The cerebellum is the main area affected in motor function organization. When the flocculonodular lobe is damaged, it leads to motor disorders similar to those caused by a vestibular apparatus lesion. These disorders include balance difficulties, gait problems, and often nystagmus. Damage to the vermis affects the trunk, while the intermediate region or hemisphere involvement results in motor disorders in the limbs. The specific part of the limbs affected depends on the location of the damage, with hemispheric lesions affecting distal muscles more than paravermal lesions.

Motor dysfunction in cerebellar disease includes disorders of coordination, equilibrium, and muscle tone. Incoordination, known as ataxia, is often observed as dysmetria, where errors in movement direction and force prevent smooth limb movement to a desired position. Ataxia can also manifest as dysdiadochokinesia, making it difficult to rapidly alternate supination and pronation of the arm. When attempting more complex movements, decomposition of movement occurs, where the movement happens in discrete steps rather than a smooth sequence. An intention tremor appears when touching a target, with the affected hand or foot developing a tremor that increases as the target is approached. Imbalance can lead to impaired balance and a tendency to fall towards the affected side, often accompanied by a wide-based stance (gait ataxia). Speech may become slow and slurred, known as scanning speech. Muscle tone may be reduced (hypotonia), except in lesions of the anterior vermis, where it may be associated with a pendular knee jerk. This can be demonstrated by eliciting a phasic stretch reflex of the quadriceps muscle through striking the patellar tendon. In contrast to the highly damped oscillation in a normal person, the leg continues to swing back and forth due to hypotonia.

These disorders partially stem from abnormal timing of muscle contractions. Normally, limb movements involve precisely timed bursts of electromyography (EMG) in both agonist and antagonist muscles. An initial burst occurs in the agonist, followed by a burst in the antagonist, and finally, a second agonist burst. With cerebellar damage, the relative timing of these bursts becomes abnormal.

The cerebellum, often referred to as the "little brain," is situated in the posterior fossa of the cranium just below the occipital lobe. It is connected to the brainstem through three cerebellar peduncles: the superior, middle, and inferior. Only the cortex is visible from the outer surface, while the white matter of the cerebellum lies beneath the cortex. Within the white matter, the four cerebellar nuclei are embedded: the fastigial, globose, emboliform, and dentate nuclei. The middle two nuclei are commonly grouped together and called the interpositus nucleus. Afferent fibers to the cerebellar cortex and nuclei primarily enter via the inferior and middle peduncles, while efferent fibers from the cerebellar nuclei exit through the superior peduncle.

The cerebellar cortex is divided into three lobes arranged in a rostrocaudal manner: the anterior lobe, posterior lobe, and flocculonodular lobe.
CHAPTER 9 Organization of Motor Function cerebellum is most affected. If the flocculonodular lobe is damaged, the motor disorders resemble those produced by a lesion of the vestibular apparatus; such disorders include difficulty in balance and in gait and often nystagmus. If the vermis is affected, the motor disturbance affects the trunk, and if the intermediate region or hemisphere is involved, motor disorders occur in the limbs. The part of the limbs affected depends on the site of damage; hemispheric lesions affect the distal muscles more than paravermal lesions do.
Types of motor dysfunction in cerebellar disease include disorders of coordination, equilibrium, and muscle tone. Incoordination is called ataxia and is often manifested as dysmetria, a condition in which errors in the direction and force of movement prevent a limb from being moved smoothly to a desired position. Ataxia may also be manifested as dysdiadochokinesia, in which rapid alternating of supination and pronation of the arm is difficult to execute. When more complicated movement is attempted, decomposition of movement occurs, in which the movement is accomplished in a series of discrete steps rather than as a smooth sequence. An intention tremor appears when the subject is asked to touch a target; the affected hand (or foot) develops a tremor that increases in magnitude as the target is approached. When equilibrium is disturbed, impaired balance may be seen, and the individual tends to fall toward the affected side and may walk with a wide-based stance (gait ataxia). Speech may be slow and slurred; such a defect is called scanning speech. Muscle tone may be diminished (hypotonia), except for lesions of the anterior vermis (see earlier section on decerebrate rigidity); the diminished tone may be associated with a pendular knee jerk. This can be demonstrated by eliciting a phasic stretch reflex of the quadriceps muscle by striking the patellar tendon. The leg continues to swing back and forth because of the hypotonia, in contrast to the highly damped oscillation in a normal person.
These disorders reflect, in part, abnormal timing of muscle contractions. Normally, limb movements involve precisely timed EMG bursts in both agonist and antagonist muscles. There is an initial agonist burst followed by a burst in the antagonist and, finally, a second agonist burst. With cerebellar damage, the relative timing of these bursts is abnormal (
Fig. 9.19
The cerebellum (“little brain”) is located in the posterior fossa of the cranium, just below the occipital lobe, and is connected to the brainstem via three cerebellar peduncles (superior, middle, and inferior). From the outer surface, only the cortex is visible. Deep to the cortex is the white matter of the cerebellum, and buried within the white matter are the four cerebellar nuclei: proceeding medially to laterally, the fastigial, globose, emboliform, and dentate nuclei. The middle two nuclei are often grouped together and referred to as the interpositus nucleus. For the most part, cerebellar afferent fibers to the cortex and nuclei enter the cerebellum •Fig. 9.19 Disruption of Cerebellar Activity Alters the Timing of EMG Responses During Movement. Thecerebellarnucleiwerecooledtoblocktheirfunctioningtemporarilywhilemonkeysperformedmovementsabouttheirelbow.LossofcerebellaractivitydisruptstherelativetimingofagonistandantagonistEMGbursts.Thisleadstoabnormalaccelerationofthelimbandamovementtrajectorythatovershootsthetargetposition(hypermetria).(DatafromFlamentD,HoreJ.J Neurophysiol. 1986;55:1221.) via the inferior and middle peduncles, and efferent fibers from the cerebellar nuclei leave via the superior peduncle.
The cerebellar cortex is subdivided into three rostrocaudally arranged lobes: the anterior lobe, the posterior lobe, and the flocculonodular lobe (