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Head, Neck & Cranial Nerves (Anatomy)

Foramina, the cavernous sinus, and localizing the twelve nerves

Anatomy & Embryology·Head, Neck & Trunk·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy
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Cranial nerve overview and skull-base foramina

Sensory, motor, or both. In order from I to XII: "Some Say Marry Money But My Brother Says Big Brains Matter More" (S = sensory, M = motor, B = both). CN I and II are really CNS tracts rather than true peripheral nerves, which is why the optic nerve is myelinated by oligodendrocytes and is involved in multiple sclerosis.

Foramina localize lesions. Nerves that share an exit are injured together, so a cluster of deficits points to one opening. V1, V2, and V3 leave through the superior orbital fissure, foramen rotundum, and foramen ovale in that order ("Standing Room Only").

Skull-base exits, front to back
OpeningContentsKey point
Cribriform plateCN IAnosmia and CSF rhinorrhea after an anterior skull-base fracture
Optic canalCN II, ophthalmic arteryMonocular vision loss with an afferent pupillary defect
Superior orbital fissureCN III, IV, V1, VI; ophthalmic veinTotal ophthalmoplegia plus forehead numbness
Foramen rotundumV2Cheek and upper lip sensation
Foramen ovaleV3Mastication; lower face and anterior tongue sensation
Foramen spinosumMiddle meningeal arteryEpidural hematoma after a pterion fracture
Internal acoustic meatusCN VII, VIIIA vestibular schwannoma can involve both
Jugular foramenCN IX, X, XI; internal jugular veinCombined IX–XI palsy from a skull-base mass
Hypoglossal canalCN XIITongue deviates toward the lesion

Cavernous sinus and eye movements

Contents. The cavernous sinus holds CN III, IV, V1, V2, and VI plus the internal carotid artery (with its sympathetic plexus). CN VI runs freely through the sinus beside the ICA and is affected first; the others sit in the lateral wall. Cavernous sinus syndrome is ophthalmoplegia with V1/V2 sensory loss; causes include pituitary tumor extension, carotid–cavernous fistula, and septic cavernous sinus thrombosis.

Infections of the facial "danger triangle" (nose and upper lip) can spread through valveless facial and ophthalmic veins to cause cavernous sinus thrombosis.

Extraocular muscles: SO4 LR6, rest III. Superior oblique = CN IV (trochlear), lateral rectus = CN VI (abducens), all others (plus levator palpebrae) = CN III (oculomotor).

  • CN IV palsy: the superior oblique depresses and intorts the adducted eye, so vertical diplopia is worst looking down and in (descending stairs, reading); patients tilt the head away from the affected side. CN IV is the only cranial nerve to exit the dorsal brainstem and the only one to fully decussate.
  • CN VI palsy: the eye is turned in with horizontal diplopia worse on looking toward the lesion; its long intracranial course makes it a false localizing sign of raised intracranial pressure.

CN III and the pupil rule. Palsy gives a "down and out" eye (unopposed SO and LR), ptosis (levator palpebrae), and mydriasis. The parasympathetic pupillomotor fibers run on the outside of the nerve. A compressive lesion (posterior communicating artery aneurysm, uncal herniation) works outside-in, so the pupil blows early; an ischemic diabetic or hypertensive infarct strikes the vulnerable central somatic fibers and spares the pupil.

Face: trigeminal and facial nerves

Mastication (CN V3). Masseter, temporalis, and medial and lateral pterygoids are all supplied by V3. The lateral pterygoid opens and protrudes the jaw; the others close it. With a V3 lesion the jaw deviates toward the weak side, pushed by the intact lateral pterygoid. V3 also carries both limbs of the jaw-jerk reflex.

Facial nerve (CN VII). Its five motor branches leave the parotid: "To Zanzibar By Motor Car" (Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical). The upper face receives bilateral cortical input, which decides how a palsy looks.

  • Upper motor neuron lesion (stroke): weakness of the contralateral lower face only; the forehead is spared.
  • Lower motor neuron lesion (Bell palsy): the entire ipsilateral half-face is paralyzed, including forehead and eye closure. Depending on the level, hyperacusis (stapedius), loss of anterior-tongue taste, and reduced tearing can accompany it. Causes include idiopathic Bell palsy, Lyme disease (may be bilateral), sarcoidosis, and parotid tumors.

Tongue and salivary glands

Tongue innervation
RegionGeneral sensationTasteMotor
Anterior 2/3V3 (lingual nerve)CN VII (chorda tympani)CN XII
Posterior 1/3CN IXCN IXCN XII
Palatoglossus is the only tongue muscle not supplied by CN XII (it is CN X); taste from the extreme posterior tongue and epiglottis also travels with CN X.

Hypoglossal lesions. A lower motor neuron CN XII lesion weakens the ipsilateral genioglossus, so the protruded tongue deviates toward the lesion, with atrophy and fasciculations on that side.

Gland secretomotor supply.

  • Parotid: CN IX, via the otic ganglion and auriculotemporal nerve. The facial nerve passes through the parotid but does not innervate it; it is at risk during parotid surgery, such as resection of a pleomorphic adenoma, and facial weakness from a parotid mass suggests malignancy.
  • Submandibular and sublingual: CN VII, via the chorda tympani and submandibular ganglion.
  • Lacrimal: CN VII, via the greater petrosal nerve and pterygopalatine ganglion.

Neck and sympathetic pathway

Triangles. The anterior triangle is bounded by the SCM, the midline, and the mandible. The posterior triangle is bounded by the SCM, trapezius, and clavicle and contains the accessory nerve (CN XI), brachial plexus roots, and subclavian vessels. CN XI crosses the posterior triangle superficially, so a lymph node biopsy there can weaken the trapezius (shoulder droop); the SCM is spared because its branch leaves before the nerve enters the triangle.

Carotid sheath (VAN). Vagus nerve (CN X), posterior and between the vessels; common or internal carotid Artery, medial; internal jugular veiN, lateral.

Horner syndrome. Loss of sympathetic supply to one side of the face gives ptosis (superior tarsal muscle), miosis, and anhidrosis. The three-neuron pathway can be interrupted anywhere from hypothalamus to orbit:

  1. First-order neuronHypothalamus → ciliospinal center (C8–T2): lateral medullary (Wallenberg) syndrome, cord lesions.
  2. Second-order neuronCord → over the lung apex → superior cervical ganglion: Pancoast tumor.
  3. Third-order neuronAlong the internal carotid to the orbit: carotid dissection (with neck pain), cavernous sinus lesions; facial sweating is largely spared.