CRANIAL NERVES

Inferior view of the brain and brain stem showing cranial nerves. An unlabelled

version is here

Latin nervus cranialis (plural: nervi craniales)

Cranial nerves are nerves that emerge directly from the brain, in contrast to spinal nerves which emerge from segments of the spinal cord. In humans, there are 12 pairs of cranial nerves. Only the first and the second pair emerge from the cerebrum; the remaining 10 pairs emerge from the brainstem.

Olfactory nerve

Nerve: Olfactory nerve

The Olfactory Nerve

Latin nervus olfactorius

The olfactory nerve, or cranial nerve I, is the first of twelve cranial nerves. It is instrumental in the sense of smell.

Anatomy

The specialized olfactory receptor neurons of the olfactory nerve are located in the olfactory mucosa of the upper parts of the nasal cavity. The olfactory nerves do not form two trunks like the remaining cranial nerves, but consist of a collection of many sensory nerve fibers that extend from the olfactory epithelium to the olfactory bulb, passing through the many openings of the Cribriform plate of the Ethmoid bone; a sieve-like structure.

Olfactory receptor neurons continue to be born throughout life and extend new axons to the olfactory bulb. Olfactory ensheathing glia wrap bundles of these axons and are thought to facilitate their passage into the central nervous system.

The sense of smell (olfaction) arises from the stimulation of olfactory (or odorant) receptors by small molecules of different spatial, chemical, and electrical properties that pass over the nasal epithelium in the nasal cavity during inhalation. These interactions are transduced into electrical activity in the olfactory bulb which then transmits the electrical activity to other parts of the olfactory system and the rest of the central nervous system via the olfactory tract.

The olfactory nerve is the shortest of the twelve cranial nerves and only one of two cranial nerves (the other being the optic nerve) that do not join with the brainstem.

Testing

To test the function of the olfactory nerve, doctors block one of the patient's nostrils and place a pungent odor (such as damp coffee essence) under the open nostril. The test is then repeated on the other nostril.

Lesions

Lesions to the olfactory nerve can occur because of blunt trauma, such a coup-contra-coup damage, meningitis and tumors of the frontal lobe. They often lead to a reduced ability to taste and smell. However, lesions of the olfactory nerve do not lead to a reduced ability to sense pain from the nasal epithelium. This is because pain from the nasal epithelium is not carried to the central nervous system by the olfactory nerve; rather, it is carried to the central nervous system by the trigeminal nerve (cranial nerve V).

Optic nerve

This article is about the anatomical structure. For the comic book series, see Optic Nerve (comic). For the album about David Wojnarowicz, see Optic Nerve (CD-ROM).

Nerve: Optic Nerve

The left optic nerve and the optic tracts.

Latin nervus opticus

The optic nerve, also called cranial nerve II, transmits visual information from the retina to the brain.

Anatomy

The optic nerve is the second of twelve paired cranial nerves but is considered to be part of the central nervous system as it is derived from an outpouching of the diencephalon during embryonic development. Consequently, the fibres are covered with myelin produced by oligodendrocytes rather than the Schwann cells of the peripheral nervous system and are encased within the meninges. Therefore the distinction of nerve is technically a misnomer, as the optic system lies within the central nervous system and nerves exist, by definition, within the peripheral nervous system. Therefore peripheral neuropathies like Guillain-Barré syndrome do not affect the optic nerve.

The optic nerve is ensheathed in all three meningeal layers (dura, arachnoid, and pia mater) rather than the epineurium, perineurium, and endoneurium found in peripheral nerves. Fibre tracks of the mammalian central nervous system (as opposed to the peripheral nervous system) are incapable of regeneration and hence optic nerve damage produces irreversible blindness. The fibres from the retina run along the optic nerve to nine primary visual nuclei in the brain, whence a major relay inputs into the primary visual cortex.

The optic nerve is composed of retinal ganglion cell axons and support cells. It leaves the orbit (eye) via the optic canal, running postero-medially towards the optic chiasm where there is a partial decussation (crossing) of fibres from the temporal visual fields of both eyes. Most of the axons of the optic nerve terminate in the lateral geniculate nucleus from where information is relayed to the visual cortex, while other axons terminate in the pretectal nucleus and are involved in reflexive eye movements and other axons terminate in the suprachiasmatic nucleus and are involved in regulating the sleep-wake cycle. Its diameter increases from about 1.6 mm within the eye, to 3.5 mm in the orbit to 4.5 mm within the cranial space. The optic nerve component lengths are 1 mm in the globe, 24 mm in the orbit, 9 mm in the optic canal and 16 mm in the cranial space before joining the optic chiasm. There, partial decussation occurs and about 53% of the fibers cross to form the optic tracts. Most of these fibres terminate in the lateral geniculate body.

From the lateral geniculate body, fibers of the optic radiation pass to the visual cortex in the occipital lobe of the brain. More specifically, fibers carrying information from the contralateral superior visual field traverse Meyer's loop to terminate in the lingual gyrus below the calcarine fissure in the occipital lobe, and fibers carrying information from the contralateral inferior visual field terminate more superiorly.

Physiology

The eye's blind spot is a result of the absence of photoreceptors in the area of the retina where the optic nerve leaves the eye.

Each optic nerve contains around 1.2 million nerve fibers, which are axons of the retinal ganglion cells of one retina. In the fovea, which has high acuity, these ganglion cells connect to as few as 5 photoreceptor cells; in other areas of retina, they connect to many thousand photoreceptors.

Role in disease

Damage to the optic nerve typically causes permanent and potentially severe loss of vision, as well as an abnormal pupillary reflex, which is diagnostically important. The type of visual field loss will depend on which portions of the optic nerve were damaged. Generally speaking:

Damage proximal to the optic chiasm causes loss of vision in the visual field of the same side only. Damage in the chiasm causes loss of vision laterally in both visual fields (bitemporal hemianopia). It may occur in large

pituitary adenomata.

Damage distal to the chiasm causes loss of vision in one eye but affecting both visual fields: the visual field affected is located on the opposite side of the lesion.

Injury to the optic nerve can be the result of congenital or inheritable problems like Leber's Her edit ary Optic Neuropathy , glaucoma, trauma, toxicity, inflammation, ischemia, infection (very rarely), or compression from tumors or aneurysms. By far, the three most common injuries to the optic nerve are from glaucoma, optic neuritis (especially in those younger than 50 years of age) and anterior ischemic optic neuropathy (usually in those older than 50).

Glaucoma is a group of diseases involving loss of retinal ganglion cells causing optic neuropathy in a pattern of peripheral vision loss, initially sparing central vision.

Optic neuritis is inflammation of the optic nerve. It is associated with a number of diseases, most notably multiple sclerosis.

Anterior Ischemic Optic Neuropathy is a particular type of infarct that affects patients with an anatomical predisposition and cardiovascular risk factors.

Optic nerve hypoplasia is the under-development of the optic nerve causing little to no vision in the affected eye.

Ophthalmologists, particularly those sub specialists who are neuro-ophthalmologists, are often best suited to diagnose and treat diseases of the optic nerve.

The International Foundation for Optic Nerve Diseases IFOND sponsors research and information on a variety of optic nerve disorders and may provide general direction.

Oculomotor nerve

Nerve: Oculomotor nerve

Nerves of the orbit. Seen from above.

Latin nervus oculomotorius

Innervates

Superior rectus, Inferior rectus, Medial rectus,

Inferior oblique, Levator palpebrae, sphincter

pupillae (parasympathetics), ciliaris muscle

(parasympathetics)

From oculomotor nucleus, Edinger-Westphal nucleus

To superior branch, inferior branch

The oculomotor nerve is the third of twelve paired cranial nerves. It controls most of the eye's movement, constriction of the pupil, and maintains an open eyelid. (Note: cranial nerves IV and VI also participate in control of eye movement.)

Path

Nuclei

The oculomotor nerve (CN III) arises from the anterior aspect of mesencephalon (midbrain). There are two nuclei for the oculomotor nerve:

The oculomotor nucleus originates at the level of the superior colliculus. The muscles it controls are the striated muscle in levator palpebrae superioris and all extraocular muscles except for the superior oblique muscle and the lateral rectus muscle.

The Edinger-Westphal nucleus supplies parasympathetic fibres to the eye via the ciliary ganglion, and thus controls the sphincter pupillae muscle (affecting pupil constriction) and the ciliary muscle (affecting accommodation).

Sympathetic postganglionic fibres also join the nerve from the plexus on the internal carotid artery in the wall of the cavernous sinus and are distributed through the nerve, e.g. to the smooth muscle of levator palpebrae superioris.

Emergence from brain

On emerging from the brain, the nerve is invested with a sheath of pia mater, and enclosed in a prolongation from the arachnoid.

It passes between the superior cerebellar (below) and posterior cerebral arteries (above), and then pierces the dura mater anterior and lateral to the posterior clinoid process, passing between the free and attached borders of the tentorium cerebelli.

It runs along the lateral wall of the cavernous sinus, above the other orbital nerves, receiving in its course one or two filaments from the cavernous plexus of the sympathetic, and a communicating branch from the ophthalmic division of the trigeminal.

Superior and inferior rami

It then divides into two branches, which enter the orbit through the superior orbital fissure, between the two heads of the lateral rectus.

Here the nerve is placed below the trochlear nerve and the frontal and lacrimal branches of the ophthalmic nerve, while the nasociliary nerve is placed between its two rami:

superior branch of oculomotor nerve inferior branch of oculomotor nerve

Testing the oculomotor nerve

Eye muscles

Cranial nerves III, IV and VI are usually tested together. The examiner typically instructs the patient to hold his head still and follow only with the eyes a finger or penlight that circumscribes a large "H" in front of the patient. By observing the eye movement and eyelids, the examiner is able to obtain more information about the extraocular muscles, the levator palpebrae superioris muscle, and cranial nerves III, IV, and VI.

Since the oculomotor nerve controls most of the eye muscles, it may be easier to detect damage to it. Damage to this nerve, termed oculomotor nerve palsy is also known by the down n' out symptoms, because of the position of the affected eye.

Pupillary reflex

The oculomotor nerve also controls the constriction of the pupils and thickening of the lens of the eye. This can be tested in two main ways. By moving a finger towards a person's face to induce accommodation, as well as them going cross-eyed, their pupils should constrict.

Shining a light into their eyes should also make their pupils constrict. Both pupils should constrict at the same time, independent of what eye the light is actually shone on.

Pathology

Paralysis of the oculomotor nerve, i.e. oculomotor nerve palsy, is a rare condition. It can arise due to:

direct trauma, demyelinating diseases (e.g. multiple sclerosis),

increased intracranial pressure (leading to uncal herniation)

o due to a space-occupying lesion (e.g. brain cancer) or a

o spontaneous subarachnoid haemorrhage (e.g. berry aneurysm), and

microvascular disease, e.g. diabetes.

In people with diabetes and older than 50 years of age, an oculomotor nerve palsy, classically, occurs with sparing (or preservation) of the pupillary reflex. This is thought to arise due the anatomical arrangement of the nerve fibers in the oculomotor nerve; fibers controlling the pupillary function are superficial and spared from ischemic injuries typical of diabetes. Conversely, a subarachnoid haemorrhage, which leads to compression of the oculomotor nerve, usually affects the superficial fibers and manifests as a palsy with loss of the pupillary reflex.[1]

Trochlear nerve

Nerve: Trochlear nerve

Path of the Trochlear nerve

Latin nervus trochlearis

The trochlear nerve (the fourth cranial nerve, also called the fourth nerve, IV) is a motor nerve (a “somatic efferent” nerve) that innervates a single muscle: the superior oblique muscle of the eye.

The trochlear nerve is unique among the cranial nerves in several respects. It is the smallest nerve in terms of the number of axons it contains. It has the greatest intracranial length. Along with the optic nerve (cranial nerve II), it is the only cranial nerve that decussates (crosses to the other side) before innervating its target[1]. Finally, it is the only cranial nerve that exits from the dorsal aspect of the brainstem.

Homologous trochlear nerves are found in all jawed vertebrates. The unique features of the trochlear nerve, including its dorsal exit from the brainstem and its contralateral innervation, are seen in the primitive brains of sharks.[2] [edit] Peripheral anatomy

The Cavernous Sinus

The trochlear nerve emerges from the dorsal aspect of the brainstem at the level of the caudal mesencephalon, just below the inferior colliculus. It circles anteriorly around the brainstem and runs forward toward the eye in the subarachnoid space. It passes between the posterior cerebral artery and the superior cerebellar artery, and then pierces the dura just under free margin of the tentorium cerebelli, close to the crossing of the attached margin of the tentorium and within millimeters of the posterior clinoid process.[3] It enters the cavernous sinus, where it is joined by the other two extraocular nerves (III and VI), the internal carotid artery, and portions of the trigeminal nerve (V). Finally, it enters the orbit through the superior orbital fissure and innervates the superior oblique muscle.

The superior oblique muscle ends in a tendon that passes through a fibrous loop, the trochlea, located anteriorly on the medial aspect of the orbit. Trochlea means “pulley” in Latin; the fourth nerve is named after this structure.

Actions of the superior oblique muscle

In order to understand the actions of the superior oblique muscle, it is useful to imagine the eyeball as a sphere that is constrained – like the trackball of a computer mouse – in such a way that only certain rotational movements are possible. Allowable movements for the superior oblique are (1) rotation in a vertical plane – looking down and up (depression and elevation of the eyeball) and (2) rotation in the plane of the face (intorsion and extorsion of the eyeball).

The body of the superior oblique muscle is located behind the eyeball, but the tendon (which is redirected by the trochlea) approaches the eyeball from the front. The tendon attaches to the top (superior aspect) of the eyeball at an angle of 51 degrees with respect to the primary position of the eye (looking straight forward). The force of the tendon’s pull therefore has two components: a forward component that tends to pull the eyeball downward (depression), and a medial component that tends to rotate the top of the eyeball toward the nose (intorsion).

The relative strength of these two forces depends on which way the eye is looking. When the eye is adducted (looking toward the nose), the force of depression increases. When the eye is abducted (looking away from the nose), the force of intorsion increases, while the force of depression decreases. When the eye is in the primary position (looking straight ahead), contraction of the superior oblique produces depression and intorsion in roughly equal amounts.

To summarize, the actions of the superior oblique muscle are (1) depression of the eyeball, especially when the eye is adducted; and (2) intorsion of the eyeball, especially when the eye is abducted. The clinical consequences of weakness in the superior oblique (caused, for example, by fourth nerve palsies) are discussed below.

This summary of the superior oblique muscle describes its most important functions. However, it is an oversimplification of the actual situation. For example, the tendon of the superior oblique inserts behind the equator of the eyeball in the frontal plane, so contraction of the muscle also tends to abduct the eyeball (turn it outward). In fact, each of the six extraocular muscles exerts rotational forces in all three planes (elevation-depression, adduction-abduction, intorsion-extorsion) to varying degrees, depending on which way the eye is looking. The relative forces change every time the eyeball moves – every time the direction of gaze changes. The central control of this process, which involves the continuous, precise adjustment of forces on twelve different tendons in order to point both eyes in exactly the same direction, is truly remarkable.

The recent discovery of soft tissue pulleys in the orbit – similar to the trochlea, but anatomically more subtle and previously missed – has completely changed (and greatly simplified) our understanding of the actions of the extraocular muscles[4]. Perhaps the most important finding is that a 2-dimensional representation of the visual field is sufficient for most purposes.

Central anatomy

Transverse Section of the Brainstem at the level of the Inferior Colliculus

The nucleus of the trochlear nerve is located in the caudal mesencephalon beneath the cerebral aqueduct. It is immediately below the nucleus of the oculomotor nerve (III) in the rostral mesencephalon.

The trochlear nucleus is unique in that its axons run dorsally and cross the midline before emerging from the brainstem. Thus a lesion of the trochlear nucleus affects the contralateral eye. Lesions of all other cranial nuclei affect the ipsilateral side (except of course the optic nerves - cranial nerves II - which innervate both eyes).

Clinical syndromes

Vertical diplopia

Injury to the trochlear nerve cause weakness of downward eye movement with consequent vertical diplopia (double vision). The affected eye drifts upward relative to the normal eye, due to the unopposed actions of the remaining extraocular muscles. The patient sees two visual fields (one from each eye), separated vertically. To compensate for this, patients learn to tilt the head forward (tuck the chin in) in order to bring the fields back together – to fuse the two images into a single visual field. This accounts for the “dejected” appearance of patients with “pathetic nerve” palsies.

As would be expected, the diplopia gets worse when the affected eye looks toward the nose – the contribution of the superior oblique muscle to downward gaze is greater in this position. Common activities requiring this type of convergent gaze are reading the newspaper and walking down stairs. Diplopia associated with these activities may be the initial symptom of a fourth nerve palsy.

Alfred Bielschowsky's head tilt test is a test for palsy of the superior oblique muscle caused by damage to cranial nerve IV (trochlear nerve).

Torsional diplopia

Trochlear nerve palsy also affects torsion (rotation of the eyeball in the plane of the face). Torsion is a normal response to tilting the head sideways. The eyes automatically rotate in an equal and opposite direction, so that the orientation of the environment remains unchanged – vertical things remain vertical.

Weakness of intorsion results in torsional diplopia, in which two different visual fields, tilted with respect to each other, are seen at the same time. To compensate for this, patients with trochlear nerve palsies tilt their heads to the opposite side, in order to fuse the two images into a single visual field.

The characteristic appearance of patients with fourth nerve palsies (head tilted to one side, chin tucked in) suggests the diagnosis, but other causes must be ruled out. For example, torticollis can produce a similar appearance.

Causes

The clinical syndromes can originate from both peripheral and central lesions.

Peripheral lesions

A peripheral lesion is a damage to the bundle of nerves, in contrast to a central lesion, which is a damage to the trochlear nucleus. Acute symptoms are probably a result of a trauma or disease, while chronic symptoms probably are congenital.

Acute palsy

The most common cause of acute fourth nerve palsy is head trauma.[5] Even relatively minor trauma can transiently stretch the fourth nerve (by transiently displacing the brainstem relative to the posterior clinoid process). Patients with minor damage to the fourth nerve will complain of “blurry” vision. Patients with more extensive damage will notice frank diplopia and rotational (torsional) disturbances of the visual fields. The usual clinical course is complete recovery within weeks to months.

Isolated injury to the fourth nerve can be caused by any process that stretches or compresses the nerve. A generalized increase in intracranial pressure – hydrocephalus, pseudotumor cerebri, hemorrhage, edema – will affect the fourth nerve, but the abducens nerve (VI) is usually affected first (producing horizontal diplopia, not vertical diplopia). Infections (meningitis, herpes zoster), demyelination (multiple sclerosis), diabetic neuropathy and cavernous sinus disease can affect the fourth nerve, as can orbital tumors and Tolosa-Hunt syndrome. In general, these diseases affect other cranial nerves as well. Isolated damage to the fourth nerve is uncommon in these settings.

Chronic palsy

The most common cause of chronic fourth nerve palsy is a congenital defect, in which the development of the fourth nerve (or its nucleus) is abnormal or incomplete. Congenital defects may be noticed in childhood, but minor defects may not become evident until adult life, when compensatory mechanisms begin to fail. Congenital fourth nerve palsies are amenable to surgical treatment.

Central lesions

Central damage is a damage to the trochlear nucleus. It affects the contralateral eye. The nuclei of other cranial nerves affect ipsilateral structures (except of course the optic nerves - cranial nerves II - which innervate both eyes).

The trochlear nucleus and its axons within the brainstem can be damaged by infarctions, hemorrhage, arteriovenous malformations, tumors and demyelination. Collateral damage to other structures will usually dominate the clinical picture.

The fourth nerve is one of the final common pathways for cortical systems that control eye movement in general. Cortical control of eye movement (saccades, smooth pursuit, accommodation) involves conjugate gaze, not unilateral eye movement.

Trigeminal nerve

Nerve: Trigeminal nerve

Trigeminal nerve, shown in yellow

Latin nervus trigeminus

To

ophthalmic nerve

maxillary nerve

mandibular nerve

The trigeminal nerve (the fifth cranial nerve, also called the fifth nerve, or simply CNV or CN5) is responsible for sensation in the face. Sensory information from the face and body is processed by parallel pathways in the central nervous system.

The fifth nerve is primarily a sensory nerve, but it also has certain motor functions (biting, chewing, and swallowing). These are discussed separately.

Function

The sensory function of the trigeminal nerve is to provide the tactile, proprioceptive, and nociceptive afference of the face and mouth. The motor function activates the muscles of mastication, the tensor tympani, tensor veli palatini, mylohyoid, and anterior belly of the digastric.

Peripheral anatomy

Dermatome distribution of the trigeminal nerve

The trigeminal nerve 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 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 sensory and motor functions.

The three branches converge on the trigeminal ganglion (also called the semilunar ganglion or gasserian ganglion), that is 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. Motor fibers of the eye are distributed (together with sensory fibers) in branches of the mandibular 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.

It is also worth noting that 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.[1]

The ophthalmic nerve 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 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 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.

o 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 fibers 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

massetertemporalis

medial pterygoid

lateral pterygoid

Others

tensor veli palatinimylohyoid

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 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

The fifth nerve is primarily a sensory nerve. The anatomy of sensation in the face and mouth is the subject of the remainder of this article. Background information on sensation is reviewed, followed by a summary of central sensory pathways. The central anatomy of the fifth nerve is then discussed in detail.

Sensation

There are two basic types of sensation: 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. Think of stepping on a pin. There is immediate awareness of stepping on something, but it takes a moment before it starts to hurt.

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, 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 certain nonhuman 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 that 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 that we 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. There are separate pathways 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 together in series:

It is noteworthy that the secondary neurons in each pathway decussate (cross to the other side of the spinal cord or brainstem). The reason for this is because initially Spinal Cord forms segmentally. Later on, decussated fibres reach and connect these segments with the Higher Centres. The main reason for Decussation is that optic chiasma occurs(Nasal fibres of the Optic Nerve cross so each cerebral hemisphere receives the contralateral vision) and to keep interneuronal connections short(responsible for processing of information) all sensory and motor pathways converge and diverge respectively to the contralateral hemisphere.(Courtesy H. Balram Krishna, excerpt from Cunningham's Manual of Practical Anatomy)

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; touch/position 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; pain/temperature information from the face is carried to the thalamus by the trigeminothalamic tract (also called the quintothalamic tract).

Pathways for touch/position sensation from the face and body merge together 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 together 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 the present time. 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 mapof the face and mouth. From the spinal 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 pain/temperature information to the thalamus from the rest of the body. 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 carry 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 main nucleus 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 leminscus, 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 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 main nucleus of V. As noted above, this information is projected bilaterally to the thalamus. It is available for conscious perception.

Activities like biting, chewing and swallowing require symmetrical, simultaneous coordination of both sides of the body. They are essentially automatic activities, to which we pay little conscious attention. They involve a sensory component (feedback about touch/position) that is 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. It is evident, therefore, that information about biting, chewing and swallowing is singled out for special processing in the vertebrate brainstem, specifically in the mesencephalic nucleus.

Lampreys and hagfishes have cells in their brainstems that can be identified as the evoutionary precursors of the mesencephalic nucleus. These "internal ganglion" cells were discovered in the latter part of the 19th century by a young medical student named Sigmund Freud.[2]

Pathways to the thalamus and the cortex

We have defined sensation 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.[3] 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 primary sensory cortex (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.

Summary

The complex processing of pain/temperature information in the thalamus and cerebral cortex (as opposed to the relatively simple, straightforward processing of touch/position information) reflects a phylogenetically older, more primitive sensory system. The rich, detailed information we receive from peripheral touch/position receptors is superimposed on a background of awareness, memory and emotions that is set, in part, by peripheral pain/temperature receptors.

The thresholds for touch/position perception are relatively easy to measure, and are similar in all humans. The thresholds for pain/temperature perception are difficult to define and even more difficult to measure. "Touch" is an objective sensation. "Pain" is a highly individualized, personal sensation that varies markedly among different people. It is conditioned by their memories and by their emotions. The fundamental anatomical differences between the pathways for touch/position perception and pain/temperature sensation help to explain why pain, especially chronic pain, is so difficult to manage.

Wallenberg syndrome

Wallenberg syndrome (also called the lateral medullary syndrome) is a classic clinical demonstration of the anatomy of the fifth nerve. It provides a useful summary of essential points about the processing of sensory information by the trigeminal nerve.

A stroke usually affects only one side of the body. If a stroke causes loss of sensation, the deficit will be lateralized to the right side or the left side of the body. The only exceptions to this rule are certain spinal cord lesions and the medullary syndromes, of which Wallenberg syndrome is the most famous example. In Wallenberg syndrome, a stroke causes loss of pain/temperature sensation from one side of the face and the other side of the body.

The explanation involves the anatomy of the brainstem. In the medulla, the ascending spinothalamic tract (which carries pain/temperature information from the opposite side of the body) is adjacent to the descending spinal tract of the fifth nerve (which carries pain/temperature information from the same side of the face). A stroke that cuts off the blood supply to this area (e.g., a clot in the posterior inferior cerebellar artery) destroys both tracts simultaneously. The result is loss of pain/temperature sensation (but not touch/position sensation) in a unique "checkerboard" pattern (ipsilateral face, contralateral body) that is entirely diagnostic.

Abducens nerve

Nerve: Abducens nerve

The path of the Abducens nerve

Inferior view of the human brain, with the cranial nerves

labelled.

Latin nervus abducens

Gray's subject #201 899

From abducens nucleus

MeSH Abducens+Nerve

The abducens nerve or abducent nerve (the sixth cranial nerve, also called the sixth nerve or simply VI) is a “somatic efferent” nerve that controls the movement of a single muscle, the lateral rectus muscle of the eye. Homologous abducens nerves are found in all vertebrates except lampreys and hagfishes.

"Abducens" and "Abducent"

The Latin name for the sixth cranial nerve is nervus abducens. The Terminologia Anatomica officially recognizes two different English translations: abducent nerve and abducens nerve.[1] Either term is correct.

“Abducens” is more common in recent literature, while “abducent” predominates in the older literature. The United States National Library of Medicine uses “abducens nerve” in its Medical Subject Heading (MeSH) vocabulary to index the vast MEDLINE and PubMed biomedical databases. The 39th edition of Gray’s Anatomy (2005) also prefers “abducens nerve.”[2]

Peripheral anatomy

The Clivus

The abducens nerve leaves the brainstem at the junction of the pons and the medulla, medial to the facial nerve. In order to reach the eye, it runs upward (superiorly) and then bends forward (anteriorly).

The nerve enters the subarachnoid space when it emerges from the brainstem. It runs upward between the pons and the clivus, and then pierces the dura mater to run between the dura and the skull. At the tip of the petrous temporal bone it makes a sharp turn forward to enter the cavernous sinus. In the cavernous sinus it runs alongside the internal carotid artery. It then enters the orbit through the superior orbital fissure and innervates the lateral rectus muscle of the eye.

The long course of the abducens nerve between the brainstem and the eye makes it vulnerable to injury at many levels. For example, fractures of the petrous temporal bone can selectively damage the nerve, as can aneurysms of the intracavernous carotid artery. Mass

lesions that push the brainstem downward can damage the nerve by stretching it between the point where it emerges from the pons and the point where it hooks over the petrous temporal bone.

Central anatomy

Axial section of the Brainstem (Pons) at the level of the Facial Colliculus

The abducens nucleus is located in the pons, on the floor of the fourth ventricle, at the level of the facial colliculus. Axons from the facial nerve loop around the abducens nucleus, creating a slight bulge (the facial colliculus) that is visible on the dorsal surface of the floor of the fourth ventricle. The abducens nucleus is close to the midline, like the other motor nuclei that control eye movements (the oculomotor and trochlear nuclei).

Motor axons leaving the abducens nucleus run ventrally and caudally through the pons. They pass lateral to the corticospinal tract (which runs longitudinally through the pons at this level) before exiting the brainstem at the pontomedullary junction.

The central anatomy of the sixth nerve predicts (correctly) that infarcts affecting the dorsal pons at the level of the abducens nucleus can also affect the facial nerve, producing an ipsilateral facial palsy together with a lateral rectus palsy. The anatomy also predicts (correctly) that infarcts involving the ventral pons can affect the sixth nerve and the corticospinal tract simultaneously, producing a lateral rectus palsy associated with a contralateral hemiparesis. These rare syndromes are of interest primarily as useful summaries of the anatomy of the brainstem.

Clinical syndromes

Peripheral lesions

Complete interruption of the peripheral sixth nerve causes diplopia (double vision), due to the unopposed action of the medial rectus muscle. The affected eye is pulled medially. In order to see without double vision, patients will rotate their heads so that both eyes are looking sideways. On formal testing, the affected eye cannot abduct past the midline – it cannot look sideways, toward the temple. Partial damage to the sixth nerve causes weak or incomplete abduction of the affected eye. The diplopia is worse on attempted lateral gaze, as would be expected (since the lateral gaze muscle is impaired).

Peripheral sixth nerve damage can be caused by tumors, aneurysms, or fractures – anything that directly compresses or stretches the nerve. Other processes that can damage the sixth nerve include strokes (infarctions), demyelination, infections (e.g. meningitis), cavernous sinus diseases and various neuropathies. Perhaps the most common overall cause of sixth nerve impairment is diabetic neuropathy.

Rare causes of isolated sixth nerve damage include Wernicke-Korsakoff syndrome and Tolosa-Hunt syndrome. Wernicke-Korsakoff syndrome is caused by thiamine deficiency, classically due to alcoholism. The characteristic ocular abnormalities are nystagmus and lateral rectus weakness. Tolosa-Hunt syndrome is an idiopathic granulomatous disease that causes painful oculomotor (especially sixth nerve) palsies.

Indirect damage to the sixth nerve can be caused by any process (brain tumor, hydrocephalus, pseudotumor cerebri, hemorrhage, edema) that exerts downward pressure on the brainstem, causing the nerve to stretch along the clivus. This type of traction injury can affect either side first. A right-sided brain tumor can produce either a right-sided or a left-sided sixth nerve palsy as an initial sign. Thus a right-sided sixth nerve palsy does not necessarily imply a right-sided cause. Sixth nerve palsies are infamous as “false localizing signs.” Isolated sixth nerve palsies in children are assumed to be due to brain tumors until proven otherwise.

Nuclear lesions

Damage to the abducens nucleus does not produce an isolated sixth nerve palsy, but rather a horizontal gaze palsy that affects both eyes simultaneously. The abducens nucleus contains two types of cells: motor neurons that control the lateral rectus muscle on the same side, and interneurons that cross the midline and connect to the contralateral oculomotor nucleus (which controls the medial rectus muscle of the opposite eye). In normal vision, lateral movement of one eye (lateral rectus muscle) is precisely coupled to medial movement of the other eye (medial rectus muscle), so that both eyes remain fixed on the same object.

The control of conjugate gaze is mediated in the brainstem by the medial longitudinal fasciculus (MLF), a nerve tract that connects the three extraocular motor nuclei (abducens, trochlear and oculomotor) into a single functional unit. Lesions of the abducens nucleus and the MLF produce observable sixth nerve problems, most notably internuclear ophthalmoplegia (INO).

Supranuclear lesions

The sixth nerve is one of the final common pathways for numerous cortical systems that control eye movement in general. Cortical control of eye movement (saccades, smooth pursuit, accommodation) involves conjugate gaze, not unilateral eye movement.

Tuberculosis

15-40% of people with tuberculosis have some resulting cranial nerve deficit. The sixth nerve is the most commonly affected cranial nerve in immunocompetent people with tuberculosi

Facial nerve

Nerve: Facial nerve

Cranial nerve VII

The nerves of the scalp, face, and side of neck.

Latin nervus facialis

The facial nerve is the seventh (VII) of twelve paired cranial nerves. It emerges from the brainstem between the pons and the medulla, and controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue and oral cavity. It also supplies preganglionic parasympathetic fibers to several head and neck ganglia.

[edit] Course

The motor part of the facial nerve arises from the facial nerve nucleus in the pons while the sensory part of the facial nerve arises from the nervus intermedius.

The motor part and sensory part of the facial nerve enters the petrous temporal bone into the internal auditory meatus (intimately close to the inner ear) then runs a tortuous course (including two tight turns) through the facial canal, emerges from the stylomastoid foramen and passes through the parotid gland, where it divides into five major branches. Though it passes through the parotid gland, it does not innervate the gland (This is the responsibility of cranial nerve IX, the glossopharyngeal nerve).

The facial nerve forms the geniculate ganglion prior to entering the facial canal.

Branches Greater petrosal nerve - provides parasympathetic innervation to lacrimal gland, sphenoid sinus, frontal sinus, maxillary

sinus, ethmoid sinus, nasal cavity, as well as special sensory taste fibers to the palate via the Vidian nerve. Nerve to stapedius - provides motor innervation for stapedius muscle in middle ear

Chorda tympani - provides parasympathetic innervation to submandibular gland and sublingual gland and special sensory taste fibers for the anterior 2/3 of the tongue.

Outside skull (distal to stylomastoid foramen) Posterior auricular nerve - controls movements of some of the scalp muscles around the ear Branch to Posterior belly of Digastric and Stylohyoid muscle

Five major facial branches (in parotid gland) - from top to bottom:

o Temporal (frontal) branch of the facial nerve

o Zygomatic branch of the facial nerve

o Buccal branch of the facial nerve

o Marginal mandibular branch of the facial nerve

o Cervical branch of the facial nerve

Embryology

The facial nerve is developmentally derived from the hyoid arch (second pharyngeal branchial arch)

Function

Efferent

Its main function is motor control of most of the muscles of facial expression. It also innervates the posterior belly of the digastric muscle, the stylohyoid muscle, and the stapedius muscle of the middle ear. All of these muscles are striated muscles of branchiomeric origin developing from the 2nd pharyngeal arch.

The facial also supplies parasympathetic fibers to the submandibular gland and sublingual glands via chorda tympani. Parasympathetic innervation serves to increase the flow of saliva from these glands. It also supplies parasympathetic innervation to the nasal mucosa and the lacrimal gland via the pterygopalatine ganglion.

The facial nerve also functions as the efferent limb of the corneal reflex and the blink reflex.

Afferent

In addition, it receives taste sensations and general sensation from the anterior two-thirds of the tongue and sends them to the gustatory portion of the solitary nucleus. The facial nerve also supplies a small amount of afferent innervation to the oropharynx below the palatine tonsil. There is also a small amount of cutaneous sensation carried by the nervus intermedius from the skin in and around the auricle (earlobe).

Location of Cell Bodies

The cell bodies for the facial nerve are grouped in anatomical areas called nuclei or ganglia. The cell bodies for the afferent nerves are found in the geniculate ganglion for both taste and general afferent sensation. The cell bodies for muscular efferent nerves are found in the facial motor nucleus whereas the cell bodies for the parasympathetic efferent nerves are found in the superior salivatory nucleus.

Pathology

People may suffer from acute facial nerve paralysis, which is usually manifested by facial paralysis. Bell's palsy is one type of idiopathic acute facial nerve paralysis, which is more accurately described as a multiple cranial nerve ganglionitis that involves the facial nerve, and most likely results from viral infection and also sometimes as a result of Lyme disease. Iatrogenic Bell's Palsy may also be as a result of an incorrectly placed dental local-anesthetic (Inferior alveolar nerve block). Although giving the appearance of a hemi-plegic stroke, effects dissipate with the drug.

Testing the facial nerve

Voluntary facial movements, such as wrinkling the brow, showing teeth, frowning, closing the eyes tightly (inability to do so is called lagophthalmos)[1] , pursing the lips and puffing out the cheeks, all test the facial nerve. There should be no noticeable asymmetry.

In an UMN lesion, called central seven, only the lower part of the face on the contralateral side will be affected, due to the bilateral control to the upper facial muscles (frontalis and orbicularis oculi).

Lower motor neuron lesions can result in a CNVII palsy (Bell's palsy is the term used to describe the idiopathic form of facial nerve palsy), manifested as both upper and lower facial weakness on the same side of the lesion.

Taste can be tested on the anterior 2/3 of the tongue. This can be tested with a swab dipped in a flavoured solution, or with electronic stimulation (similar to putting your tongue on a battery).

Corneal reflex. The afferent arc is mediated by the General Sensory afferents of the Trigeminal Nerve. The efferent arc occurs via the Facial Nerve. The reflex involves consensual blinking of both eyes in response to stimulation of one eye. This is due to the Facial Nerve's innervation of the muscles of facial expression, namely Orbicularis Oculi, responsible for blinking. Thus, the corneal reflex effectively tests the proper functioning of both Cranial Nerves V and VII.

Vestibulocochlear nerve

Nerve: Vestibulocochlear nerve

The course and connections of the facial nerve in the temporal

bone

To cochlear nerve, vestibular nerve

The vestibulocochlear nerve (also known as the auditory or acoustic nerve) is the eighth of twelve cranial nerves, and is responsible for transmitting sound and equilibrium (balance) information from the inner ear to the brain.

Structure and function

This is the nerve along which the sensory cells (the hair cells) of the inner ear transmit information to the brain. It consists of the cochlear nerve, carrying information about hearing, and the vestibular nerve, carrying information about balance. It emerges from the medulla oblongata and exits the inner skull via the internal acoustic meatus (or internal auditory meatus) in the temporal bone

Innervations

The vestibulocochlear nerve consists mostly of bipolar neurons and splits into two large divisions – the cochlear nerve and the vestibular nerve.

The cochlear nerve travels away from the cochlea of the inner ear where it starts as the spiral ganglia. Processes from the organ of Corti conduct afferent transmission to the spiral ganglia . It is the inner hair cells of the organ of Corti that are responsible for activation of afferent receptors in response to pressure waves reaching the basilar membrane through the transduction of sound. The exact mechanism by which sound is transmitted by the neurons of the cochlear nerve is uncertain; the two competing theories are place theory and temporal theory.

The vestibular nerve travels from the vestibular system of the inner ear. The vestibular ganglion houses the cell bodies of the bipolar neurons and extends processes to five sensory organs. Three of these are the cristae located in the ampullae of the semicircular canals. Hair cells of the cristae activate afferent receptors in response to rotational acceleration. The other two sensory organs supplied by the vestibular neurons are the maculae of the saccule and utricle. Hair cells of the maculae activate afferent receptors in response to linear acceleration.

Symptoms of damage

Damage to the vestibulocochlear nerve may cause the following symptoms:

hearing loss vertigo

false sense of motion

loss of equilibrium (in dark places)

nystagmus

motion sickness

gaze-evoked tinnitus.[1]

Glossopharyngeal nerve

Nerve: Glossopharyngeal nerve

Plan of upper portions of glossopharyngeal, vagus, and

accessory nerves.

Course and distribution of the glossopharyngeal, vagus, and

accessory nerves. (Label for glossopharyngeal is at upper right.)

Latin nervus glossopharyngeus

Innervates stylopharyngeus

To tympanic nerve

The glossopharyngeal nerve is the ninth (IX) of twelve pairs of cranial nerves (24 nerves total). It exits the brainstem out from the sides of the upper medulla, just rostral (closer to the nose) to the vagus nerve.

Functions

There are a number of functions of the glossopharyngeal nerve:

It receives general sensory fibers (ventral trigeminothalamic tract) from the tonsils, the pharynx, the middle ear and the posterior 1/3 of the tongue.

It receives special sensory fibers (taste) from the posterior one-third of the tongue.

It receives visceral sensory fibers from the carotid bodies.

It supplies parasympathetic fibers to the parotid gland via the otic ganglion.

It supplies motor fibers to stylopharyngeus muscle, the only motor component of this cranial nerve.

It contributes to the pharyngeal plexus.

1. Cranial Nerve IX – Glossopharyngeal Overview.

The glossopharyngeal nerve consists of five components with distinct functions: Brancial motor (special visceral efferent) - supplies the stylopharyngeus muscle. Visceral motor (general visceral efferent) provides parasympathetic innervation of the smooth muscle and glands of the pharynx, larynx, and viscera of the thorax and abdomen. Visceral sensory (general visceral afferent) carries visceral sensory information from the carotid sinus and body. General sensory (general somatic afferent) provides general sensory information from the skin of the external ear, internal surface of the tympanic membrane, upper pharynx, and the posterior one-third of the tongue. Special sensory (special afferent) provides taste sensation from the posterior one-third of the tongue.

2. Overview of Branchial Motor Component.

The branchial motor component of CN IX provides voluntary control of the stylopharyngeus muscle which elevates the pharynx during swallowing and speech. Origin and Central Course - Branchial Motor Component. The branchial motor component originates from the nucleus ambiguus in the reticular formation of the medulla Rostral medulla. Fibers leaving the nucleus ambiguus travel anteriorly and laterally to exit the medulla, along with the other components of CN IX, between the olive and the inferior cerebellar peduncle. Intracranial Course - Branchial Motor Component. Upon emerging from the lateral aspect of the medulla the branchial motor component joins the other components of CN IX to exit the skull via the jugular foramen. The glossopharyngeal fibers travel just anterior to the cranial nerves X and XI which also exit the skull via the jugular foramen. Extra-cranial course and final innervation. Upon exiting the skull the branchial motor fibers descend deep to the styloid process and wrap around the posterior border of the stylopharyngeus muscle before innervating it. Branchial motor component - voluntary control of the stylopharyngeus muscle. Signals for the voluntary movement of stylopharyngeus muscle originate in the pre-motor and motor cortex (in association with other cortical areas) and pass via the corticobulbar tract in the posterior limb of the internal capsule to synapse bilaterally on the ambiguus nuclei in the medulla.

3. Overview of visceral motor component.

Parasympathetic component of the glossopharyngeal nerve which innervates the ipsilateral parotid gland. Origin and central course - visceral motor component. The preganglionic nerve fibers originate in the inferior salivatory nucleus of the rostral medulla and travel anteriorly and laterally to exit the brainstem between the olive and the inferior cerebellar peduncle with the other components of CN IX. Note: These neurons do not form a distinct nucleus visible on cross-section of the brainstem. The position indicated on the diagram is representative of the location of the cell bodies of these fibers. Intracranial course - visceral motor component. Upon emerging from the lateral aspect of the medulla, the visceral motor fibers join the other components of CN IX to enter the jugular foramen. Within the jugular foramen there are two glossopharyngeal ganglia which contain nerve cell bodies which mediate general, visceral, and special sensation. The visceral motor fibers pass through both ganglia without synapsing and exit the inferior ganglion with CN IX general sensory fibers as the tympanic nerve. Before exiting the jugular foramen, the tympanic nerve enters the petrous portion of the temporal and ascends via the inferior tympanic canaliculus to the tympanic cavity. Within the tympanic cavity the tympanic nerve forms a plexus on the surface of the promontory of the middle ear to provide general sensation. The visceral motor fibers pass through this plexus and merge to become the lesser petrosal nerve. The lesser petrosal nerve re-enters and travels through the temporal bone to emerge in the middle cranial fossa just lateral to the greater petrosal nerve. It then proceeds anteriorly to exit the skull via the foramen ovale along with the mandibular component of CN V (V3). Visceral motor component - extra-cranial course and final innervations. Upon exiting the skull, the lesser petrosal nerve synapses in the otic ganglion which is suspended from the mandibular nerve immediately below the foramen ovale. Postganglionic fibers from the otic ganglion travel with the auriculotemporal branch of CN V3 to enter the substance of the parotid gland. Hypothalamic Influence - visceral motor component. Fibers from the hypothalamus and olfactory system project via the dorsal longitudinal fasciculus to influence the output of the inferior salivatory nucleus. Examples include: 1) dry mouth in response to fear (mediated by the hypothalamus); 2) salivation in response to smelling food (mediated by the olfactory system)

4. Overview of visceral sensory component.

This component of CN IX innervates the baroreceptors of the carotid sinus and chemoreceptors of the carotid body. Peripheral and intracranial course. Sensory fibers arise from the carotid sinus and carotid body at the bifurcation of the common carotid artery, ascend in the sinus nerve, and join the other components of CN IX at the inferior hypoglossal ganglion. The cell bodies of these neurons reside in the inferior ganglion. The central processes of these neurons enter the skull via the jugular foramen. Central course - visceral sensory component. Once inside the skull, the visceral sensory fibers enter the lateral medulla between the olive and the inferior cerebellar peduncle and descend in the tractus solitarius to synapse in the caudal nucleus solitarius. From the nucleus solitarius, connections are made with several areas in the reticular formation and hypothalamus to mediate cardiovascular and respiratory reflex responses to changes in blood pressure, and serum concentrations of CO2 and O2.

5. Overview of general sensory component.

This component of CN IX carries general sensory information (pain, temperature, and touch) from the skin of the external ear, internal surface of the tympanic membrane, the walls of the upper pharynx, and the posterior one-third of the tongue. Peripheral course. Sensory fibers from the skin of the external ear initially travel with the auricular branch of CN X, while those from the middle ear travel in the tympanic nerve as discussed above (CN IX visceral motor section). General sensory information from the upper pharynx and posterior one-third of the tongue travel via the pharyngeal branches of CN IX. These peripheral processes have cell their cell body in either the superior or inferior glossopharyngeal ganglion. Central course - general sensory component. The central processes of the general sensory neurons exit the glossopharyngeal ganglia and pass through the jugular foramen to enter the brainstem at the level of the medulla. Upon entering the medulla these fibers descend in the spinal trigeminal tract and synapse in the caudal spinal nucleus of the trigeminal. Central course - general sensory component. Ascending secondary neurons originating from the spinal nucleus of CN V project to the contralateral ventral posteromedial (VPM) nucleus of the thalamus via the anterolateral system (ventral trigeminothalamic tract). Tertiary neurons from the thalamus project via the posterior limb of the internal capsule to the sensory cortex of the post-central gyrus. Clinical correlation. The general sensory fibers of CN IX mediate the afferent limb of the pharyngeal reflex in which touching the back of the pharynx stimulates the patient to gag (i.e. the gag reflex). The efferent signal to the musculature of the pharynx is carried by the branchial motor fibers of the vagus nerve.

6. Overview of Special Sensory Component.

The special sensory component of CN IX provides taste sensation from the posterior one-third of the tongue. Peripheral course. Special sensory fibers from the posterior one-third of the tongue travel via the pharyngeal branches of CN IX to the inferior glossopharyngeal ganglion where their cell bodies reside. Central course - special sensory component. The central processes of these neurons exit the inferior ganglion and pass through the jugular foramen to enter the brainstem at the level of the rostral medulla between the olive and inferior cerebellar peduncle. Upon entering the medulla these fibers ascend in the tractus solitarius and synapse in the caudal nucleus solitarius. Taste fibers from CN VII and X also ascend and synapse here. Ascending secondary neurons originating in nucleus solitarius project bilaterally to the ventral posteromedial (VPM) nuclei of the thalamus via the central tegmental tract. Tertiary neurons from the thalamus project via the posterior limb of the internal capsule to the inferior one-third of the primary sensory cortex (the gustatory cortex of the parietal lobe).

Brainstem connections

The glossopharyngeal nerve is mostly sensory. The glossopharyngeal nerve also aids in tasting, swallowing and salivary secretions. Its superior and inferior (petrous) ganglia contain the cell bodies of pain fibers. It also projects into many different structures in the brainstem:

Solitary nucleus : Taste from the posterior one-third of the tongue and information from carotid baroreceptors and carotid body chemoreceptors

Spinal nucleus of the trigeminal nerve : Somatic sensory fibers from the middle ear.

Lateral Nucleus of Ala Cinerea : Visceral pain.

Nucleus ambiguus : The lower motor neurons for the stylopharyngeus muscle.

Inferior salivatory nucleus : Parasympathetic input to the parotid and mucous glands.

Path

From the anterior portion of the medulla oblongata, the glossopharyngeal nerve passes laterally across or below the flocculus, and leaves the skull through the central part of the jugular foramen. From the superior and inferior ganglia in jugular foramen it has its own sheath of dura mater. The inferior ganglion on the inferior surface of petrous part of temporal is related with a triangular deppression into which the aqueduct of cochlea opens. Inferiorly the glossopharyngeal nerve is lateral and anterior to the vagus nerve and accessory nerve.

In its passage through the jugular foramen it passes between the internal jugular vein and internal carotid artery. It descends in front of the latter vessel, and beneath the styloid process and the muscles connected with it, to the lower border of the stylopharyngeus. It then curves forward, forming an arch on the side of the neck and lying upon the stylopharyngeus and middle pharyngeal constrictor muscle. From there it passes under cover of the hyoglossus muscle, and is finally distributed to the palatine tonsil, the mucous membrane of the fauces and base of the tongue, and the mucous glands of the mouth

Branches Tympanic Stylopharyngeal

Tonsillar

Nerve to carotid sinus

Branches to the posterior third of tongue

Lingual branches

A communicating branch to the Vagus nerve

Note: The glossopharyneal nerve contributes in the formation of the pharyngeal plexus along with the vagus nerve.

Testing the glossopharyngeal nerve

The integrity of the glossopharyngeal nerve may be evaluated by testing the patient's general sensation and that of taste on the posterior third of the tongue. The gag reflex can also be used to evaluate the glossphyaryngeal nerve, but also tests the vagus nerve, as only the afferent fibres involved in the reflex are carried by the glossopharyngeal nerve.

Vagus nerve

Nerve: Vagus nerve

Plan of upper portions of glossopharyngeal, vagus, and

accessory nerves.

Course and distribution of the glossopharyngeal, vagus, and

accessory nerves.

Latin nervus vagus

Innervates Levator veli palatini, Salpingopharyngeus,

Palatoglossus, Palatopharyngeus, Superior

pharyngeal constrictor, Middle pharyngeal

constrictor, Inferior pharyngeal constrictor, viscera

The vagus nerve (pronounced /ˈveɪɡəs/, US dict: vā′·gəs), also called pneumogastric nerve or cranial nerve X, is the tenth of twelve (excluding CN0) paired cranial nerves. Upon leaving the medulla between the olivary nucleus and the inferior cerebellar peduncle, it extends through the jugular foramen, then passing into the carotid sheath between the internal carotid artery and the internal jugular vein down below the head, to the neck, chest and abdomen, where it contributes to the innervation of the viscera. Besides output to the various organs in the body the vagus nerve conveys sensory information about the state of the body's organs to the central nervous system. 80-90% of the nerve fibers in the vagus nerve are afferent (sensory) nerves communicating the state of the viscera to the brain.[1]

The medieval Latin word vagus means literally "Wandering" (the words vagrant, vagabond, and vague come from the same root). Sometimes the branches are spoken of in the plural and are thus called vagi (pronounced /ˈveɪdʒaɪ/, US dict: vā′·jī). The vagus is also called the pneumogastric nerve since it innervates both the lungs and the stomach.

Branches Auricular nerve Pharyngeal nerve

Superior laryngeal nerve

Superior cervical cardiac branches of vagus nerve

Inferior cervical cardiac branch

Recurrent laryngeal nerve

Thoracic cardiac branches

Branches to the pulmonary plexus

Branches to the esophageal plexus

Anterior vagal trunk

Posterior vagal trunk

Hering-Breuer reflex in alveoli

The vagus runs posterior to the common carotid artery and internal jugular vein inside the carotid sheath.

Innervation

Both right and left vagus nerves descend from the brain in the carotid sheath, lateral to the carotid artery.

The right vagus nerve gives rise to the right recurrent laryngeal nerve which hooks around the right subclavian artery and ascends into the neck between the trachea and esophagus. The right vagus then crosses anteriorly to the right subclavian artery and runs posterior to the superior vena cava and descends posterior to the right main bronchus and contributes to cardiac, pulmonary and esophageal plexuses. It forms the posterior vagal trunk at the lower part of the esophagus and enters the diaphragm through the esophageal hiatus.

The left vagus nerve enters the thorax between left common carotid artery and left subclavian artery and descends on the aortic arch. It gives rise to the left recurrent laryngeal nerve which hooks around the aortic arch to the left of the ligamentum arteriosum and ascends between the trachea and esophagus. The left vagus further gives off thoracic cardiac branches, breaks up into pulmonary plexus, continues into the esophageal plexus and enters the abdomen as the anterior vagal trunk in the esophageal hiatus of the diaphragm. Both the vagal nerves have their cell bodies contained in the two nodose ganglia.

The vagus nerve supplies motor parasympathetic fibers to all the organs except the suprarenal (adrenal) glands, from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles, namely:

Cricothyroid muscle Levator veli palatini muscle

Salpingopharyngeus muscle

Palatoglossus muscle

Palatopharyngeus muscle

Superior, middle and inferior pharyngeal constrictors

Muscles of the larynx (speech).

This means that the vagus nerve is responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, and quite a few muscle movements in the mouth, including speech (via the recurrent laryngeal nerve) and keeping the larynx open for breathing (via action of the posterior cricoarytenoid muscle, the only abductor of the vocal folds). It also has some afferent fibers that innervate the inner (canal) portion of the outer ear, via the Auricular branch (also known as Alderman's nerve) and part of the meninges. This explains why a person may cough when tickled on their ear (such as when trying to remove ear wax with a cotton swab).

The vagus nerve and the heart

Fibres of the vagus nerve (right/bottom of image) innervate the sinoatrial node tissue (central and left of image). H&E stain.

Parasympathetic innervation of the heart is controlled by the vagus nerve. Specifically, the vagus nerve acts to lower the heart rate. The right vagus innervates the sinoatrial node. Parasympathetic hyperstimulation predisposes those affected to bradyarrhythmias. The left vagus when hyperstimulated predisposes the heart to atrioventricular (AV) blocks.

At this location neuroscientist Otto Loewi first proved that nerves secrete substances called neurotransmitters which have effects on receptors in target tissues. Loewi described the substance released by the vagus nerve as vagusstoff, which was later found to be acetylcholine. Drugs that inhibit the muscarinic cholinergic receptor (anticholinergics) such as atropine and scopolamine are called vagolytic because they inhibit the action of the vagus nerve on the heart, gastrointestinal tract and other organs. Anticholinergic drugs increase heart rate and are used to treat bradycardia (slow heart rate) and asystole, which is when the heart has no electrical activity.

Medical treatment involving the vagus nerve

Vagus nerve stimulation (VNS) therapy using a pacemaker-like device implanted in the chest is a treatment used since 1997 to control seizures in epilepsy patients and has recently been approved for treating drug-resistant cases of clinical depression.[2] A non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon undergo trials.[citation

needed]

VNS may also be achieved by one of the vagal maneuvers: holding the breath for a few seconds, dipping the face in cold water, coughing, or tensing the stomach muscles as if to bear down to have a bowel movement.[3] Patients with supraventricular tachycardia,[3] atrial fibrillation, and other illnesses may be trained to perform vagal maneuvers (or find one or more on their own).

Vagus nerve blocking (VBLOC) therapy is similar to VNS but only used during the day. In a six month open-label trial involving three medical centers in Australia, Mexico, and Norway, vagus nerve blocking has helped 31 obese participants lose an average of nearly 15 percent of their excess weight. A year long 300 participant double-blind, phase II trial has begun.[4]

Vagotomy (cutting of the vagus nerve) is a now-obsolete therapy that was performed for peptic ulcer disease. Vagotomy is currently being researched as a less invasive alternative weight loss procedure to gastric bypass surgery.[5] The procedure curbs the feeling of hunger and is sometimes performed in conjunction with putting bands on patients' stomachs, resulting in average weight loss of 43% at six months with diet and exercise.[6]

One serious side effect of a Vagotomy is a Vitamin B12 deficiency later in life - i.e. 10 years - that is similar to Pernicious Anaemia. As one gets older, the stomach produces less acid. The acid, and one of its components called Intrinsic Factor, is needed to metabolize B12 from food. The vagotomy reduces the acid that ultimately leads to the deficiency which, if left untreated, causes nerve damage, tiredness, dementia, paranoia and ultimately death.[7]

Physical and emotional effects

Activation of the vagus nerve typically leads to a reduction in heart rate, blood pressure, or both. This occurs commonly in the setting of gastrointestinal illness such as viral gastroenteritis or acute cholecystitis, or in response to other stimuli, including carotid sinus massage, Valsalva maneuver, or pain from any cause, particularly having blood drawn. When the circulatory changes are great enough, vasovagal syncope results. Relative dehydration tends to amplify these responses.

Excessive activation of the vagal nerve during emotional stress, which is a parasympathetic overcompensation of a strong sympathetic nervous system response associated with stress, can also cause vasovagal syncope because of a sudden drop in blood pressure and heart rate. Vasovagal syncope affects young children and women more often. It can also lead to temporary loss of bladder control under moments of extreme fear.

Research has shown that women who have complete transection of the spinal cord can experience orgasms through the vagus nerve, which can go from the uterus, cervix and probably the vagina to the brain.[8][9]

Effects of vagus nerve lesions

The patient complains of hoarse voice, difficulty in swallowing (dysphagia) and choking when drinking fluid. There is also loss of gag reflex. Uvula deviates away from the side of lesion and there is failure of palate elevation.

Accessory nerve

Nerve: Accessory nerve

Plan of upper portions of glossopharyngeal, vagus, and

accessory nerves.

Latin nervus accessorius

Innervates sternocleidomastoid muscle, trapezius muscle

In anatomy, the accessory nerve is a nerve that controls specific muscles of the neck. As a part of it was formerly believed to originate in the brain, it is considered a cranial nerve. Based on its location relative to other such nerves, it is designated the eleventh of twelve cranial nerves, and is thus abbreviated CN XI. Although anatomists typically refer to the accessory nerve in singular, there are in reality two accessory nerves, one on each side of the body.

Traditional descriptions of the accessory nerve divide it into two parts: a spinal part and a cranial part.[1] But because the cranial component rapidly joins the vagus nerve and serves the same function as other vagal nerve fibers, modern descriptions often consider the cranial component part of the vagus nerve and not part of the accessory nerve proper.[2] Thus in contemporary discussions of the accessory nerve, the common practice is to dismiss the cranial part altogether, referring to the accessory nerve specifically as the spinal accessory nerve.

The spinal accessory nerve provides motor innervation from the central nervous system to two muscles of the neck: the sternocleidomastoid muscle and the trapezius muscle. The sternocleidomastoid muscle tilts and rotates the head, while the trapezius muscle has several actions on the scapula, including shoulder elevation and adduction of the scapula.

Range of motion and strength testing of the neck and shoulders can be measured during a neurological examination to assess function of the spinal accessory nerve. Limited range of motion or poor muscle strength are suggestive of damage to the spinal accessory nerve, which can result from a variety of causes. Injury to the spinal accessory nerve is most commonly caused by medical procedures that involve the head and neck.[3]

Anatomy

Course

Upon exiting the skull via the jugular foramen, the spinal accessory nerve pierces the sternocleidomastoid muscle before terminating on the trapezius muscle.

Like other cranial nerves, the spinal accessory nerve begins in the central nervous system and exits the cranium through a specialized hole (or foramen). However, unlike all other cranial nerves, the spinal accessory nerve begins outside the skull rather than inside. In particular, in the majority of individuals, the fibers of the spinal accessory nerve originate solely in neurons situated in the upper spinal cord.[4] These fibers coalesce to form spinal rootlets, roots, and finally the spinal accessory nerve itself, which enters the skull through the foramen magnum, the large opening at the base of the skull. The nerve courses along the inner wall of the skull towards the jugular foramen, through which it exits the skull with the glossopharyngeal (CN IX) and vagus nerves (CN X). Owing to its peculiar course, the spinal accessory nerve is notable for being the only cranial nerve to both enter and exit the skull.

Traditionally, the accessory nerve is described as having a small cranial component that descends from the medulla oblongata and briefly connects with the spinal accessory component before branching off of the nerve to join the vagus nerve. A recent study of twelve subjects suggests that in the majority of individuals, this cranial component does not make any distinct connection to the spinal component; the roots of these distinct components were separated by a fibrous sheath in all but one subject.[4]

Once the cranial component has detached from the spinal component, the spinal accessory nerve continues alone and heads posteriorly (backwards) and inferiorly (downwards) upon exiting the skull. It pierces the sternocleidomastoid muscle while sending it motor branches, then continues inferiorly until it reaches the trapezius muscle to provide motor innervation to its upper portion.

Origin

The fibers that form the spinal accessory nerve are formed by lower motor neurons located in the upper segments of the spinal cord. This cluster of neurons, called the spinal accessory nucleus, is located in the lateral horn of the spinal cord. This is in contrast to most other motor neurons, whose cell bodies are found in the spinal cord's anterior horn. The lateral horn of high cervical segments appears to be continuous with the nucleus ambiguus of the medulla oblongata, from which the cranial component of the accessory nerve is derived.

Classification

Among investigators there is disagreement regarding the terminology used to describe the type of information carried by the accessory nerve. As the trapezius and sternocleidomastoid muscles are derived from the branchial arches, some investigators believe the spinal accessory nerve that innervates them must carry branchiomeric (special visceral efferent, SVE) information.[5] This is in line with the observation that the spinal accessory nucleus appears to be continuous with the nucleus ambiguus of the medulla. Others, notably Haines, consider the spinal accessory nerve to carry general somatic efferent (GSE) information.[6] Still others believe it is reasonable to conclude that the spinal accessory nerve contains both SVE and GSE components.[7]

Function

The nerve functions to control the sternocleidomastoid and trapezius muscles.

Clinical relevance

Injury

Injury to the spinal accessory nerve can cause an accessory nerve disorder or spinal accessory nerve palsy, which results in diminished or absent function of the sternocleidomastoid muscle and upper portion of the trapezius muscle.

The distal part of the spinal accessory nerve is most susceptible to injury. Throughout much of its course, the nerve is protected from injury by the muscles it innervates. It is in the interval between protection from these muscles, which corresponds to the distal part of the nerve, that the spinal accessory nerve is most vulnerable to injury.

Assessment of function

As physical examination cannot directly assess the functioning of nerves, assessment of spinal accessory nerve function is usually done indirectly. This is often accomplished through gross observation, range of motion testing, and strength testing, with specific attention to the trapezius and sternocleidomastoid muscles which are innervated by the spinal accessory nerve.

The trapezius muscle is tested by asking the patient to shrug their shoulders with and without resistance. A one-sided weakness is indicative of an injury to the spinal accessory nerve on the same side (termed ipsilateral) of the body being assessed. The sternocleidomastoid muscle is tested by asking the patient to turn their head to the left or right against resistance. Weakness in head-turning suggests injury to the contralateral spinal accessory nerve: a weak leftward turn is indicative of a weak right sternocleidomastoid muscle (and thus right spinal accessory nerve injury), while a weak rightward turn is indicative of a weak left sternocleidomastoid muscle (and thus left spinal accessory nerve).

Gross observation may identify other findings associated with spinal accessory nerve injury. Patients with spinal accessory nerve palsy may exhibit signs of lower motor neuron disease such as diminished muscle mass (atrophy) and fasciculations of the sternocleidomastoid and trapezius muscles.

History and etymology

In 1848, Jones Quain described the nerve as the "spinal nerve accessory to the vagus", recognizing that while a minor component of the nerve joins with the larger vagus nerve, the majority of accessory nerve fibers originate in the spinal cord.[8] Quain also suggested spinal accessory nerve as a shortened form of the term; this term, and its more abbreviated variant, accessory nerve, have persisted to modern times. Throughout this interval, the nerve has never had a consistent name among investigators and medical practitioners.

Some use accessory nerve and spinal accessory nerve interchangeably; others distinguish between spinal accessory nerve and cranial accessory nerve; still others use accessory nerve to refer to both spinal and cranial components of the nerve.

Hypoglossal nerve

Nerve: Hypoglossal nerve

Hypoglossal nerve, cervical plexus, and their branches.

Latin nervus hypoglossus

Innervates genioglossus, hyoglossus, styloglossus

The hypoglossal nerve is the twelfth cranial nerve (XII), leading to the tongue. The nerve arises from the hypoglossal nucleus and emerges from the medulla oblongata in the preolivary sulcus separating the olive and the pyramid. It then passes through the hypoglossal canal. On emerging from the hypoglossal canal, it gives off a small meningeal branch and picks up a branch from the anterior ramus of C1. It spirals behind the vagus nerve and passes between the internal carotid artery and internal jugular vein lying on the carotid sheath. After passing deep to the posterior belly of the digastric muscle, it passes to the submandibular region to enter the tongue.

It supplies motor fibres to all of the muscles of the tongue, except the palatoglossus muscle which is innervated by the vagus nerve (cranial nerve X) or, according to some classifications, by fibers from the glossopharyngeal nerve (cranial nerve IX) that "hitchhike" within the vagus.

Testing the hypoglossal nerve

To test the function of the nerve, a person is asked to poke out their tongue. If there is a loss of function on one side (unilateral paralysis) the tongue will point towards the affected side.

The strength of the tongue can be tested by getting the person to poke the inside of their cheek, and feeling how strongly they can push a finger pushed against their cheek - a more elegant way of testing than directly touching the tongue.

The tongue can also be looked at for signs of lower motor neuron disease, such as fasciculation and atrophy.

Paralysis/paresis of one side of the tongue results in ipsilateral curvature of the tongue (apex toward the impaired side of the mouth) i.e., the tongue will move towards the affected side.

Cranial Nerve XII is innervated by the contralateral cortex, so a purely upper motor neuron lesion will cause the tongue to deviate away from the cortical lesion.