Left View of the human brain from below, showing origins of cranial nerves. Right Juxtaposedskull base withforamina through which many nerves exit the skull.
Cranial nerves as they pass through the skull base to the brain
Cranial nerves are thenerves that emerge directly from thebrain (including thebrainstem), of which there are conventionally considered twelve pairs. Cranial nerves relay information between the brain and parts of the body, primarily to and from regions of thehead and neck, including thespecial senses ofvision,taste,smell, andhearing.[1]
There are conventionally twelve pairs of cranial nerves, which are described withRoman numerals I–XII. Some considered there to be thirteen pairs of cranial nerves, including the non-pairedcranial nerve zero. The numbering of the cranial nerves is based on the order in which they emerge from the brain and brainstem, from front to back.[2]
The cranial nerves are considered components of theperipheral nervous system (PNS),[3] although on a structural level the olfactory (I), optic (II), and trigeminal (V) nerves are more accurately considered part of the central nervous system (CNS).[4]
Cranial nerves are generally named according to their structure or function. For example, the olfactory nerve (I) supplies smell, and the facial nerve (VII) supplies the muscles of the face. BecauseLatin was thelingua franca of the study ofanatomy when the nerves were first documented, recorded, and discussed, many nerves maintain Latin orGreek names, including the trochlear nerve (IV), named according to its structure, as it supplies a muscle that attaches to a pulley (Greek:trochlea). The trigeminal nerve (V) is named in accordance with its three components (Latin:trigeminus meaningtriplets),[6] and the vagus nerve (X) is named for its wandering course (Latin:vagus).[7]
Cranial nerves are numbered based on their position from front to back (rostral-caudal) of their position on the brain,[8] as, when viewing the forebrain and brainstem from below, they are often visible in their numeric order. For example, the olfactory nerves (I) and optic nerves (II) arise from the base of theforebrain, and the other nerves, III to XII, arise from the brainstem.[8]
Cranial nerves have paths within and outside theskull. The paths within the skull are called "intracranial" and the paths outside the skull are called "extracranial". There are many holes in the skull called "foramina" by which the nerves can exit the skull. All cranial nerves arepaired, which means they occur on both the right and left sides of the body. The muscle, skin, or additional function supplied by a nerve, on the same side of the body as the side it originates from, is anipsilateral function. If the function is on the opposite side to the origin of the nerve, this is known as acontralateral function.[9]
Grossly, all cranial nerves have anucleus. With the exception of the olfactory nerve (I) and optic nerve (II), all the nuclei are present in the brainstem.[2]
Themidbrain has the nuclei of the oculomotor nerve (III) and trochlear nerve (IV); thepons has the nuclei of the trigeminal nerve (V), abducens nerve (VI), facial nerve (VII) and vestibulocochlear nerve (VIII); and themedulla has the nuclei of the glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI) and hypoglossal nerve (XII).[10] The olfactory nerve (I) emerges from theolfactory bulb, and depending slightly on division the optic nerve (II) is considered to emerge from thelateral geniculate nuclei.[10]
Because each nerve may have several functions, thenerve fibres that make up the nerve may collect in more than onenucleus. For example, the trigeminal nerve (V), which has a sensory and a motor role, hasat least four nuclei.[10][11]
With the exception of the olfactory nerve (I) and optic nerve (II), the cranial nerves emerge from thebrainstem. The oculomotor nerve (III) and trochlear nerve (IV) emerge from themidbrain, the trigeminal (V), abducens (VI), facial (VII) and vestibulocochlear (VIII) from thepons, and the glossopharyngeal (IX), vagus (X), accessory (XI) and hypoglossal (XII) emerge from themedulla.[12]
The olfactory nerve (I) and optic nerve (II) emerge separately. The olfactory nerves emerge from theolfactory bulbs on either side of thecrista galli, a bony projection below thefrontal lobe, and the optic nerves (II) emerge from the lateral colliculus, swellings on either side of thetemporal lobes of the brain.[12]
The cranial nerves give rise to a number ofganglia, collections of thecell bodies of neurons in the nerves that are outside of the brain. These ganglia are both parasympathetic and sensory ganglia.[10]
The ganglion of the sensory nerves, which are similar in structure to the dorsal root ganglion of thespinal cord, include:[13]
Thetrigeminal ganglia of the trigeminal nerve (V), which occupies a space in thedura mater calledMeckel's cave. This ganglion contains only the sensory fibres of the trigeminal nerve.
After emerging from the brain, the cranial nerves travel within theskull, and some must leave it in order to reach their destinations. Often the nerves pass through holes in the skull, calledforamina, as they travel to their destinations. Other nerves pass through bony canals, longer pathways enclosed by bone. These foramina and canals may contain more than one cranial nerve and may also contain blood vessels.[13]
The terminal nerve (0) is a thin network of fibers associated with the dura and lamina terminalis running rostral to the olfactory nerve, with projections through the cribriform plate.
The olfactory nerve (I) passes through perforations in thecribriform plate part of theethmoid bone. The nerve fibres end in the upper nasal cavity.
The oculomotor nerve (III), trochlear nerve (IV), abducens nerve (VI) and the ophthalmic branch of the trigeminal nerve (V1) travel through thecavernous sinus into thesuperior orbital fissure, passing out of the skull into theorbit.
The maxillary division of the trigeminal nerve (V2) passes throughforamen rotundum in the sphenoid bone.
The mandibular division of the trigeminal nerve (V3) passes throughforamen ovale of the sphenoid bone.
The facial nerve (VII) and vestibulocochlear nerve (VIII) both enter theinternal auditory canal in thetemporal bone. The facial nerve then reaches the side of the face by using the stylomastoid foramen, also in the temporal bone. Its fibers then spread out to reach and control all of the muscles of facial expression. The vestibulocochlear nerve reaches the organs that control balance and hearing in the temporal bone and therefore does not reach the external surface of the skull.
The glossopharyngeal (IX), vagus (X) and accessory nerve (XI) all leave the skull via the jugular foramen to enter the neck. The glossopharyngeal nerve provides sensation to the upper throat and the back of the tongue, the vagus supplies the muscles in thelarynx and continues downward to supply parasympathetic supply to the chest and abdomen. The accessory nerve controls the trapezius and sternocleidomastoid muscles in the neck and shoulder.
Schematic 3D model of the cranial nervesThe hypoglossal nerve (XII) exits the skull using the hypoglossal canal in theoccipital bone.
The cranial nerves are formed from the contribution of two specialized embryonic cell populations,cranial neural crest and ectodermal placodes. The components of the sensory nervous system of the head are derived from the neural crest and from an embryonic cell population developing in close proximity, the cranial sensory placodes (the olfactory, lens, otic, trigeminal, epibranchial and paratympanic placodes). The dual origin cranial nerves are summarized in the following table:[15]
Contributions of neural crest cells and placodes to ganglia and cranial nerves
Cranial nerve
Ganglion and type
Origin of neurons
CNI – olfactory
(Ensheating glia of olfactory nerves)
Telencephalon/olfactory placode; NCCs at forebrain
CNIII – oculomotor
(m)
Ciliary, visceral efferent
NCCs at forebrain-midbrain junction (caudal diencephalon and the anterior mesencephalon)
CNV – trigeminal
(mix)
Trigeminal, general afferent
NCCs at forebrain-midbrain junction (from r2 into 1st PA), trigeminal placode
CNVII – facial
(mix)
-Superior, general and special afferent
-Inferior: geniculate, general and special afferent
-Sphenopalatine, visceral efferent
-Submandibular, visceral efferent
-Hindbrain NCCs (from r4 into 2nd PA), 1st epibranchial placode
-1st epibranchial placode (geniculate)
-Hindbrain NCCs (2nd PA)
-Hindbrain NCCs (2nd PA)
CNVIII – Vestibulocochlear
(s)
-Acoustic: cochlear, special afferent; and vestibular, special afferent
-Otic placode and hindbrain (from r4) NCCs
CNIX – glossopharyngeal
(mix)
-Superior, general and special afferent
-Inferior, petrosal, general and special afferent
-Otic, visceral efferent
-Hindbrain NCCs (from r6 into 3rd PA)
-2nd epibranchial placode (petrosal)
-Hindbrain NCCs (from r6 into 3rd PA)
CNX – vagus
(mix)
Superior laryngeal branch; and recurrent laryngeal branch
Abbreviations: CN, cranial nerve; m, purely motor nerve; mix, mixed nerve (sensory and motor); NC, neural crest; PA, pharyngeal (branchial) arch; r, rhombomere; s, purely sensory nerve. * There is no known ganglion of the accessory nerve. The cranial part of the accessory nerve sends occasional branches to the superior ganglion of the vagus nerve.
The cranial nerves provide motor and sensory supply mainly to the structures within the head and neck. The sensory supply includes both "general" sensation such as temperature and touch, and "special" senses such astaste,vision,smell, balance andhearing.[11] The vagus nerve (X) provides sensory and autonomic (parasympathetic) supply to structures in the neck and also to most of the organs in the chest and abdomen.[3][2]
Theterminal nerve (0) may not have a role in humans,[3] although it has been implicated in hormonal responses to smell, sexual response and mate selection.[5]
Theolfactory nerve (I) conveys information giving rise to the sense of smell.[16]
Damage to the olfactory nerve (I) can cause an inability to smell (anosmia), a distortion in the sense of smell (parosmia), or a distortion or lack of taste.[16][17]
Damage to the optic nerve (II) affects specific aspects of vision that depend on the location of the damage. A person may not be able to see objects on their left or right sides (homonymous hemianopsia), or may have difficulty seeing objects from their outer visual fields (bitemporal hemianopsia) if theoptic chiasm is involved. Inflammation (optic neuritis) may impact the sharpness of vision or color detection[16]
The oculomotor (III), troclear (IV) and abducens (VI) nerves supply the muscle of the eye. Damage will affect the movement of the eye in various ways, shown here.
Theoculomotor nerve (III),trochlear nerve (IV) andabducens nerve (VI) coordinateeye movement. The oculomotor nerve (III) controls all muscles of the eye except for thesuperior oblique muscle controlled by the trochlear nerve (IV), and thelateral rectus muscle controlled by the abducens nerve (VI). This means the ability of the eye to look down and inwards is controlled by the trochlear nerve (IV), the ability to look outwards is controlled by the abducens nerve (VI), and all other movements are controlled by the oculomotor nerve (III)[16]
Damage to these nerves may affect the movement of the eye. Damage may result in double vision (diplopia) because the movements of the eyes are not synchronized. Abnormalities of visual movement may also be seen on examination, such as jittering (nystagmus).[17]
Damage to the oculomotor nerve (III) can cause double vision and inability to coordinate the movements of both eyes (strabismus), also eyelid drooping (ptosis) and pupil dilation (mydriasis).[18] Lesions may also lead to inability to open the eye due to paralysis of thelevator palpebrae muscle. Individuals suffering from a lesion to the oculomotor nerve, may compensate by tilting their heads to alleviate symptoms due to paralysis of one or more of the eye muscles it controls.[17]
Damage to the trochlear nerve (IV) can also cause double vision with the eye adducted and elevated.[18] The result will be an eye which can not move downwards properly (especially downwards when in an inward position). This is due to impairment in the superior oblique muscle.[17]
Damage to the abducens nerve (VI) can also result in double vision.[18] This is due to impairment in the lateral rectus muscle, supplied by the abducens nerve.[17]
Thetrigeminal nerve (V) and its three main branches the ophthalmic (V1), maxillary (V2), and mandibular (V3) provide sensation to the skin of the face and also controls the muscles ofchewing.[16]
Damage to the trigeminal nerve leads to loss of sensation in an affected area. Other conditions affecting the trigeminal nerve (V) includetrigeminal neuralgia, herpes zoster, sinusitis pain, presence of adental abscess, andcluster headaches.[19][16]
The facial nerve (VII) supplies the muscles of facial expression. Damage to the nerve causes a lack of muscle tone on the affected side, as can be seen on the right side of the face here.
Thefacial nerve (VII) controls most muscles of facial expression, supplies the sensation of taste from the front two-thirds of the tongue, and controls thestapedius muscle.[16] Most muscles are supplied by the cortex on the opposite side of the brain; the exception is thefrontalis muscle of the forehead, in which the left and the right side of the muscle both receive inputs from both sides of the brain.[16]
Damage to the facial nerve (VII) may causefacial palsy. This is where a person is unable to move the muscles on one or both sides of their face.[16] The most common cause of this isBell's palsy, the ultimate cause of which is unknown.[16] Patients with Bell's palsy often have a drooping mouth on the affected side and often have trouble chewing because thebuccinator muscle is affected.[3] The facial nerve is also the most commonly affected cranial nerve inblunt trauma.[20]
Thevestibulocochlear nerve (VIII) supplies information relating to balance and hearing via its two branches, thevestibular andcochlear nerves. The vestibular part is responsible for supplying sensation from thevestibules andsemicircular canal of theinner ear, including information aboutbalance, and is an important component of thevestibuloocular reflex, which keeps the head stable and allows the eyes to track moving objects. The cochlear nerve transmits information from thecochlea, allowing sound to be heard.[2]
When damaged, the vestibular nerve may give rise to the sensation of spinning and dizziness (vertigo). Function of the vestibular nerve may be tested by putting cold and warm water in the ears and watching eye movementscaloric stimulation.[3][17] Damage to the vestibulocochlear nerve can also present as repetitive and involuntary eye movements (nystagmus), particularly when the eye is moving horizontally.[17] Damage to the cochlear nerve will cause partial or completedeafness in the affected ear.[17]
Thevagus nerve (X) provides sensory and parasympathetic supply to structures in the neck and also to most of the organs in the chest and abdomen.[2]
Loss of function of the vagus nerve (X) will lead to a loss of parasympathetic supply to a very large number of structures. Major effects of damage to the vagus nerve may include a rise in blood pressure and heart rate. Isolated dysfunction of only the vagus nerve is rare, but – if the lesion is located above the point at which the vagus first branches off – can be indicated by a hoarse voice, due to dysfunction of one of its branches, therecurrent laryngeal nerve.[10]
Damage to this nerve may result in difficulties swallowing.[17]
The accessory nerve (XI) supplies the sternocleidomastoid and trapezius muscles. Damage to the nerve may cause awinged scapula, shown here.
The hypoglossal nerve (XII) supplies the muscles of the tongue. A damaged hypoglossal nerve will result in an inability to stick the tongue out straight; here seen in an injury resulting frombranchial cyst surgery.[21]
Damage to the accessory nerve (XI) will lead to weakness in the trapezius muscle on the same side as the damage. The trapezius lifts the shoulder whenshrugging, so the affected shoulder will not be able to shrug and the shoulder blade (scapula) will protrude into awinged position.[3] Depending on the location of the lesion there may also be weakness present in the sternocleidomastoid muscle, which acts to turn the head so that the face points to the opposite side.[16]
Thehypoglossal nerve (XII) supplies the intrinsic muscles of the tongue, controlling tongue movement.[16] The hypoglossal nerve (XII) is unique in that it is supplied by themotor cortices of both hemispheres of the brain.[17]
Damage to the nerve may lead to fasciculations or wasting (atrophy) of the muscles of the tongue. This will lead to weakness of tongue movement on that side. When damaged and extended, the tongue will move towards the weaker or damaged side, as shown in the image.[17] The fasciculations of the tongue are sometimes said to look like a "bag of worms". Damage to the nerve tract or nucleus will not lead to atrophy or fasciculations, but only weakness of the muscles on the same side as the damage.[17]
Doctors,neurologists and other medical professionals may conduct acranial nerve examination as part of aneurological examination to examine the cranial nerves. This is a highly formalised series of steps involving specific tests for each nerve.[16] Dysfunction of a nerve identified during testing may point to a problem with the nerve or of a part of the brain.[16]
A cranial nerve exam starts with observation of the patient, as some cranial nerve lesions may affect the symmetry of the eyes or face.[16] Vision may be tested by examining thevisual fields, or by examining theretina with anophthalmoscope, using a process known asfunduscopy. Visual field testing may be used to pin-point structural lesions in the optic nerve, or further along the visual pathways.[17] Eye movement is tested and abnormalities such asnystagmus are observed for. The sensation of the face is tested, and patients are asked to perform different facial movements, such as puffing out of the cheeks. Hearing is checked by voice andtuning forks. The patient'suvula is examined. After performing a shrug and head turn, the patient's tongue function is assessed by various tongue movements.[16]
Smell is not routinely tested, but if there is suspicion of a change in the sense of smell, each nostril is tested with substances of known odors such as coffee or soap. Intensely smelling substances, for exampleammonia, may lead to the activation ofpain receptors of the trigeminal nerve (V) located in the nasal cavity and this can confound olfactory testing.[16][17]
An increase in intracranial pressure may lead to impairment of the optic nerves (II) due to compression of the surrounding veins and capillaries, causing swelling of the eyeball (papilloedema).[24] A cancer, such as anoptic nerve glioma, may also impact the optic nerve (II). Apituitary tumour may compress the optic tracts or theoptic chiasm of the optic nerve (II), leading to visual field loss. A pituitary tumour may also extend into the cavernous sinus, compressing the oculomotor nerve (III), trochlear nerve (IV) and abducens nerve (VI), leading to double-vision andstrabismus. These nerves may also be affected by herniation of thetemporal lobes of the brain through thefalx cerebri.[22]
The cause oftrigeminal neuralgia, in which one side of the face is exquisitely painful, is thought to be compression of the nerve by an artery as the nerve emerges from the brain stem.[22] Anacoustic neuroma, particularly at the junction between the pons and medulla, may compress the facial nerve (VII) and vestibulocochlear nerve (VIII), leading to hearing and sensory loss on the affected side.[22][25]
Occlusion of blood vessels that supply the nerves or their nuclei, anischemicstroke, may cause specific signs and symptoms relating to the damaged area. If there is a stroke of themidbrain,pons ormedulla, various cranial nerves may be damaged, resulting in dysfunction and symptoms ofa number of different syndromes.[26]Thrombosis, such as acavernous sinus thrombosis, refers to a clot (thrombus) affecting the venous drainage from thecavernous sinus, affects the optic (II), oculomotor (III), trochlear (IV), ophthalmic branch of the trigeminal nerve (V1) and the abducens nerve (VI).[25]
Inflammation of a cranial nerve can occur as a result of infection, such as viral causes like reactivatedherpes simplex virus, or can occur spontaneously. Inflammation of the facial nerve (VII) may result inBell's palsy.[27]
The Graeco-Roman anatomistGalen (AD 129–210) named seven pairs of cranial nerves.[7] Much later, in 1664, English anatomist SirThomas Willis suggested that there were actually 9 pairs of nerves. Finally, in 1778, German anatomistSamuel Soemmering named the 12 pairs of nerves that are generally accepted today.[7] However, because many of the nerves emerge from the brain stem as rootlets, there is continual debate as to how many nerves there actually are, and how they should be grouped.[7] For example, there is reason to consider both the olfactory (I) and optic (II) nerves to be brain tracts, rather than cranial nerves.[7]
Dog-fish brain in two projections. top;ventral bottom;lateral The accessory nerve (XI) and hypoglossal nerve (XII) cannot be seen, as they are not always present in all vertebrates.
Cranial nerves are also present in othervertebrates. Otheramniotes (non-amphibiantetrapods) have cranial nerves similar to those of humans. Inanamniotes (fishes and amphibians), the accessory nerve (XI) and hypoglossal nerve (XII) do not exist, with the accessory nerve (XI) being an integral part of the vagus nerve (X); the hypoglossal nerve (XII) is represented by a variable number of spinal nerves emerging from vertebral segments fused into the occiput. These two nerves only became discrete nerves in the ancestors of amniotes.[28] The very smallterminal nerve (nerve N or O) exists in humans but may not be functional. In other animals, it appears to be important to sexual receptivity based on perceptions ofpheromones.[3][29]
The cranial nerves in the horse
Ventral view of asheep's brain. The exits of the various cranial nerves are marked with red.
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^abcNorton, Neil (2007).Netter's head and neck anatomy for dentistry. Philadelphia, Pa.: Saunders Elsevier. p. 78.ISBN978-1-929007-88-2.
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