THE CEREBELLUM AND MOTOR CONTROL

 The cerebellum comprises a bilaterally symmetrical expansion of the superior dorsal lip of the hindbrain, which is divided by deep horizontal fissures into an anterior lobe, large posterior lobe, and a small flocculo-nodular lobe. Two longitudinal grooves running through both anterior and posterior lobes, demarcate a mid-line vermis, flanked on each side by the intermediate zones. Most laterally in the posterior lobe, are the lateral hemispheres. The cerebellar surface is covered by a three layered mantle or cortex of grey matter. The cortex is thrown into extensive, parallel, horizontal folds or folia which increase the surface area. The total surface area of cerebellar cortex, is equal to that of the cerebral cortex. (Right hemisphere removed to show peduncles).

 The innermost layer of the cerebellar cortex is the granule cell layer containing the small granule cells whose axons run up to the surface, bifurcate and run along the folia as parallel fibres in the outermost layer of the cortex - the molecular layer. Between these two layers is the Purkinje Cell layer with the cell bodies of the large Purkinje cells. The large, fan-like dendritic trees of these cells lie in the molecular layer, oriented across the folia, and receiving excitatory synaptic contact from the parallel fibres. Basket and stellate cells in the molecular layer mediate lateral inhibition across the folia. Most inputs to the cerebellar cortex terminate on granule cells as excitatory mossy fibers. Inputs from the inferior olive terminate directly on the Purkinje cells as strongly excitatory climbing fibres. These fibres are strongly activated during the learning new motor activity; their activity is minimal when well-rehearsed tasks are carried out. Axons from the Purkinje cells, the sole outputs from the cortex, run through the granule cell layer, to make inhibitory (GABA-ergic) synapses on the cells of the deep nuclei (see below). The cells of the deep nuclei give rise to the outputs from the cerebellum.

Within the cerebellum is white matter, in which are trapped nuclei of gray matter, the deep nuclei (fastigial, interposed, dentate - See Fig 1). Inputs going to the cerebellar cortex, all send collaterals to excite the cells of the deep nucleus to which the target cortical area projects. The Purkinje cells from the target area of cortex then feed back inhibition to the cells of the deep nucleus which were just previously excited by the input. Outputs from the vermis synapse in the fastigial nuclei, which in turn project to reticular formations, vestibular nuclei and motor cortex (via the ventrolateral/ventral anterior thalamus), to control tone and ongoing activity in the axial and proximal musculature. From the intermediate zones, outputs synapse in the interposed nuclei, which project to the magnocellular red nucleus and the motor cortex (via the VL thalamus), to regulate tone and ongoing activity in the muscles of the limbs. From the lateral hemispheres outputs synapse in the dentate nucleus, which relays to the parvocellular red nucleus (then to the inferior olive, which feeds back to the cerebellum) and to the premotor cortex, to control the timing and planning of complex movements.

The most primitive function of the cerebellum was probably the coordination, in fish, of movements in 3D space (water), based upon inputs from the vestibular apparatus to the VESTIBULO-CEREBELLUM or archicerebellum (the flocculonodular lobe). Not surprisingly, inputs from the vestibular apparatus project directly into the vestibulo-cerebellum, and the vestibular nuclei behave like cerebellar deep nuclei, receiving output directly from the cerebellar cortex (Purkinje cells). Via the vestibulospinal tract and medial longitudinal fasciculus these outputs help to regulate eye movements and control of balance.

As animals moved onto land and the reptiles raised themselves off the ground, it became important to maintain the upright posture against gravity, and to move over irregular terrain without falling over. Information from the proprioceptors was clearly essential, and to process the information from these spinal afferents, the cerebellum expanded by addition of the SPINO-CEREBELLUM or paleocerebellum (anterior lobe, vermis and intermediate areas of hemispheres). Spinal afferents from the axial portions of the body; facial, visual and auditory and vestibular inputs - project to the vermis. Afferents from the limbs project to intermediate zones. Both these areas also receive somatotopically organised inputs from the contralateral motor cortex. Two somatotopic maps exist in the spinocerebellum: one in the anterior lobe and one in the posterior.

In mammals, as the neocortex developed to become a major controlling centre in the cerebral hemispheres, strong connections were formed between motor cortical "association areas" (premotor cortex) and the cerebellum, in order to allow planning, programming and the smoothly integrated execution of complex activities.

 The cerebellum has input/output relations with the ipsilateral body; the cerebral hemispheres with the contralateral. To connect the two, functionally (not somatotopically) organised fibres from the contralateral pre-motor cortex synapse in the pontine nuclei and decussate into a new expanded area, the lateral cerebellar hemispheres. The lateral cerebellar hemispheres, which evolve alongside the neocortex and pons in mammals, constitute the CEREBRO-CEREBELLUM or neocerebellum.

Input to the cerebellar cortex enters the cerebellum via the superior, the middle and the inferior peduncles. Input axons give collaterals which project to & excite the cells of the deep nuclei while the main branches pass on to the cortex. The cortex processes the incoming signals and generates output in the Purkinje cells, which inhibits the recently excited deep nuclei, so sculpting and modifying the pattern of output activity from the deep nuclei.

Inputs into the cerebellum come from three types of sources:

(1) Peripheral inputs from receptors excited by movements, (dorsal spinocerebellar tract; vestibular apparatus, eyes)

(2) Descending inputs from collaterals of descending pathways, to provide information about commands which will result in movements (cortico-ponto-cerebellar tracts)

(3) Mixed inputs from brainstem nuclei (e.g. inferior olive) and spinal motor centers (ventral spinocerebellar tract) which receive convergent input from ascending and descending sources, to provide immediate "comparisons" of differences between efferent messages, and the re-afference created as the commands are executed (?).

 

 

The cerebellum is integrally involved in motor learning- adjusting and re-tooling reflex responses. A good example of this is the adjustment of vestibulo-ocular reflexes and hand-eye co-ordination when wearing prismatic lenses. Perhaps as a consequence of this ability to relearn, cerebellar lesions in non-progressive disorders, tend to have only transient effects, particularly in the young, as the system re-organises and learns new ways of controlling motor activity.

Once the distributions of inputs and outputs and the functional divisions of the cerebellum are understood, the consequences of lesions in the different parts can be rationalised. In general, cerebellar lesions are associated with ipsilateral hypotonia, lack of check, pendular reflexes, ataxia, dysmetria, dysdiadochokinesia, decomposition of movement (asynergia), action tremor, motor Romberg's sign.

Midline lesions affect axial (gait, balance) and facial/oral coordination (speech - dysarthria) and may cause tremor of the trunk and difficulty in sitting upright, while the distal muscles are spared (e.g. alcoholic cerebellar syndrome). Intermediate zone lesions affect limb coordination (gait, heel-shin test, finger-nose test). Lateral hemispheric lesions lead to delays in timing and decomposition of movement (dysdiadochokinesia). Flocculonodular lobe lesions lead to vertigo, ataxia, nystagmus. Note that lesions in different areas can cause ataxia (gait disturbance) with slightly different characteristics, for different reasons.

Lesions which include damage to the superior peduncles and/or deep nuclei cause the most severe forms of cerebellar dysfunction.

Read: SOMJEN, Neurophysiology - the essentials, Chapter 18.3

GANONG, Review of Medical Physiology, Chapter 12 (relevant section)

BERNE & LEVY: Physiology, Chapter 16; Principles of Physiology, Pg.131-135.

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Segment of a folium of the cerebellar cortex showing the relationships between the cellular elements.

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