorsolateral brainstem (e.g., loss of pain and temperature sensation in the face is part of lateral medullary syndrome along with contralateral loss of pain and temperature in the body, Horner’s syndrome, ataxia, nausea, vomiting, vertigo, dysarthria, and dysphagia)
VPM of the thalamus
The lateral postcentral gyrus (facial region of the somatosensory cortex)
The subcortical white matter connecting VPM and somatosensory cortex
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Isolated facial sensory loss is most likely to be due to a lesion of the trigeminal nerve, the entry zone of the nerve in the pons, or a small cortical lesion because lesions at all other sites would likely cause other deficits due to involvement of adjacent structures:
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A brainstem lesion causing facial sensory loss will often also affect other cranial nerve nuclei.
A cavernous sinus lesion causing facial sensory loss (which will only affect V1 and V2 divisions since V3 does not pass through the cavernous sinus) will often also affect CNs 3, 4, and/or 6 (see Ch. 11).
A thalamic lesion causing facial sensory loss will often also cause sensory loss beyond the face.
A subcortical lesion causing facial sensory loss will often also affect additional adjacent sensory fibers representing other parts of the body.
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Since the face and hand have the most cortical sensory representation, a common pattern of numbness for cortical, subcortical, and small thalamic lesions is contralateral face and hand numbness (cheiro-oral pattern).
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Facial numbness due to an isolated trigeminal nerve lesion can be caused by:
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Malignancy: skull base tumor, cerebellopontine angle tumor, leptomeningeal metastasis
Inflammatory disease: Sjögren’s syndrome, sarcoidosis
Spread of head and neck cancers along the trigeminal nerve (perineural spread), most commonly caused by squamous cell cancer of the skin on the face
Dental pathology
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Numb chin sign—Numbness of the chin (numb chin sign) should raise concern for metastatic malignancy affecting the mandibular (V3) division of the trigeminal nerve in the skull base or the distal trigeminal branches in the mandible (usually the mental nerve, a branch of the inferior alveolar nerve, which is a branch of V3). The numb chin sign may be the presenting feature of systemic malignancy or metastatic disease in a patient with known cancer. Breast cancer and lymphoma are among the most common malignancies causing the numb chin sign. When patients present with this symptom, history for other symptoms of malignancy should be elicited (e.g., weight loss, night sweats). The differential diagnosis includes dental etiologies and systemic causes of trigeminal neuropathy (e.g., Sjögren’s syndrome, sarcoidosis). Evaluation should include panoramic dental x-ray, CT scan or bone scan of the jaw (to evaluate the mandible), CT scan of the head (to evaluate for a skull base lesion), and/or MRI of the brain with contrast (to evaluate the trigeminal nerve itself).
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In trigeminal neuralgia, brief lightening-like paroxysms of pain shoot through the face. These may be spontaneous or may be triggered by contacting the face (e.g., brushing the teeth). Trigeminal neuralgia is most commonly unilateral and most commonly affects the lower face (V2 and/or V3 regions). The condition may be idiopathic, or it can be caused by multiple sclerosis, a compressive vascular loop, any of the above-listed etiologies of trigeminal pathology, or it may begin after dental work (ostensibly due to irritation of the most distal branches of the trigeminal nerve).
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If trigeminal neuralgia is present in a young woman and/or bilaterally, multiple sclerosis should be considered and MRI obtained. How can trigeminal neuralgia be caused by multiple sclerosis if multiple sclerosis is a central nervous system disease and the trigeminal nerves are peripheral nerves? When multiple sclerosis causes trigeminal neuralgia, the lesion is in the trigeminal entry zone in the pons, which is part of the central nervous system.
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In idiopathic trigeminal neuralgia, facial sensation is generally normal. If facial sensation is diminished in a patient with trigeminal neuralgia, this is atypical and a structural lesion should be sought with neuroimaging.
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Antiepileptics are used for pain control in trigeminal neuralgia, with the most supportive evidence being for carbamazepine. If neuroimaging reveals a vascular loop compressing the trigeminal nerve in a patient with trigeminal neuralgia, microvascular decompression can be considered if the patient does not respond to medications. In refractory cases of trigeminal neuralgia, surgical ablation of or radiotherapy to the gasserian ganglion may be considered.