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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.
Details
Latin nervus cranialis
(pl: nervi craniales)
Identifiers
TA A14.2.01.001
A14.2.00.038
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).[4]

Anatomy[edit]

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]

Terminology[edit]

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),[5] and the vagus nerve (X), named for its wandering course (Latin: vagus).[6]

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.[7]

Cranial nerves have paths within and outside of the skull. The paths are 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 pass to exit the skull. All cranial nerves are paired, which means that they occur on both the right and left sides. If a nerve supplies a muscle, skin, or has another function on the same side of the body as where it originates, this is called an ipsilateral course. If the course is opposite to the nucleus of the nerve, this is known as a contralateral course.[8]

Intracranial course[edit]

Nuclei[edit]

Main article: Cranial nerve nuclei

The cell bodies of many of the cells of most of the cranial nerves are contained in one or more nuclei in the brainstem. These nuclei are important relative to cranial nerve dysfunction because damage to these nuclei such as from a stroke or trauma can mimic damage to one or more branches of a cranial nerve. In terms of specific cranial nerve nuclei, the midbrain of the brainstem 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). The fibers of these cranial nerves exit the brainstem from these nuclei. [1]


Ganglia[edit]

Main article: Cranial nerve ganglia

Some of the cranial nerves have sensory or parasympathetic ganglia or, collections of cell bodies of neurons, which are located outside of the brain (but can be inside or outside of the skull). [9]

The sensory ganglia are directly correspondent to dorsal root ganglia of spinal nerves and are known as cranial sensory ganglia. [7] Sensory ganglia exist for nerves with sensory function: V, VII, VIII, IX, X.[3] There are also parasympathetic ganglia, which are part of the autonomic nervous system for cranial nerves III, VII, IX and X.


Exiting the skull and Extracranial Course[edit]

Exits of cranial nerves from the skull.[9][10]
Location Nerve
cribriform plate Olfactory nerve (I)
optic foramen Optic nerve (II)
superior orbital fissure Oculomotor (III)
Trochlear (IV)
Abducens (VI)
Trigeminal V1
(ophthalmic)
Foramen rotundum Trigeminal V2
(maxillary)
Foramen ovale Trigeminal V3
(mandibular)
internal auditory canal Facial (VII)
Vestibulocochlear (VIII)
jugular foramen Glossopharyngeal (IX)
Vagus (X)
Accessory (XI)
hypoglossal canal Hypoglossal (XII)

After emerging from the brain, the cranial nerves travel within the skull, and some must leave this bony compartment in order to reach their destinations. Often the nerves pass through holes in the skull, called foramina, 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 additional blood vessels.[10]

  • The olfactory nerve (I), actually composed of many small separate nerve fibers, passes through perforations in the cribiform plate part of the ethmoid bone. These fibers terminate in the upper part of the nasal cavity and function to convey impulses containing information about odors to the brain.
  • The optic nerve (II) passes through the optic foramen in the sphenoid bone as it travels to the eye. It conveys visual information to the brain.
  • The oculomotor nerve (III), trochlear nerve (IV), abducens nerve (VI) and the ophthalmic branch of the trigeminal nerve (V1) travel through the cavernous sinus into the superior orbital fissure, passing out of the skull into the orbit. These nerves control the small muscles that move the eye and also provide sensory innervation to the eye and orbit.
  • The maxillary division of the trigeminal nerve (V2) passes through foramen rotundum in the sphenoid bone to reach the face and supply the skin of the middle of the face.
  • The mandibular division of the trigeminal nerve (V3) passes through foramen ovale of the sphenoid bone to supply the lower face with sensory innervation. This nerve also sends branches to almost all of the muscles that control chewing.
  • The facial nerve (VII) and vestibulocochlear nerve (VIII) both pass through the internal auditory canal in the temporal 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 leave 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 innervation to the upper throat and the back of the tongue, the vagus provides innervation to the muscles in the voicebox, and continues downward to supply parasympathetic innervation to the chest and abdomen. The accessory nerve controls two muscles in the neck and shoulder.
  • The hypoglossal nerve (XII) exits the skull using the hypoglossal canal in the occipital bone and reaches the tongue to control almost all of the muscles involved in movements of this organ. [1]

Extracranial course (images)[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.


Function[edit]

The cranial nerves provide motor and sensory innervation mainly to the structures within the head and neck. The sensory innervation includes both "general" sensation such temperature and touch, and "special" innervation such as such as taste, vision, smell, balance and hearing[1] [14]

The vagus nerve (X) provides sensory and autonomic (parasympatheic) motor innervation to structures in the neck and also to the abdominal organs (though not pelvic), and thoracic organs.[1] [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. 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 pain receptors (nociceptors) of the trigeminal nerve that are located in the nasal cavity.[15]

Vision (II)[edit]

The optic nerve (II) transmits visual information.[3][14]

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.[16]: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.[15]

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 to nerves III, IV, or VI may affect the movement of the eyeball (globe). Both or one eye may be affected; in either case double vision (diplopia) will likely occur because the movements of the eyes are no longer synchronized. Nerves III, IV and VI are tested 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.[15] If the eyes do not work together, the most likely cause is damage to a specific cranial nerve or nuclei.[15]

Damage to the oculomotor nerve (III) can cause double vision (diplopia) with lateral strabismus, also eyelid drooping (ptosis) and pupil dilation (mydriasis).[16][16]:84 Lesions may also lead to inability to open the eye due to paralysis of the levator palpebrae muscle. Individuals suffering from 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.[15]

Damage to the trochlear nerve (IV) can also cause diplopia with the eye adducted and elevated.[16]: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.[15]

Damage to the abducens nerve (VI) can also result in diplopia.[16]:84 This is due to impairment in the lateral rectus muscle, which is innervated by the abducens nerve.[15]

Facial sensation (V)[edit]

The trigeeminal nerve (V) provides sensation to the skin of the face and also controls the muscles of mastication (chewing). [1] Conditions affecting the trigeminal nerve (V) include trigeminal neuralgia,[9] cluster headache,[17] and trigeminal zoster.[9] Trigeminal neuralgia occurs later in life, from middle age onwards, most often after an age of 60, and is a condition typically associated with very strong pain distributed over the area innervated by the maxillary or mandibular nerve divisions of this nerve (V2 and V3).[18]

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. A very common and generally temporarily facial palsy is known as Bell's palsy. Bell's Palsy is the result of an idiopathic, unilateral lower motor neurone lesion of the facial nerve and is characterised by an inability to move the ipsilateral muscles of facial expression, including elevation of the eyebrow and furrowing of the forehead. Upper motor neurone lesions affecting the facial nerve usually spare the forehead because the lower motor neurones supplying the frontalis muscle receive bilateral innervation from upper motor neurones of both hemispheres, at the level of the facial nerve nuclei.[1]

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.[15] Damage to the vestibulocochlear nerve can also present as repetitive and involuntary eye movements (nystagmus), particularly when looking in a horizontal plane.[15] The cochlear nerve will cause partial or complete deafness in the affected ear.[15]

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.[19] The glossopharyngeal nerve also provides parasympathetic innervation to the parotid gland (though the submandibular and sublingual glands are innervated by the facial nerve).

Unilateral absence of a gag reflex suggests a lesion of CN IX, and perhaps CN X.[20]

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.[9]

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).[15] Damage to this nerve may result in difficulties swallowing.[15]

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.[15] Weakness or an inability to elevate the scapula may be present, since the levator scapulae is alone in providing this function.[18] 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.[15]

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.[15]

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.[15]

Clinical significance[edit]

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

Examination[edit]

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.[21] 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.[21]

Damage[edit]

Compression[edit]

Nerves may be compressed because of increased intercranial pressure, a mass effect of an intracerebral haemorrhage, or tumour that presses against the nerves.[22] 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.[9] Mononeuropathy of a cranial nerve may sometimes be the first symptom of an intracranial or skull base cancer.[23]

An increase in intercranial pressure may lead to swelling of the optic nerves (II) and compression of the surrounding veins and capillaries, causing papilloedema.[24] 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.[22]

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.[22] 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.[22][25]

Stroke[edit]

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.[26] 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).[25]

Inflammation[edit]

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.[27]

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

Other[edit]

Trauma to the skull, disease of bone, such as Paget's disease, and injury to nerves during surgery are other causes of nerve damage.[25]

History[edit]

The cranial nerves were originally given their numerals by Galen millennia ago, in the rostro-caudal (or anterio-posterior) order still employed today.[28]

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.[29] 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.[30] 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.[31]

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).[32]

See also[edit]

References[edit]

  1. ^ a b c d e f g h i j k l 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 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. ^ Board Review Series – Neuroanatomy, Fourth Edition, Lippincott Williams & Wilkins, Maryland 2008, p. 177. ISBN 978-0-7817-7245-7.
  5. ^ Harper, Douglas. nerve "Trigeminal Nerve". Online Etymology Dictionary. Retrieved 2 May 2014. 
  6. ^ 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. 
  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. ^ Albert, Daniel (2012). Dorland's Illustrated Medical Dictionary. (32nd ed.). Philadelphia, PA: Saunders/Elsevier. ISBN 978-1416062578. 
  9. ^ a b c d e f 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. 
  10. ^ a b 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. 
  11. ^ Fuller GN, Burger PC (1990). "Nervus terminalis (cranial nerve zero) in the adult human". Clinical Neuropathology 9 (6): 279–83. PMID 2286018. 
  12. ^ 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. 
  13. ^ 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. 
  14. ^ a b 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. 
  15. ^ a b c d e f g h i j k l m n o p 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. 
  16. ^ 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
  17. ^ Nesbitt AD, Goadsby PJ (Apr 11, 2012). "Cluster headache". BMJ (Clinical research ed.) (Review) 344: e2407. doi:10.1136/bmj.e2407. PMID 22496300. 
  18. ^ a b 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. 
  19. ^ 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. 
  20. ^ Bickley, Lynn S., Peter G. Szilagyi, and Barbara Bates. Bates' Guide to Physical Examination and History-taking. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013. Print.
  21. ^ 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. 
  22. ^ 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. 
  23. ^ 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. 
  24. ^ 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. 
  25. ^ 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. 
  26. ^ 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. 
  27. ^ 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. 
  28. ^ 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. 
  29. ^ 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. 
  30. ^ Vilensky JA, The neglected cranial nerve: nerves terminus (Cranial nerve N). Clin Anat. 2014 Jan;27(1) PMID 22836597
  31. ^ Fuller GN and Burger PC, Nervus terminals (cranial nerve zero) in the adult human. Clin Neuropathol.1990 Nov–Dec;9(6) PMID 2286018
  32. ^ Quiring, Daniel Paul (1950). Functional anatomy of the vertebrates. New York: McGraw-Hill. p. 249. 

External links[edit]