Cerebellum

Function

• The basic function of cerebellum is to calibrate the detailed form of a movement, not to initiate movements or to decide which movements to execute. Therefore cerebellar damage causes decreased precision, producing erratic, uncoordinated, or incorrectly timed movements

• Cerebellar cognitive affective syndrome or Schmahmann's syndrome

• Damage to the flocculonodular lobe: Loss of equilibrium and in particular an altered, irregular walking gait, with a wide stance due to balancing difficulties.
• Damage to the lateral zone: Problems in skilled Voluntary / Planned movements which can cause errors in the Force/ Direction / Speed / Amplitude of movements.
• Other manifestations include hypotonia, dysarthria, dysmetria, dysdiadochokinesia, impaired check reflex or rebound phenomenon, and intention tremor
• Midline portion handle whole-body movements, whereas lateral portion is more likely involved in fine movements of the hands or limbs.
• Damage to the upper parts cause Gait impairments / Leg coordination
• Damage to the lower parts cause Uncoordinated / Slowed / Poorly aimed movements of Arms / Hands
• This complex of motor symptoms is called ataxia.

Etiology

• Chronic degenerative conditions such as olivopontocerebellar atrophy.
• Prion diseases
• Miller Fisher syndrome
• Viral cerebellar ataxia

Pain

• Cerebellum is involved in pain processing.
• Cerebellum receives pain input from both descending cortico-cerebellar pathways and ascending spino-cerebellar pathways, through the pontine nuclei and inferior olives. Some of this information is transferred to the motor system inducing a conscious motor avoidance of pain, graded according to pain intensity.

These direct pain inputs, as well as indirect inputs, are thought to induce long-term pain avoidance behavior that results in chronic posture changes and consequently, in functional and anatomical remodeling of vestibular and proprioceptive nuclei. As a result, chronic neuropathic pain can induce macroscopic anatomical remodeling of the hindbrain, including the cerebellum. The magnitude of this remodeling and the induction of neuron progenitor markers suggest the contribution of adult neurogenesis to these changes.