Much of what we know about cerebellar function comes from studies of patients whose cerebellums have been injured. Patients with uncoordinated voluntary movements and problems maintaining balance and posture are prevalent. The following are some of the signs of cerebellar damage:
Decomposition of movement. Most of our motions necessitate the coordinated activity of numerous muscle groups and joints to achieve a smooth trajectory of the body part across space. Patients with cerebellar impairment are unable to perform these smooth, coordinated motions. They usually break down movements into their component pieces in order to attain the appropriate trajectory. Touching one’s finger to one’s nose, for example, involves shoulder, elbow, and wrist joint synchronisation. Cerebellar patients must move their shoulders first, then their elbows, and finally their wrists in that order, rather than all at once.
When Cerebellar patients move toward a target, they usually exhibit an involuntary tremor that increases as they get closer to the object. This is known as intentional tremor. When reaching for a cup, for example, the hand travels straight toward the cup at first, but as it gets closer, it begins to move back and forth as it seeks to make contact with the cup.
Dysdiadochokinesia. Patients have difficulty performing quick alternate actions, such as frequently slapping a surface with the palm and back of the hand.
Impaired motor learning. According to studies, cerebellar damage causes motor learning impairments in both human patients and experimental animals. A well-known experimental model is the vestibuloocular reflex (VOR). This reaction allows us to maintain our concentration on an object when the head is rotated. Vestibular signals detect head movement and deliver impulses to the eye muscles via the cerebellum, precisely counteracting the rotation and maintaining the centre of vision. The cerebellum appears to be in charge of ensuring that motor commands to the eyes are correctly calibrated throughout time. The volunteers in the studies wore prisms that magnified the visual image. When the subjects’ heads were moved, the VOR caused the visual picture on the retina to shift rather than remain constant. When the head was rotated, the VOR, on the other hand, progressively adjusted over time, providing appropriate compensating eye movements to keep the retinal image stable. Experimental animals with cerebellar lesions are unable to adjust the VOR.
A second example of cerebellum-dependent motor learning is the execution of precise, coordinated movements. Subjects were instructed to toss balls towards a wall target while wearing prism goggles that shifted the visual image to the right.
The respondents’ accuracy was originally quite low due to the prisms, as the balls usually hit to the left of the target. As they practised more, people improved their accuracy at hitting the target. Because their motor programmes had been re-calibrated to employ the new visual information, the participants began to toss the balls to the right of the target when the goggles were removed. They gradually improved their accuracy over time once more. Because their balls consistently landed to the left of the goal while wearing the goggles, patients with cerebellar injury never learned to correct for the prism. When the goggles were removed, they were immediately accurate at striking the target since they had never made any compensations for the prior prism trials.
A third example is Pavlovian classical conditioning of the eye blink reflex. In this task, a neutral stimulus (like a tone) is coupled with a noxious stimulus (like a puff of air into the eye) to cause reflexive eye blinking. When the tone is heard, the experimental animals will gradually learn to close their eyelids in anticipation of the air puff. When it comes to peaking at the desired puff moment, this taught eyelid closure is incredibly exact. Cerebellar damage makes it impossible for animals to learn to close their eyelids in response to a tone.