Cranial Nerve Lesions

Which nerve? Where's the lesion? What gives it away?
The board loves clinical vignettes · learn the exam findings, not just the list.

Q1 of 4 · Which nerve, which mechanism?
A 55-year-old man with uncontrolled T2DM presents with acute right eye pain and a drooping right eyelid. Exam shows ptosis, the right eye is deviated "down and out," and the right pupil is 4 mm and reactive (same as the left). He denies headache.
Right. Diabetic CN III palsy spares the pupil · ischemia hits the inner vasa nervorum (motor fibers), sparing the outer pupilomotor fibers that run on the surface. PCA aneurysm does the opposite: compression hits those outer fibers first → fixed dilated pupil before ptosis develops. When you see CN III + normal pupil → diabetes or HTN until proven otherwise.
Not quite. The key is that reactive pupil. CN III palsy from a PCA aneurysm or uncal herniation compresses the outer pupilomotor fibers first → blown (fixed, dilated) pupil. Diabetic CN III is a microvascular infarct of the inner nerve · motor fibers die, pupil is spared. CN VI palsy causes failure to abduct (not ptosis). Horner has ptosis + miosis + anhidrosis, not an extraocular movement problem.
Q2 of 4 · Localize the lesion
A 30-year-old woman has sudden severe headache and is brought to the ED. She has left-sided facial droop. On exam, she cannot raise her left eyebrow and cannot close her left eye. Corneal reflex is absent on the left. Upper and lower face are equally affected.
Yes. The forehead gives it away. The forehead receives bilateral cortical input · so an UMN (cortical) stroke only causes contralateral lower face weakness (forehead spared). LMN lesions at the nerve itself (Bell's palsy, parotid tumor, CPA lesion) affect ALL ipsilateral facial muscles including the forehead. Can't raise brow + can't close eye = LMN on that same side.
Not quite. The key is the forehead. UMN (cortical stroke) spares the forehead because the forehead has bilateral cortical representation · even if the left cortex is damaged, the right cortex keeps it moving. LMN lesions (at CN VII itself) have no such backup: whole ipsilateral face goes down. Can't raise left eyebrow + can't close left eye = left LMN lesion. CN V lesion would affect sensation, not motor.
Q3 of 4 · Where is it deviating?
A 70-year-old man with HTN and new-onset dysarthria and dysphagia is examined. When he opens his mouth and says "ahhh," the uvula deviates to the right. He also has hoarseness. Which nerve is affected, and on which side?
Correct. Uvula deviates away from the CN X lesion (toward the intact side). The intact side's soft palate pulls the uvula toward it. Here: uvula goes right → left CN X is down. Contrast with CN XII: tongue deviates toward the lesion (the genioglossus on the damaged side can't push, so the tongue falls toward that side). One points away, one points toward · classic boards trick.
Not quite. The rule: uvula goes away from the CN X lesion. The intact side lifts the soft palate and pulls the uvula toward it. So uvula right → left CN X lesion. Compare with CN XII: tongue deviates toward the lesion (weak side). These two deviate in opposite directions relative to the lesion · know both.
Q4 of 4 · False localizing sign
A 45-year-old woman with a history of pseudotumor cerebri presents with diplopia. She has a lateral rectus palsy on the left. MRI shows no mass lesion near the left lateral rectus or CN VI. What explains the CN VI palsy?
Yes. CN VI is the classic false localizing sign of raised ICP. It has the longest intracranial course of any cranial nerve · runs from the pons, over the petrous apex, through the cavernous sinus. Raised ICP stretches it anywhere along that path, causing unilateral or bilateral lateral rectus palsy with no local lesion. Any bilateral CN VI palsy = assume elevated ICP until proven otherwise.
Not quite. CN VI = false localizing sign for elevated ICP. It has the longest intracranial course, making it uniquely vulnerable to stretch from raised pressure · no mass needed at the site. An INO (internuclear ophthalmoplegia) is a MLF lesion and produces adduction failure with nystagmus of the abducting eye, not simply a lateral rectus palsy.
The 12 Nerves
Tap a card to flip it. One pearl and one board trap per nerve.
The Five Rules
High-yield traps the boards love to test. One fact per card.
CN III palsy · Pupil is EVERYTHING
Blown pupil (fixed, dilated) → compressive = aneurysm, uncal herniation. Pupil-sparing → microvascular = diabetes, HTN. The pupil is how you tell life-threatening from benign.
UMN vs LMN VII · Forehead is EVERYTHING
Forehead spared (still raises brow) → UMN, contralateral cortical stroke. Forehead involved (can't raise brow, can't close eye) → LMN, ipsilateral (Bell's palsy, CPA tumor, parotid).
Uvula vs Tongue · Opposite Directions
Uvula → AWAY from lesion (toward intact CN X). Tongue → TOWARD lesion (weak genioglossus can't push it away, falls ipsilaterally).
CN VI palsy + no mass = elevated ICP
Longest intracranial course → most vulnerable to stretch. Bilateral CN VI palsy is basically a reflex finding of papilledema/pseudotumor until proven otherwise.
Internuclear Ophthalmoplegia (INO)
MLF lesion = ipsilateral adduction failure + contralateral abduction nystagmus. Bilateral INO in young woman = MS. Unilateral INO in elderly = brainstem stroke.
Mnemonic for sensory vs motor: "Some Say Marry Money But My Brother Says Bad Business Marry Money" · S S M M B M B S B B M M → CN I through XII: I=S, II=S, III=M, IV=M, V=B, VI=M, VII=B, VIII=S, IX=B, X=B, XI=M, XII=M.
Cavernous Sinus
What runs through it and what happens when it goes wrong.

Contents: CN III, IV, VI, V1, V2 + Internal Carotid

Cavernous sinus syndrome = ipsilateral ophthalmoplegia (III, IV, VI) + facial sensory loss (V1/V2). It does NOT include CN VII, IX, X.

  • Causes: pituitary apoplexy, thrombosis (post-facial/nasal infection), carotid-cavernous fistula, meningioma
  • Classic boards presentation: painful ophthalmoplegia + V1/V2 numbness in a diabetic = mucormycosis until proven otherwise
  • Tolosa-Hunt syndrome = idiopathic granulomatous cavernous sinus inflammation, steroid-responsive, diagnosis of exclusion

CN Villain Cards

Each villain is a cranial nerve lesion pattern. Tap to reveal the board lock.

💀
The Blown Pupil
CN III + fixed dilated pupil. You have hours, not days.
tap to flip
💀 The Blown Pupil

CN III palsy with a fixed, dilated pupil = compressive cause. Pupilomotor fibers run on the OUTER surface of CN III. A mass (PCA aneurysm, uncal herniation) compresses the outside first.

Break it down: Blown pupil + CN III = emergency CT/CTA. Rule out PCA aneurysm NOW. Diabetic CN III is pupil-SPARING.

🙄
The Forehead Liar
Facial droop. But can they raise their eyebrow?
tap to flip
🙄 The Forehead Liar

UMN (cortical stroke) spares the forehead. Bilateral cortical input to the forehead means one side can go down and the forehead still moves. LMN (Bell's palsy) hits ALL ipsilateral face muscles.

Break it down: Can't raise the brow = LMN on that side. Can raise the brow = UMN, contralateral stroke.

📍
The False Localizer
CN VI palsy. No mass anywhere near it.
tap to flip
📍 The False Localizer

CN VI has the longest intracranial course of any cranial nerve. Elevated ICP stretches it along its path from pons to cavernous sinus. Lateral rectus palsy with no local lesion = raised ICP until proven otherwise.

Break it down: Bilateral CN VI palsy = elevated ICP is the cause. Always check for papilledema.

💨
The Uvula Deceiver
Uvula goes right. Which nerve is down?
tap to flip
💨 The Uvula Deceiver

Uvula deviates AWAY from the CN X lesion. The intact side pulls the soft palate and uvula toward it. If uvula goes right, the LEFT CN X is the lesion.

Break it down: Uvula AWAY from lesion (CN X). Tongue TOWARD lesion (CN XII). They go opposite directions - know both or you get both wrong.

🧠
The MLF Hijacker
Eye won't cross the midline. The other eye is bouncing.
tap to flip
🧠 The MLF Hijacker

INO = medial longitudinal fasciculus (MLF) lesion. Ipsilateral adduction failure + contralateral abduction nystagmus. The MLF connects the CN VI nucleus (pontine) to the contralateral CN III nucleus (midbrain).

Break it down: Bilateral INO in a young woman = MS. Unilateral INO in an elderly patient = brainstem stroke. Never forget this split.

🌐
The Cave Syndicate
Painful ophthalmoplegia + V1/V2 numbness in a diabetic.
tap to flip
🌐 The Cave Syndicate

Cavernous sinus contains CN III, IV, VI, V1, V2 + internal carotid. Syndrome: ipsilateral ophthalmoplegia + V1/V2 sensory loss. CN VII, IX, X are NOT involved.

Break it down: Painful ophthalmoplegia + V1/V2 numbness in a diabetic = mucormycosis until proven otherwise. Steroid-responsive granulomatous version = Tolosa-Hunt.

CN Lesion Localizer

CN III palsy walks into the ED. Follow the branches to the diagnosis.

CN III palsy (ptosis + eye down and out)
Is the pupil involved?
(fixed, dilated = "blown")
YES · Pupil blown
Compressive cause
PCA aneurysm / uncal herniation
CTA head NOW. Outer pupilomotor fibers compressed first by mass.
NO · Pupil spared
Microvascular ischemia
Diabetes, HTN
Check HbA1c, BP. Inner motor fibers die from ischemia. Outer pupil fibers survive.
Lateral rectus palsy (CN VI)
Is there a local mass/lesion at CN VI on imaging?
YES
Direct compression
Tumor, cavernous sinus
NO
FALSE LOCALIZING SIGN
Elevated ICP · check for papilledema

Memory Hooks

Tap any highlighted phrase to reveal the hook.

To remember the sensory vs motor classification"Some Say Marry Money But My Brother Says Bad Business Marry Money" = S S M M B M B S B B M M for CN I-XII of all 12 cranial nerves, one sentence runs the whole sequence from CN I to XII.

The cavernous sinus contents"O TOM CAT" = CN III (Oculomotor), IV (Trochlear), Ophthalmic (V1), Maxillary (V2), CN VI (Abducens), internal caroTid. CN VII is NOT in the cavernous sinus. are tested by asking what's missing after a cavernous sinus thrombosis. O TOM CAT gets you through the door.

For uvula vs tongue deviationUvula goes AWAY (CN X lesion opposite side). Tongue goes TOWARD (CN XII lesion same side). Remember: "Tongue points blame at the criminal (the lesion). Uvula runs away from it.", they go in opposite directions relative to the lesion. Boards test this constantly.

When you see CN III + diabetic + pupil sparedIschemia hits INNER vasa nervorum (motor fibers). Outer pupilomotor fibers survive. Remember: ischemia kills from the inside out. Compression kills from the outside in., the mechanism is microvascular ischemia of the inner nerve trunk. This is the single most board-tested CN III distinction.

Bilateral INO in a young womanMS. MLF = Myelinated tract. MS = demyelinating disease. Young woman + bilateral INO = MS until proven otherwise. Unilateral INO in elderly = stroke. points to one diagnosis above all others. The MLF is a myelinated tract and MS attacks myelin.

What It Looks Like

Real imaging and anatomy. Tap any image to enlarge.

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CN palsy localization

Which CN is affected? Follow the branches to the diagnosis.

Which CN is affected?
Pupil involved = surgical CN3
Posterior communicating artery aneurysm compresses outer parasympathetic fibers first. Emergent CTA head.

Pupil spared = medical CN3
Diabetes (ischemia spares outer fibers). Glucose control. Can follow clinically.
Unilateral: local mass or ischemia. Check for increased ICP.

Bilateral: increased ICP until proven otherwise. Emergent CT. False localizing sign: CN VI has the longest intracranial course and gets stretched first when ICP rises.
UMN (forehead spared, can wrinkle): central lesion (stroke, tumor), contralateral side. Forehead has bilateral cortical input.

LMN (entire face including forehead): Bell's palsy (idiopathic, HSV?) treat with acyclovir + prednisone. Also Lyme disease, parotid tumor.
BPPV: Dix-Hallpike positive, Epley maneuver.

Acoustic neuroma: NF2 if bilateral. Unilateral sensorineural hearing loss + tinnitus.

Labyrinthitis: viral, acute onset, resolves spontaneously.
Bulbar palsy (LMN): flaccid, atrophy, fasciculations of tongue and palate.

Pseudobulbar palsy (UMN): spastic, hyperreflexia, emotional lability (pathological laughing/crying).

Wallenberg (PICA stroke): ipsilateral face sensory loss + contralateral body sensory loss + dysphagia + Horner.
Tongue deviates toward the side of the LMN lesion.

The intact side pushes harder. Tongue falls toward weakness.

LMN signs (atrophy, fasciculations) confirm nerve or nucleus lesion. Causes: skull base tumor, carotid dissection, motor neuron disease.

CN Lesion Quiz

8 questions. Original vignettes only. Answer before the explanation unlocks.

Board-Style Walkthrough

Board-Style Walkthrough

Original board-style vignettes. Shuffled, never-repeat, full explanations for every choice.