Hypoglossal Nerve (CN XII)

The hypoglossal nerve is the twelfth and final cranial nerve, providing motor innervation to the tongue muscles. Its name means "under the tongue" in Greek. It controls all intrinsic tongue muscles and most extrinsic tongue muscles, essential for speech, chewing, and swallowing.

Origin

Hypoglossal nucleus in medulla (floor of fourth ventricle)

Foramina

Hypoglossal canal

Course

Exits medulla between pyramid and olive → hypoglossal canal → descends between internal carotid and internal jugular → loops forward to tongue

Functions

•Tongue protrusion
•Tongue retraction
•Tongue shape changes
•Essential for speech articulation
•Assists in chewing and swallowing

Branches

Lingual branches to intrinsic and extrinsic tongue muscles

Structures Innervated

→Intrinsic tongue muscles (superior/inferior longitudinal, transverse, vertical)
→Genioglossus (protrudes tongue)
→Hyoglossus (depresses tongue)
→Styloglossus (retracts tongue)

Clinical Testing

Inspect tongue at rest for atrophy, fasciculations, asymmetry. Have patient protrude tongue - deviates toward weak side. Test lateral tongue movement against resistance.

Clinical Relevance

CN XII palsy causes tongue deviation TOWARD the lesion side on protrusion (weak genioglossus can't push tongue away). LMN lesions cause atrophy and fasciculations. UMN lesions cause spastic weakness without atrophy. Bilateral damage severely impairs speech and swallowing.

Study Tips

✓Tongue deviates toward the lesion (weak side can't push tongue away)
✓CN XII = Tongue motor; Lingual nerve (V3) = Tongue sensation
✓LMN: atrophy + fasciculations; UMN: no atrophy, spastic
✓"Twelve = Two-L's" - hypoglossal moves tongue which has two L's

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Hypoglossal Nerve (CN XII) FAQs

Common questions about this cranial nerve

The genioglossus muscle protrudes the tongue by pushing it forward and to the opposite side. When one CN XII is damaged, the intact side's genioglossus pushes the tongue toward the weak side (the tongue "points to the lesion").

LMN lesions (nerve or nucleus damage) cause tongue atrophy, fasciculations, and deviation toward the lesion. UMN lesions (cortical or corticobulbar tract) cause spastic weakness without atrophy, deviation away from the cortical lesion (toward the weak tongue).

Bulbar palsy is LMN weakness of CN IX, X, XII (atrophy, fasciculations, flaccid). Pseudobulbar palsy is bilateral UMN lesions causing spastic dysarthria, dysphagia, and emotional lability, but no atrophy. Both affect speech and swallowing.