The basilar artery gives off numerous perforating branches to the pons from its posterior surface — the paramedian perforators (supplying the medial pons including the corticospinal tracts, PPRF, CN VI nucleus, and medial lemniscus) and the short circumferential perforators (supplying the anterolateral tegmentum). These small vessels (0.1-0.5 mm diameter) cannot be visualised on conventional angiography but are demonstrated on high-resolution vessel wall MRI.
Basilar perforator occlusion from in-situ thrombosis, pontine lipohyalinosis (hypertensive small vessel disease), or embolism produces characteristic pontine lacunar syndromes: paramedian pontine perforator occlusion causes the locked-in syndrome (bilateral corticospinal tract infarction with preserved consciousness) or pure motor hemiplegia. Short circumferential branch occlusion causes lateral tegmental syndromes (internuclear ophthalmoplegia, ipsilateral facial palsy, contralateral limb ataxia). Basilar artery atherosclerotic disease may produce in-situ thrombosis of the perforators at their ostia.
Bilateral pontine paramedian infarction from basilar perforator thrombosis or embolism destroys the corticospinal tracts bilaterally in the ventral pons, producing complete motor paralysis except vertical eye movements and blinking (preserved dorsal midbrain); consciousness is maintained via the intact ascending reticular system and patients communicate by vertical gaze coding.
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