Cranial nerve palsies

Last updated: May 9, 2022

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Cranial nerve palsy is characterized by a decreased or complete loss of function of one or more cranial nerves. Cranial nerve palsies can be congenital or acquired. Multiple cranial neuropathies are commonly caused by tumors, trauma, ischemia, or infections. While diagnosis can usually be made based on clinical features, further investigation is often warranted to determine the specific etiology. Contrast-enhanced MRI is usually the preferred imaging modality to evaluate the affected nerve and any soft tissue abnormalities. A CT scan may be indicated to evaluate for bony lesions and fractures that may be compressing the nerve. Management is mainly aimed at treating the underlying etiology. Surgery may be indicated for individuals with severe disability (e.g., acute traumatic cranial nerve palsies, persistent symptoms despite conservative measures). Spontaneous resolution over months may occur, especially in cranial nerve palsies secondary to microangiopathy.

Facial nerve palsy is covered in detail separately.

Overview of cranial nerves and their function [1]
Cranial nerve Nerve type Function
I Olfactory nerve
  • Sensory
II Optic nerve
  • Sensory
III Oculomotor nerve
  • Motor (somatic)
IV Trochlear nerve
  • Motor
V Trigeminal nerve
  • Sensory
VI Abducens nerve
  • Motor
VII Facial nerve
  • Sensory
  • Motor (somatic)
VIII Vestibulocochlear nerve
  • Sensory
  • Balance and equilibrium: vestibular nerve
  • Hearing: cochlear nerve
IX Glossopharyngeal nerve
  • Sensory
  • Motor (somatic)
X Vagus nerve
  • Sensory (somatic)
  • Motor (somatic)
XI Accessory spinal nerve
  • Motor
XII Hypoglossal nerve
  • Motor

Some Say Marry Money, But My Brother Says Big Brain Matters More:” CN I is sensory, CN II is sensory, CN III is motor, CN IV is motor, CN V is both (mixed), CN VI is motor, CN VII is both (mixed), CN VIII is sensory, CN IX is both (mixed), CN X is both (mixed), CN XI is motor, and CN XII is motor.

CN VII (Seven) controls Salivation by innervating Submandibular and Sublingual glands.

Gross anatomy

Origin and pathways of the cranial nerves

Cranial nerve

Nerve origin Foramina/Structures Cranial nerve nuclei Destination Pathway
CN I
  • -
CN II
CN III
  • Ocular and orbital muscles
CN IV
CN V
CN VI
CN VII
CN VIII
CN IX
  • Medulla
CN X
CN XI
CN XII

CN I–IV are located in the midbrain, V–VIII in the pons,and IX–XII in the medulla.

The nuclei located in the medial brainstem are factors of 12, except 1 and 2 (i.e., CN III, CN IV, CN VI, and CN XII).

“Standing Room Only”: CN V1 exits through Superior orbital fissure, CN V2 exits through foramen Rotundum, and CN V3 exits through foramen Ovale.

The sulcus limitans in the 4th ventricle separates the CN Motor nuclei in the Medial part of the brain stem (basal plate) from the sensory nuclei in the Lateral part (aLar plate).

3D Anatomy

  • Confirm the diagnosis clinically with a cranial nerve examination.
  • Consider further evaluation for underlying etiology based on clinical suspicion.
  • Consult neurology and other relevant specialties.
  • Management depends on addressing underlying etiology; spontaneous recovery may occur.

Etiology

Clinical features [16][19]

Diagnostics [16][17][20][21]

Cranial nerve examination

Diagnosis is clinical and based on:

  • Comprehensive history
  • Cranial nerve examination: inability to identify certain smells (e.g., peppermint, coffee) [20]
  • Assess for common differential diagnoses of olfactory dysfunction, such as sinonasal pathology. [21]

Further evaluation [20]

Evaluate for the underlying etiology.

  • Imaging [16][17][18]
    • CT maxillofacial region (with IV contrast): preferred for trauma or suspected sinonasal pathology not confirmed on nasal endoscopy
    • MRI head (without and with IV contrast): preferred for a suspected primary neurological etiology [18]
  • Laboratory studies as needed : to evaluate for other etiologies as guided by clinical probability

Treatment

  • Consult neurology.
  • Address any treatable causes identified.
  • Consider a trial of olfactory training. [20][22][23]
    • A self-administered therapy in which the patient exposes themselves to 4 different odors for ∼10 seconds twice daily for about 12–24 weeks.
    • Associated with improved olfactory sensitivity, especially in olfactory dysfunction secondary to trauma, infections, and neurodegenerative diseases.
  • Spontaneous recovery (typically over months to years) can occur in up to half the patients with anosmia. [20][21]

Counsel patients on coping strategies such as monitoring for signs of spoiled food and installing smoke and gas detectors. [24]

Etiology

Clinical features [16]

Diagnostics [16][26]

Cranial nerve examination

Diagnosis is clinical and based on a comprehensive ocular examination as part of the cranial nerve examination, which includes:

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings.

Treatment [16][26]

  • Address any underlying etiologies identified.
  • Consult neurosurgery and/or ophthalmology.
  • Traumatic CN II palsy: Options include surgery, high-dose corticosteroids, and observation.

Etiology

Etiology of CN III palsy
Structure

Etiology

Clinical features
Oculomotor nuclei
Basilar segment
Intracavernous segment
Intraorbital segment
Isolated oculomotor nerve palsy

Parasympathetic fibers of CN III are located superficially and motor fibers are located centrally. Parasympathetic fibers are more susceptible to compressive lesions (e.g., uncal herniation, aneurysm of the posterior communicating artery). Motor fibers are more susceptible to ischemia (e.g., vasculitis, diabetes, atherosclerosis).

Clinical features [30]

  • Horizontal diplopia that worsens when the head is turned away from the side of the lesion
  • Ptosis
  • Light sensitivity
  • Additional features may be present, depending on the etiology and the level of the oculomotor nerve lesion.

Diagnostics [16][30]

Cranial nerve examination

Diagnosis is clinical and based on a comprehensive ocular examination as part of the cranial nerve examination.

Oculomotor nerve palsy leaves you down and out.

Impaired pupillary reaction with relative sparing of motor function is typically seen in compressive lesions. Prominent motor dysfunction with sparing of the pupil is typically seen in ischemic lesions. However, pupillary findings cannot reliably distinguish between the etiologies of oculomotor palsy. [27][31][32]

Further evaluation

Evaluate for underlying etiology based on clinical findings.

Clinical findings Likely underlying etiology Further evaluation

Complete palsy with dilated pupil
OR
Incomplete palsy regardless of pupillary findings

Complete palsy with a normal pupillary reflex (pupillary sparing)

MRI brain and orbits should also be obtained in patients ≤ 50 years old with a history of cancer and additional neurologic findings, including nonisolated cranial nerve palsy. [33]

Treatment [16][30]

Motor fibers are in the Middle of CN III, while Parasympathetic fibers are on the Periphery of the nerve.

Etiology

Clinical features

  • Vertical or oblique diplopia
  • Exacerbated on downgaze (e.g., reading, walking downstairs) away from side of affected muscle [37]
  • Worsens when patient turns the head towards the paralyzed muscle → compensatory head tilt to the opposite side of the lesion

With damage to the CN IV, you cannot look at the floor.

Diagnostics

Cranial nerve examination

Diagnosis is clinical, based on cranial nerve examination, which includes: [37][38]

Imaging [17][33]

  • Not routinely required
  • Consider MRI brain and orbits in consultation with a neurologist in the following situations
    • History of trauma
    • Patients ≤ 50 years old with a history of cancer and additional neurologic findings, including nonisolated cranial nerve palsy
    • Persistent palsy after 3 months (in all age groups)
    • Progression of symptoms

Treatment [16][39]

  • Consult neurology and ophthalmology.
  • Symptoms often resolve spontaneously within six months of onset.
  • Prism glasses or an eye patch can be used to improve diplopia while awaiting resolution.
  • Surgical realignment may be needed for persistent CN IV palsy.

Etiology

Clinical features

Clinical features depend on the site of the lesion and can include (see “Localizing features of CN V palsy” for details):

Diagnostics [16][40]

Cranial nerve examination

Diagnosis is clinical, based on ear examination, nose and throat examination, and cranial nerve examination.

Localizing features of CN V palsy
Peripheral trigeminal nerve lesions Ophthalmic nerve (CN V1
Maxillary nerve (CN V2)
Mandibular nerve (CN V3
Lesion of the tensor tympani branch
  • Hearing impairment (particularly affecting low-pitched sounds)
Lesions of the trigeminal nerve nuclei (depending on the nuclei affected)

The primary features of trigeminal neuropathy are numbness and/or weakness in the areas of trigeminal nerve innervation, whereas the primary feature of trigeminal neuralgia is intermittent sharp pain in the same area without sensory or motor deficits. [40]

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings.

Treatment [16][40]

Etiology [10][41]

Abducens nerve palsy is the most common ocular cranial nerve palsy.

Clinical features

  • Horizontal diplopia that worsens when looking at distant objects
  • Inability to look laterally in the affected eye
  • Features of the underlying cause

Diagnostics [41][43]

Cranial nerve examination

Diagnosis is clinical, based on the examination of the extraocular muscles as part of the cranial nerve examination.

Further evaluation [41]

Evaluate for underlying etiology based on clinical findings.

Treatment

Etiology

Clinical features

Diagnostics [46][47]

Cranial nerve examination

Diagnosis is clinical, based on a comprehensive examination of the ears, hearing, and vestibular system, as part of the cranial nerve examination.

If a tuning fork is unavailable, a hum test may be used as an alternative to the Weber test [47]In patients with sudden hearing loss, audiometry should be performed within 14 days from the onset of symptoms. [47]

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings.

Treatment [47]

  • Consult neurology and/or otolaryngology.
  • Treatment is aimed at resolving underlying causes (e.g., surgical excision and/or radiation for a tumor).
  • Consider expectant management with scheduled repeat audiometry to assess for spontaneous recovery.
  • For severe sensorineural hearing loss, consider initial treatment with prednisone within two weeks of symptom onset. [47]

Etiology

Clinical features

Isolated CN IX palsy is rare and may be asymptomatic due to shared sensory and motor nuclei with adjacent nerves. [48]

Lesions that affect the glossopharyngeal nerve typically also affect the vagus nerve because the two nerves exit the jugular foramen in close proximity. [16][48]

Diagnostics [48]

Cranial nerve examination

Diagnosis is clinical, based on the cranial nerve examination.

Further evaluation

  • Consider high-resolution MRI orbit, face, and neck, in conjunction with MRI head (without and with IV contrast) to assess for underlying etiology. [17][18][49]

Treatment

Etiology

Clinical features

Lesions that affect the vagus nerve typically also affect the glossopharyngeal nerve because the two nerves exit the jugular foramen in close proximity. [16][48]

Diagnostics [16][48][50]

Cranial nerve examination

Isolated palsy of the recurrent laryngeal nerve(s) indicates that the site of the lesion is most likely distal to the hyoid bone. More proximal lesions manifest with dysphagia, nasal speech, palatal paralysis, and uvular deviation. [17][48]

Dysphonia in a patient with a neck mass, dyspnea, stridor, progressive neurological symptoms, history of tobacco use, or history of surgery on the head, neck, or chest requires urgent evaluation by an otolaryngology specialist to evaluate for a potentially serious underlying etiology. [50]

Further evaluation [16][17][18]

Based on clinical and laryngoscopic findings, consult neurology and consider further evaluation, including:

Treatment

Depending on the etiology and severity of symptoms may include: [48][50]

Bilateral vocal cord palsy with stridor and dyspnea is a potentially airway-threatening condition. Consult otolaryngology urgently to secure the airway (e.g., via tracheostomy). [51]

Etiology

Clinical features [52]

  • Shoulder pain and heaviness
  • Difficulty or inability to raise hand overhead
  • Neckline asymmetry

Diagnostics [16][17]

Cranial nerve examination

Diagnosis is clinical, based on the cranial nerve examination.

Muscular atrophy is a late sequelae of CN XI palsy. [52]

Further evaluation

Consider further evaluation for underlying etiology based on clinical findings. Studies may include:

  • Imaging (i.e.,MRI orbit, face, neck or CT neck with IV contrast): to evaluate for possible underlying compressive etiology (e.g., malignancy) [17][18]
  • Electromyography (EMG): to assess severity of impairment

Accessory nerve palsy should be part of the differential diagnosis of neck and shoulder pain.

Treatment [16]

  • Consult neurology and/or head and neck or plastic surgery.
  • Conservative measures can be considered for patients with mild dysfunction and/or evidence of improvement on follow-up. [52]
  • Surgical measures (e.g., nerve grafting, neurolysis) [52][53]
    • May be preferred for acute traumatic causes with severe dysfunction
    • Consider within 6 months of onset if there is poor response to conservative management

Etiology

Clinical features

Diagnostics [17]

Cranial nerve examination

Diagnosis is clinical, based on the cranial nerve examination. Ask the patient to:

Further evaluation

Consider further evaluation to identify lesion location and underlying etiology based on clinical findings. Studies may include:

  • Imaging [17][18]
    • MRI head and neck (without and with IV contrast) : to locate nerve lesion and possible etiologies
    • CT skull base and neck with IV contrast: may be performed in conjunction with MRI to evaluate the foramina and skull base (e.g., for fractures, skull base tumors)
  • Electromyography (EMG): to assess severity of of nerve damage

Treatment [16]

  • Consult neurology and speech language pathology.
  • Consider early surgery in acute nerve injury. [16]
  • Unilateral nerve injury
    • May spontaneously resolve within 6 months.
    • Advise patients to chew on the unaffected side.
  • Bilateral nerve injury: Consider enteral feeding strategies for swallowing difficulty.
Overview of multiple cranial neuropathies [55][56][57]
Condition Affected cranial nerve Etiology Clinical features
Chronic meningitis
  • Any
  • Insidious or subacute headache, fever, and neck stiffness
  • Additional symptoms depend on which CN is involved
Jugular foramen syndrome
Cavernous sinus syndrome
Cerebellopontine angle syndrome
Guillain-Barré syndrome
Multiple sclerosis
  1. Erman AB, Kejner AE, Hogikyan ND, Feldman EL. Disorders of cranial nerves IX and X. Semin Neurol. 2009; 29 (1): p.85–92. doi: 10.1055/s-0028-1124027 . | Open in Read by QxMD
  2. Tubbs RS. Nerves and Nerve Injuries. Academic Press ; 2015
  3. Khaku A, Patel V, Zacharia T, Goldenberg D, McGinn J. Guidelines for Radiographic Imaging of Cranial Neuropathies. Ear Nose Throat J. 2017; 96 (10-11): p.E23-E39. doi: 10.1177/0145561317096010-1106 . | Open in Read by QxMD
  4. Blumenfeld A, Nikolskaya G. Glossopharyngeal Neuralgia. Curr Pain Headache Rep. 2013; 17 (7). doi: 10.1007/s11916-013-0343-x . | Open in Read by QxMD
  5. Policeni B et al.. ACR Appropriateness Criteria ® Cranial Neuropathy. J Am Coll Radiol. 2017; 14 (11): p.S406-S420. doi: 10.1016/j.jacr.2017.08.035 . | Open in Read by QxMD
  6. Morillon P, Bremner F. Trochlear nerve palsy.. Br J Hosp Med (Lond). 2017; 78 (3): p.C38-C40. doi: 10.12968/hmed.2017.78.3.C38 . | Open in Read by QxMD
  7. Sharma AK, Kim DD, Fraser JA. Pearls & Oy-sters: Paradoxical Head Tilt in a Congenital Fourth Nerve Palsy. Neurology. 2021; 97 (3): p.e320-e323. doi: 10.1212/wnl.0000000000012082 . | Open in Read by QxMD
  8. Murchison AP. Neuroimaging and Acute Ocular Motor Mononeuropathies. Arch Ophthal. 2011; 129 (3): p.301. doi: 10.1001/archophthalmol.2011.25 . | Open in Read by QxMD
  9. Lueck CJ. Infranuclear ocular motor disorders. Elsevier ; 2011 : p. 281-318
  10. The abducens nerve (CN VI). https://teachmeanatomy.info/head/cranial-nerves/abducens-nerve/. Updated: March 13, 2019. Accessed: April 2, 2019.
  11. Elder C, Hainline C, Galetta SL, Balcer LJ, Rucker JC. Isolated Abducens Nerve Palsy: Update on Evaluation and Diagnosis. Curr Neurol Neurosci Rep. 2016; 16 (8). doi: 10.1007/s11910-016-0671-4 . | Open in Read by QxMD
  12. Duane syndrome. https://rarediseases.org/rare-diseases/duane-syndrome/. . Accessed: April 6, 2017.
  13. Chan J, Albretson J. Causes of isolated recurrent ipsilateral sixth nerve palsies in older adults: a case series and review of the literature. Clinical Ophthalmology. 2015 : p.373. doi: 10.2147/opth.s78319 . | Open in Read by QxMD
  14. Peragallo JH, Bruce BB, Hutchinson AK, et al. Functional and Motor Outcomes of Strabismus Surgery for Chronic Isolated Adult Sixth Nerve Palsy. Neuro-Ophthalmology. 2014; 38 (6): p.320-325. doi: 10.3109/01658107.2014.957780 . | Open in Read by QxMD
  15. Stachler RJ, Francis DO, Schwartz SR, et al. Clinical Practice Guideline: Hoarseness (Dysphonia) (Update). Otolaryngology–Head and Neck Surgery. 2018; 158 (1_suppl): p.S1-S42. doi: 10.1177/0194599817751030 . | Open in Read by QxMD
  16. Li Y, Garrett G, Zealear D. Current Treatment Options for Bilateral Vocal Fold Paralysis: A State-of-the-Art Review. Clinical and experimental otorhinolaryngology. 2017; 10 (3): p.203-212. doi: 10.21053/ceo.2017.00199 . | Open in Read by QxMD
  17. Chandawarkar RY, Cervino LA, Pennington GA. Management of Iatrogenic Injury to the Spinal Accessory Nerve. Plast Reconstr Surg. 2003; 111 (2): p.611-617. doi: 10.1097/01.prs.0000041943.47622.eb . | Open in Read by QxMD
  18. Olarte M, Adams D. Accessory nerve palsy.. Journal of Neurology, Neurosurgery & Psychiatry. 1977; 40 (11): p.1113-1116. doi: 10.1136/jnnp.40.11.1113 . | Open in Read by QxMD
  19. Setter K, Voloshin I, Bigliani L. Operative Treatment of Spinal Accessory Nerve Palsy. Techniques in Shoulder and Elbow Surgery. 2004; Volume 5 (Issue 1): p.25-36.
  20. Smith JH, Cutrer FM. Numbness matters: A clinical review of trigeminal neuropathy. Cephalalgia. 2011; 31 (10): p.1131-1144. doi: 10.1177/0333102411411203 . | Open in Read by QxMD
  21. Shah AC, Barnes C, Spiekerman CF, Bollag LA. Hypoglossal nerve palsy after airway management for general anesthesia: an analysis of 69 patients. Anesth Analg. 2015; 120 (1): p.105-120. doi: 10.1213/ANE.0000000000000495 . | Open in Read by QxMD
  22. Blumenfeld H. Neuroanatomy Through Clinical Cases. Wiley-Blackwell ; 2010
  23. Yanovitch T, Buckley E. Diagnosis and management of third nerve palsy. Curr Opin Ophthalmol. 2007; 18 (5): p.373-378. doi: 10.1097/icu.0b013e328270b8db . | Open in Read by QxMD
  24. Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. Lippincott Williams & Wilkins ; 2013
  25. Tamhankar MA, Biousse V, Ying G-S, et al. Isolated Third, Fourth, and Sixth Cranial Nerve Palsies from Presumed Microvascular versus Other Causes. Ophthalmology. 2013; 120 (11): p.2264-2269. doi: 10.1016/j.ophtha.2013.04.009 . | Open in Read by QxMD
  26. Fang C, Leavitt JA, Hodge DO, Holmes JM, Mohney BG, Chen JJ. Incidence and Etiologies of Acquired Third Nerve Palsy Using a Population-Based Method. JAMA Ophthalmology. 2017; 135 (1): p.23. doi: 10.1001/jamaophthalmol.2016.4456 . | Open in Read by QxMD
  27. Sadagopan KA, Wasserman BN. Managing the patient with oculomotor nerve palsy. Curr Opin Ophthalmol. 2013; 24 (5): p.438-447. doi: 10.1097/icu.0b013e3283645a9b . | Open in Read by QxMD
  28. Steiner T, Juvela S, Unterberg A, Jung C, Forsting M, Rinkel G. European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage. Cerebrovasc Dis. 2013; 35 (2): p.93-112. doi: 10.1159/000346087 . | Open in Read by QxMD
  29. Thompson BG, Brown RD, Amin-Hanjani S, et al. Guidelines for the Management of Patients With Unruptured Intracranial Aneurysms. Stroke. 2015; 46 (8): p.2368-2400. doi: 10.1161/str.0000000000000070 . | Open in Read by QxMD
  30. Carroll CG, Campbell WW. Multiple Cranial Neuropathies. Seminars in Neurology. 2009; 29 (1): p.53-65.
  31. Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet. 2016; 388 : p.717-727. doi: 10.1016/ S0140-6736(16)00339-1 . | Open in Read by QxMD
  32. Multiple Sclerosis (MS). https://www.merckmanuals.com/professional/neurologic-disorders/demyelinating-disorders/multiple-sclerosis-ms. Updated: August 1, 2016. Accessed: April 6, 2017.
  33. Peripheral Vestibular Nystagmus. https://www.aao.org/bcscsnippetdetail.aspx?id=d20f8ad8-845e-46fc-b7ed-7d00216c2726. . Accessed: April 6, 2017.
  34. Thomas Brandt, Marianne Dieterich. The dizzy patient: don't forget disorders of the central vestibular system. Nature Reviews Neurology. 2017; 13 (6): p.352-362. doi: 10.1038/nrneurol.2017.58 . | Open in Read by QxMD
  35. Chandrasekhar SS, Tsai Do BS, Schwartz SR, et al. Clinical Practice Guideline: Sudden Hearing Loss (Update). Otolaryngology–Head and Neck Surgery. 2019; 161 (1_suppl): p.S1-S45. doi: 10.1177/0194599819859885 . | Open in Read by QxMD
  36. The olfactory nerve (CN I) and olfactory pathway. https://teachmeanatomy.info/head/cranial-nerves/olfactory-cni/. Updated: December 24, 2018. Accessed: April 2, 2019.
  37. The optic nerve (CN II) and visual pathway. https://teachmeanatomy.info/head/cranial-nerves/optic-cnii/. Updated: October 19, 2018. Accessed: April 2, 2019.
  38. The oculomotor nerve (CN III). https://teachmeanatomy.info/head/cranial-nerves/oculomotor/. Updated: March 13, 2019. Accessed: April 2, 2019.
  39. The trochlear nerve (CN IV). https://teachmeanatomy.info/head/cranial-nerves/trochlear-nerve/. Updated: March 13, 2019. Accessed: April 2, 2019.
  40. The opthalmic division of the trigeminal nerve (CNV1). https://teachmeanatomy.info/head/nerves/ophthalmic-nerve/. Updated: December 22, 2017. Accessed: April 3, 2019.
  41. The opthalmic division of the trigeminal nerve (CNV2). https://teachmeanatomy.info/head/nerves/maxillary-nerve/. Updated: December 24, 2018. Accessed: April 3, 2019.
  42. The opthalmic division of the trigeminal nerve (CNV3). https://teachmeanatomy.info/head/nerves/mandibular-nerve/. Updated: April 2, 2018. Accessed: April 3, 2019.
  43. The facial nerve (CN VII). https://teachmeanatomy.info/head/cranial-nerves/facial-nerve/. Updated: December 31, 2017. Accessed: April 4, 2019.
  44. The vestibulocochlear nerve (CN VIII). https://teachmeanatomy.info/head/cranial-nerves/vestibulocochlear/. Updated: August 7, 2018. Accessed: April 4, 2019.
  45. The glossopharyngeal nerve (CN IX). https://teachmeanatomy.info/head/cranial-nerves/glossopharyngeal-nerve/. Updated: January 2, 2018. Accessed: April 4, 2019.
  46. The accessory nerve (CN XI). https://teachmeanatomy.info/head/cranial-nerves/accessory/. Updated: January 2, 2018. Accessed: April 4, 2019.
  47. The hypoglossal nerve (CN XII). https://teachmeanatomy.info/head/cranial-nerves/hypoglossal/. Updated: January 20, 2019. Accessed: April 4, 2019.
  48. Bähr M, Frotscher M. Duus' Topical Diagnosis in Neurology. Thieme Medical Pub ; 2012
  49. Ahmed HU. A case of mistaken muscles. BMJ. 2002; 324 (7343): p.962-962. doi: 10.1136/bmj.324.7343.962 . | Open in Read by QxMD
  50. Wrobel BB, Leopold DA. Smell and taste disorders.. Facial Plast Surg Clin North Am. 2004; 12 (4): p.459-68, vii. doi: 10.1016/j.fsc.2004.04.006 . | Open in Read by QxMD
  51. Bromley SM. Smell and taste disorders: a primary care approach.. Am Fam Physician. 2000; 61 (2): p.427-36, 438.
  52. Malaty J, Malaty IA. Smell and taste disorders in primary care. Am Fam Physician. 2013; 88 (12): p.852-9.
  53. Pellegrino R, Han P, Reither N, Hummel T. Effectiveness of olfactory training on different severities of posttraumatic loss of smell. Laryngoscope. 2019; 129 (8): p.1737-1743. doi: 10.1002/lary.27832 . | Open in Read by QxMD
  54. Pekala K, Chandra RK, Turner JH. Efficacy of olfactory training in patients with olfactory loss: a systematic review and meta-analysis. International Forum of Allergy & Rhinology. 2015; 6 (3): p.299-307. doi: 10.1002/alr.21669 . | Open in Read by QxMD
  55. Pinto JM. Olfaction. Proc Am Thorac Soc. 2011; 8 (1): p.46-52. doi: 10.1513/pats.201005-035rn . | Open in Read by QxMD
  56. Vodopivec I, Rizzo JF. Ophthalmic manifestations of giant cell arteritis. Rheumatology. 2018; 57 (suppl_2): p.ii63-ii72. doi: 10.1093/rheumatology/kex428 . | Open in Read by QxMD
  57. Riordan-Eva P. Clinical assessment of optic nerve disorders. Eye (Lond). 2004; 18 (11): p.1161-1168. doi: 10.1038/sj.eye.6701575 . | Open in Read by QxMD
  58. Behbehani R. Clinical approach to optic neuropathies.. Clin Ophthalmol. 2007; 1 (3): p.233-46.
  59. DIAGNOSIS: How are vestibular disorders diagnosed?. https://vestibular.org/understanding-vestibular-disorder/diagnosis. . Accessed: April 4, 2019.
  60. The vagus nerve (CN X). https://teachmeanatomy.info/head/cranial-nerves/vagus-nerve-cn-x/. Updated: January 28, 2019. Accessed: April 4, 2019.
  61. Gastroparesis Diagnosis. https://www.ucsfhealth.org/conditions/gastroparesis/diagnosis.html. . Accessed: April 9, 2019.
  62. Bedside Water-Swallow Testing for Dysphagia. https://www.jwatch.org/na41936/2016/07/28/bedside-water-swallow-testing-dysphagia. Updated: July 28, 2016. Accessed: April 9, 2019.

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