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You are here: Home / Neurology / 128: Cranial Nerves 6-12

128: Cranial Nerves 6-12

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CN VI (Abducens Nerve Palsy)

Definition/Overview

  • Dysfunction of the abducens nerve (CN VI), which innervates the lateral rectus muscle
  • Leads to inability to abduct (move eye laterally), resulting in horizontal diplopia
  • CN VI has a long intracranial course, making it vulnerable to increased intracranial pressure (ICP)

Clinical Presentation

  • Horizontal diplopia, worsens with gaze toward the affected side
  • Medial deviation (esotropia) at rest due to unopposed medial rectus
  • May have headache, papilledema if associated with increased ICP

Physical Exam

  • EOM testing → Limited abduction of the affected eye
  • Cover test → Eye drifts medially
  • Check for signs of increased ICP → Papilledema, headache, vomiting

Labs, Studies, and Imaging

  • MRI with contrast → Rule out tumor, stroke, demyelination (MS)
  • CT head → If acute trauma or suspected increased ICP
  • Lumbar puncture (LP) with opening pressure for ICP
  • ESR, CRP → Rule out giant cell arteritis in elderly patients

Common Causes

  • Increased ICP – idiopathic intracranial hypertension (IIH), hydrocephalus, mass effect
  • Microvascular disease – diabetes, hypertension
  • Trauma – skull fractures
  • Demyelination – multiple sclerosis
  • Brainstem stroke

Treatment

  • Address underlying cause
  • Increased ICP → Acetazolamide, weight loss (IIH), shunt or surgery if necessary
  • Microvascular – diabetes, hypertension → Observation, improves over months
  • Prism glasses for persistent diplopia
  • Strabismus surgery if severe and unresolved

Key Takeaways

  • Most common cause = increased ICP, especially in young obese females with IIH
  • Diplopia worsens when looking toward the affected side
  • If bilateral → Think increased ICP or brainstem pathology

CN VII (Facial Nerve Palsy)

Definition/Overview

  • Dysfunction of the facial nerve (CN VII), which controls facial expression, lacrimation, salivation, and taste (anterior 2/3 of tongue)
  • Can be peripheral (Bell’s palsy, Ramsay Hunt) or central (stroke, tumor)

Clinical Presentation

  • Unilateral facial weakness – unable to close eye, flattening of nasolabial fold
  • Loss of forehead movement in peripheral palsy
  • Loss of taste – anterior 2/3 of tongue (chorda tympani involvement)
  • Hyperacusis – increased sensitivity to sound due to stapedius dysfunction
  • Decreased lacrimation if greater petrosal nerve affected

Physical Exam

  • Facial asymmetry
  • Peripheral lesion – Bell’s palsy, Ramsay Hunt → Entire side affected
  • Central lesion – stroke → Forehead spared, lower face affected
  • Eyelid closure testing → Inability to close affected eye (peripheral palsy)
  • Taste testing → Loss on anterior 2/3 of tongue
  • Hyperacusis test → Ask about increased sensitivity to sound

Labs, Studies, and Imaging

  • Clinical diagnosis in classic cases (Bell’s palsy)
  • MRI brain → If concern for stroke, tumor, or demyelination (MS)
  • CT head → If trauma suspected
  • Lyme titers → If recent tick bite or endemic area
  • VZV PCR or serology → If vesicles present (Ramsay Hunt syndrome)

Common Causes

  • Bell’s palsy
  • Ramsay Hunt syndrome – VZV reactivation, with vesicles in ear
  • Stroke
  • Lyme disease
  • Acoustic neuroma
  • Sarcoidosis

Treatment

  • Bell’s palsy → Prednisone within 72 hours, artificial tears for eye protection
  • Ramsay Hunt → Prednisone + acyclovir or valacyclovir
  • Lyme disease → Doxycycline (early), IV ceftriaxone (severe cases)
  • Stroke → Neurovascular evaluation
  • Eye care → Lubricating drops, tape eyelid shut at night to prevent corneal injury

Key Takeaways

  • Forehead involvement = Peripheral (Bell’s, Ramsay Hunt, Lyme, trauma)
  • Forehead sparing = Central (stroke, tumor)
  • Vesicles in ear = Ramsay Hunt (treat with steroids + antivirals)
  • Bilateral facial palsy? Think Lyme disease or Guillain-Barré

CN VIII (Vestibulocochlear Nerve Palsy)

Definition/Overview

  • Dysfunction of the vestibulocochlear nerve (CN VIII), responsible for hearing (cochlear branch) and balance (vestibular branch)
  • Presents with hearing loss, tinnitus, vertigo, and balance issues

Clinical Presentation

  • Sensorineural hearing loss – unilateral or bilateral
  • Tinnitus – ringing in the ears
  • Vertigo – room-spinning dizziness
  • Gait instability, falls
  • Nystagmus – if vestibular component involved

Physical Exam

  • Weber test → Lateralizes to unaffected ear (sensorineural hearing loss)
  • Rinne test
    • Air conduction > bone conduction → Normal or sensorineural loss
    • Bone conduction > air conduction → Conductive loss (not CN VIII)
  • Dix-Hallpike maneuver (if vertigo present)
    • Positive → Benign paroxysmal positional vertigo (BPPV)
  • Head impulse test (for vestibular neuritis/labyrinthitis)
    • Corrective saccade when turning head toward affected side

Labs, Studies, and Imaging

  • Audiometry → Confirms type and severity of hearing loss
  • MRI brain with contrast → If concern for acoustic neuroma (vestibular schwannoma)
  • CT temporal bone → If trauma or congenital malformation suspected
  • Viral serologies (HSV, CMV, VZV, syphilis, Lyme) → If infectious cause suspected

Common Causes

  • Acoustic neuroma (vestibular schwannoma) → Gradual unilateral hearing loss + imbalance
  • Meniere’s disease → Episodic vertigo + fluctuating hearing loss + tinnitus
  • Labyrinthitis (viral/post-infectious) → Vertigo + hearing loss following URI
  • Vestibular neuritis → Acute vertigo without hearing loss
  • Ototoxic drugs – Aminoglycosides, cisplatin, loop diuretics → Bilateral sensorineural hearing loss
  • Stroke (posterior circulation) → Sudden vertigo, ataxia, diplopia, weakness

Treatment

  • Acoustic neuroma → Observation vs. surgical excision or radiation
  • Meniere’s disease → Low-sodium diet, diuretics (HCTZ-triamterene), vestibular rehab
  • Labyrinthitis → Self-limited, supportive care
  • Vestibular neuritis → Vestibular rehab, steroids if severe
  • Ototoxicity → Discontinue offending agent

Key Takeaways

  • Unilateral sensorineural hearing loss + imbalance? Think acoustic neuroma
  • Episodic vertigo + hearing loss + tinnitus? Meniere’s disease
  • Acute vertigo without hearing loss? Vestibular neuritis
  • Ototoxic drugs – aminoglycosides, cisplatin → Bilateral hearing loss

CN IX & X (Glossopharyngeal & Vagus Nerve Palsy)

Definition/Overview

  • CN IX (Glossopharyngeal Nerve): Controls taste (posterior 1/3 of tongue), swallowing, and the gag reflex.
  • CN X (Vagus Nerve): Controls swallowing, phonation (voice), autonomic functions (heart, lungs, GI), and the gag reflex.
  • Dysfunction of these nerves leads to dysphagia, voice changes, and loss of gag reflex.

Clinical Presentation

  • Dysphagia (trouble swallowing)
  • Hoarseness or nasal voice (CN X dysfunction)
  • Loss of gag reflex (CN IX sensory, CN X motor)
  • Uvula deviation away from the lesion (CN X lesion)
  • Palate elevation asymmetry
  • Syncope (if vagal dysfunction affects autonomic tone)

Physical Exam

  • Gag reflex testing → Absent if CN IX or CN X affected
  • Palatal elevation test → Uvula deviates away from affected side
  • Voice quality → Hoarseness or breathiness suggests CN X involvement
  • Swallow assessment → Risk of aspiration with CN IX/X palsy

Labs, Studies, and Imaging

  • MRI brainstem → If concern for stroke, tumor, or MS
  • CT head/neck → If trauma or skull base mass (schwannoma, metastasis)
  • Laryngoscopy → If persistent hoarseness (assess vocal cord paralysis)
  • ESR, CRP → If inflammatory cause suspected (GCA, Guillain-Barré)

Common Causes

  • Brainstem stroke (lateral medullary syndrome/Wallenberg syndrome) → CN IX/X involvement with dizziness, ataxia, Horner’s syndrome
  • Guillain-Barré syndrome (GBS) → Progressive dysphagia, autonomic instability
  • Tumors → Skull base, vagal schwannoma, metastasis
  • Neurosyphilis (tabes dorsalis) → Rare cause
  • Trauma → Carotid dissection, surgical injury
  • Iatrogenic → Thyroid, neck, or ENT surgeries

Treatment

  • Stroke (Wallenberg syndrome) → Supportive care, swallow precautions
  • GBS → IVIG or plasmapheresis
  • Tumors → Neurosurgical or oncologic management
  • Vocal cord paralysis → Speech therapy, possible surgical intervention
  • Aspiration risk → Modified diet, potential PEG tube placement if severe

Key Takeaways

  • Uvula deviation → Away from the lesion (CN X involvement)
  • Loss of gag reflex → CN IX sensory or CN X motor deficit
  • Dysphagia + hoarseness + lateral medullary signs → Think Wallenberg syndrome
  • Guillain-Barré can cause bulbar dysfunction (CN IX, X involvement)

CN XI (Accessory Nerve Palsy)

Definition/Overview

  • Dysfunction of the spinal accessory nerve (CN XI), which innervates the sternocleidomastoid (SCM) and trapezius muscles.
  • Leads to weakness in head turning and shoulder shrugging.

Clinical Presentation

  • Weakness turning head against resistance (SCM dysfunction)
  • Head turns away from the affected side
  • Shoulder droop on affected side (trapezius weakness)
  • Difficulty shrugging shoulder against resistance
  • Scapular winging (if trapezius involvement is severe)
  • Neck or shoulder pain (if traumatic or compressive cause)

Physical Exam

  • SCM testing → Ask patient to rotate head against resistance; weakness on affected side
  • Trapezius testing → Ask patient to shrug shoulders against resistance; affected side is weaker
  • Scapular positioning → Winged scapula if chronic nerve dysfunction

Labs, Studies, and Imaging

  • MRI cervical spine or brainstem → If concern for tumor, stroke, or trauma
  • CT neck → If suspected iatrogenic injury or trauma
  • Electromyography (EMG) → To assess chronic nerve dysfunction
  • Nerve conduction studies (NCS) → To differentiate nerve injury from muscle disease

Common Causes

  • Iatrogenic (most common) → Neck surgery, lymph node dissection, carotid endarterectomy
  • Trauma → Blunt or penetrating neck injury
  • Tumors → Skull base, cervical, or spinal cord lesions
  • Neurodegenerative diseases → ALS, peripheral neuropathy
  • Idiopathic → Rare but possible isolated palsy

Treatment

  • Physical therapy → Strengthen remaining muscle function
  • Nerve repair or grafting → If traumatic nerve transection
  • Pain management → NSAIDs, muscle relaxants if discomfort present
  • Surgical decompression → If compressive lesion causing palsy

Key Takeaways

  • Weak shoulder shrug + weak head turning → CN XI palsy
  • Most common cause → Iatrogenic injury from neck surgery

CN XII (Hypoglossal Nerve Palsy)

Definition/Overview

  • Dysfunction of the hypoglossal nerve (CN XII), which controls tongue movement.
  • Leads to tongue weakness, atrophy, and deviation.
  • Can be unilateral or bilateral, depending on the cause.

Clinical Presentation

  • Tongue deviation toward the affected side (due to unopposed muscles on the intact side)
  • Dysarthria (difficulty with speech)
  • Dysphagia (difficulty swallowing if severe)
  • Tongue atrophy and fasciculations (if lower motor neuron lesion)

Physical Exam

  • Tongue protrusion test → Deviates toward the lesion
  • Inspect for atrophy and fasciculations
  • Assess speech → Slurred articulation
  • Assess swallowing function → Risk of aspiration if severe

Labs, Studies, and Imaging

  • MRI brainstem → If concern for stroke, tumor, or neurodegenerative disease
  • CT head/neck → If trauma or suspected mass
  • Electromyography (EMG) → To assess chronic denervation (ALS, GBS)
  • Lumbar puncture → If concern for Guillain-Barré or infection

Common Causes

  • Brainstem stroke (medial medullary syndrome) → CN XII involvement with contralateral hemiparesis
  • Amyotrophic lateral sclerosis (ALS) → Progressive tongue fasciculations + limb weakness
  • Guillain-Barré syndrome (GBS) → Can cause bulbar weakness
  • Tumors → Brainstem, skull base, hypoglossal schwannoma
  • Trauma → Base of skull, neck injury, surgical damage
  • Multiple sclerosis (MS) → If demyelination affects CN XII pathways

Treatment

  • Address underlying cause
  • Speech therapy → To assist with articulation deficits
  • Swallow precautions → Prevent aspiration in severe cases
  • Physical therapy → If associated hemiparesis (stroke-related cases)

Key Takeaways

  • Tongue deviation toward the lesion (ipsilateral deficit)
  • Tongue fasciculations + atrophy? Think lower motor neuron disease (ALS, GBS)
  • Stroke with tongue involvement? Consider medial medullary syndrome
  • Bilateral involvement = High risk for aspiration (ALS, brainstem pathology)

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