Aetiology
There are 12 paired cranial nerves, named and numbered according to the rostral-caudal order of attachment to the brain. They serve a variety of functions, and predominantly provide the motor and sensory innervation to the head. The effects of a mononeuropathy depend on where in its pathway the nerve is affected and the aetiology.
Olfactory (I)
Most chronic anosmia or hyposmia is due to aetiologies that do not damage the olfactory nerve itself. These include upper respiratory tract infection (including COVID-19), head trauma, nasal/paranasal sinus disease, and toxins such as hydrogen sulfide.[34][35] Factors such as age, sex, and smoking behaviour can influence olfaction.[5]
Olfactory disturbances secondary to olfactory nerve involvement include the following.
Head trauma: the prevalence of precedent head trauma in olfactory dysfunction is 4% to 15% and up to 20% in those who attend a specialised chemosensory centre.[35] Occipital and side impacts are most likely to result in olfactory deficits; frontal impacts, the least.[36] Olfactory dysfunction is related to coup-contrecoup forces that cause a shearing of the olfactory filaments as they pass through the cribriform plate. Less than half of patients show any subsequent recovery in their olfaction.[36][37] In those that do have some improvement, the process typically takes many months.
Neurodegenerative disease: olfactory dysfunction is a cardinal feature of several neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease.[38] Deficits are present in 85% to 90% of people with early-stage disease and are associated with decreased activation of central olfactory elements.[39] The magnitude of dysfunction is not associated with disease stage, severity of motor symptoms, or neurocognitive function. Multiple sclerosis (MS) can result in smell dysfunction proportional to plaque burden.[40] In these cases, olfactory dysfunction waxes and wanes during periods of remission and exacerbation.
Congenital: patients with apparent congenital anosmia usually lack or have hypoplasia of the olfactory bulbs.[2] Kallmann's syndrome is a genetic disorder that results in dysplasia of the olfactory bulbs and hypothalamopituitary axis abnormalities.[41]
Intracranial mass lesion: olfactory groove meningiomas and mass lesions of the frontal lobe can result in anosmia ipsilateral to the lesion. Foster Kennedy syndrome is ipsilateral anosmia associated with optic atrophy with contralateral papilloedema.[42]
Hereditary: Refsum's disease (hereditary motor and sensory neuropathy type IV) is a rare cause of anosmia.
Optic (II)
Given the critical importance of sight, the optic nerve is perhaps the most important of the cranial nerves. Disorders affecting its function demand rapid and thorough evaluation.[6]
Ischaemic optic neuropathy is the most common optic neuropathy in adults >50 years old.[43] Non-arteritic anterior ischaemic neuropathy is the most common subtype. Risk factors for microvascular disease are common in this population of patients.[44] About 15% of patients with ischaemic optic neuropathy will develop involvement of the contralateral eye within 5 years.[6][45] Arteritis accounts for 6% to 14% of cases of ischaemic optic neuropathy, primarily in patients >65 years old.[46] Arteritic optic neuropathy, usually giant cell arteritis, can result in severe loss of vision. Varicella zoster vasculopathy has been identified as a potential mimic of giant cell arteritis in biopsy-negative cases.[47]
MS is one of the major causes of optic neuritis, occurring in 50% of patients at some point in their illness.[48] Population-based data suggest optic neuritis incidence of approximately 4 per 100,000 person-years; women are affected more than men.[49][50] Those affected are usually between the ages of 18 and 40 years. Visual acuity largely recovers in 2 to 12 weeks, and recovery is hastened (although not improved) by treatment with intravenous methylprednisolone.[51]
Other autoimmune/inflammatory conditions: optic neuropathy is a complication in 5% to 15% of patients with sarcoidosis and can be the initial presentation.[52] Optic neuritis is a rare manifestation of systemic autoimmune disorders, including systemic lupus erythematosus (SLE), Sjogren's syndrome, granulomatosis with polyangiitis, and Behcet's disease.[50] Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein-associated disorder (MOGAD) are demyelinating conditions affecting the optic nerves and central nervous system that are pathophysiologically distinct from MS and associated with serological markers.[53] NMOSD and MOGAD are both commonly associated with optic neuritis and longitudinally extensive myelitis. A relapsing course is more common with NMOSD while monophasic course is seen in half of the patients among MOGAD. While both can have aggressive and severe attacks, patients with MOGAD can have more favourable recovery compared with patients with NMOSD.[54]
Viral infections: can cause isolated infection of the eye and produce neuroretinitis, which results in a triad of visual loss, swollen optic disc, and a macular star.[6] Visual loss can be mild or severe, but vision recovers completely in 90% of patients. Post-viral optic neuritis has been associated with measles, mumps, chickenpox, and influenza, and typically follows the clinical infection by 1 to 3 weeks. It has also been reported as a post-immunisation phenomenon.
Optic canal trauma: injury may be caused by a tear, avulsion, contusion, or haemorrhage within the optic canal. Trauma is frequently to the outer brow or adjacent temporal bone.[55] Spontaneous recovery is well documented, occurring in about 50% of patients, and probably reflects a conduction block rather than a transection.
Compressive lesions are usually neoplastic. Optic nerve sheath meningiomas can originate anywhere along the retrobulbar optic nerve, and predominantly affect women of middle age.[6] Optic nerve gliomas occur mainly in the first and second decades of life, and about one third of patients have neurofibromatosis.[56] Sellar and parasellar masses (craniopharyngioma, meningioma, and pituitary tumours) can compress the optic nerve and chiasm, resulting in slowly progressive visual loss in the bitemporal visual fields.[6]
Idiopathic intracranial hypertension results in swelling of the optic disc in most patients, but not all experience symptoms. It can affect all ages but typically affects young women, particularly those with obesity.
Hereditary optic neuropathies, such as dominant optic atrophy (DOA) and Leber’s hereditary optic neuropathy (LHON), are causes of progressive visual loss.[57] They are both ultimately bilateral but may present asymmetrically. LHON predominantly affects young men and is inherited from the maternal side through mitochondrial DNA mutations.[57][58]
IgG4 disease causing pachymeningitis is a rare cause of optic neuropathy.[59][60] IgG4 disease is an inflammatory condition which can affect a variety of systems/organs (e.g., pancreato-biliary tract, retroperitoneum/aorta, and salivary glands), but it can also produce infiltrates at the base of the skull, which affect the cranial nerves. The imaging appearances can mimic other causes of basal skull infiltration, such as a tumour or granulomatous disease. Diagnosis is by biopsy and IgG4 disease is usually highly responsive to corticosteroid and immune treatment.[59][60]
Drugs such as ethambutol, infliximab, sildenafil, and amiodarone have all been implicated in optic neuropathy.[61]
Nutritional deficits have a presumed role in endemic outbreaks of optic neuropathy in situations of deprivation. Vitamins B1 (thiamine), B2 (riboflavin), B9 (folate), and B12 (cobalamin) have been implicated.[62] Chronic excessive alcohol can also result in vitamin deficiencies.
Oculomotor (III), trochlear (IV), and abducens (VI)
Dysfunction of the third cranial nerve can result from a lesion anywhere along its path between the midbrain nucleus and innervation of the extraocular muscles in the orbit.[63]
Isolated third nerve palsies can be divided into acquired, traumatic, and congenital.
Acquired third nerve palsy
Can be further subdivided according to pupillary involvement and degree of extraocular muscle dysfunction:[64]
Normal pupillary function with complete ophthalmoplegia (occurs when the lesion is confined to the inner somatomotor fibres of the nerve innervating the extraocular muscles, and does not disrupt the outer pupillomotor fibres)
Normal pupillary function with incomplete ophthalmoplegia (may be due to intracranial aneurysm or vascular malformation, disrupting the outer pupillomotor fibres of the oculomotor nerve)
Pupillary dysfunction with partial or complete ophthalmoplegia (most often due to compressive lesions or meningeal infiltration).
Drugs may cause an acquired third nerve palsy with normal pupillary sphincter and complete ophthalmoplegia. These may follow use of sildenafil and cocaine.[65][66]
Migraines can lead to temporary third nerve mononeuropathy with headache, photophobia, and nausea, but consciousness is not impaired.[67]
Traumatic third nerve palsy
Raises suspicion for an underlying cerebral lesion in a patient with minor head trauma, and should prompt immediate further work-up.
Congenital third nerve palsy
Rare, and are usually diagnosed in the first 3 months of life.[9] They may occur in isolation or be associated with other neurological or systemic congenital abnormalities. Congenital fourth and sixth nerve palsies are extremely rare.[9][68]
Dysfunction of third, fourth, or sixth cranial nerve
Progressive symptoms of third, fourth, or sixth nerve palsy may be due to a compressive intracranial lesion. A third nerve palsy can indicate serious underlying pathology such as subarachnoid haemorrhage or uncal herniation.[69] Structural anomalies such as pituitary or skull base base tumours, cavernous sinus thrombosis, or a vascular malformation (such as a cerebral aneurysm or a cavernous-carotid fistula) may compress cranial nerves III, IV, or VI.
Meningitis (viral, bacterial, fungal, tuberculous, sarcoid, or carcinomatous) may result in meningismus and cause third, fourth, or sixth nerve palsy. Third nerve palsy typically presents with pupillary dysfunction and partial or complete extra-ocular muscle palsy. Cranial nerve palsies are seen in 9% of cases of community-acquired bacterial meningitis, and are predictive of a less favourable outcome when present.[70] Infrequently, sixth nerve palsies can occur after an LP.[71][72]
IgG4 disease causing pachymeningitis is a rare cause of abducens neuropathy.[59][60] IgG4 disease is an inflammatory condition which can affect a variety of systems/organs (e.g., pancreato-biliary tract, retroperitoneum/aorta, and salivary glands), but it can also produce infiltrates at the base of the skull, which affects cranial nerves. The cranial nerves II to VI are commonly affected.[60][73] The imaging appearances can mimic other causes of basal skull infiltration, such as a tumour or granulomatous disease. Diagnosis is by biopsy and IgG4 disease is usually highly responsive to corticosteroid and immune treatment.[59][60]
Risk factors for ischaemia and microvasculopathy include diabetes mellitus, hypertension, and tobacco use. A third nerve palsy with normal pupillary sphincter and complete ophthalmoplegia is most commonly the result of ischaemia (50% to 60%), especially when associated with diabetes mellitus.[9][63] Arteritic involvement (giant cell arteritis) should be considered in older adults.[74] Sixth nerve palsies as a result of ischaemia typically improve in 1-3 months, and fourth nerve palsies often resolve spontaneously within 6 months.[9][75]
Idiopathic intracranial hypertension can affect all ages but typically affects young women, particularly those with obesity, and compresses cranial nerves as they leave the brainstem.[76] The sixth nerve is most commonly affected.
The lengthy course of the fourth cranial nerve makes it particularly susceptible to traumatic injury, and this is the most common known cause of isolated fourth nerve palsy. Trauma would usually be severe enough to cause loss of consciousness.[77][78] The sixth nerve has the longest subarachnoid course, and is also susceptible to traumatic damage.
Trigeminal (V)
Lesions can affect the nuclei of the trigeminal nerve within the brainstem (intra-axial) or the trigeminal nerve itself (extra-axial). Trigeminal mononeuropathy is more often the result of extra-axial lesions. Intra-axial lesions often result in additional neurological and cranial nerve deficits due to the close anatomical proximity of other critical structures.
Meningitis (bacterial, fungal, tuberculous, sarcoid, or carcinomatous) may result in meningismus and/or fever with trigeminal nerve palsy.
Posterior inferior cerebellar artery stroke can cause lateral medullary (Wallenberg's) syndrome. This is characterised by sensory deficits on the opposite side of the body and affects the ipsilateral cranial nerves, facial sensation, and motor supply. The effects on the trigeminal nucleus result in loss of ipsilateral facial sensation and the corneal reflex. It does not cause an isolated fifth nerve neuropathy.
Trigeminal neuralgia may be caused by any lesion that compresses the trigeminal nerve as it traverses the cerebellopontine and prepontine cisterns.[79] Compression of the nerve by an aberrant vascular structure is thought to be responsible for most idiopathic cases. These include aberrant vessels (in particular the superior cerebellar artery) or an unruptured intracranial aneurysm.[80] Diagnosis is usually clinical, but onset in a patient aged <55 years should be investigated with cerebral imaging.[81] Incidence of trigeminal neuralgia peaks at age >60 years.[82][83][84]
Pontine haemorrhage due to a vascular malformation may cause sudden and enduring trigeminal sensory impairment in the absence of any other neurological findings. A second form, termed symptomatic, is caused by lesions other than vascular compression, typically meningioma, schwannoma, epidermoid and arachnoid cysts, or malignant neoplasm, that can be demonstrated on brain MRI.[85] These patients are more likely to have concomitant neurological deficits.
MS may cause a demyelinating lesion in the pons. Trigeminal neuralgia is rarely the presenting symptom, as it tends to occur in advanced disease.
High cervical spinal cord lesions can affect the spinal trigeminal tract as it extends caudally to the level of C2.
Metastasis from extracranial tumours, such as nasopharyngeal carcinoma and neck malignancies, may spread along the course of the trigeminal nerve to Meckel's cave. Numb chin syndrome may occur due to metastasis to the mandible involving the mental nerve (a branch of the inferior alveolar nerve).
Local infections, such as a skull-base osteomyelitis, can cause trigeminal neuropathy. A dental abscess near the third molar tooth can result in a neuropathy of the mandibular division.
Herpes zoster can cause severe neuralgia in the trigeminal distribution, most commonly in the ophthalmic division. The condition is self-limiting and remits in 3-4 days, but in a few patients (about 10%) pain can persist for several months and is known as postherpetic neuralgia.[86]
Autoimmune trigeminal neuropathy is rare but causes include Sjogren's syndrome, systemic lupus erythematosus (SLE), and systemic sclerosis.[87]
IgG4 disease causing pachymeningitis is a rare cause of trigeminal neuropathy.[59][60] IgG4 disease is an inflammatory condition which can affect a variety of systems/organs (e.g., pancreato-biliary tract, retroperitoneum/aorta, and salivary glands), but it can also produce infiltrates at the base of the skull, which affects cranial nerves. The cranial nerves II to VI are commonly affected.[60][73] The imaging appearances can mimic other causes of basal skull infiltration, such as a tumour or granulomatous disease. Diagnosis is by biopsy, and IgG4 disease is usually highly responsive to corticosteroid and immune treatment.[59][60]
Orbital, mid-face, mandibular, or skull-base fractures can result in trigeminal neuropathy.
Congenital causes include aplasia or hypoplasia of the trigeminal nerve and Chiari type I and II malformations.
Iatrogenic injury may occur to the inferior alveolar nerve (V3 division) during oral surgery or cosmetic liquid nitrogen procedures.[88]
A rare cause of trigeminal neuropathy is Tolosa-Hunt syndrome. It is a non-specific inflammation of the superior orbital fissure, often extending into the cavernous sinus with sparing of the pupillary function.[89] This often includes painful ophthalmoplegia (due to involvement of nerves III, IV, and VI). Symptoms last for days to weeks with spontaneous remission and recurrent attacks but no systemic involvement.
Facial (VII)
This is the most frequently diagnosed cranial neuropathy, with myriad potential aetiologies.[90]
It affects patients of both sex and at any age.
Bell's palsy is the most common aetiology of facial paralysis, accounting for up to 70% of all facial neuropathies.[91] It is a diagnosis of exclusion and is defined as a facial palsy with no known cause or associated neurology. It is thought to be due to a viral demyelinating neuritis, likely to be secondary to herpes simplex virus reactivation in the geniculate ganglion.[92][93]
Ramsay Hunt syndrome accounts for about 3% to 18% of cases of peripheral facial paralysis.[94][95] It is a rare neurological condition characterised by reactivation of the varicella zoster virus involving the facial nerve, and less commonly other cranial nerves (e.g., V, IX, and X).[96] Patients often present with a triad of symptoms: sudden-onset (<72 hours) ipsilateral peripheral facial palsy, severe ear/facial pain, and vesicular ear rash.[96] However, many patients do not present with all three classic features concomitantly; vesicles can precede, co-exist, or follow facial palsy. Other cranial nerves, particularly VIII (with hearing loss and tinnitus), IX, and X, may also be involved, differentiating this aetiology from Bell's palsy.
Central facial palsy is most commonly the result of a lesion in the contralateral motor strip (precentral gyrus) or corticobulbar tract, usually from ischaemic stroke. A nuclear facial palsy may also result from a lesion involving the facial nucleus, such as ischaemia or a neoplasm. Involvement of adjacent structures often results in additional neurological findings, such as ipsilateral sixth cranial nerve (abducens) palsy or contralateral limb weakness.
Basal skull fracture is another common cause of an isolated facial nerve palsy. It can result in injury proximal to the origin of chorda tympani. Temporal bone fracture can also result in facial nerve paralysis.
Meningitis (bacterial, fungal, tuberculous, sarcoid, or carcinomatous) may result in meningismus and/or fever with a resulting facial nerve palsy. Other cranial nerves may also be affected.
Cerebellopontine angle tumours/cysts can compress the facial nerve. The most common tumours responsible are benign schwannomas. Other, less common masses include arachnoid cysts, meningiomas, and epidermoid cysts.
Iatrogenic injury to one or more of the branches of the facial nerve is a risk of parotid gland and otological surgery, due to the nerve’s close proximity.
Local infections such as otitis media or mastoid infection can affect the facial nerve. Neuropathy usually responds to treatment of the underlying infection.[97]
Tumours of the parotid gland may also cause facial weakness through involvement of some (but often not all) terminal branches of the facial nerve.
Facial neuropathy may be associated with human immunodeficiency virus (HIV). It may develop as an isolated finding or in combination with peripheral neuropathy.
Lyme disease is a frequent cause of bilateral facial neuropathy and accounts for 50% of patients with neurological involvement.[98]
IgG4 disease causing pachymeningitis is a rare cause of facial neuropathy.[59][60] IgG4 disease is an inflammatory condition which can affect a variety of systems/organs (e.g., pancreato-biliary tract, retroperitoneum/aorta, and salivary glands), but it can also produce infiltrates at the base of the skull, which affects cranial nerves. The cranial nerves V, VI, and VII seem most commonly affected, with subacute or chronic symptoms.[60] The imaging appearances can mimic other causes of basal skull infiltration, such as a tumour or granulomatous disease. Diagnosis is by biopsy; and IgG4 disease is usually highly responsive to corticosteroid and immune treatment.[59][60]
Other causes of facial nerve palsy include Guillain-Barré syndrome and its variants (often bilateral), diabetes mellitus, pregnancy, amyloidosis, and neurosarcoidosis.[99] Metastasis to the temporal bone can compress the nerve in the facial canal.
Vestibulocochlear (VIII)
Vestibulocochlear nerve dysfunction is a frequent cause of hearing loss, tinnitus, or vertigo resulting from damage to either the cochlear or the vestibular portion of the eighth cranial nerve between the inner ear and its entry into the brainstem at the pontomedullary junction.
Sudden sensorineural hearing loss is defined as loss of >30 decibels in 3 sequential frequencies within 72 hours.[100] It is due to dysfunction of the cochlea or the vestibulocochlear nerve itself, but the underlying aetiology is unknown.
Known causes of eighth nerve dysfunction and/or palsy include the following:
Vestibular neuritis (also known as vestibular neuronitis, labyrinthitis, and acute peripheral vestibulopathy) that is usually secondary to acute viral or post-viral inflammation of the vestibular division of the eighth cranial nerve.[101] It is a self-limiting condition.
Neural presbycusis, an age-related hearing loss caused by atrophy of nerve cells in the cochlea. It is characterised by high-frequency loss and profound reduction in speech discrimination.[102]
A tumour/cyst in the cerebellopontine angle can compress the eighth nerve.[18] The most common mass is a schwannoma arising from the vestibular division of the nerve. A history of neurofibromatosis may support this diagnosis. Other masses that can produce similar symptoms include meningiomas, arachnoid cysts, and epidermoid cysts.
IgG4 disease causes pachymeningitis and is a rare cause of vestibulocochlear neuropathy.[59][60] IgG4 disease is an inflammatory condition which can affect a variety of systems/organs (e.g., pancreato-biliary tract, retroperitoneum/aorta, and salivary glands), but it can also produce infiltrates at the base of the skull, which affects cranial nerves. The imaging appearances can mimic other causes of basal skull infiltration, such as a tumour or granulomatous disease. Diagnosis is by biopsy; IgG4 disease is usually highly responsive to corticosteroid and immune treatment.[59][60]
Ototoxic drugs include aminoglycosides, platinum-based antineoplastic agents, salicylates, quinine, and loop diuretics.[102] Hearing loss from drug toxicity is usually irreversible.[103]
Glossopharyngeal (IX) and vagus (X)
Factors that help to differentiate between specific aetiologies for cranial nerve IX and X neuropathies include the duration since onset and a history of recent head or neck surgery.
The single most common tenth nerve lesion is iatrogenic injury to the right or left recurrent laryngeal nerve during neck or thoracic surgery. It accounts for about one third of all vocal cord paralysis.[20]
Tumours/cysts, including cerebellopontine angle masses, schwannomas of the eighth or ninth nerve, meningiomas, arachnoid cysts, and epidermoid cysts, can cause compression, but other cranial nerves are often affected. Compression may also be caused by masses of the jugular foramen and parapharyngeal space, including glomus jugulare tumours and carotid body tumours (both paragangliomas). Apical lung tumours or high thoracic tumours may impinge on the recurrent laryngeal nerve (particularly the left side), resulting in hoarseness.
Meningitis (bacterial, fungal, tuberculous, sarcoid, or carcinomatous) may result in meningismus and/or fever. Other cranial nerves may also be affected.
Local infections, including in the skull base and parapharyngeal space, can affect the ninth and tenth cranial nerves.
Skull-base fracture can affect these nerves, although ninth or tenth cranial neuropathy is unlikely to be an isolated finding.
Eagle's syndrome is an irritation of the ninth cranial nerve by an elongated styloid process. It may result in glossopharyngeal neuralgia, which is characterised by paroxysmal episodes of unilateral pain in the base of the tongue and deep neck, and is usually elicited by chewing or swallowing.[104]
Cardiovocal syndrome is hoarseness due to impingement of the left recurrent laryngeal nerve as it passes between the aorta and the pulmonary artery. It can be seen in a range of cardiovascular conditions, including left atrial enlargement due to mitral stenosis.[105]
Spinal accessory (XI)
The spinal accessory nerve innervates the sternocleidomastoid and trapezius muscles. Injury to this nerve is uncommon.
Iatrogenic injury is the most common cause of isolated eleventh nerve injury. This usually occurs during surgery in the posterior triangle of the neck during lymph node biopsy or radical neck dissection.[27] Damage may also occur during jugular vein cannulation, carotid endarterectomy, or cosmetic rhytidectomy (face lift).[106][107]
Blunt or penetrating trauma may also result in an isolated spinal accessory palsy.
Tumours/cysts may include lesions of the cerebellopontine angle extending downwards towards the foramen magnum, rostral intrinsic spinal cord tumours (typically the tenth nerve is also affected), and jugular foramen tumours. Jugular foramen tumours can produce 3 characteristic syndromes involving the spinal accessory nerve:[18][108]
Vernet's syndrome (neuropathy of IX, X, and XI)
Collet-Sicard syndrome (neuropathy of IX, X, and XI, plus cerebellar disturbance)
Villaret's syndrome (neuropathy of IX, X, XI, and XII).
Hypoglossal (XII)
Mononeuropathy of the twelfth cranial nerve is rare. Causes can be nuclear (affecting the nucleus of the nerve in the caudal medulla) or infranuclear (lesions of the nerve itself as it travels from the brainstem to its target muscles). Additionally, motor neurone disease or progressive bulbar palsy (a bulbar form of motor neurone disease) can result in dysfunction. Causes of twelfth nerve dysfunction include the following.[18][109]
Nuclear (medullary) lesions, including ischaemic lesions resulting in a brainstem stroke and medullary neoplasms. The progressive bulbar palsy variant of motor neurone disease and Chiari malformations can also result in a nuclear hypoglossal nerve palsy. Due to the close anatomical proximity of other structures in this region, other neurological findings are common.
Multiple types of tumours and masses at the skull base. These include metastatic tumours, meningioma, glomus jugulare tumour, chordoma, osteoma, sarcoma, nerve sheath tumours, epidermoid or dermoid cysts, arachnoid cyst, and carcinoma of the tongue or nasopharynx.
Meningitis (bacterial, fungal, tuberculous, sarcoid, or carcinomatous) may result in meningismus and/or fever. Other cranial nerves may also be affected.
Local infections may include skull-base osteomyelitis and neck abscess.
Skull-base fracture and penetrating injuries to the neck (such as gunshot wounds) can cause isolated hypoglossal injury.
Iatrogenic injuries can result from irradiation of the neck, from surgical injury during neck dissection or carotid endarterectomy, or during central venous line placement.
Vascular malformations, such as a dural arteriovenous fistula, or internal carotid artery aneurysm or dissection may present as an isolated twelfth nerve palsy.
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