Cranial Nerve Lesions — Bone Wizardry

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 Any to Expand ›

Board Traps ›

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 deviation — they go 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 M S M B M B S S B M M → CN I through XII alternating S (sensory), M (motor), or B (both).

Cavernous Sinus — What Runs Through It ›

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