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Neurology · Neuro

Cranial Nerve Palsies & Vertigo

A board-focused walkthrough of cranial nerve palsies (III, IV, VI, VII) and vertigo, built around localization, classic vignette buzzwords, and next-best-step decisions—from the pupil-involving CN III aneurysm emergency to the HINTS exam for acute vestibular syndrome.

14 min readHigh yield

Localization is the whole game

Cranial nerve (CN) palsies and vertigo are high-yield because the exam rewards precise localization. A deficit can arise anywhere along a nerve's path: nucleus (brainstem) → fascicle → subarachnoid space → cavernous sinus → superior orbital fissure/orbit. Accompanying long-tract signs or other CN deficits point to a brainstem lesion; an isolated CN deficit favors a peripheral (nerve) process.

The ocular motor nerves (III, IV, VI) move the eye; their failure produces binocular diplopia that resolves when either eye is covered. CN VII controls facial expression—separating an upper motor neuron pattern (forehead spared) from a lower motor neuron pattern (whole hemiface) is a classic testing point.

Vertigo—an illusion of spinning—splits into peripheral (labyrinth/CN VIII: usually benign, often with auditory symptoms) and central (brainstem/cerebellum: dangerous, e.g., stroke). The board task is almost always: localize, name the classic cause, then choose the next best step—imaging, a bedside maneuver, or treatment.

Inferior (ventral) view of the human brain with all twelve cranial nerves color-coded and labeled at their brainstem exit points.
Base of the brain: tracing a nerve from where it exits helps separate a brainstem (nuclear) lesion from a peripheral one. · Wikimedia Commons — Brain_human_normal_inferior_view.svg: Patrick J. Lynch, medical illustrator derivative work: Beao — CC BY 2.5, via Wikimedia Commons
Ocular motor palsies (III, IV, VI)
  • CN III (oculomotor): eye rests "down and out," with ptosis and mydriasis if pupil-involved. Parasympathetic fibers run superficially, so a compressive lesion (posterior communicating artery aneurysm, uncal herniation) blows the pupil early—a neurosurgical emergency.
  • Pupil-sparing CN III palsy → microvascular ischemia (diabetes, HTN); central fibers infarct while surface parasympathetics are spared. Typically recovers in ~3 months.
  • CN IV (trochlear): vertical diplopia worse on downgaze (trouble reading, descending stairs); the patient tilts the head away from the lesion. Longest intracranial course and only nerve exiting dorsally → vulnerable to head trauma.
  • CN VI (abducens): horizontal diplopia, esotropia, cannot abduct the eye. Long subarachnoid course → false localizing sign of raised ICP. Also think cavernous sinus disease and Gradenigo syndrome (petrous apicitis: CN VI palsy + ear discharge + retro-orbital pain).
Pupil-sparing vs pupil-blown CN III

Vignette: A 62-year-old with poorly controlled diabetes has sudden binocular diplopia. The right eye rests down and out with ptosis; the pupil is 3 mm and reactive (spared). No headache.

  • Dx: Ischemic (microvascular) CN III palsy—pupil-sparing.
  • Next step: Control vascular risk factors and observe; expect resolution in ~3 months. Emergent angiography is not required for a complete, pupil-sparing palsy—but recheck the pupil over the next several days, since a compressive lesion can involve it late. Image any incomplete or progressing palsy (the "rule of the pupil" only applies once the palsy is complete).

Contrast: A 45-year-old with thunderclap headache, a down-and-out eye, and a fixed, dilated (blown) pupil.

  • Dx: Compressive CN III palsy—suspect a PCom artery aneurysm.
  • Next best step: CT angiography (or MRA) emergently. Pupil involvement means compression until proven otherwise.

Pearl: In any patient ≥50 with acute painful ophthalmoplegia, also consider giant cell arteritis and check ESR/CRP.

CN III vs IV vs VI

FeatureCN III (oculomotor)CN IV (trochlear)CN VI (abducens)
Muscle(s)All extraocular except SO & LR; levator; pupilSuperior obliqueLateral rectus
Eye at rest"Down and out," ptosisSlightly elevated, extortedEsotropia (adducted)
DiplopiaVariable; ptosis may mask itVertical, worse on downgazeHorizontal, worse at distance
Head postureTilt away from lesionFace turn toward lesion
Classic causesPCom aneurysm (pupil +), DM/HTN (pupil −), herniationTrauma, congenital↑ICP (false localizing), DM, cavernous sinus
Red flagPupil involvement = compressionVertical diplopia after traumaBilateral → raised ICP
CN VII: Bell palsy and its mimics
  • UMN facial palsy (cortical stroke): forehead spared (upper face has bilateral cortical input); often with limb weakness. LMN palsy (Bell): entire hemiface, including forehead and eye closure.
  • Bell palsy: acute idiopathic LMN CN VII palsy (HSV-1 reactivation implicated). May include hyperacusis (stapedius), loss of taste on the anterior ⅔ of the tongue, and decreased tearing.
  • Treatment: oral corticosteroids within 72 h (prednisone) speed recovery; add antivirals for severe/complete palsy (antivirals alone are not recommended). Eye protection—artificial tears, lubricating ointment, nighttime taping—prevents exposure keratopathy.
  • Ramsay Hunt syndrome: VZV reactivation—facial palsy + vesicles in the ear canal/auricle ± vertigo and hearing loss; treat with steroids + antivirals (more severe than Bell).
  • Bilateral facial palsy → think Lyme disease (neuroborreliosis), sarcoidosis, or Guillain-Barré.
Photograph of a patient with unilateral Bell's palsy showing a flattened forehead and nasolabial fold and incomplete eye closure on the affected side.
Lower motor neuron CN VII palsy involves the entire hemiface, including the forehead—unlike a cortical (UMN) lesion, which spares it. · Wikimedia Commons — James Heilman, MD — CC BY-SA 3.0, via Wikimedia Commons
Acute continuous vertigo: is it a stroke?

Vignette: A 68-year-old with hypertension has continuous vertigo, nausea, and unsteadiness for 6 hours, with nystagmus on exam. You must exclude posterior-circulation stroke.

Bedside HINTS exam (for the acute vestibular syndrome—continuous vertigo, not brief positional spells):

  • Peripheral (reassuring): abnormal head-impulse test (corrective saccade), unidirectional horizontal nystagmus, and no skew.
  • Central (dangerous): normal head impulse, direction-changing nystagmus, and skew deviation present.
  • Next step: If HINTS is central, other neuro signs appear, or the patient cannot sit/stand unaided → MRI with DWI (early CT misses posterior stroke).
  • Pearl: In trained hands, HINTS is more sensitive than early MRI for posterior-circulation stroke. Vertical or direction-changing nystagmus is central until proven otherwise.

Peripheral vs central vertigo

ConditionDuration / triggerHearingKey findingManagement
BPPVSeconds, positional (rolling in bed)NormalDix-Hallpike → fatigable upbeat-torsional nystagmusEpley repositioning maneuver
Vestibular neuritisDays, continuous; post-viralNormalUnidirectional nystagmus; peripheral HINTSShort-term vestibular suppressants/antiemetics; early vestibular rehab (steroids not routine)
LabyrinthitisDays, continuousReducedVertigo + hearing lossSymptomatic ± steroids
MénièreMinutes–hours, episodicFluctuating SNHLTinnitus + aural fullness (endolymphatic hydrops)Salt restriction, diuretics
Central (stroke)ContinuousUsually normalCentral HINTS; cerebellar/CN signsMRI-DWI, stroke pathway
Classics worth memorizing
  • "Down and out" = the eye position in a CN III palsy (unopposed lateral rectus + superior oblique).
  • HINTS → "INFARCT" flags a central (stroke) cause: Impulse Normal, Fast-phase Alternating (direction-changing), Refixation on Cover Test (skew). Any one component → think stroke.
  • Forehead spared = stroke (UMN); whole face = Bell (LMN).
  • Cranial nerve types—"Some Say Marry Money But My Brother Says Big Brains Matter More" (S = sensory, M = motor, B = both, for CN I–XII). Note III, IV, and VI are all Motor.

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