Blood supply to the brainstem and cerebellum comes from both vertebral arteries and the basilar artery (Fig. 8.1). There are many small penetrating arterioles that enter the brainstem from these major vessels. The arterioles generally supply one side of the medial brainstem (paramedian arteriole) or one lateral side (circumferential arteriole). Three arteries (superior cerebellar artery, anterior inferior cerebellar artery, and posterior inferior cerebellar artery) supply the cerebellum with blood and also may have branches to the brainstem.

A variety of diseases affect the brainstem but with a lower frequency than the same diseases affecting other brain regions. Brainstem tumors are most often astrocytic and slower growing than astrocytic tumors in the cortex. Bacterial abscesses are rare and most viruses causing encephalitis involve the brainstem less intensely. Hemorrhages involving the brainstem are uncommon. Ischemic strokes of the brainstem occur as lacunes or occlusions of penetrating brainstem arteries and are the most common brainstem disease. However, brainstem strokes are less common than hemispheric or basal ganglia strokes.

The cerebellum occupies about 10 % of the brain volume but contains more neurons than the entire rest of the brain. The cerebellum is divided into the three functional divisions of spinocerebellum, cerebrocerebellum, and flocculonodular lobe (Fig. 8.2). Each division in the cerebellar cortex sends Purkinje cell axons to specific deep cerebellar nuclei and has different functions (Table 8.2). Most input to the highly organized and redundant cerebellar cortex comes from many brainstem nuclei via excitatory mossy fibers that terminate on myriads of granule cells. These granule cell neurons then send inhibitory impulses to Purkinje cells. The inferior olive also sends excitatory input directly to Purkinje cells. Purkinje cells, the only output of the cerebellar cortex, send inhibitory impulses via a GABA neurotransmitter to neurons in the deep cerebellar nuclei that then send output to the brainstem and cerebral cortex.

Cerebellar neurons do not directly produce motor movements but act more as a comparator that compensates for errors in movement by comparing intention with performance and making subtle adjustments. As such, patients with cerebellar diseases do not have weakness or sensory loss. Cerebellar clinical problems are expressed as impaired coordination, imbalance, and even vertigo (Table 8.3). Dysfunction of midline cerebellar structures (vermis of spinocerebellum) produces imbalance problems of midline body structures such as gait and truncal ataxia while cerebellar hemisphere dysfunction produces ataxia of limbs. Unlike the cerebral cortex, damage to one cerebellar hemisphere produces ipsilateral dysfunction.