(Maintained by David P. Crockett. E-mail suggestions to crockett@umdnj.edu.)


(Revised 2/12/97)

David P. Crockett, M.A., Ph.D.

Department of Neuroscience and Cell Biology

UMDNJ-Robert Wood Johnson Medical School

Room R-306, Telephone: 235-3404


Notes on the cerebellum


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I. Introduction:

1. Cerebellum = 'little brain'; by weight is only 10% of the total brain and yet it contains more than half of all the neurons in the brain.

2. Highly regular, almost crystalline organization.

3. Cerebellar functions:

The cerebellum acts as a 'comparator'; i.e., a device that compensates for errors by comparing intention with performance. The cerebellum is said to compare the central commands for movement with the actual movements themselves. Three features are important to keep in mind:

a. The cerebellum receives information from brain sites that are involved in the planning of movements and commands for movements: corollary discharge.

b. The cerebellum receives information about motor performance; i.e., the results of the movement command, through sensory feedback arising in the periphery during the course of movement: reafference. The cerebellum is then in a position to compare the corollary discharge with reafference (the sensory feedback associated with the movement); if there is a mismatch, corrections may be made.

c. The cerebellum projects to the descending motor systems.

4. The cerebellum is important in the timing of movements and it has been shown to play an important role in learning of complex motor skills.

5. Cerebellar disease are recognized in the patient's inability to perform coordinated movements; i.e., ataxia

II. Cytoarchitecture and Organization of Cerebellum:

1. The cerebellum is composed of (1) an outer mantle of grey: the cerebellar cortex (which is composed of three layers: molecular, Purkinje and granular); (2) internal white matter and three pairs of deep cerebellar nuclei: the fastigial nucleus, the interposed nucleus (made up of the globose and emboliform nuclei) and the dentate nucleus.

2. Input to cerebellum comes from three sources: the periphery, the brainstem and the cerebral cortex.

3. Cerebellar peduncles carry all input and output of cerebellum: inferior cerebellar peduncle (restiform body) middle cerebellar peduncle (brachium pontis) and superior cerebellar peduncle (brachium conjunctivum)

4. The cerebellum is divided into three lobes by two deep transverse fissures: Anterior and posterior lobe by the primary fissure; posterior lobe is separated from the flocculonodular lobe by the posterolateral fissure.

5. The cerebellum may be divided into three sagittal divisions: the vermis (=worm), intermediate and lateral regions:

6. Cerebellar cortex: Three layers with five types of cells: stellate, basket, Purkinje, Golgi, and granule cells.

a. Molecular layer:

b. Purkinje Cell layer: Sole output cells of the cerebellar cortex

c. The granular cell layer:

7. Input to cerebellar cortex:

a. Mossy fibers:

b. Climbing fibers:

III. The three functional divisions of the Cerebellum:

1. Vestibulocerebellum (archicerebellum):

a. Flocculonodular lobe. (controls medial descending system)

2. Spinocerebellum (paleocerebellum):

a. Vermis and intermediate zone of anterior and posterior lobes.

i. Vermal output: fastigial nucleus

ii. Part of the medial descending system: axial and proximal musculature.

b. Intermediate zone: interposed nuclei:

i. Part of the lateral descending systems

c. Two principle functions: the control of the execution of movement; to regulate muscle tone.

3. Cerebrocerebellum (neocerebellum):

a. Input: wide areas of the cerebral cortex and does not receive peripheral sensory input.

b. Output: via the dentate nucleus

c. Participates in the programming (planning) of movement and in cognitive and perception of times:

IV. Diseases of the Cerebellum:

A. Signs and symptoms:

1. Synergia: Cerebellar diseases may lead to asynergia (i.e., limb ataxia).

2. Dysmetria. There may be hypometria or hypermetria.

4. Instead of smooth movements, there is a decomposition of movement.

5. Dysdiadochokinesia refers to an inability to produce rapid alternating movements.

6. Cerebellar diseases often lead to hypotonia of the muscles.

7. Lack of check refers to the fact that the limb may overshoot its target rather than stopping smoothly

8. Intention tremor, common following lesions to the superior cerebellar peduncle, is most pronounced at the end of the movement. Titubation is a tremor of the trunk and may be present when the patient is standing or sitting.

9. Dysarthria (scanning speech).

10. Nystagmus, oscillatory movements of the eyes is a sign of vestibular dysfunction and or lesions involving the flocculonodular lobe (vestibulocerebellum).

B: Lesions of different regions of the cerebellum produce different constellation of signs

1. Flocculonodular Lobe:

Equilibrium: ataxic gait, compensatory wide-based stance. Nystagmus is also seen.

2. Spinocerebellum:

Anterior lobe: alcoholism, particularly the leg areas and vermis: impaired gait, with relative sparing of the arms. Use of the heel-shin test. Ataxia is not improved if the body is supported unlike flocculonodular lobe lesions.

3. Cerebrocerebellar disease:

Asynergia of the ipsilateral limbs. Abnormalities of the finger-to-nose and heel-shin tests, dysmetria, dysdiadochokinesia, lack of check and hypotonia. Scanning speech may be seen with bilateral involvement.

V. Four principles in localizing decease:

1. Lesions result in ipsilateral deficits (limbs).

2. Due to somatotopy: Lesions laterally produce deficits in the limbs (asynergia); lesions medially (in vermis) produce disorders of the trunk or gait ataxia.

3. Lesion in the deep cerebellar nuclei are more intense than those just involving cortex (superior cerebellar peduncle lesions are also very severe)

4. Symptoms tend to improve with time (that is if the decease process stops); more improvement if the lesion occurs in childhood.


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