Cranial nerves

32 named structures.

Draft — not yet clinically reviewed. The structure of this map is checked automatically, but its wording has not been fact-checked against a textbook. Do not rely on it for an exam answer yet.

Clinical detail

Common questions

Which cranial nerves pass through the superior orbital fissure, and how does that differ from the cavernous sinus?

The superior orbital fissure transmits III, IV, V1 (lacrimal, frontal and nasociliary branches) and VI with the superior ophthalmic vein. The cavernous sinus immediately behind it contains the same nerves plus V2, with III, IV, V1 and V2 in its lateral wall and VI running free beside the internal carotid artery. A cavernous sinus lesion therefore adds V2 numbness of the cheek and upper lip and tends to hit VI first; an orbital apex lesion adds optic nerve involvement with visual loss.

How do you tell an upper from a lower motor neurone facial palsy, and where is the lesion in Bell's palsy?

The forehead has bilateral cortical input, so a stroke or tumour above the facial nucleus weakens only the contralateral lower face and the patient can still raise both eyebrows. A lesion of the nucleus or nerve weakens the whole hemiface including the forehead. Bell's palsy is a lower motor neurone lesion in the facial canal of the temporal bone, which is why it is commonly accompanied by hyperacusis (nerve to stapedius), loss of taste on the anterior tongue (chorda tympani) and sometimes a dry eye (greater petrosal), whereas a parotid lesion at the stylomastoid foramen causes weakness alone.

Why does a compressive third nerve palsy involve the pupil while a diabetic one usually spares it?

The parasympathetic pupillomotor fibres run on the outer dorsomedial surface of the nerve and are fed by pial vessels, so an expanding posterior communicating artery aneurysm or a herniating uncus compresses them first, giving a painful palsy with a dilated unreactive pupil. Microvascular ischaemia in diabetes or hypertension infarcts the vasa nervorum in the core of the nerve, sparing the surface fibres, so ptosis and a down-and-out eye occur with a normal pupil. A pupil-involving palsy is an aneurysm until CT angiography proves otherwise; a pupil-sparing palsy in an older vasculopath can be observed but must be imaged if the pupil becomes involved or it fails to recover.

Which way do the tongue, jaw and uvula deviate with a lower motor neurone lesion?

Tongue and jaw deviate towards the lesion; the uvula deviates away. Genioglossus pushes the tongue forward and across, so the healthy side pushes the tongue towards the weak side (XII). The lateral pterygoid pulls the jaw forward and across, so the healthy side pushes the jaw towards the weak side (V3). The palate is lifted by levator veli palatini, so the healthy side pulls the uvula away from the weak side (X). Fasciculation and wasting confirm the lesion is lower motor neurone; an upper motor neurone lesion deviates the tongue away from the lesion without wasting.

What is jugular foramen syndrome and what causes it?

Vernet syndrome is a unilateral palsy of IX, X and XI where they pass through the jugular foramen: absent gag reflex and loss of posterior-tongue taste, palatal weakness with the uvula deviating away, hoarseness and dysphagia, and weakness of sternocleidomastoid and trapezius. Adding XII from the neighbouring hypoglossal canal, with the tongue deviating towards the lesion, makes it Collet–Sicard syndrome. Causes are glomus jugulare paraganglioma (with pulsatile tinnitus), schwannoma, meningioma, nasopharyngeal carcinoma or metastasis at the skull base, skull base osteomyelitis and fractures.