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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)
