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Cranial nerves

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Cranial nerves
Skull brain human normal.svg
Left Inferior view of the human brain, showing origins of cranial nerves.
Right Juxtaposed skull base with foramina in which many nerves exit the skull.
Skull and brainstem inner ear.svg
Cranial nerves as they pass through the skull base to the brain.
Latin nervus cranialis
(pl: nervi craniales)
TA A14.2.01.001
FMA 5865
Anatomical terms of neuroanatomy

Cranial nerves are nerves emerging directly from the brain, which is in contrast to spinal nerves (which emerge from various segments of the spinal cord).[1] Cranial nerves exchange information between the brain and parts of the body, primarily to and from regions of the head and neck.[2]

Spinal nerves emerge regularly from the spinal cord with the nerve closest to the head emerging in the space above the first cervical vertebra with the nerve C1, with the cranial nerves filling corresponding roles above this level.[3] Each cranial nerve is paired and is present on both sides. Depending on definition there are in humans twelve or thirteen cranial nerves pairs, which are assigned Roman numerals I–XII, and zero assigned to cranial nerve zero, (or the terminal nerve). Their number is based on the order in which they emerge from the brain, front to back (brainstem).[1]

The terminal nerves, olfactory nerves (I) and optic nerves (II) emerge from the cerebrum or forebrain, and the remaining ten pairs arise from the brainstem.[1]

The cranial nerves are considered components of the peripheral nervous system (PNS),[1] although on a structural level the olfactory, optic and terminal nerves are more accurately considered part of the central nervous system (CNS).


Inferior view of the human brain showing the cranial nerves on an autopsy specimen
Inferior schematic view of the brain and brainstem showing the cranial nerves, numbered from olfactory to hypoglossal after the order in which they emerge
The brainstem, with deeper cranial nerve nuclei and tracts inside the brain-stem shaded red.

Traditionally, humans are considered to have twelve pairs of cranial nerves, which are numbered I–XII. They are the following: the olfactory nerve (I), the optic nerve (II),oculomotor nerve (III), trochlear nerve (IV), trigeminal nerve (V), abducens nerve (VI), facial nerve (VII), vestibulocochlear nerve (VIII), glossopharyngeal nerve (IX), vagus nerve (X), accessory nerve (XI), and hypoglossal nerve (XII). There may be a thirteenth cranial nerve, the terminal nerve, which is very small and may or may not be functional in humans[3][1]


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 motor innervation to the face. As Latin was the lingua franca of the study of Anatomy when the nerves were first documented, recorded, and discussed, many nerves maintain Latin (or Greek) 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) named according to its three heads (Latin: tri-geminus meaning triplets),[4] and the vagus nerve (X), named for its wandering course (Latin: vagus).[5]

Cranial nerves are numbered based on their rostral-caudal (front-back) position,[1] as, when viewing the brain from below. If the brain is carefully removed from the skull the nerves are typically visible in their numeric order.

Cranial nerves have intrancranial and extrancranial paths. The intracranial paths are within the skull and the extracranial pathos are outside the skull. There are many holes in the skull (foramina) that the nerves use to exit the skull. The nerves are paired, which means that they occur on both the right and left sides.

Intracranial course[edit]

Exiting the brainstem[edit]

With the exception of the olfactory nerve (I) and optic nerve (II) (and terminal nerve), the cranial nerves emerge from nuclei (collections of cell bodies) in the brainstem. The oculomotor nerve (III) and trochlear nerve (IV) emerge from the midbrain within the brainsterm, the trigeminal (V), abducens (VI), facial (VII) and vestibulocochlea (VIII) from the pons, and the glossopharyngeal (IX), vagus (X), accessory (XI) and hypoglossal (XII) emerge from the medulla.[1]

The olfactory nerve (I) nerve emerges from the olfactory bulbs 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 temporal lobes of the brain.[1]


Main article: Cranial nerve ganglia

The cranial nerves give rise to a number of ganglia, collections of the cell bodies of neurons in the nerves that are outside of the brain. These ganglia are both parasympathetic and sensory ganglia.[6]

Similar to the dorsal root ganglia of the spinal nerves and parasympathetic ganglia of the sacral parasympathetic system, the sensory cranial nerves have a number of ganglia outside the central nervous system. The sensory ganglia are directly correspondent to dorsal root ganglia and are known as cranial sensory ganglia. They can be found along the course of the cranial nerves, outside the brain and skull.[7] Sensory ganglia exist for nerves with sensory function: V, VII, VIII, IX, X.[3] There are also a number of parasympathetic cranial nerve ganglia. Sympathetic ganglia innervating the head and neck reside in the upper regions of the sympathetic trunk, and do not belong to the cranial nerves.[6]

The ganglion of the sensory nerves, which are similar in structure to the dorsal root ganglion of the spinal cord, include:[8]

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).[9]

Exiting the skull[edit]

Exits of cranial nerves from the skull.[6][8]
Location Nerve
cribiform plate Olfactory nerve (I)
optic foramen Optic nerve (II)
superior orbital fissure Oculomotor (III)
Trochlear (IV)
Abducens (VI)
Trigeminal V1
Foramen rotundum Trigeminal V2
Foramen ovale Trigeminal V3
internal auditory canal Facial (VII)
Vestibulocochlear (VIII)
jugular foramen Glossopharyngeal (IX)
Vagus (X)
Accessory (XI)
hypoglossal canal Hypoglossal (XII)

After emerging from the brainstem, the cranial nerves travel within the skull, but must leave this bony compartment in order to reach their destinations. Some nerves pass through holes in the skull, called foramina, as they travel to their destination. 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 additional blood vessels.[8]

  • The olfactory nerve (I) passes through the cribiform plate, many small perforations in the part of the ethmoid bone.
  • The optic nerve (II) passes through the optic foramen as it travels to the eye.
  • The oculomotor nerve (III), trochlear nerve (IV), abducens nerve (VI) and the opthalamic branch of the trigeminal nerve (V1) travel through the cavernous sinus into the superior orbital fissure, passing out of the skull into the orbit.
  • The maxillary division of the trigeminal nerve (V2) passes through foramen rotundum.
  • The mandibular division of the trigeminal nerve (V3) passes through foramen ovale.
  • The facial nerve (VII) and vestibulocochlear nerve (VIII) both pass through the internal auditory canal.

The cranial nerves commonly enter and exit the skull together, for example nerves II, III, IV, V, and VI all pass through foramina near the pituitary fossa.[3]

The facial nerve enters the temporal bone at the internal acoustic meatus, but exits the skull via the stylomastoid foramen while the vestibulocochlear nerve never actually exits the skull.[6]

Extracranial course[edit]

The following images show the cranial nerves schematically showing their respective exits from the CNS or brain-stem (not including the optic nerve, which, being part of the CNS, does not leave it), and their path, as well as conceptual innervation targets.


Postero-lateral or dorso-lateral aspect of the brainstem showing sensory nuclei in blue.
Postero-lateral or dorso-lateral aspect of the brainstem showing motor nuclei in red.
Brainstem showing motor nuclei in red, and sensory nuclei in blue.

Brainstem nuclei with associated functions are often found in similar areas of the brainstem. These are also known as functional columns.[6] Functional columns are a result of the development of the spinal cord. Four columns of gray matter are present in the spinal cord during embryological development. Each column represents a different function, and contributes neurons to different nerves. Each nerve is innervated by neurons from one or more of the columns.[13]

As the spinal cord develops, it originally consists of four bilateral columns as follows: a general somatic efferent column, a general visceral efferent column, a general visceral afferent column a general somatic afferent column. They also extend into the brainstem, but are there subdivided further.[13] The brainstem has seven columns:[13]

Four 'general' columns which contain fibres which supply sensation or control muscles:[8]

There are three additional columns which innervate organs and tissues developing from the branchial arches and inner ear, of which are the following:


The cranial nerves innervate the head and neck area,[7] including both somatic and autonomic motor innervation as well as sensory innervation. Together the cranial nerves supply sensory innervation of the special senses, such as taste, vision, smell, and hearing. They also supply afferents of the somatic senses: visceral sensation of the head and neck, balance, and proprioception, combining vestibular perception with proprioceptive information from the head and neck.[13]

Two nerves, the glossopharyngeal nerve (IX) and vagus nerve (X), innervate both motor and sensory synapses pertaining to abdominal organs (though not pelvic), as well as structures of the neck and chest.[3]

Unlike the spinal nerves, the cranial nerves are not strictly bound to certain segments of the body (as in dermatomes), but rather organize by function; hence, the innervated areas overlap significantly more than those of spinal nerves.[3]

The accessory nerve (XI) is considered either a cranial nerve or a spinal nerve, and arrises on level of the brain-stem.[3]

Smell (I)[edit]

The olfactory nerve (I) conveys the sense of smell.

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. Specific testing is performed when an individual perceives lack of taste or affected taste. The smell from each nostril is tested individually, and with consideration of airflow. Different substances are used, and these include coffee or soap. Using stronger smelling substances, for example ammonia, may lead to the activation of nociceptors of the trigeminal nerve.[14]

Vision (II)[edit]

The optic nerve (II) transmits visual information.[3][13]

Damage to the optic nerve (II) affects vision. Vision is affected depending on the location of the lesion. A person may not be able to see things on their left or right side (homonymous hemianopsia), or may have difficulty seeing things on their outer visual fields (bitemporal hemianopsia) if the optic chiasm is involved.[15]:82 Vision may be tested using a number of different tests, examining the visual field, 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 optic nerve, or further along the visual pathways.[14]

Eye movement (III, IV, VI)[edit]

Various deviations of the eyes due to abnormal function of the targets of the cranial nerves

The oculomotor nerve (III), trochlear nerve (IV) and abducens nerve (VI) coordinate eye movement.

Damage or lesion of nerves III, IV, or VI may affect the movement of the eye or pupil. Either both or one eye may be affected, and if both eyes are affected no double vision (diplopia) will occur. These nerves might be examined by observing how the eye follows an object in different directions. This object may be a finger or a pin, and may be moved at different directions to test for pursuit velocity.[14] If the eyes do not work together, the most likely cause is damage to a specific cranial nerve or nuclei.[14]

Damage to the oculomotor nerve (III), such as from a palsy can cause double vision (diplopia) with lateral strabismus, and also ptosis and mydriasis.[15][15]:84 All but specific deviations may be due to damage in this nerve or any of the muscles it innervates, (though not internuclear ophthalmoplegia). Lesion may also lead to inability to open the eye due to disrupted innervation of the levator palpebrae (unlike in Horner syndrome, which only results in a droopy eyelid). Individuals suffering from lesion or damage to the oculomotor nerve may compensate by tilting their heads to alleviate symptoms due to lack of control from oblique muscles when the eye is not adducted.[14]

Damage to the trochlear nerve (IV) can also cause diplopia with the eye adducted and elevated.[15]:84 The result will be an eye which can not move downwards or inwards properly (especially downwards when in an inward position). This is due to impairment in the superior oblique muscle, which is innervated by the trochlear nerve.[14]

Damage to the abducens nerve (VI) can also result in diplopia with medial strabismus.[15]:84 This is due to impairment in the lateral rectus muscle, which is innervated by the abducens nerve.[14]

Facial sensation (V)[edit]

Conditions affecting the trigeminal nerve (V) include trigeminal neuralgia,[6] cluster headache,[16] and trigeminal zoster.[6] Trigeminal neuralgia occurs later in life, from middle age onwards, most often after an age of 60, and is a condition associated with very strong pain distributed over the area innervated by the trigeminal nerve. Often, the pain follows the distribution of the maxillary or mandibular nerve (branches V2 and V3).[17] The trigeminal nerve is also present in the tendon reflexive jaw jerk. The reflex gives rise to twitch in some of the muscles involved in closing the jaw, and occurs when the jaw is tapped from a precise angle. A stronger reflex may be present if there is a supranuclear lesion of the trigeminal nerves motor nucleus, for example in pseudobulbar palsy.[17] In Parkinson's disease, the trigeminal nerve is involved in the glabellar reflex which causes involuntary eye-blinking.

Facial expression (VII)[edit]

Lesions of the facial nerve (VII) may manifest as facial palsy. This is where a person is unable to move the muscles on one or both sides of their face. If only the peripheral nerve itself is affected, this may cause Bell's palsy. Palsy that occurs is on the same side of the affected nerve. Central facial palsy will manifest in a similar fashion. If the nerve is damaged only on one side, a person will still be able to raise the eyebrows and crease the forehead on that side. That is because the frontalis muscle is innervated by both the left and the right cranial nerve. The effect is most often unilateral, and indicates contralateral damage or engagement of the cerebrum.[6]

Hearing and balance (VIII)[edit]

The vestibulocochlear nerve (VIII) splits into the vestibular and cochlear nerve. The vestibular part is responsible for innervating the vestibules and semicircular canal of the inner ear; this structure transmits information about balance, and is an important component of the vestibuloocular reflex, which keeps the head stable and allows the eyes to track moving objects. The cochlear nerve transmits information from the cochlea, allowing sound to be heard.[3]

When damaged, the vestibular nerve may give rise to the sensation of spinning and dizziness, and may cause rotatory nystagmus. Function of the vestibular nerve may be tested through caloric stimulation.[14] Damage to the vestibulocochlear nerve can also present as repetitive and involuntary eye movements (nystagmus), particularly when looking in a horizontal plane.[14] The cochlear nerve will cause partial or complete deafness in the affected ear.[14]

Oral sensation, taste, and salivation (IX)[edit]

Deviating uvula due to cranial nerve IX lesion

The glossopharyngeal nerve (IX) is almost exclusively sensory and supplies five afferent nuclei of the brainstem, providing sensory innervation to the oropharynx and back of the tongue.[18] The glossopharyngeal nerve also provides parasympathetic innervation to the parotid gland (though the submandibular and sublingual glands are innervated by the facial nerve).

Damage to the glossopharyngeal nerve (IX) can be assessed by asking the subject to say "Ah", and observing if during phonation the uvula deviates. A positive sign that is indicative of unilateral damage is a finding of an asymmetrically deviating uvula, deviating towards the side, with an intact or healthy nerve.[14]

Vagus nerve (X)[edit]

Loss of function of the vagus nerve (X) will lead to a loss of parasympathetic innervation 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 can be diagnosed by a hoarse voice, due to dysfunction of the superior laryngeal nerve.[6]

Testing of function may be performed by assessing ability to drink liquids. Choking on either saliva or liquids may indicate neurological damage to the vagus nerve (X).[14] Damage to this nerve may result in difficulties swallowing.[14]

Shoulder elevation and head-turning (XI)[edit]

Winged scapula may occur due to lesion of the spinal accessory.

Damage to the accessory nerve (XI) may lead to contralateral weakness in the trapezius. This can be tested by asking the subject to raise their shoulders or shrug, upon which the scapula will move out into a winged position if the nerve is damaged.[14] Weakness or an inability to elevate the scapula may be present, since the levator scapulae is alone in providing this function.[17] There may also be weakness present of the sternocleidomastoid muscle, but as it received cortical innervation from the ipsilateral side, any damage will give rise to ipsilateral weakness.[14]

Tongue movement (XII)[edit]

A damaged hypoglossal nerve will result in an inability to stick the tongue out straight.

The hypoglossal nerve (XII) is unique in that it is innervated bilaterally from both hemispheres motor cortex. Damage to the nerve at lower motor neuron level may lead to fasciculations or atrophy of the musculature of the tongue. The fasciculations of the tongue are sometimes said to look like a "bag of worms". Upper motor neuron damage will not lead to atrophy or fasciculations, but only weakness of the innervated muscles.[14]

When the nerve is damaged, it will lead to unilateral weakness and the tongue, when extended, will move towards the weaker or damaged side, as shown in the image.[14]

Clinical significance[edit]

Use of a Snellen chart to examine the optic nerve (II) may constitute one part of the cranial nerve examination.


Doctors, neurologists and other medical professionals may conduct a cranial nerve examination as part of a neurological examination to examine the cranial nerves. This is a highly formalised series of steps involving specific tests for each nerve, testing the function of the olfactory nerve (I) first, and progressing sequentially for each nerve.[19] Knowledge of cranial nerve function is an important, as it may indicate which portion of the brainstem is damaged. It is of clinical importance to know the path and origin of the cranial nerves, both intracranially as well as extracranially.[3]

A cranial nerve exam starts with observation of the patient, as some cranial nerve lesions may affect the symmetry of the eyes or face. The eyes are examined and the visual acuity is tested through reading a Snellen chart. The visual fields are tested for nerve lesions or nystagmus via a task to perform specific eye movements . 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 tuning forks. The patient's uvula is examined. After performing a shrug and head turn, the patient's tongue function assessed by various tongue movements.[19]



Nerves may be compressed because of increased intercranial pressure, a mass effect of an intracerebral haemorrhage, or tumour that presses against the nerves.[20] The cranial nerves are often the first structures to be affected by different forms of brain injury, such as hemorrhaging or tumors, partly because they are sensitive to compression.[6] Mononeuropathy of a cranial nerve may sometimes be the first symptom of an intracranial or skull base cancer.[21]

An increase in intercranial pressure may lead to swelling of the optic nerves (II) and compression of the surrounding veins and capillaries, causing papilloedema.[22] A glioma, such as an optic glioma, may also impact on the optic nerve (II). A pituitary tumour may compress the optic tracts or the optic chiasm of the optic nerve (II), leading to visual loss. A pituitary tumour may also extend into the cavernous sinus, compressing the oculuomotor nerve (III), trochlear nerve (IV) and abducens nerve (VI), leading to double-vision and strabismus. These nerves may also be affected by herniation of the temporal lobes of the brain through the falx cerebri.[20]

The cause for trigeminal neuralgia, in which one side of the face is exquisitely tender, is thought to be compression of the nerve by the superior cerebellar artery, one of the arteries supplying the cerebellum.[20] 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.[20][23]


Occlusion of blood vessels that supply the nerves or their nuclei, an ischemic stroke, may cause specific signs and symptoms that can localise where the occlusion occurred. If there is a stroke of the midbrain, pons or medulla, various cranial nerves may be damaged, resulting in dysfunction and symptoms of a number of different syndromes.[24] Thrombosis, such as a cavernous sinus thrombosis, refers to a thrombus affecting the venous drainage from the cavernous sinus, affects the optic (II), oculomotor (III), trochlear (IV), opthalamic branch of the trigeminal nerve (V1) and the abducens nerve (VI).[23]


Inflammation can be a result of infection, such as viral causes like reactivated herpes simplex virus, or can occur spontaneously. Inflammation of the facial nerve (VII) may result in Bell's palsy.[25]

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.[25] Other rarer inflammatory causes affecting the function of multiple cranial nerves include sarcoidosis, miliary tuberculosis, and inflammation of arteries, such as granulomatosis with polyangiitis.[23]


Trauma to the skull, disease of bone, such as Paget's disease, and injury to nerves during surgery are other causes of nerve damage.[23]


The cranial nerves were originally given their numerals by Galen millennia ago, in the rostro-caudal (or anterio-posterior) order still employed today.[26]

Terminal nerve controversy[edit]

Main article: Terminal nerve

The terminal nerve, often called cranial nerve zero, CN 0 (or cranial nerve nulla or N, since there is no Roman numeral for zero), has been largely neglected from textbooks, even though it was first clearly identified over a century ago. It was first shown to be present in the shark, but its presence in humans (and other mammals) remained somewhat controversial.[27] More recent studies have shown the nerve to be quite distinct in human fetuses and infants, and has also regularly been seen in the adult brain. The nerve axons are unmyelinated and arise from ganglia. The terminal nerve has also been shown to release luteinising hormone.[28] Another study has shown the terminal nerve to be a microscopic plexus of unmyelinated fibres in the frontal lobes. It was concluded in the study, confirming earlier findings by light microscope, that this nerve is a common finding in the human brain.[29]

Other animals[edit]

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 other vertebrates. Other amniotes (non-amphibian tetrapods) have cranial nerves similar to those of humans. In anamniotes (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 (non-amphibian tetrapods).[30]

See also[edit]


  1. ^ a b c d e f g h Vilensky, Joel; Robertson, Wendy; Suarez-Quian, Carlos (2015). The Clinical Anatomy of the Cranial Nerves: The Nerves of "On Olympus Towering Top". Ames, Iowa: Wiley-Blackwell. ISBN 978-1118492017. 
  2. ^ Standring, Susan; Borley, Neil R. (2008). "Overview of cranial nerves and cranial nerve nuclei". Gray's anatomy: the anatomical basis of clinical practice (40th ed.). [Edinburgh]: Churchill Livingstone/Elsevier. ISBN 978-0-443-06684-9. 
  3. ^ a b c d e f g h i j Kandel, Eric R. (2013). Principles of neural science (5 ed.). Appleton and Lange: McGraw Hill. pp. 1019–1036. ISBN 978-0-07-139011-8. 
  4. ^ Harper, Douglas. nerve "Trigeminal Nerve". Online Etymology Dictionary. Retrieved 2 May 2014. 
  5. ^ Davis, Matthew C.; Griessenauer, Christoph J.; Bosmia, Anand N.; Tubbs, R. Shane; Shoja, Mohammadali M. "The naming of the cranial nerves: A historical review". Clinical Anatomy 27 (1): 14–19. doi:10.1002/ca.22345. 
  6. ^ a b c d e f g h i j Keith L. Moore, Anne M.R. Agur, Arthur F. Dalley (2010). Clinically oriented anatomy (6th ed.). Philadelphia: Lippincott Williams & Wilkins, Wolters Kluwer. pp. 1055–1082. ISBN 978-1-60547-652-0. 
  7. ^ a b Mallatt, Elaine N. Marieb, Patricia Brady Wilhelm, Jon (2012). Human anatomy (6th ed. media update. ed.). Boston: Benjamin Cummings. pp. 431–432. ISBN 978-0-321-75327-4. 
  8. ^ a b c d Drake, Richard L.; Vogl, Wayne; Tibbitts, Adam W.M. Mitchell; illustrations by Richard; Richardson, Paul (2005). Gray's anatomy for students. Philadelphia: Elsevier/Churchill Livingstone. pp. 800–807. ISBN 978-0-8089-2306-0. 
  9. ^ Purves, Dale, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, James O. McNamara, and Leonard E. White (2008). Neuroscience. 4th ed. Sinauer Associates. pp. 12–13. ISBN 978-0-87893-697-7. 
  10. ^ Fuller GN, Burger PC (1990). "Nervus terminalis (cranial nerve zero) in the adult human". Clinical Neuropathology 9 (6): 279–83. PMID 2286018. 
  11. ^ Bordoni B, Zanier E (2013). "Cranial nerves XIII and XIV: nerves in the shadows". Journal of Multidisciplinary Healthcare 6: 87–91. doi:10.2147/JMDH.S39132. PMC 3601045. PMID 23516138. 
  12. ^ Vilensky JA (January 2014). "The neglected cranial nerve: nervus terminalis (cranial nerve N)". Clinical Anatomy 27 (1): 46–53. doi:10.1002/ca.22130. PMID 22836597. 
  13. ^ a b c d e f Mtui, M.J. Turlough FitzGerald, Gregory Gruener, Estomih (2012). Clinical neuroanatomy and neuroscience (6th ed. ed.). [Edinburgh?]: Saunders/Elsevier. p. 198. ISBN 978-0-7020-3738-2. 
  14. ^ a b c d e f g h i j k l m n o p q Kandel, Eric R. (2013). Principles of neural science (5. ed. ed.). Appleton and Lange: McGraw Hill. pp. 1533–1549. ISBN 978-0-07-139011-8. 
  15. ^ a b c d e Norton, Neil (2007). Netter's head and neck anatomy for dentistry. Philadelphia, Pa.: Saunders Elsevier. ISBN 978-1-929007-88-2. :78
  16. ^ Nesbitt AD, Goadsby PJ (Apr 11, 2012). "Cluster headache". BMJ (Clinical research ed.) (Review) 344: e2407. doi:10.1136/bmj.e2407. PMID 22496300. 
  17. ^ a b c Fitzgerald, M.J. Turlough FitzGerald, Gregory Gruener, Estomih Mtui (2012). Clinical neuroanatomy and neuroscience (6th ed. ed.). [Edinburgh?]: Saunders/Elsevier. p. 235. ISBN 978-0-7020-3738-2. 
  18. ^ Mtui, M.J. Turlough FitzGerald, Gregory Gruener, Estomih (2012). Clinical neuroanatomy and neuroscience (6th ed. ed.). [Edinburgh?]: Saunders/Elsevier. pp. 220–222. ISBN 978-0-7020-3738-2. 
  19. ^ a b O'Connor, Nicholas J. Talley, Simon (2009). Clinical examination : a systematic guide to physical diagnosis (6th ed.). Chatswood, N.S.W.: Elsevier Australia. pp. 330–352. ISBN 978-0-7295-3905-0. 
  20. ^ a b c d Britton, the editors Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston ; illustated by Robert (2010). Davidson's principles and practice of medicine. (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 787, 1215–1217. ISBN 978-0-7020-3085-7. 
  21. ^ Kumar (), Vinay et al. (2010). Robbins and Cotran pathologic basis of disease (8th ed.). Philadelphia, PA: Saunders/Elsevier. p. 1266. ISBN 978-1-4160-3121-5. 
  22. ^ Britton, the editors Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston ; illustated by Robert (2010). Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. p. 1166. ISBN 978-0-7020-3085-7. 
  23. ^ a b c d Fauci, Anthony S.; Harrison, T. R., eds. (2008). Harrison's principles of internal medicine (17th ed.). New York: McGraw-Hill Medical. pp. 2583–2587. ISBN 978-0-07-147693-5. 
  24. ^ Fauci, Anthony S.; Harrison, T. R., eds. (2008). Harrison's principles of internal medicine (17th ed.). New York: McGraw-Hill Medical. pp. 2526–2531. ISBN 978-0-07-147693-5. 
  25. ^ a b Britton, the editors Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston ; illustated by Robert (2010). Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 1164–1170, 1192–1193. ISBN 978-0-7020-3085-7. 
  26. ^ Paradiso, Mark F. Bear, Barry W. Connors, Michael A. (2007). Neuroscience: exploring the brain (3rd ed.). Philadelphia, PA: Lippincott Williams & Wilkins. p. 173. ISBN 978-0-7817-6003-4. 
  27. ^ Whitlock, KE (2004). "Development of the nervus terminalis: origin and migration". Microscopy Research and Technique 65 (1–2): 2–12. doi:10.1002/jemt.20094. PMID 15570589. 
  28. ^ Vilensky JA, The neglected cranial nerve: nerves terminus (Cranial nerve N). Clin Anat. 2014 Jan;27(1) PMID 22836597
  29. ^ Fuller GN and Burger PC, Nervus terminals (cranial nerve zero) in the adult human. Clin Neuropathol.1990 Nov–Dec;9(6) PMID 2286018
  30. ^ Quiring, Daniel Paul (1950). Functional anatomy of the vertebrates. New York: McGraw-Hill. p. 249. 

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