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Deficits in motor coordination were observed by scientists in the early 1900s when damage occurred to the cerebellum. This type of damage does not cause paralysis, loss of sensation, or an inability to comprehend tasks. Instead, it results in a lack of proficiency in performing movements. Despite the extensive understanding of the cerebellum's anatomical and physiological organization, the exact role it plays in generating movement remains difficult to define. It is believed that the cerebellum is crucial for learning and executing both voluntary and reflex movements. However, these hypotheses face challenges that hinder their complete acceptance. This section will discuss the behavioral effects of cerebellar damage, its connectivity within the central nervous system (CNS), and its activity.

The behavioral consequences of cerebellar damage are manifested as impaired motor function on the same side of the body as the damaged cerebellum. This is due to the double crossing of most cerebellum-related output as it travels to the motor neurons. The first crossing typically occurs in the cerebellar efferent pathway, while the second crossing takes place in the descending motor pathways. For instance, the cerebellum projects to the opposite motor cortex through the thalamus, and the corticospinal pathway recrosses the midline at the lower medulla.

The specific motor deficits resulting from cerebellar lesions depend on the functional component of the cerebellum that is damaged.

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In the early 1900s, scientists showed that damage to the cerebellum led to deficits in motor coordination. That is, damage or loss of the cerebellum does not lead to paralysis, loss of sensation, or an inability to understand the nature of a task; rather, it leads to an inability to perform movements well. Yet it has been hard to define the precise role or 45 135 225 315° Direction of movement • Fig. 9.18 A, Experimental setup in which a monkey holds onto the arm of the apparatus and captures light spots with the distal end of the arm. The monkey first captures the central light spot and then captures whichever of the surrounding targets that becomes illuminated. B, Raster plots showing the activity of one motor cortex cell during movement in eight different directions. T indicates the time at which the target light turns on, whereas M indicates the time at the onset of movement, which is at the center of each raster. Each mark on a raster represents a spike of a motor cortex cell, and each row of marks shows the cell’s activity during one trial. C, Cosine function was fit to the firing level as a function of the direction of movement. The horizontal bar indicates the average spontaneous firing rate in the absence of an upcoming movement. Note that for most directions, the activity in the periods just before and during movement changed significantly from baseline.
•Fig. 9.18, cont’d D, Vectormodelofpopulationactivityinthemotorcortex.Black lines representindividualcellvectors.Whenallofthemaresummedforaparticulardirectionofmovement,theresultingpopulationvector(red) pointsinessentiallythedirectionoftheupcomingmovement.(B andC, ModifiedfromGeorgopoulosAP,etal.J Neurosci. 1982;2:1527.D, ModifiedfromGeorgopoulosAP,etal.InMassionJ,etal[eds].Experimental Brain Research Series, vol.7:Neuronal Coding of Motor Performance. Berlin:Springer-Verlag;1983.) roles of the cerebellum in generating movement, although, paradoxically, scientists have more detailed knowledge of its deceptively simple anatomic and physiological organization than of any other CNS region. The cerebellum is proposed to play a critical role in the learning and execution of both voluntary and certain reflex movements. However, hypotheses about these roles face significant challenges that prevent their complete acceptance. In this section, the behavioral effects of damaging the cerebellum are discussed, followed by a description of its connectivity, both intrinsic and with the rest of the CNS, and then finally a discussion of its activity.
Behavioral Consequences of Cerebellar Damage
Damage to one side of the cerebellum impairs motor function on the ipsilateral side of the body. This reflects a double crossing of most cerebellum-related output as it travels to the motor neurons. The first crossing typically occurs in the cerebellar efferent pathway, whereas the second crossing takes place in the descending motor pathways. For example, the cerebellum projects to the contralateral motor cortex, via the thalamus, and the corticospinal pathway recrosses the midline at the lower medulla.
The specific motor deficits that result from cerebellar lesions depend on which functional component of the