superior cerebellar artery

**Anatomy** - Origin: distal basilar artery, just caudal to the basilar bifurcation into the posterior cerebral arteries (PCAs). CN III passes between the SCA (below) and PCA (above). - Course: wraps around the upper pons, runs below the tentorium cerebelli, and reaches the superior surface of the cerebellum. - Territory: superior cerebellar hemisphere and superior vermis; deep cerebellar nuclei (especially the dentate); superior and middle cerebellar peduncles; dorsolateral rostral pons (including the lateral spinothalamic tract, lateral lemniscus, and descending sympathetic fibers). - Does not supply the medulla. The AICA supplies the anterior-inferior cerebellum and lateral caudal pons. The PICA supplies the posterior-inferior cerebellum and lateral medulla. Basilar branches in order from caudal to rostral: AICA, labyrinthine (internal auditory) artery, pontine branches, SCA, then the PCAs.

**Clinical significance: SCA syndrome (rostral dorsolateral pontine syndrome)** - Ipsilateral: limb ataxia, dysmetria, intention tremor, and gait ataxia (cerebellar hemisphere and peduncles). Nausea, vomiting, dysarthria, and nystagmus may also occur. Ipsilateral Horner syndrome (miosis, ptosis, anhidrosis) results from damage to descending sympathetic fibers. - Contralateral: loss of pain and temperature sensation in the body and face (lateral spinothalamic tract and ventral trigeminothalamic tract). Hearing loss can occur (lateral lemniscus), but it is less prominent than in AICA infarcts. - Key point: no facial paralysis and no prominent hearing loss or vertigo, unlike AICA infarction. - Large cerebellar infarcts can cause edema, brainstem compression, and obstructive hydrocephalus (fourth ventricle). This can require suboccipital decompression.

**Comparison with other posterior circulation syndromes** - AICA (lateral pontine): ipsilateral facial paralysis, deafness, tinnitus, vertigo, facial sensory loss, and Horner syndrome. Contralateral loss of pain and temperature in the body. - PICA (lateral medullary or Wallenberg): dysphagia, hoarseness, ipsilateral Horner syndrome, ipsilateral facial pain and temperature loss, and contralateral body pain and temperature loss. Vertigo and nystagmus also occur. - Basilar tip occlusion ("top of the basilar") affects the SCA and PCA territories. It causes vertical gaze palsy, altered consciousness, and visual deficits.

**Other associations** - Neurovascular compression: SCA loops are a classic cause of **trigeminal neuralgia** (compression of CN V at the root entry zone in the pons). Treatment is carbamazepine first-line, with microvascular decompression for refractory cases. - Aneurysms: SCA aneurysms are uncommon and typically occur at the basilar-SCA junction or on the SCA itself. - Etiology of SCA infarct: embolic (cardioembolic or vertebral artery dissection) or atherosclerotic/thrombotic. Vertebrobasilar risk factors are the usual ones (hypertension, diabetes, atrial fibrillation, smoking). - Imaging: MRI with diffusion-weighted imaging is more sensitive than CT for posterior fossa infarcts. CTA or MRA assesses the vertebrobasilar system.

**Mnemonic** - "Superior = top of the pons, near CN III; the SCA and PCA sandwich CN III." Aneurysm or compression here can cause CN III palsy.