7-19 Cerebellar corticonuclear fibers arise from all regions of the cortex and terminate in an orderly (mediolateral and rostrocaudal) sequence in the ipsilateral cerebellar nuclei. For example, corticonuclear fibers from the vermal cortex terminate in the fastigial nucleus, those from the intermediate cortex terminate in the emboliform and globo-sus nuclei, and those from the lateral cortex terminate in the dentate nucleus. Also, cerebellar corticonuclear fibers from the anterior lobe typically terminate in more rostral regions of these nuclei while those from the posterior lobe terminate more caudally. Cerebellar corticovestibu-lar fibers originate primarily from the vermis and flocculonodular lobe, exit the cerebellum via the juxtarestiform body, and end in the ipsilat-eral vestibular nuclei. These projections arise from Purkinje cells.
Nucleocortical processes originate from cerebellar nuclear neurons and pass to the overlying cortex in a pattern that basically reciprocates that of the corticonuclear projection; they end as mossy fibers. Some nucleocortical fibers are collaterals of cerebellar efferent axons. The cerebellar cortex may influence the activity of lower motor neurons through, for example, the cerebellovestibular-vestibulospinal route.
Neurotransmitters: Gamma-aminobutyric acid (GABA) ( —) is found in Purkinje cells and is the principal transmitter substance present in cerebellar corticonuclear and corticovestibular projections. However, taurine (—) and motilin (—) are also found in some Purk-inje cells. GABA-ergic terminals are numerous in the cerebellar nuclei and vestibular complex. Some of the glutamate-containing mossy fibers in the cerebellar cortex represent the endings of nucleocortical fibers that originate from cells in the cerebellar nuclei.
Clinical Correlations: Numerous disease entities can result in cerebellar dysfunction including viral infections (echovirus), hereditary diseases (see Figure 7—18), trauma, tumors (glioma, medulloblastoma), occlusion of cerebellar arteries (cerebellar stroke), arteriovenous malformation of cerebellar vessels, developmental errors (such as the DandyWalker syndrome or the Arnold-Chiari deformity), or the intake of toxins. Usually, damage to only the cortex results in little or no dysfunction unless the lesion is quite large or causes an increase in intracranial pressure. However, lesions involving both the cortex and nuclei, or only the nuclei, will produce obvious cerebellar signs.
Lesions involving midline structures (vermal cortex, fastigial nuclei) and/or the flocculonodular lobe result in truncal ataxia (titubation or tremor), nystagmus, and head tilting. These patients may also have a wide-based (cerebellar) gait, are unable to walk in tandem (heel to toe), and may be unable to walk on their heels or on their toes. Generally, midline lesions result in bilateral motor deficits affecting axial and proximal limb musculature.
Damage to the intermediate and lateral cortices and the globose, emboliform, and dentate nuclei results in various combinations of the following deficits: dysarthria, dysmetria (hypometria, hypermetria), dysdi-adochokinesia, tremor (static, kinetic, intention), rebound phenomenon, unsteady and wide-based (cerebellar) gait, and nystagmus. One of the more commonly observed deficits in patients with cerebellar lesions is an intention tremor, which is best seen in the finger-nose test. The finger-to-finger test is also used to demonstrate an intention tremor and to assess cerebellar function. The heel-to-shin test will show dysmetria in the lower extremity. If the heel-to-shin test is normal in a patient with his/her eyes open, the cerebellum is intact. If this test is repeated in the same patient with eyes closed and is abnormal, this would suggest a lesion in the posterior column-medial lemniscus system.
Cerebellar damage in intermittent and lateral areas (nuclei or cortex plus nuclei) causes movement disorders on the side of the lesion with ataxia and gait problems on that side; the patient may tend to fall toward the side of the lesion. This is because the cerebellar nuclei project to the contralateral thalamus, which projects to the motor cortex on the same side, which projects to the contralateral side of the spinal cord via the corticospinal tract. Other circuits (cerebellorubal-rubospinal) and feedback loops (cerebelloolivary-olivocerebellar) follow similar routes. Consequently, the motor expression of unilateral cerebellar damage is toward the lesioned side because of these doubly crossed pathways.
Lesions of cerebellar efferent fibers, after they cross the midline in the decussation of the superior cerebellar peduncle, will give rise to motor deficits on the side of the body (excluding the head) contralateral to the lesion. This is seen in midbrain lesions such as the Claude syndrome.
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