Examining the consequences of damage to the the cerebellum provides the strongest clues to its function. Animals and humans with cerebellar dysfunction show problems with motor control. They can still generate motor activity, but lose precision and produce erratic, uncoordinated, or incorrectly timed movements. Functional imaging studies have also shown cerebellar activation in relation to language, attention, and mental imagery. Additionally, correlation studies have shown interactions between the cerebellum and non-motor areas of the cerebral cortex.

Principles of Cerebellar Function

The comparative simplicity and regularity of the cerebellar anatomy led to an early hope that a similar simplicity of computational function could be implied. This was expressed in one of the first books on cerebellar electrophysiology, The Cerebellum as a Neuronal Machine by John C. Eccles, Masao Ito, and Janos Szentágothai. Although a full understanding of cerebellar function has remained elusive, at least four principles have been identified as important: feedforward processing, divergence and convergence, modularity, and plasticity.

1. Feedforward processing: The cerebellum differs from other parts of the brain (especially the cerebral cortex) in that the signal processing is almost entirely feedforward. This means signals move unidirectionally through the system from input to output with very little recurrent internal transmission. The small amount of recurrence that does exist consists of mutual inhibition. There are no mutually excitatory circuits. This feedforward mode of operation means that the cerebellum, in contrast to the cerebral cortex, cannot generate self-sustaining patterns of neural activity. Signals enter the circuit, are processed by each stage in sequential order, and then leave. This provides a quick, concise response to any combination of inputs.

2. Divergence and convergence: In the human cerebellum, information from 200 million mossy fiber inputs is expanded to 40 billion granule cells. This neural divergence is followed by parallel fiber outputs that converge onto 15 million Purkinje cells. Due to their longitudinal alignment, the approximately 1000 Purkinje cells belonging to a microzone may receive input via neural convergence from as many as 100 million parallel fibers. The cells then focus their own output down to a group of less than 50 deep nuclear cells. Therefore, the cerebellar network only receives a modest number of inputs to process and send results via a limited number of output cells.

3. Modularity: The cerebellar system is functionally divided into thousands of independent modules. All modules have a similar internal structure but different inputs and outputs. A module consists of a small cluster of neurons in the inferior olivary nucleus, a set of long narrow strips of Purkinje cells in the cerebellar cortex (microzones), and a small cluster of neurons in one of the deep cerebellar nuclei. Different modules share input, but also appear to function independently. The output of one module does not seem to significantly influence the activity of other modules.

4. Plasticity: The synapses between parallel fibers and Purkinje cells and between mossy fibers and deep nuclear cells are both susceptible to modification of their strength. In a single cerebellar module, input from as many as a billion parallel fibers converge onto a group of less than 50 deep nuclear cells, and the influence of each parallel fiber on those nuclear cells is adjustable. This arrangement gives tremendous flexibility for fine-tuning the relationship between cerebellar inputs and outputs.

Role of the Cerebellum in Motor Learning

There is considerable evidence that the cerebellum plays an essential role in some types of motor learning, most clearly in tasks in which fine adjustments must be made to an action's performance. There has been much dispute about whether learning takes place within the cerebellum itself, or whether it merely serves to provide signals that promote learning in other brain structures. 

One of the most extensively studied cerebellar learning tasks is the eyeblink conditioning paradigm. A blink response is elicited when a neutral conditioned stimulus, such as a tone or a light, is repeatedly paired with an unconditioned stimulus, such as an air puff. After many conditioned-unconditioned stimuli (CS-US) pairings, an association is formed whereby a learned blink, or conditioned response, occurs and precedes US onset. The magnitude of learning is measured by the percentage of all paired CS-US trials that result in a CR.

Experiments showed that lesions localized either to a specific part of the interpositus nucleus (one of the deep cerebellar nuclei), or to a few specific points in the cerebellar cortex, abolished learning of a correctly timed blink response. If cerebellar outputs are pharmacologically inactivated while leaving the inputs and intracellular circuits intact, learning takes place even while the animal fails to show any response. However, if intracerebellar circuits are disrupted, no learning takes place; these facts taken together make a strong case that learning occurs inside the cerebellum and that its cells exhibit neuroplasticity.

Clinical Relevance

Motor abnormalities are the primary symptoms of cerebellar dysfunction, and the nature of those depends on the part of the cerebellum affected. 

Example Symptoms of Cerebellar Dysfunction

Damage to the flocculonodular lobe (vestibulocerebellum) - loss of equilibrium causing an altered walking gait

Lateral zone damage - problems with skilled voluntary and planned movements leading to errors in intended movements (eg., dysdiadochokinesia, the inability to perform rapid alternating movements).

Damage to the midline portion – disruption of whole-body movements

Damage to the upper part of the cerebellum - gait impairments and other problems with leg coordination (ie, ataxia).