Mixed cranial nerves
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|Definition||Mixed cranial nerves are the nerves that consist of motor and sensory nerve fibers.|
Trigeminal nerve (CN V)
Facial nerve (CN VII)
Glossopharyngeal nerve (CN IX)
Vagus nerve (CN X)
|Clinical relations||Trigeminal neuralgia, surgical removal of the parotid Gland, facial nerve palsy, inferior medial pontine syndrome, glossopharyngeal neuralgia, lateral pontine syndrome, lateral medullary syndrome, syringobulbia|
- Cranial nerves
- Trigeminal nerve (CN V)
- Facial nerve (CN VII)
- Glossopharyngeal nerve (CN IX)
- Vagus nerve (CN X)
- Mixed cranial nerves and reflexes
- Clinical notes
- Related diagrams and images
Cranial nerves are the 12 nerves of the peripheral nervous system that innervate the structures of the head and neck. Vagus nerve (CN X) is the only cranial nerve that innervates the structures beyond the head and neck region. Except for the spinal accessory nerve (CN XI) which has origin in the spinal cord, all the other cranial nerves emerge from the brain.
These 12 paired nerves are summarized in this table.
|Cranial nerve 1||Olfactory nerve (CN I) - sensory|
|Cranial nerve 2||Optic nerve (CN II) - sensory|
|Cranial nerve 3||Oculomotor nerve (CN III) - motor|
|Cranial nerve 4||Trochlear nerve (CN IV) - motor|
|Cranial nerve 5||
Trigeminal nerve (CN V) - mixed
- Ophthalmic branch (V1)
- Maxillary branch (V2)
- Mandibular branch (V3)
|Cranial nerve 6||Abducens nerve (CN VI) - motor|
|Cranial nerve 7||Facial nerve (CN VII) - mixed|
|Cranial nerve 8||Vestibulocochlear nerve (CN VIII) - sensory|
|Cranial nerve 9||Glossopharyngeal nerve (CN IX) - mixed|
|Cranial nerve 10||Vagus nerve (CN X) - mixed|
|Cranial nerve 11||Spinal accessory nerve (CN XI) - motor|
|Cranial nerve 12||Hypoglossal nerve (CN XII) - motor|
Cranial nerves have various functions;
- The olfactory nerve, the optic nerve, the facial nerve, the vestibulocochlear nerve, the glossopharyngeal nerve, and the vagus nerve each play roles in special sensory functions (i.e. olfaction, vision, gustation, audition, and balance).
- Trigeminal (all three branches) and glossopharyngeal nerves play roles in somatic sensory functions.
- Oculomotor, facial, glossopharyngeal, and vagus nerves have important autonomic functions.
- Oculomotor nerve, trochlear, mandibular branch of the trigeminal nerve (V3), abducens, facial, glossopharyngeal, vagus, spinal accessory and hypoglossal nerves are responsible for motor functions.
Understand better the anatomy of cranial nerves with our cranial nerves quizzes and labeling exercises.
According to their functions, cranial nerves are either motor, sensory or both (mixed). To remember if a nerve is sensory, motor or both in numerical order, remember this mnemonic: Some say money matters, but my brother says big brains matter most.
Cranial nerves anatomy starter pack is waiting for you here.
Trigeminal nerve (CN V)
The trigeminal nerve (CN V) is a mixed nerve containing both general sensory (afferent) fibers and somatic motor (efferent) fibers. The fibers originate from the nuclei in the brainstem and spinal cord; principal sensory nucleus of trigeminal nerve, spinal nucleus of trigeminal nerve, mesencephalic nucleus of trigeminal nerve and the motor nucleus of trigeminal nerve. CN V forms the trigeminal ganglion near the apex of the petrous part of the temporal bone.
From the trigeminal ganglion, the trigeminal nerve divides into three divisions; ophthalmic nerve (CN V1), maxillary nerve (CN V2) and mandibular nerve (CN V3). Ophthalmic divison exits the skull through the superior orbital fissure, maxillary through the foramen rotundum and the mandibular nerve exits via the foramen ovale.
The general sensory component sends information about pain, touch, pressure, and temperature sensation from the anterior two-thirds of the head, including the face. The smaller somatic efferent component innervates the skeletal muscles derived from the first branchial arch; the mylohyoid muscles, tensor tympani, tensor veli palatini, anterior belly of the digastric muscle and the muscles of mastication (the masseter, temporalis, medial pterygoid, and lateral pterygoid muscles). Because of its size, the trigeminal nerve can be easily seen where it emerges from the pons near the middle cerebral peduncle.
Ophthalmic division (CN V1)
The ophthalmic divison of the trigeminal nerve (CN V1) transmits sensory signals from receptors on the: forehead, cornea, upper eyelid, dorsal surface of the nose and the mucous membranes of the nasal and frontal sinuses.
The signals then travel along nerve fibers which enter the skull through the superior orbital fissure (along with the oculomotor, trochlear, and abducens nerves).
Find out more about the ophthalmic nerve here.
Maxillary division (CN V2)
The maxillary division of the trigeminal nerve (CN V2) transmits sensory signals from receptors on the: lateral surface of the nose, upper teeth, hard palate, upper cheek and mucous membranes of the upper teeth, nose, and roof of the mouth.
Signals generated by these receptors then travel along the nerve fibers into the skull via the foramen rotundum.
Learn more about the maxillary nerve here.
Mandibular division (CN V3)
The mandibular division of the trigeminal nerve (CN V3) transmits sensory signals from receptors on the: lower jaw, lower teeth, chin, parts of the posterior cheek, temple, external ear, anterior two-thirds of the tongue and the floor of the mouth.
It also supplies motor innervation to the muscles of mastication and a few other muscles in the lower face (listed previously). These fibers enter the skull via the foramen ovale.
Cover the anatomy of the mandibular branch here.
Facial nerve (CN VII)
Facial nerve carries general and special fibers. It originates from the brainstem as two separate divisions; a larger primary motor root, and a smaller intermediate nerve carrying sensory and parasympathetic fibers. The former originates from the motor nucleus of facial nerve, while the latter stemms from the nuclei of solitary tract, spinal nucleus of trigeminal nerve and the superior salivatory nucleus.
The two divisions leave the cranial cavity through the internal acoustic meatus and then travel through the facial canal. Here they join and leave the cranium together through the stylomastoid foramen. Facial nerve innervates the muscles of facial expression and salivary glands via its major branches; temporal, zygomatic, buccal, mandibular and cervical branches. It also provides the taste sensation from the anterior two thrids of the tongue.
Sensory branches innervate the middle ear, nasal cavity, soft palate (general visceral afferent); anterior two-thirds of the tongue (special visceral afferent); external auditory meatus (general somatic afferent). Motor fibers supply lacrimal, submandibular, sublingual, basal, palatine glands (general visceral efferent); muscles of facial expression (special visceral efferent).
Learn more about the facial nerve with our study materials.
Glossopharyngeal nerve (CN IX)
Glossopharyngeal nerve is another multimodal nerve. It originates from the brainstem and leaves the skull through the jugular foramen. Its fibers originate from four nuclei; nucleus ambiguus, inferior salivatory nucleus, nuclei of solitary tract and spinal nucleus of trigeminal nerve. This nerve enables swallowing, salivation, taste sensation and blood gas levels regulation.
Its motor fibers supply the stylopharyngeus and pharyngeal constrictors (special visceral efferent); parotid gland (general visceral efferent). Sensory fibers supply posterior one-third of the tongue (special visceral afferent); middle ear, pharynx, epiglottis, carotid body, carotid sinus (general visceral afferent); posterior one-third of the tongue and soft palate (general somatic afferent).
Learn more about the glossopharyngeal nerve here.
Vagus nerve (CN X)
Vagus nerve is also a multimodal nerve, containing somatic and visceral fibers. It originates from multiple nuclei in the brainstem, and exits the skull through the jugular foramen. Its nuclei are the posterior nucleus of vagus nerve (dorsal motor nucleus), nucleus ambiguus, nuclei of solitary tract and spinal nucleus of trigeminal nerve.
Vagus nerve provides parasympathetic supply to the thoracic and abdominal viscera and it is the only cranial nerve that leaves the head and neck region. Its motor fibers supply the thoracic and abdominal viscera (general visceral efferent); laryngeal and pharyngeal muscles (special visceral efferent). Sensory fibers supply the epiglottis (special visceral afferent); thoracic and abdominal viscera and carotid body (general visceral afferent); external acoustic meatus, retroauricular skin and posterior part of meninges (general somatic afferent).
We have covered the vagus nerve anatomy in detail here.
Mixed cranial nerves and reflexes
The corneal reflex, also called the blink reflex, is the involuntary response of blinking the eyelids when the cornea is stimulated. The trigeminal nerve comprises the afferent (sensory) limb of the corneal reflex, while the facial nerve comprises the efferent (motor) limb.
Stimulation of sensory receptors in the cornea sends signals along the ophthalmic division of the trigeminal nerve and into the brainstem. The trigeminal nerve axons descend via the spinal trigeminal tract and synapse with neurons in the pars caudalis of the spinal trigeminal nucleus. Axons from these neurons subsequently project to the contralateral VPM thalamic nucleus.
Collateral axons from pars caudalis neurons are sent bilaterally to synapse with neurons in the facial nerve motor nuclei. As part of the facial nerve, the axons of motor neurons in these nuclei exit the skull via the stylomastoid foramen, and innervate the orbicularis oculi muscles in the eyelids as part of the zygomatic branch of the facial nerve. Innervation of the orbicularis oculi muscles leads the eyes to blink. Because both left and right facial nerve motor nuclei receive input from sensory stimulation of the trigeminal nerve on either side, the corneal reflex is both direct (in the stimulated eye) and indirect (in the opposite eye, also called a consensual reflex). The blink does, however, tend to be stronger on the stimulated side.
Stimulation of the cornea, of course, is also ultimately perceived as painful; this occurs due to transmission of the noxious information via ascending fibers in the anterior trigeminothalamic tract.
The mandibular reflex, otherwise known as the jaw jerk reflex, is a version of the muscle stretch reflex mediated through the trigeminal nerve.
Tapping on the chin stretches muscle spindle fibers in the temporalis and masseter muscles, which triggers action potentials in A-alpha (primary) muscle spindle fibers and A-beta (secondary) muscle spindle fibers. These afferent fibers travel along the sensory root of the trigeminal nerve to both synapse on cell bodies in the mesencephalic nucleus, and send collaterals bilaterally to synapse on motor neurons in the trigeminal motor nuclei. As part of the motor root of the trigeminal nerve, axons of these motor neurons innervate the temporalis and masseter muscles, resulting in contraction of these muscles and closure of the jaw.
The gag reflex has an afferent limb mediated by the glossopharyngeal nerve and an efferent limb mediated by the glossopharyngeal and vagus nerves. The gag reflex allows for constriction and elevation of the pharynx in response to irritation in the back of the throat, at the base of the tongue and/or in the soft palate in the back of the roof of the mouth, functioning to push out the object that is irritating the area. These regions between the mouth and pharynx are called the fauces; for this reason, the gag reflex may also be referred to as the faucial reflex.
When there is stimulation of A-delta fibers and C fibers in the fauces, signals are sent along the glossopharyngeal nerve to cell bodies in its superior ganglion. The signals are then transmitted via interneurons to the nucleus ambiguus, the origination of the efferent limb of the reflex. Efferent signals then travel along the glossopharyngeal nerve to innervate the stylopharyngeus muscle, and along the vagus nerve to innervate the pharyngeal constrictor muscles and other muscles which move the palate.
Carotid body chemoreceptor reflex
Increase in carbon dioxide levels, decrease in oxygen levels, or alterations in pH in the blood stimulate afferent fibers in the glossopharyngeal nerve, ultimately activating reticulospinal neurons in the reticular formation. Fibers then descend in the spinal cord to synapse on ventral horn cells in the cervical spinal cord, specifically in cervical levels 3, 4, and 5.
Axons from these ventral horn cells form the phrenic nerve, which innervates the muscles of the diaphragm and causes reflex contractions of the diaphragmatic muscles. This increases respiratory rate, which ultimately reduces the amount of carbon dioxide in the blood.
The baroreceptor reflex functions to maintain a person’s blood pressure and cardiac output when mean arterial pressure changes. For example, when a person suddenly stands up from a sitting or lying position, blood pressure drops; this leads to decreased firing by receptors in the carotid body and aortic arch. Signals originating in the carotid body are transmitted by the glossopharyngeal nerve, whereas signals originating in the aortic arch are transmitted by the vagus nerve. The decreased signalling rate ultimately results in disinhibition of the sympathetic nervous system, which leads to an increase peripheral vascular tone, cardiac rate, and cardiac output.
A number of infantile reflexes are mediated by the trigeminal, facial, glossopharyngeal, and vagus nerves, as well as the hypoglossal nerve. The snout, sucking, and rooting reflexes, known as the primitive reflexes, typically disappear within the first few months of life; although they have been observed to reappear in some individuals with dementia, or degeneration or dysfunction of the frontal lobe. In infants, however, these reflexes are essential for survival by facilitating feeding.
The trigeminal nerve makes up the afferent limb of the primitive reflexes, and is activated by touching around or in the mouth. Signals travel along afferent trigeminal fibers to the spinal trigeminal ganglion in the brain stem, terminating in the spinal trigeminal nucleus and principal sensory nucleus. Fibers from these nuclei, as they travel to the VPM nucleus of the thalamus, give off collaterals which either travel directly or indirectly via interneurons to the facial nucleus, nucleus ambiguus, accessory nucleus, and hypoglossal nucleus. This leads to innervation of the infant’s facial muscles via the facial nucleus; orientation of the head toward or away from the stimulus via the accessory nucleus; and contraction of the laryngeal and pharyngeal muscles to allow for sucking via the hypoglossal nucleus.
Trigeminal neuralgia, otherwise known as tic douloureux, is a painful condition caused by irritation of the trigeminal nerve. It can occur due to infection or inflammation of the nerve, a tumor compressing the nerve, or a vascular lesion affecting blood supply to the nerve. Trigeminal neuralgia is usually associated with a specific branch of the trigeminal nerve, and therefore tends to localize to the region of the ipsilateral side of the face supplied by that branch.
Surgical removal of the parotid gland
The five terminal branches of the facial nerve–the temporal, zygomatic, buccal, marginal mandibular, and cervical branches–are closely anatomically related to the parotid gland: they emerge from the parotid gland’s upper, anterior, and lower borders. Because of this close association, removal of the parotid gland (i.e. in the removal of an adenoma or neoplasm) without damaging these branches is a particularly delicate procedure. Damage to any of these five branches would result in weakness or paralysis of the muscles supplied.
Facial nerve palsy
Facial nerve palsy can be associated with a variety of etiologies and syndromes. Additional symptoms depend on the level at which the lesion occurs. Although most facial nerve palsies are considered idiopathic, common causes include infection, trauma, iatrogenic injury, and neoplasia. The incidence of facial palsy in neonates is reported to be 0.6–1.8 per 1000 live births, but is primarily associated with forceps delivery. The incidence in adults ranges between 17-35 per 100000.
Vascular damage to the facial nerve usually occurs at the supranuclear, pontine, and (rarely) cerebellopontine angle. Upper motor neuron (UMN) lesions occur in strokes and can easily be differentiated with lower motor neuron (LMN) lesions by their presentation. A LMN lesion causes paralysis of the whole side of face, while an UMN lesion results in sparing of the forehead. The muscles in the forehead remain unaffected because they receive input from both the left and right cerebral hemispheres: input from the ipsilateral hemisphere maintains the function of the muscles in the upper face even when input from the contralateral hemisphere is lost. This is unlike the muscles in the lower part of the face, which receive input from the contralateral hemisphere only.
Lesions at the level of the geniculate ganglion typically result in weakness or paralysis of the muscles on the entire ipsilateral side of the face. Because the greater petrosal nerve and chorda tympani have not yet branched off of the facial nerve at that level, lacrimation, salivation, and taste sensation in the anterior two-thirds of the tongue are also likely to be affected.
If the facial nerve itself is damaged prior to dividing into the temporal, zygomatic, buccal, marginal mandibular, and cervical branches, the muscles of facial expression in the entire side of the face supplied by the damaged nerve may be weakened or paralyzed. This is most commonly associated with viral inflammation of the facial nerve before it exits the stylomastoid foramen. If the lesion occurs distally to the branching of the greater petrosal nerve and chorda tympani, lacrimation, salivation, and taste sensation in the anterior two-thirds of the tongue will be unaffected.
When the stapedius muscle, the nerve to stapedius, or the facial nerve is damaged, paralysis of the stapedius muscle may lead to hyperacusis. In this condition, loss of inhibition of oscillation of the stapes results in its excessive vibration: as a result, sounds that would otherwise be considered of normal volume are perceived as being uncomfortably loud.
Bell’s palsy is the most common form of peripheral facial nerve palsy. Although there is usually no detectable cause (i.e. idiopathic), some evidence suggests that latent infection with herpes simplex virus type 1 (HSV-1) plays a role, causing inflammation of the nerve and subsequent symptoms. It presents with sudden onset of impairment of facial expression, typically on one side. It is frequently preceded by periauricular paraesthesia or otalgia and may be associated with dry eyes, xerostomia, tinnitus, and hyperacusis.
Ramsay Hunt Syndrome results from reactivation of the varicella zoster virus in the geniculate ganglion. It presents as a triad of facial nerve palsy, vertigo, and vesicles in the ipsilateral external ear, palate or anterior tongue. Treatment typically consists of steroids and antivirals.
Facial nerve paralysis secondary to acute otitis media is more common in young children. The most common cause of otitis media is the gram-positive bacteria Streptococcus pneumoniae, and the majority of cases resolve with antibiotics.
Facial nerve paralysis is also a feature of skull-base osteomyelitis, a condition which occurs primarily in elderly / immunocompromised patients. The characteristic features are severe pain, aural discharge, and progressive cranial neuropathies.
As in an infant injured during a forceps delivery, facial nerve palsy in an adult can also be due to any trauma affecting the temporal bone.
Inferior medial pontine syndrome
Inferior medial pontine syndrome, also called Foville syndrome, typically occurs when there is occlusion of the paramedian branches of the basilar artery and subsequent ischemia of the medial aspect of the pons. This can result in damage to a number of structures, including:
- the corticospinal fibers, resulting in contralateral hemiplegia
- the medial lemniscus, resulting in contralateral diminution or potential loss of vibration, proprioception, and fine touch sensation;
- the PPRF, abducens nucleus, or abducens nerve, resulting in ipsilateral paralysis of the lateral rectus muscle and subsequently diplopia, or a potential loss of conjugate gaze toward the side of the lesion via interruption of communication between the abducens nucleus of one side of the brain with the oculomotor nucleus on the opposite side.
If the lesion is in the caudal pons and extends laterally, in may involve:
- the lateral lemniscus, resulting in hyperacusis
- the middle cerebellar peduncle, resulting in ataxia
- the motor nucleus of the facial cranial nerve, resulting in ipsilateral facial paralysis
- the spinal trigeminal nucleus and tract, resulting in ipsilateral loss of pain and temperature sensation in the face
- the anterolateral system resulting in contralateral loss of pain and temperature sensation in the body.
A lesion at this level resulting in corticospinal deficits on one side of the body with motor cranial nerve deficits on the opposite side of the face is referred to as a middle alternating hemiplegia.
If the lesion is in the rostral pons and extends medially, it may involve:
- the part of the medial lemniscus that contains fibers carrying sensory information from the upper extremity, leading to contralateral loss of vibration, proprioception, and fine touch sensation in the upper extremity;
- the trigeminal motor nucleus, resulting in ipsilateral paralysis of the muscles of mastication;
- the anterolateral system and parts of the spinal trigeminal tract and nucleus, resulting in contralateral loss of pain and temperature sensation in the body and ipsilateral loss of pain and temperature sensation in the face, respectively.
Glossopharyngeal neuralgia, also called glossopharyngeal tic, is a rare condition in which a person experiences idiopathic pain (i.e. pain without identifiable cause) localized to the parts of the mouth with sensory innervation from the glossopharyngeal nerve (the tonsillar area, posterior pharynx, and posterior tongue). The pain may be exacerbated by speaking or swallowing.
Lateral pontine syndrome
Occlusion of the long circumferential branches of the basilar artery and subsequent ischemia of the lateral aspect of the pons is associated with lateral pontine syndrome. This results in damage to a number of structures, including:
- the middle and superior cerebellar peduncles, resulting in ataxia and gait instabilities, with a tendency to fall toward the side of the lesion
- the vestibular and cochlear nuclei and nerves, resulting in vertigo, nausea or vomiting, nystagmus, deafness, or tinnitus
- the facial motor nucleus, resulting in ipsilateral paralysis of the muscles of facial expression
- the trigeminal motor nucleus, resulting in ipsilateral paralysis of the muscles of mastication
- descending hypothalamospinal fibers, resulting in ptosis, miosis, and anhidrosis (a.k.a. Horner syndrome)
- the anterolateral system and parts of the spinal trigeminal tract and nucleus, resulting in contralateral loss of pain and temperature sensation in the body and ipsilateral loss of pain and temperature sensation in the face, respectively
- the PPRF, resulting in loss of conjugate gaze toward the side of the lesion.
The precise constellation of symptoms observed depends significantly on whether the lesion occurs in the rostral or caudal regions of the pons. Lesions of the lateral pons and their associated clinical presentations are often referred to as Gubler syndrome, or Miller-Gubler syndrome; but basilar pontine lesions specifically involving the trigeminal root may also be referred to as mid pontine base syndrome.
Lateral medullary syndrome
Lateral medullary syndrome, otherwise known as Wallenberg syndrome, results when the posterior inferior cerebellar artery (PICA), supplying the dorsolateral medulla, is occluded. It can also occur when the vertebral artery, which supplies the PICA, is occluded. Such occlusion results in loss of blood flow, or ischemia, to the structures receiving blood supply from the PICA. Among these is the spinal trigeminal tract and nucleus, damage to which leads to loss of pain and temperature sensation in the side of the face ipsilateral to the lesion. Also damaged in this syndrome are the nucleus ambiguus, and the roots of the glossopharyngeal and vagus nerves, resulting in dysphagia, paralysis of the soft palate, hoarseness, and reduction or loss of the gag reflex.
Other symptoms of Wallenberg syndrome include:
- contralateral loss of pain and temperature sensation in the body, caused by damage to the anterolateral system
- ipsilateral Horner syndrome (i.e. miosis, ptosis, anhidrosis, and facial flushing), caused by damage to the descending hypothalamospinal tract
- nausea, diplopia, nystagmus, vertigo, and a tendency to fall toward the lesioned side, caused by damage to the vestibular nuclei
- ataxia on the side of the lesion, caused by damage to the restiform body and spinocerebellar tract.
The term syringobulbia refers to the formation of a cavity within the brainstem, typically the medulla. This may occur in addition to or as an extension of syringomyelia, a cavitation in the spinal cord, or it may occur completely on its own. While the cavity in syringomyelia usually forms in the middle of the spinal cord, the cavity in syringobulbia tends to be off to one side of the midline. Enlargement of this cavity can affect the surrounding structures.
Pressure to or damage of the hypoglossal nucleus or nerve is associated with weakened tongue muscles, leading to deviation of the tongue toward the side of the lesion upon protrusion. Pressure or damage to the nucleus ambiguus can cause weakness in the pharyngeal muscles, muscles of the palate, and vocal muscles, and presents with deviation of the uvula away from the side of the lesion. Nystagmus can result if the vestibular nuclei are affected, and damage to or pressure on the spinal trigeminal tract, nucleus, or fibers as they cross the midline can result in loss of pain and temperature sensation on the ipsilateral face.
A 67 year-old man visits his primary care physician with the complaint of fever, headache, fatigue, and a painful red rash on his face. He tells you the rash appeared only a day ago, but it was preceded by a few days of burning pain in the same region. On inspection, you note that the rash is erythematous, with a mix of fluid-filled blisters and ulcerated, crusting lesions. It is sensitive to touch, and only presents on the left upper third of his face, including his left eyelid.
Trigeminal neuralgia can have a variety of causes, one of which can be herpes zoster, otherwise known as shingles. Herpes zoster occurs in those with a history of infection with the varicella-zoster virus (VZV)–an enveloped, double-stranded DNA virus–which causes chickenpox. Chickenpox is one of the most common viral exanthems of childhood, and it is extremely virulent (i.e. infectious): by adulthood, over 95% of people will have contracted it. In a usual first infection (again, typically occurring in childhood) chickenpox is characterized by a pruritic (i.e. itchy) full-body rash of blisters, commonly described as having a “dew-drop on a rose petal” type of appearance. These blisters display what is referred to as temporal heterogeneity: new blisters erupt while old blisters simultaneously ulcerate and crust over.
In those with a history of chickenpox, the virus can enter and establish latency in the dorsal root ganglia of the spinal cord, including the trigeminal ganglia. Because of this, the virus can periodically reactivate, resulting in shingles, a painful skin rash which appears in a dermatomal distribution. Shingles occurs most frequently in those who are elderly or immunocompromised.
When trigeminal neuralgia is caused by reactivation of latent herpes zoster infection in the trigeminal ganglia, the infection and subsequent rash and other symptoms tend to primarily affect the ophthalmic branch of the trigeminal nerve. If this is the case, the condition is called ophthalmic zoster.
As of 1995, a live-attenuated chickenpox vaccine became available to the public for use in children 12 months of age and older. Although the current recommendations are that all children be vaccinated between 12 and 18 months of age with a booster vaccination between 11 and 12 years of age, adolescents and adults who have never been infected are also eligible to receive this vaccination.