Home » Themes: Trigeminal, facial and vestibular-cochlear nerves, symptoms of their lesions

Themes: Trigeminal, facial and vestibular-cochlear nerves, symptoms of their lesions

June 10, 2024

Themes: Trigeminal, facial and vestibular-cochlear nerves, symptoms of their lesions. Neuralgia of trigeminal nerve, its partial form. Neuropathy of trigeminal nerve and its branches.

The Fifth Nerve (Trigeminal Nerve)

The trigeminal nerve supplies sensation to the face, the buccal and nasal mucosa, sinuses, contents of the orbit, teeth, gums, and part of the scalp. The motor root supplies the muscles of mastication.

The trigeminal nerve (the fifth cranial nerve, also called the fifth nerve, or simply CNV) is a nerve responsible for sensation in the face and certain motor functions such as biting and chewing. It is the largest of the cranial nerves. Its name (“trigeminal” = tri- or three, and -geminus or twin, or thrice twinned) derives from the fact that each trigeminal nerve, one on each side of the pons, has three major branches: the ophthalmic nerve (V₁), the maxillary nerve (V₂), and the mandibular nerve (V₃). The ophthalmic and maxillary nerves are purely sensory. The mandibular nerve has both cutaneous and motor functions.

Sensory information from the face and body is processed by parallel pathways in the central nervous system. The motor division of the trigeminal nerve is derived from the basal plate of the embryonic pons, while the sensory division originates from the cranial neural crest.

Anatomy The trigeminal (gasserian) ganglion is located on the floor of the middle fossa and contains the unipolar cells subserving touch, pain, and temperature sensation. The peripheral fibers leaving the ganglion enter the three major subdivisions of the trigeminal nerve, the ophthalmic, maxillary, and mandibular nerves. The proximal fibers enter the lateral pons at the junction of the pons and middle cerebellar peduncle. Fibers that carry discriminatory touch information ascend and synapse in the chief sensory nucleus of the trigeminal complex. The mesencephalic nucleus contains the cells of origin subserving proprioception.

The peripheral fibers are located in the maxillary division and carry proprioceptive information from the muscles of mastication. Fibers that carry pain, temperature, and crude touch descend and synapse in the nucleus of the spinal tract of the trigeminal nerve, which extends to the upper cervical portion of the spinal cord. The nucleus of the tract is divided into three portions: the oralis, which extends from the mid-pons to olive; the interpolaris, which extends from the olive to the pyramidal decussation; and the caudalis,

which extends from the decussation to the C2 level. Axons carrying pain information synapse in the caudalis, while axons carrying temperature information synapse in all three portions. Fibers carrying crude touch information synapse in the oralis and interpolaris. Fibers from the mandibular portion of the nerve are most dorsal in the tract; fibers from the ophthalmic portion are most ventral. The maxillary fibers occupy an intermediate position. The dorsal trigeminothalamic tract arises from the chief sensory nucleus, contains crossed and uncrossed fibers, and ascends to the posteromedial ventral nucleus of the thalamus. Tertiary neurons send fibers through the posterior limb of the internal capsule to the lower one-third to one-half of the postcentral gyrus. Fibers arising in the spinal nucleus decussate and form the ventral trigeminothalamic tract, which ascends in the medial aspect of the medial lemniscus to synapse in the posteromedial ventral nucleus of the thalamus. Pain, temperature, and crude touch sensations are then relayed through the posterior limbs of the internal capsule to the postcentral portion of the parietal lobe.

The motor neurons of the motor nucleus of the trigeminal nerve lie in the midpons, central and slightly medial to the chief sensory nucleus. Axons of the motor neurons pass in the motor portion of the trigeminal nerve to exit from the pons and pass beneath the trigeminal ganglion to join the mandibular division.

The three divisions of the trigeminal nerve are distributed as follows:

1. The ophthalmic division passes along the lateral wall of the cavernous sinus, enters the orbit through the superior orbital fissure, and divides into a number of branches which supply the frontal and ethmoid sinuses, the conjunctiva, cornea, upper lid, bridge of nose, forehead, and the scalp posteriorly as far as the vertex of the skull.

2. The maxillary division enters the lateral wall of the cavernous sinus and leaves the middle cranial fossa through the foramen rotundum to enter the sphenomaxillary fossa. The nerve enters the orbit through the inferior orbital fissure, passes through the floor of the orbit in the inferior orbital canal, and emerges below the orbit through the inferior orbital foramen. The maxillary division supplies sensation to the skin of the cheek, the sphenoid and maxillary sinuses, the lateral aspect of the nose, the upper teeth, and the mucous membrane covering the nasal pharynx, hard palate, uvula, and inferior part of the nasal cavity.

3. The mandibular division leaves the middle cranial fossa through the foramen ovale accompanied by the motor branch of the trigeminal nerve. Sensory

fibers are distributed to the skin over the chin and lower jaw, extending as far back as the pinna of the ear; the anterior portion of the external auditory meatus; the anterior two-thirds of the tongue; the lower teeth; the gums and floor of the mouth; and the buccal surface of the cheek. The motor fibers supply the muscles of mastication, tensor tympani, anterior belly of the digastric, and mylohyoid.

The three major branches of the trigeminal nerve, the ophthalmic nerve (V₁), the maxillary nerve (V₂), and the mandibular nerve (V₃) converge on the trigeminal ganglion (also called the semilunar ganglion or gasserian ganglion), located within Meckel’s cave, and contains the cell bodies of incoming sensory nerve fibers. The trigeminal ganglion is analogous to the dorsal root ganglia of the spinal cord, which contain the cell bodies of incoming sensory fibers from the rest of the body.

From the trigeminal ganglion, a single large sensory root enters the brainstem at the level of the pons. Immediately adjacent to the sensory root, a smaller motor root emerges from the pons at the same level.

Motor fibers pass through the trigeminal ganglion on their way to peripheral muscles, but their cell bodies are located in the nucleus of the fifth nerve, deep within the pons.

Dermatome distribution of the trigeminal nerve

The areas of cutaneous distribution (dermatomes) of the three branches of the trigeminal nerve have sharp borders with relatively little overlap (unlike dermatomes in the rest of the body, which show considerable overlap). Injection of local anesthetics such as lidocaine results in the complete loss of sensation from well-defined areas of the face and mouth. For example, the teeth on one side of the jaw can be numbed by injecting the mandibular nerve. Occasionally, injury or disease processes, though, may affect two or all three branches of the trigeminal nerve, and in these cases the involved branches may be termed:

V1/V2 distribution – referring to the ophthalmic and maxillary branches
V2/V3 distribution – referring to the maxillary and mandibular branches
V1-V3 distribution – referring to all three branches

Notably, nerves on the left side of the jaw outnumber slightly the number of nerves on the right side of the jaw.

Sensory branches of the trigeminal nerve

Dermatome distribution of the trigeminal nerve

The ophthalmic, maxillary and mandibular branches leave the skull through three separate foramina: the superior orbital fissure, the foramen rotundum and the foramen ovale. The mnemonic standing room only can be used to remember that V₁ passes through the superior orbital fissure, V₂ through the foramen rotundum, and V₃ through the foramen ovale.

The ophthalmic nerve (V₁) carries sensory information from the scalp and forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose (including the tip of the nose, except alae nasi), the nasal mucosa, the frontal sinuses, and parts of the meninges (the dura and blood vessels).

The maxillary nerve (V₂) carries sensory information from the lower eyelid and cheek, the nares and upper lip, the upper teeth and gums, the nasal mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses, and parts of the meninges.

The mandibular nerve (V₃) carries sensory information from the lower lip, the lower teeth and gums, the chin and jaw (except the angle of the jaw, which is supplied by C2-C3), parts of the external ear, and parts of the meninges. The mandibular nerve carries touch/position and pain/temperature sensation from the mouth. It does not carry taste sensation (chorda tympani is responsible for taste), but one of its branches, the lingual nerve, carries multiple types of nerve fibre that do not originate in the mandibular nerve.

Motor branches of the trigeminal nerve

Motor branches of the trigeminal nerve are distributed in the mandibular nerve. These fibers originate in the motor nucleus of the fifth nerve, which is located near the main trigeminal nucleus in the pons. Motor nerves are functionally quite different from sensory nerves, and their association in the peripheral branches of the mandibular nerve is more a matter of convenience than of necessity.

In classical anatomy, the trigeminal nerve is said to have general somatic afferent (sensory) components, as well as special visceral efferent (motor) components. The motor branches of the trigeminal nerve control the movement of eight muscles, including the four muscles of mastication.

Muscles of mastication

Others

tensor veli palatini

mylohyoid

anterior belly of digastric

tensor tympani

With the exception of tensor tympani, all of these muscles are involved in biting, chewing and swallowing. All have ‘bilateral’ cortical representation. A unilateral central lesion (e.g., a stroke), no matter how large, is unlikely to produce any observable deficit. Injury to the peripheral nerve can cause paralysis of muscles on one side of the jaw. The jaw deviates to the paralyzed side when it opens. This direction of the mandible is due to the action of normal pterygoids on the opposite side.

Central anatomy

Sensation

The two basic types of sensation are touch/position and pain/temperature. They are distinguished, roughly speaking, by the fact that touch/position input comes to attention immediately, whereas pain/temperature input reaches the level of consciousness only after a perceptible delay. When stepping on a pin, awareness of stepping on something is immediate, but the pain associated with it is delayed.

In general, touch/position information is carried by myelinated (fast-conducting) nerve fibers, whereas pain/temperature information is carried by unmyelinated (slow-conducting) nerve fibers. The primary sensory receptors for touch/position (Meissner’s corpuscles, Merkel’s receptors, Pacinian corpuscles, Ruffini’s corpuscles, hair receptors, muscle spindle organs, and Golgi tendon organs) are structurally more complex than the primitive receptors for pain/temperature, which are bare nerve endings.

The term “sensation”, as used in this article, refers to the conscious perception of touch/position and pain/temperature information. It does not refer to the so-called “special senses” (smell, sight, taste, hearing and balance), which are processed by different cranial nerves and sent to the cerebral cortex through different pathways. The perception of magnetic fields, electrical fields, low-frequency vibrations and infrared radiation by certaionhuman vertebrates is processed by the equivalent of the fifth cranial nerve in these animals.

The term “touch”, as used in this article, refers to the perception of detailed, localized tactile information, such as “two-point discrimination” (the difference between touching one point and two closely spaced points) or the difference between grades of sandpaper (coarse, medium and fine). People who lack touch/position perception can still “feel” the surface of their bodies, and can therefore perceive “touch” in a crude, yes-or-no way, but they lack the rich perceptual detail others normally experience.

The term “position”, as used in this article, refers to conscious proprioception. Proprioceptors (muscle spindle organs and Golgi tendon organs) provide information about joint position and muscle movement. Much of this information is processed at an unconscious level (mainly by the cerebellum and the vestibular nuclei). However, some of this information is available at a conscious level.

The two types of sensation in humans, touch/position and pain/temperature, are processed by different pathways in the central nervous system. The distinction is hard-wired, and it is maintained all the way to the cerebral cortex. Within the cerebral cortex, sensations are further hard-wired to (associated with) other cortical areas.

Sensory pathways

Sensory pathways from the periphery to the cortex are summarized below. Pathways are separate for touch/position sensation and pain/temperature sensation. All sensory information is sent to specific nuclei in the thalamus. Thalamic nuclei, in turn, send information to specific areas in the cerebral cortex.

Each pathway consists of three bundles of nerve fibers, connected in series:

The ‘secondary’ neurons in each pathway decussate (cross to the other side of the spinal cord or brainstem), because the spinal cord initially forms segmentally. Later on, decussated fibres reach and connect these segments with the higher centres. The main reason for decussation is the optic chiasma occurs (nasal fibres of the optic nerve cross so each cerebral hemisphere receives the contralateral vision) to keep interneuronal connections short (responsible for processing of information), and all sensory and motor pathways converge and diverge respectively to the contralateral hemisphere.

Sensory pathways are often depicted as chains of ‘individual’ neurons connected in series; this is an oversimplification. Sensory information is processed and modified at each level in the chain by interneurons and by input from other areas of the nervous system. For example, cells in the main trigeminal nucleus (“Main V” in the diagram) receive input (not shown) from the reticular formation and from the cerebral cortex. This information contributes to the final output of the cells in Main V to the thalamus.

Touch/position information from the body is carried to the thalamus by the medial lemniscus; this information from the face is carried to the thalamus by the trigeminal lemniscus. Pain/temperature information from the body is carried to the thalamus by the spinothalamic tract; this information from the face is carried to the thalamus by the trigeminothalamic ‘ (or quintothalamic) tract.

Pathways for touch/position sensation from the face and body merge in the brainstem. A single touch/position sensory map of the entire body is projected onto the thalamus. Likewise, pathways for pain/temperature sensation from the face and body merge in the brainstem. A single pain/temperature sensory map of the entire body is projected onto the thalamus.

From the thalamus, touch/position and pain/temperature information is projected onto various areas of the cerebral cortex. Exactly where, when, and how this information becomes conscious is entirely beyond our understanding at present. The explanation of consciousness is one of the great unsolved mysteries in science.

The details of the pathways connecting the lower body to the cerebral cortex are beyond the scope of this article. The details of the pathways connecting the face and mouth to the cerebral cortex are discussed below.

Trigeminal nucleus

Brainstem nuclei: Red = Motor; Blue = Sensory; Dark Blue = Trigeminal Nucleus

It is not widely appreciated that all sensory information from the face (all touch/position information and all pain/temperature information) is sent to the trigeminal nucleus. In classical anatomy, most sensory information from the face is carried by the fifth nerve, but sensation from certain parts of the mouth, certain parts of the ear and certain parts of the meninges is carried by “general somatic afferent” fibers in cranial nerves VII (the facial nerve), IX (the glossopharyngeal nerve) and X (the vagus nerve).

Without exception, however, all sensory fibers from these nerves terminate in the trigeminal nucleus. On entering the brainstem, sensory fibers from V, VII, IX, and X are sorted out and sent to the trigeminal nucleus, which thus contains a complete sensory map of the face and mouth. The spinal counterparts of the trigeminal nucleus (cells in the dorsal horn and dorsal column nuclei of the spinal cord) contain a complete sensory map of the rest of the body.

The trigeminal nucleus extends throughout the entire brainstem, from the midbrain to the medulla, and continues into the cervical cord, where it merges with the dorsal horn cells of the spinal cord. The nucleus is divided anatomically into three parts, visible in microscopic sections of the brainstem. From caudal to rostral (i.e., going up from the medulla to the midbrain) they are the spinal trigeminal nucleus, the main trigeminal nucleus, and the mesencephalic trigeminal nucleus.

The three parts of the trigeminal nucleus receive different types of sensory information. The spinal trigeminal nucleus receives pain/temperature fibers. The main trigeminal nucleus receives touch/position fibers. The mesencephalic nucleus receives proprioceptor and mechanoreceptor fibers from the jaws and teeth.

Spinal trigeminal nucleus

The spinal trigeminal nucleus represents pain/temperature sensation from the face. Pain/temperature fibers from peripheral nociceptors are carried in cranial nerves V, VII, IX, and X. On entering the brainstem, sensory fibers are grouped together and sent to the spinal trigeminal nucleus. This bundle of incoming fibers can be identified in cross sections of the pons and medulla as the spinal tract of the trigeminal nucleus, which parallels the spinal trigeminal nucleus itself. The spinal tract of V is analogous to, and continuous with, Lissauer’s tract in the spinal cord.

The spinal trigeminal nucleus contains a pain/temperature sensory map of the face and mouth. From the spinal trigeminal nucleus, secondary fibers cross the midline and ascend in the trigeminothalamic (quintothalamic) tract to the contralateral thalamus. Pain/temperature fibers are sent to multiple thalamic nuclei. As discussed below, the central processing of pain/temperature information is markedly different from the central processing of touch/position information.

Somatotopic representation

Onion skin distribution of the trigeminal nerve

Exactly how pain/temperature fibers from the face are distributed to the spinal trigeminal nucleus has been a subject of considerable controversy. The present understanding is that all pain/temperature information from all areas of the human body is represented (in the spinal cord and brainstem) in an ascending, caudal-to-rostral fashion. Information from the lower extremities is represented in the lumbar cord. Information from the upper extremities is represented in the thoracic cord. Information from the neck and the back of the head is represented in the cervical cord. Information from the face and mouth is represented in the spinal trigeminal nucleus.

Within the spinal trigeminal nucleus, information is represented in an onion skin fashion. The lowest levels of the nucleus (in the upper cervical cord and lower medulla) represent peripheral areas of the face (the scalp, ears and chin). Higher levels (in the upper medulla) represent more central areas (nose, cheeks, lips). The highest levels (in the pons) represent the mouth, teeth, and pharyngeal cavity.

The onion skin distribution is entirely different from the dermatome distribution of the peripheral branches of the fifth nerve. Lesions that destroy lower areas of the spinal trigeminal nucleus (but which spare higher areas) preserve pain/temperature sensation in the nose (V₁), upper lip (V₂) and mouth (V₃) while removing pain/temperature sensation from the forehead (V₁), cheeks (V₂) and chin (V₃). Analgesia in this distribution is “nonphysiologic” in the traditional sense, because it crosses over several dermatomes. Nevertheless, analgesia in exactly this distribution is found in humans after surgical sectioning of the spinal tract of the trigeminal nucleus.

The spinal trigeminal nucleus sends pain/temperature information to the thalamus. It also sends information to the mesencephalon and the reticular formation of the brainstem. The latter pathways are analogous to the spinomesencephalic and spinoreticular tracts of spinal cord, which send pain/temperature information from the rest of the body to the same areas. The mesencephalon modulates painful input before it reaches the level of consciousness. The reticular formation is responsible for the automatic (unconscious) orientation of the body to painful stimuli.

Main trigeminal nucleus

The main trigeminal nucleus represents touch/position sensation from the face. It is located in the pons, close to the entry site of the fifth nerve. Fibers carrying touch/position information from the face and mouth (via cranial nerves V, VII, IX, and X) are sent to the main trigeminal nucleus when they enter the brainstem.

The main trigeminal nucleus contains a touch/position sensory map of the face and mouth, just as the spinal trigeminal nucleus contains a complete pain/temperature map. The maiucleus is analogous to the dorsal column nuclei (the gracile and cuneate nuclei) of the spinal cord, which contain a touch/position map of the rest of the body.

From the main trigeminal nucleus, secondary fibers cross the midline and ascend in the trigeminal lemniscus to the contralateral thalamus. The trigeminal lemniscus runs parallel to the medial lemniscus, which carries touch/position information from the rest of the body to the thalamus.

Some sensory information from the teeth and jaws is sent from the main trigeminal nucleus to the ipsilateral thalamus, via the small dorsal trigeminal tract. Thus touch/position information from the teeth and jaws of one side of the face is represented bilaterally in the thalamus (and hence in the cortex). The reason for this special processing is discussed below.

Mesencephalic trigeminal nucleus

The mesencephalic trigeminal nucleus is not really a “nucleus”; rather, it is a sensory ganglion (like the trigeminal ganglion) that happens to be embedded in the brainstem. The mesencephalic “nucleus” is the sole exception to the general rule that sensory information passes through peripheral sensory ganglia before entering the central nervous system.

Only certain types of sensory fibers have cell bodies in the mesencephalic nucleus: proprioceptor fibers from the jaw and mechanoreceptor fibers from the teeth. Some of these incoming fibers go to the motor nucleus of V, thus entirely bypassing the pathways for conscious perception. The jaw jerk reflex is an example. Tapping the jaw elicits a reflex closure of the jaw, in exactly the same way that tapping the knee elicits a reflex kick of the lower leg. Other incoming fibers from the teeth and jaws go to the maiucleus of V. As noted above, this information is projected bilaterally to the thalamus. It is available for conscious perception.

Activities such as biting, chewing and swallowing require symmetrical, simultaneous coordination of both sides of the body. They are essentially automatic activities, requiring little conscious attention. They involve a sensory component (feedback about touch/position), processed at a largely unconscious level.

The unusual anatomy of “mesencephalic V” has been found in all vertebrates, with the exception of lampreys and hagfishes. Lampreys and hagfishes are the only vertebrates without jaws. Information about biting, chewing and swallowing evidently is singled out for special processing in the vertebrate brainstem, specifically in the mesencephalic nucleus.

Pathways to the thalamus and the cortex

Sensation has beed defined herein as the conscious perception of touch/proprioception and pain/temperature information. With the sole exception of smell, all sensory input (touch/position, pain/temperature, sight, taste, hearing, and balance) is sent to the thalamus before being sent to the cortex.

The thalamus is anatomically subdivided into a number of separate nuclei. The thalamic nuclei involved in sensation, and their cortical projections, are discussed below.

Touch/position sensation

The sensory homunculus

Touch/position information from the body is sent to the ventral posterolateral nucleus (VPL) of the thalamus. Touch/position information from the face is sent to the ventral posteromedial nucleus (VPM) of the thalamus. From the VPL and VPM, information is projected to the primary sensory cortex (SI) in the postcentral gyrus of the parietal lobe.

The representation of sensory information in SI is organized somatotopically. Adjacent areas in the body are represented by adjacent areas in the cortex. When body parts are drawn in proportion to the density of their innervation, however, the result is a strangely distorted “little man”, the sensory homunculus.

Many textbooks reproduce the classic Penfield-Rasmussen diagram, which is now outdated. For example, the toes and genitals are shown in the classic diagram on the mesial surface of the cortex, when in fact they are represented on the convexity.^[5] What is more important, the classic diagram implies a single primary sensory map of the body, when in fact there are multiple primary maps. At least four separate, anatomically distinct sensory homunculi have been identified in SI. They represent different blends of input from surface receptors, deep receptors, rapidly adapting receptors, and slowly adapting peripheral receptors. For example, smooth objects will activate certain cells, whereas edged objects will activate other cells.

Information from all four maps in the SI is sent to the secondary sensory cortex (SII) in the parietal lobe. SII contains two more sensory homunculi.

In general, information from one side of the body is represented on the opposite side in SI, but on both sides in SII. Functional MRI imaging of a defined stimulus (e.g., stroking the skin with a toothbrush) “lights up” a single focus in SI and two foci in SII.

Pain/temperature sensation

Pain/temperature information is sent to the VPL (body) and VPM (face) of the thalamus (the same nuclei that receive touch/position information). From the thalamus, pain/temperature and touch/position information is projected onto SI.

In marked contrast to touch/position information, however, pain/temperature information is also sent to other thalamic nuclei, and is projected onto additional areas of the cerebral cortex. Some pain/temperature fibers are sent to the medial dorsal thalamic nucleus (MD), which projects to the anterior cingulate cortex. Other fibers are sent to the ventromedial (VM) nucleus of the thalamus, which projects to the insular cortex. Finally, some fibers are sent to the intralaminar (IL) nuclei of the thalamus via the reticular formation. The IL project diffusely to all parts of the cerebral cortex.

The insula and cingulate cortex are areas of the brain that represent our perception of touch/position and pain/temperature in the context of other simultaneous perceptions (sight, smell, taste, hearing and balance), and in the context of our memories and present emotional state. It is noteworthy that peripheral pain/temperature information is channeled directly into the brain at these deep levels, without prior processing. This contrasts markedly with the way that touch/position information is handled.

Diffuse thalamic projections from the IL and other thalamic nuclei are responsible for one’s overall level of consciousness. The thalamus and reticular formation “activate” the entire brain. It is noteworthy that peripheral pain/temperature information feeds directly into this system as well.

Examination of the Trigeminal Nerve

Examination of the trigeminal nerve includes evaluation of the corneal reflex, sensation over the face and scalp, motor function, and the jaw jerk.

CORNEAL REFLEX This reflex is tested by the light application of cotton to the cornea. The examiner takes a cotton applicator and pulls the cotton head into a fine point. The patient is asked to look upward, and the cotton is brought toward the eye from a lateral position and gently applied to the cornea (Fig. 1-10). Application should produce a prompt bilateral reflex closure of the eyelids. The response is compared on the two sides, and the patient is asked whether the sensation appears to be equal on the two sides. The afferent loop of this reflex is via the ophthalmic division of the trigeminal nerve. The efferent side of the reflex is conducted through the facial nerve.

SENSATION OVER THE FACE AND SCALP

The patient is asked to close the eyes and to respond if touched. The cotton is applied to the forehead on one side, followed by application to the forehead in a similar position on the other side, then to the cheeks on the two sides, then to the jaws on the two sides. The patient’s responses are monitored, and the patient is asked whether the sensation appears to be equal on the two sides of the face. The same test is then repeated using a sharp pin with gentle application in the ophthalmic, maxillary, and mandibular area, alternating between the two sides. The examiner then touches each cheek simultaneously with a sharp pin (Fig. 1-11) and asks the patient to identify the site of pinpricks. The correct answer—both sides. There may be failure of appreciation of pinprick on one side even though the patient has appreciated pinprick when applied unilaterally to the face. The phenomenon termed extinction occurs occasionally in early lesions affecting the opposite parietal lobe or the thalamoparietal connections.

MOTOR function

The examiner places the fingers over the temporalis muscles and asks the patient to clench the teeth or bite. The temporalis muscles will be felt to contract under the examiner’s hands on both sides. A similar maneuver is performed with the fingers over the masseter muscles (Fig 1-12). The pterygoids can be tested by having the patient deviate the jaw to one side against resistance In unilateral lesions the jaw deviates toward the side of the lesion.

JAW jerk The jaw jerk is tested by lightly tapping the anterior, lower jaw with the reflex hammer (Fig. 1-13). Normally, there is a slight upward movement of the mandible. The jaw jerk is increased in destructive or compressive lesions involving the corticopontine pathways and is discussed in more detail below.

Signs of lesion V nerve (trigeminal)

l facial pain

l sensory disturbance in the face

l corneal reflex is decreased or absent

l temporal and masseter muscles are atrophic or hypotrophic, atonic or hypotonic

l jaw is seen to deviated toward the side of the weakened muscle

The Seventh Nerve (Facial Nerve)

The seventh nerve innervates the facial muscles and supplies taste sensation to the anterior two-thirds of the tongue and general sensation to a small portion of the external ear.

Anatomy

The motor neurons of the seventh nerve are located in the facial nucleus in the tegmentum of the pons. The motor fibers pass dorsally and medially from the nucleus, loop around the nucleus of the sixth cranial nerve, and then proceed in a ventrolateral and caudal direction to emerge at the lateral pontomedullary junction. The Facial nerve immediately enters the internal auditory meatus in association with the eighth cranial nerve. The seventh nerve leaves the internal auditory canal, enters the facial canal, and passes through the facial canal to emerge through the stylomastoid foramen at the inferior border of the temporal bone. The nerve then penetrates the parotid gland and divides into several branches, which supply the muscles of the face, the stylohyoid, the buccinator, the posterior belly of the digastric muscle, and the platysma. The facial nerve also gives off a branch to the stapedius muscle in the facial canal.

The Facial nerve carries parasympathetic motor fibers that arise from the superior salivatory nucleus in the pons. These fibers leave the facial nerve via the greater superficial petrosal nerve and pass to the sphenopalatine ganglion. The postganglionic fibers innervate the glands and mucous membranes of the palate, nasopharynx, and paranasal sinuses. The remaining parasympathetic fibers leave the facial nerve via the chorda tympani and terminate in the submaxillary ganglion. Postganglionic fibers innervate the sublingual and submaxillary salivary glands.

The sensory neurons of the seventh nerve are located in the geniculate ganglion, which is situated in the proximal portion of the facial canal. The peripheral branches of these nerve cells transmit taste sensation from the anterior two-thirds of the tongue and reach the geniculate ganglion via the lingual nerve, chorda tympani, and a short portion of the facial nerve. The central branches pass from the geniculate ganglion, form a separate bundle called the nerve of Wrisberg, enter the pons, and terminate in the nucleus of the tractus solitarius.

The Facial nerve has a relatively small general somatic sensory component. These sensory fibers supply sensation to a small portion of the external ear, and the impulses are transmitted to the unipolar cells in the geniculate ganglion and through the Facial nerve into the pons.

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Examination of the Facial Nerve

The patient is asked to contract the facial muscles and show the teeth. The contraction should be symmetrical on the two sides and simultaneously performed. The patient is then asked to close the eyes tightly and the examiner attempts to open the lids (Fig. 1-14). Normally this is not possible even when the examiner uses considerable force. Finally, the patient is asked to wrinkle the forehead in an upward direction. Again, this should be symmetrical on the two sides.

Two types of facial weakness may be observed:

1. Upper motor neuron lesions involving the corticobulbar pathways will produce weakness of the lower portion of the face with normal function when the patient is asked to wrinkle the forehead. The lower portion of the face has unilateral innervation from cortical centers, while the forehead is bilaterally innervated from cortical centers.

2. Involvement of the facial nucleus in the pons or the facial nerve will produce total involvement of the facial muscles on the same side, and the lower facial muscles and forehead are equally involved in the process.

There are three forms of taste sensation: sweet, sour, and bitter. The sense of taste is tested by placing a test substance, sugar (sweet), vinegar (sour), or quinine (bitter), on the tongue. The test is best conducted by asking the patient to protrude the tongue, exposing one side. The side of the tongue is then dried and the test substance that has been prepared in solution is gently applied with a cotton applicator. The patient signals when the test substance is identified and can then draw the tongue back into the mouth and verbally identify the solution.

Signs of lesion of the VII nerve (Facial)

l Facial asymmetry

l patient can’t wrinkle the forehead, close eyes, purse the lips, retract the buccal angles in a smile

l impairment of taste on the anterior two third of the tongue

l Bell’s symptom

l corneal reflex is decreased or absent

Alternate pond’ syndromes:

Raymond syndrome – a fallout of sensation on the face according to the segmental type on the side of the lesion both fallout pain and thermoesthesia on a trunk and extremities on opposite side.

Miyar-Gubler syndrome – peripheral palsy of the facial muscles on the site of the lesion and a contralateral hemiplegia.

Fovill syndrome – peripheral palsy of the facial muscles and the external rectus eyes’ muscle on the site of the lesion and a contralateral hemiplegia.

Fig. Peripheral paresis of right mimic musles $F:\Заняття_4_Каудальна_група_ЧМН_Нейропатія.files\image071.jpg$

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Fig. Examination of taste on the tounge $F:\Заняття_4_Каудальна_група_ЧМН_Нейропатія.files\image081.gif$

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Fig. Examination of m. buccalis

The Eighth Nerve (Acoustic Nerve)

The eighth nerve, or acoustic nerve, is a compound nerve with two divisions: the cochlear, subserving hearing, and the vestibular, subserving motion, balance, and an awareness of position in space.

Anatomy

THE COCHLEAR NERVE

The ganglion cells in the spiral ganglia of the cochlea have short peripheral and long central processes. The peripheral processes terminate around the hair cells of the organ of Corti, while the central processes pass to the cochlear nuclei in the brainstem. The cochlear nerve and the vestibular nerve form a common trunk, the acoustic nerve, which is closely related to the facial nerve in the internal auditory meatus. The two divisions of the acoustic nerve separate, and the cochlear nerve enters the brainstem lateral to the vestibular nerve at the junction of the pons and medulla. On entering the pons, the cochlear nerve divides, and fibers synapse in the dorsal and ventral cochlear nuclei.

Axons from cells in the ventral cochlear nucleus enter the trapezoid body and pass to the contralateral lateral lemniscus and medial longitudinal fasciculus and to the ipsilateral superior olivary nucleus and then to the medial longitudinal fasciculus and the nucleus of the sixth cranial nerve.

Axons from neurons in the dorsal cochlear nucleus cross the midline immediately below the fourth ventricle and enter the contralateral lateral lemniscus. The lateral lemniscus is a multisynaptic pathway, and the fibers within the structure may synapse as they pass through the pons and lower midbrain and ascend to the inferior colliculus. Several commissural connections cross between the two lateral lemnisci. The inferior colliculus is a relay station in the auditory pathway, which may also be concerned with the interpretation of sound stimuli. Consequently, the majority of fibers from the lateral lemniscus enter and synapse with cells in the inferior colliculus, while a few fibers bypass the inferior colliculus and enter the brachium of the medial geniculate to terminate ieurons within this latter structure. Fibers arising from neurons in the inferior colliculus also terminate in the medial geniculate body.

The axons of neurons within the medial geniculate body form the auditory radiation, which passes through the sublenticular portion of the posterior limb of the internal capsule to the superior transverse temporal gyri. These structures constitute the primary auditory reception areas of the cerebral cortex and are located on the opercular surface of the superior temporal gyrus.

THE VESTIBULAR NERVE

The vestibular ganglion is attached to the vestibular nerve and is situated just within the internal auditory meatus. The ganglion contains bipolar cells with peripheral processes distributed to the maculae of the utricle and saccule and to the ampullae of the superior, lateral, and posterior semicircular canals. The central processes form the vestibular nerve, which accompanies the cochlear nerve and enters the brainstem. The vestibular nerve then passes dorsomedially between the inferior cerebellar peduncle and the spinal tract of the fifth cranial nerve to reach the vestibular nuclei. The vestibular nuclei consist of four separate structures: the medial vestibular nucleus, which extends from mid medulla to the inferior pons forming the vestibular area of the fourth ventricle; the lateral vestibular nucleus, which extends from the medulla, caudally, to the level of the sixth cranial nerve in the pons; the inferior (spinal) vestibular nucleus, located almost entirely within the medulla; and the superior vestibular nucleus, which is situated in the floor of the fourth ventricle and extends through the pons into the lower portion of the midbrain.

Efferent fibers from the vestibular nuclei pass to the medial longitudinal fasciculus, which brings the vestibular system into communication with other cranial nerve nuclei. Other fibers enter the pontine reticular formation or descend into the upper spinal cord to communicate with motor neurons. There are additional connections to the cerebellum and an ascending fiber system, which takes an unknown course and terminates in the temporal cortex in the posterior aspects of the superior temporal gyrus.

Tests of Auditory Function

Testing for hearing at the bedside is inaccurate. Audiograms should be obtained in all cases where there is doubt about the patient’s ability to hear properly.

Conduction tests are useful, however, because in the normal state, air conduction is much more sensitive than bone conduction. Testing is carried out b} placing a tuning fork over the mastoid process am asking the patient to indicate when the sound is m longer audible (Fig. 1-15). At this point the fork i placed at the level of the external auditory meatus an the patient is asked whether the sound is audible. Ur der normal circumstances this will be so, because a conduction is better than bone conduction.

This test the Rinne test, is said to be positive when air condu tion is more sensitive than bone conduction. In cone tions where bone conduction is more sensitive th; air conduction, the Rinne test is negative. This inc cates some obstruction of transmission of sound 1 disease involving the external auditory meatus, su as foreign bodies or wax, some malfunction of t drum, or some malfunction of the middle ear. D eases of the cochlea or cochlear nerve produce i pairment of hearing, and both air and bone condition are diminished, but the Rinne test rema positive.

The examination continues with the perl mance of the Weber test, in which the tuning forl placed on the center of the forehead and the pati is asked to indicate the location of the sound (1 1-16). This will usually be heard equally in both < or appreciated at the site of the tuning fork on forehead. When there is impairment of air conduc on one side, the Weber lateralizes to that ear. On other hand, if there is disease of the cochle; cochlear nerve, the Weber will lateralize to the opposite the diseased ear.

Test of Vestibular Function

The vestibular system is an extremely sensitive system, and disturbances of function of the vestibular system oi vestibular division of the eighth nerve are accounted by vertigo. Vertigo is a sensation of movement which objects seem to be moving in a rotating ion around the subject or when the subject has; lusion of rotation. Occasionally vertigo may pr with an illusion of tilting of objects in a horizon vertical plane without a rotary component. Vertigo: always accompanied by nystagmus because c connections between the vestibular system and fourth, and sixth nerves via the medial longitudinalis fasciculus. This anatomical pathway can be test follows.

BARANY TEST

Labyrinthine nystagmus may be induced by rotating the subject in a Barany chair. The patient’s eyes are closed and the head is inclined forward 30° to test the lateral semicircular canal, or extended backward 60° to test the anterior canal. Under these circumstances, the canal to be tested is in the horizontal plane. The chair is then rotated 10 times in 20 s, which produces stimulation of the cristae in the canal. When the movement of the chair is stopped, the inertia of the endolymph continues to stimulate the cristae, producing a sensation of vertigo in the direction opposite to the previous rotation of the chair. This is accompanied by nystagmus, past-pointing, and deviation of the eyes in the direction of the previous rotation. The sensation of vertigo usually lasts about 35 s under normal circumstances. Vertigo is reduced in disease of the stimulated canal or vestibular nerve. The vertigo may be increased in certain conditions that produce dysfunction of the vestibular system.

CALORIC TESTING

Caloric testing can be performed by tilting the head of a supine patient forward 30° and irrigating the external auditory canal of one side with 10 to 15 mL of iced water or warm water for 30 s. The larger volume should be used in testing comatose individuals for presence or absence of brainstem function. The effect of caloric stimulation is reduced in disease of the external auditory canal, the vestibular apparatus or the vestibular nerve, and the central connections.

Trigeminal Neuralgia (Tic Douloureux)

Definition Trigeminal neuralgia is a condition characterized by sudden, severe, lancinating pain occurring in the distribution of the trigeminal nerve.

Etiology and Pathology Trigeminal neuralgia is probably syndromic and may be due to:

1. Degenerative changes in the trigeminal (gasserian) ganglion, producing paroxysmal discharge of neurons.

2. Pressure on the trigeminal nerve root by an aberrant or arteriosclerotic vessel, by a tumor, particularly a meningioma located in the posterior fossaor by displacement of the brainstem by a contralateral tumor with compression of the trigeminal nerve against a bony structure.

3. Increased angulation of the nerve root over the petrous bone caused by demineralization at the base of the skull in the elderly with upward movement of the petrous pyramid.

4. Demyelination of the most proximal portion of the trigeminal nerve root or demyelination affecting the spinal tract in the brainstem in patients with multiple sclerosis. (A similar condition occurs in patients with tabes dorsalis).

5. Familial trigeminal neuropathy has been described in the setting of hereditary peripheral neuropathies, especially HMSN type I, Charcot-Marie-Tooth disease.

6. Paroxysmal discharges of the neurons of the spinal nucleus of the trigeminal nerve. (This concept suggests that trigeminal neuralgia is a form of seizure activity occurring at the brainstem level secondary to degenerative or vascular changes affecting the neurons of the spinal nucleus.)

Trigeminal neuralgia is a neuropathic pain syndrome and one of the most common causes of facial pain, typically affecting patients older than 50 years
Disorder involving one or more sensory divisions of trigeminal nerve that often produces unilateral, abrupt, brief but severe lancinating pain, which becomes more frequent over time; successive occurrences can lead to incapacitation
Pain may arise spontaneously but is often associated with particular triggers such as sensory stimulus to face
Most patients respond well to pharmacologic therapy; those who do not may require surgical intervention

Description

Trigeminal neuralgia is a prototypic neuropathic pain syndrome and one of the most common causes of facial pain
Typically affects patients older than 50 years
Disorder involving one or more sensory divisions of the trigeminal nerve that often produces brief but severe lancinating pain
Attacks are abrupt but brief, lasting only seconds but becoming more frequent over time; successive occurrences can lead to incapacitation
Facial pain is unilateral, and pain is generally limited to distribution of trigeminal nerve
Pain may arise spontaneously but is often associated with particular triggers such as sensory stimulus to face
Pain episode is typically triggered by facial touching but also chewing or talking
Following a paroxysm of pain, refractory period occurs during which pain cannot be triggered
Constant, dull pain can develop between bouts of acute pain
Pain only rarely occurs during sleep
Pathophysiology of trigeminal neuralgia is not well understood, but many cases are hypothesized to be the result of compression of trigeminal nerve root near dorsal root entry zone
Neurologic examination often shows no abnormalities except in cases in which there is an underlying lesion
Carbamazepine is effective initial treatment in most cases
Referral to neurologist or neurosurgeon is necessary if diagnosis is difficult or if pain is refractory to pharmacologic treatment

Classification:

Trigeminal neuralgia may be classified either as classic or secondary
Classic trigeminal neuralgia includes all cases for which no definite etiology can be found or those that may have vascular anomaly compressing nerve
Secondary trigeminal neuralgia are those cases caused by underlying structural lesion excluding vascular compression
Pain of secondary trigeminal neuralgia is indistinguishable from classic trigeminal neuralgia except for absence of a refractory period
Secondary trigeminal neuralgia may have accompanying sensory loss of masticatory weakness

International Headache Society Classification:

A. Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting one or more divisions of trigeminal nerve and fulfilling criteria B and C
B. Pain has at least one of the following characteristics:

Intense, sharp, superficial, or stabbing
Precipitated from trigger areas or trigger factors

C. Attacks are stereotyped in individual patient
D. There is no clinically evident neurologic deficit
E. Not attributable to another disorder

Epidemiology

Incidence and prevalence:

Incidence is 12.6 per 100,000 person years in U.S.
Prevalence is 155 cases/1,000,000 in U.S.

Demographics:

Predominantly found in those older than 50 years
Female to male ratio about 3:2
No significant genetic associations have been identified; clustering within families is rarely found

Causes and risk factors

Common causes:

There is no single pathophysiology for trigeminal neuralgia. Known causes include focal demyelination of trigeminal nerve or ganglia, and extrinsic and intrinsic tumors that lie near the Gasserian ganglia
Most cases of classic or ‘idiopathic’ trigeminal neuralgia are probably due to an anomalous blood vessel impinging on trigeminal nerve root near dorsal root entry zone. This state is referred to as microvascular compression
Mechanism of pain is postulated to be result of compression producing demyelination of afferent trigeminal nerve fibers leading to ephaptic transmission between light touch and pain fibers

Rare causes:

Secondary causes include aneurysm, syringomyelia, post-medullary infarction, and sarcoidosis

Serious causes:

Tumors include schwannoma, cholesteatoma, acoustic neuroma, epidermoid, meningioma, and metastases
Multiple sclerosis plaques surrounding the root entry region of the trigeminal nerve

Clinical Features The disease predominantly occurs in middle-aged and elderly patients. The occurrence of trigeminal neuralgia in the younger individual suggests the diagnosis of multiple sclerosis, tumor, or aneurysm. The disorder is somewhat more common in women. The condition is characterized by paroxysms of pain occurring in the maxillary or mandibular division of the trigeminal nerve with later spread from one division to involve the other division. Involvement of the ophthalmic division is rare and occurs in less than 5 percent of cases. Trigeminal neuralgia may involve both sides of the face, but paroxysms never occur simultaneously on the two sides. In established cases the pain may be provoked by touching the face, chewing, talking, drinking, brushing the teeth, shaving, or the movement of air across the affected side of the face. Patients recognize certain “trigger points,” which will produce a typical paroxysm of pain if stimulated. Established cases exhibit sudden, severe paroxysms of pain with cessation of speech and contortion of the face often accompanied by a cry of distress. The attacks are short-lived with long periods of freedom in the early stages, but the paroxysms gradually become longer and closer together in time. This leads to constant dread of the next attack with depression, suicidal thoughts, and weight loss.

The neurological examination is normal.

Diagnostic Procedures

1. The patient should have radiographs or a CT scan of the base of the skull with visualization of the foramen ovale. Enlargement of the foramen ovale suggests the possibility of intracranial or extracranial tumor.

2. If there is a suspicion of the presence of tumor or aneurysm, a high-resolution computed tomography (CT) scan of the base of the skull and posterior fossa should be performed.

Treatment Medical treatment using carbamazepine (Tegretol) is successful in most cases. It should be given in small doses initially and gradually increased to effect, beginning with 100 mg at night and increasing by 100 mg every 3 days until the patient is receiving 800 to 1600 mg in three divided doses daily. The slow introduction of carbamazepine will permit the establishment of therapeutic levels of the drug, without the development of unpleasant adverse effects.

Phenytoin (Dilantin) is less effective than earbamazepine in the control of trigeminal neuralgia but should be used to treat patients who are unable to tolerate carbamazepine. Phenytoin is also useful as an adjunct when earbamazepine produces significant but incomplete control of pain. The dosage of phenytoin should be sufficient to produce therapeutic plasma concentrations of the drug.

Baclofen, benzodiazepines, gabapentin, or pimozide 4 to 12 mg daily are occasionally effective when carbamazepine and phenytoin fail to control trigeminal neuralgia.

A number of surgical procedures are currently advocated for the treatment of trigeminal neuralgia. These include alcohol injection of individual nerves or the trigeminal ganglion. This form of treatment relieves pain, but the patient must clearly understand that alcohol injection produces anesthesia, and pain loss is associated with loss of sensation in the affected area of the face. Nerve regeneration often occurs after 6 months with return of the pain in some cases. Other surgical procedures include percutaneous radiofrequency or glycerol trigeminal gangliolysis and suboccipital craniotomy with microvascular decompression of the trigeminal nerve, which has the advantage of relieving pain without producing anesthesia. When the latter is not feasible, partial sensory rhizotomy with sectioning of one-third to one-half of the cross-section area of the sensory root, 2 to 5 mm from the pons, produces complete relief from neuralgic pain in about 50 percent of cases.

Prognosis The majority of cases of trigeminal neuralgia can be controlled medically with carbamazepine but many patients have to continue taking the drug for a prolonged period. An attempt at withdrawal should be made when the patient has been pain free for 6 months. This is successful in some cases.

Herpes Zoster (Shingles)

Definition Herpes zoster is an acute, painful mononeuropathy associated with a vesicular eruption in the distribution of the affected nerve.

Etiology and Pathology The infective agent is the varicella virus. Herpes zoster may represent an infection by recently acquired varicella virus in an individual who has a declining immunity to the virus or a recrudescence of activity by latent varicella virus in the presence of declining immunity.

The viral activity is predominantly located in the dorsal root ganglia or sensory ganglia of the cranial nerves. The ganglia are swollen and show areas of necrosis. There is a marked inflammatory response with necrosis of neurons. The ventral (motor) nerve root is occasionally involved, and inflammatory changes may spread to the spinal cord or brainstem. The vesicles in the skin contain herpes virus, and the surrounding area shows a polymorphonuclear infiltration due to secondary bacterial infection.

Clinical Features Herpes zoster is a disease of adults and rarely affects children. There is an increased incidence in patients with altered immunity due to such conditions as malignancy, HIV infection, Hodgkin disease, and leukemia. The condition presents with fever followed by pain in the distribution of the involved nerve. Vesicles appear in the affected area within 24 h and are soon involved by secondary bacterial infection, which results in severe regional lymphodermatitis. The pain usually begins to subside after a few days but may persist for months (postherpetic neuralgia). The pustules heal, and crusts separate after about 3 weeks, leaving pigmented scars.

Herpes zoster is not confined to sensory symptoms. Motor weakness from ventral root involvement occurs in 5 to 10 percent of patients.

Complications

1. Involvement of the ophthalmic division of the fifth cranial nerve is frequently associated with corneal ulceration (Herpes zoster ophthalmicus) and may result in severe damage to the cornea. This condition is occasionally followed by retinal and intracranial arteritis, producing additional visual loss and contralateral hemiparesis.

2. Herpes zoster involvement of the geniculate ganglion produces a painful vesicular rash involving the pinna, external auditory meatus, and eardrum followed by ipsilateral facial paralysis (Ramsay-Hunt syndrome).

3. Sacral nerve involvement may be associated with loss of bladder and anal sphincter control.

4. Herpes zoster encephalitis is probably more common than has been thought in the past. Careful neurological examination may reveal subtle signs of intention tremor or gait ataxia, which should be regarded as encephalitic in origin. However, it is not unusual to find a CSF pleocytosis in the early stages of herpes zoster mononeuropathy.

5. Retrograde spread of the virus from the posterior root ganglion into the spinal cord occasionally produces an acute transverse myelitis. This may result in permanent cord damage with major neurological deficits. Herpes zoster myelitis usually occurs in immunocompromised individuals.

Differential Diagnosis It is extremely difficult to diagnose herpes zoster before the characteristic vesicles appear. The pain may mimic many acutely painful conditions such as pleurisy, pericarditis, perforated peptic ulcer, appendicitis, renal colic, and herniated lumbar disc.

Diagnostic Procedures

1. The white blood cell count is often elevated in the presence of secondary infection.

2. Lumbar puncture will reveal a lymphocytic pleocytosis in many cases. If there is clinical evidence of CNS involvement, the CSF abnormality is indicative of encephalitis.

Treatment

1. Herpes zoster is a systemic illness and patients should be treated with bed rest.

2. Adequate analgesia is mandatory. Narcotics are often required in the early stages.

3. Acyclovir 800 mg q4h orally or famciclovir 500 mg q8h is very effective in aborting an attack of herpes zoster.

4. A course of corticosteroids such as prednisone 80 mg daily for 7 days will produce rapid relief from pain in many cases. However, these antiviral agents must be given within 48 h of onset of herpes zoster.

5. Local application of calamine lotion or calodion, or application of a cream containing acyclovir or capsaicin, and avoidance of contact with clothing or bedclothes help to relieve pain and itching.

6. Herpes zoster encephalitis should be treated with acyclovir or famciclovir intravenously.

7. The rare occurrence of transverse myelitis or vasculitis may respond to intravenous acyclovir or famciclovir.

8. Postherpetic neuralgia is a most debilitating condition, particularly in elderly patients. The condition may persist for many months, but the patient should be informed that it will eventually subside. There is no single effective remedy, but some patients obtain relief from topical capsaicin cream or subcutaneous interferon injections. Carbamazepine (Tegretol), gabapentin 300 mg q8h increasing to 3600 mg per day if necessary for pain control, or phenytoin (Dilantin) may also be effective. These drugs may be used in combination if necessary. Alternatives include amitriptyline (Elavil) beginning 10 mg q.h.s. and slowly increasing by 10-mg increments up to 175-200 mg if necessary. A rapid increase in dosage leads to unacceptable dry mouth, resulting in rejection of the medication, particularly by elderly patients.

Neuropathy of the trigeminal nerve

can involve its full course, from its nuclei in the brain stem to its peripheral branches. The nerve can be divided into four segments–brain stem, cistern, the Meckel cave and cavernous sinus, and extracranial–and consideration of the pathologic entities by these locations simplifies the differential diagnosis. Multiple sclerosis, infarct, and glioma are the most common abnormalities in the brain stem leading to trigeminal neuropathy. The most common cisternal cause is neurovascular compression, followed by acoustic and trigeminal schwannomas, meningiomas, epidermoid cysts, lipomas, and metastases. Trigeminal neuropathy arising from the Meckel cave and cavernous sinus is frequently due to meningiomas, trigeminal schwannomas, epidermoid cysts, metastases, pituitary adenomas, and aneurysms. Malignant tumors, which may demonstrate perineural tumor spread, are the most common extracranial cause. Because the clinical findings do not permit accurate lesion localization, magnetic resonance imaging must be used to visualize the entire course of the fifth cranial nerve. The standard study should include T2-weighted images of the whole brain and high-resolution axial and coronal T1-weighted images of the skull base obtained with and without contrast material enhancement.