Cranial nerves are the that emerge directly from the brain (including the brainstem), 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 the head and neck, including the special senses of vision, taste, Olfaction, and hearing.
The cranial nerves emerge from the central nervous system above the level of the first vertebra of the vertebral column. Each cranial nerve is paired and is present on both sides.
There are conventionally twelve pairs of cranial nerves, which are described with Roman numerals I–XII. Some considered there to be thirteen pairs of cranial nerves, including the non-paired cranial 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.
The (0), (I) and (II) emerge from the cerebrum, and the remaining ten pairs arise from the brainstem, which is the lower part of the brain.
The cranial nerves are considered components of the peripheral nervous system (PNS), 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). Board Review Series – Neuroanatomy, Fourth Edition, Lippincott Williams & Wilkins, Maryland 2008, p. 177. .
The cranial nerves are in contrast to , which emerge from segments of the spinal cord.
Cranial nerves are numbered based on their position from front to back (rostral-caudal) of their position on the brain,
Cranial nerves have paths within and outside the Human Skull. 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 are paired, 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 an ipsilateral function. If the function is on the opposite side to the origin of the nerve, this is known as a contralateral function.
The midbrain has the nuclei of the oculomotor nerve (III) and trochlear nerve (IV); the pons has the nuclei of the trigeminal nerve (V), abducens nerve (VI), facial nerve (VII) and vestibulocochlear nerve (VIII); and the medulla has the nuclei of the glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI) and hypoglossal nerve (XII).
Because each nerve may have several functions, the that make up the nerve may collect in more than one nucleus. For example, the trigeminal nerve (V), which has a sensory and a motor role, has at least four nuclei.
The olfactory nerve (I) and optic nerve (II) emerge separately. The olfactory nerves emerge from the on either side of the crista galli, a bony projection below the frontal lobe, and the optic nerves (II) emerge from the lateral colliculus, swellings on either side of the of the brain.
The sensory ganglia of the cranial nerves, directly correspond to the dorsal root ganglia of and are known as cranial nerve ganglia. Sensory ganglia exist for nerves with sensory function: V, VII, VIII, IX, X. There are also a number of parasympathetic cranial nerve ganglia. Sympathetic ganglia supplying the head and neck reside in the upper regions of the sympathetic trunk, and do not belong to the cranial nerves.
The ganglion of the sensory nerves, which are similar in structure to the dorsal root ganglion of the spinal cord, include:
Additional ganglia for nerves with parasympathetic function exist, and include the ciliary ganglion of the oculomotor nerve (III), the pterygopalatine ganglion of the maxillary nerve (V2), the submandibular ganglion of the lingual nerve, a branch of the facial nerve (VII), and the otic ganglion of the glossopharyngeal nerve (IX).
After emerging from the brain, the cranial nerves travel within the skull, and some must leave it in order to reach their destinations. Often the nerves pass through holes in the skull, called foramen, 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.
Contributions of neural crest cells and placodes to ganglia and cranial nerves
(Ensheating glia of olfactory nerves)
(m)
(mix)
(mix)
-Inferior: geniculate, general and special afferent
-Sphenopalatine, visceral efferent
-Submandibular, visceral efferent
-1st epibranchial placode (geniculate)
-Hindbrain NCCs (2nd PA)
-Hindbrain NCCs (2nd PA)
(s)
(mix)
-Inferior, petrosal, general and special afferent
-Otic, visceral efferent
-2nd epibranchial placode (petrosal)
-Hindbrain NCCs (from r6 into 3rd PA)
(mix)
Superior laryngeal branch; and recurrent laryngeal branch
-Inferior: nodose, general and special afferent
-Vagal: parasympathetic, visceral efferent
-Hindbrain NCCs (4th& 6th PA); 3rd (nodose) and 4th epibranchial placodes
-Hindbrain NCCs (4th & 6th PA)
(m)
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.
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 the optic chiasm is involved. Inflammation (optic neuritis) may impact the sharpness of vision or color detection
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).
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). Lesions may also lead to inability to open the eye due to paralysis of the levator 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.
Damage to the trochlear nerve (IV) can also cause double vision with the eye adducted and elevated. 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.
Damage to the abducens nerve (VI) can also result in double vision. This is due to impairment in the lateral rectus muscle, supplied by the abducens nerve.
Damage to the trigeminal nerve leads to loss of sensation in an affected area. Other conditions affecting the trigeminal nerve (V) include trigeminal neuralgia, herpes zoster, sinusitis pain, presence of a dental abscess, and .
Damage to the facial nerve (VII) may cause facial palsy. This is where a person is unable to move the muscles on one or both sides of their face. The most common cause of this is Bell's palsy, the ultimate cause of which is unknown. Patients with Bell's palsy often have a drooping mouth on the affected side and often have trouble chewing because the buccinator muscle is affected. The facial nerve is also the most commonly affected cranial nerve in blunt trauma.
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 movements caloric stimulation. Damage to the vestibulocochlear nerve can also present as repetitive and involuntary eye movements (nystagmus), particularly when the eye is moving horizontally. Damage to the cochlear nerve will cause partial or complete deafness in the affected ear.
Damage to the nerve may cause failure of the gag reflex; a failure may also be seen in damage to the vagus nerve (X).
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, the recurrent laryngeal nerve.
Damage to this nerve may result in difficulties swallowing.
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 when , so the affected shoulder will not be able to shrug and the shoulder blade (scapula) will protrude into a winged scapula position. 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.
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. 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.
A cranial nerve exam starts with observation of the patient, as some cranial nerve lesions may affect the symmetry of the eyes or face. Vision may be tested by examining the , or by examining the retina with an ophthalmoscope, using a process known as funduscopy. Visual field testing may be used to pin-point structural lesions in the optic nerve, or further along the visual pathways. Eye movement is tested and abnormalities such as nystagmus 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 and . The patient's uvula is examined. After performing a shrug and head turn, the patient's tongue function is assessed by various tongue movements.
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 example ammonia, may lead to the activation of Nociceptor of the trigeminal nerve (V) located in the nasal cavity and this can confound olfactory testing.
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).
The cause of trigeminal 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. An acoustic 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.
Multiple sclerosis, an inflammatory process resulting in a loss of the myelin sheathes which surround the cranial nerves, may cause a variety of shifting symptoms affecting multiple cranial nerves. Inflammation may also affect other cranial nerves. Other rarer inflammatory causes affecting the function of multiple cranial nerves include sarcoidosis, miliary tuberculosis, and vasculitis, such as granulomatosis with polyangiitis.
Anatomy
Terminology
Intracranial course
Nuclei
Exiting the brainstem
Ganglia
Exiting the skull and extracranial course
+ Exits of cranial nerves from the skull. Terminal nerve (0) Olfactory nerve (I) Optic nerve (II) Oculomotor (III)
Trochlear (IV)
Abducens (VI)
Trigeminal V1
(Ophthalmic nerve)Trigeminal V2
(maxillary nerve)Trigeminal V3
(Mandibular nerve)Facial nerve (VII) Vestibulocochlear (VIII) Glossopharyngeal (IX)
Vagus (X)
Accessory (XI)Hypoglossal (XII)
Development
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.
CNI – olfactory
Telencephalon/olfactory placode; NCCs at forebrain CNIII – oculomotor
Ciliary, visceral efferent NCCs at forebrain-midbrain junction (caudal diencephalon and the anterior mesencephalon) CNV – trigeminal
Trigeminal, general afferent NCCs at forebrain-midbrain junction (from r2 into 1st PA), trigeminal placode CNVII – facial
-Superior, general and special afferent
-Hindbrain NCCs (from r4 into 2nd PA), 1st epibranchial placode
CNVIII – Vestibulocochlear
-Acoustic: cochlear, special afferent; and vestibular, special afferent -Otic placode and hindbrain (from r4) NCCs CNIX – glossopharyngeal
-Superior, general and special afferent
-Hindbrain NCCs (from r6 into 3rd PA)
CNX – vagus
-Superior, general afferent
-Hindbrain NCCs (from r7-r8 to 4th & 6th PA)
CNXI – accessory
No ganglion * Hindbrain (from r7-r8 to PA 4); NCCs (4th PA)
Function
Terminal nerve (0)
Smell (I)
Vision (II)
Eye movement (III, IV, VI)
Trigeminal nerve (V)
Facial expression (VII)
Hearing and balance (VIII)
Oral sensation, taste, and salivation (IX)
Vagus nerve (X)
Shoulder elevation and head-turning (XI)
Tongue movement (XII)
Clinical significance
Examination
Damage
Compression
Stroke
Inflammation
Other
History
Other animals
See also
External links
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