Understanding Cerebellar Disorders: Behavioral Signs, Clinical Signs, and Treatment

1. Lecture 33: Cerebellar Disorders Behavioral signs: • Delay in movement initiation (clumsiness, but movement execution is not prevented) • Incomplete and inaccurate movement forms (errors of force, velocity, and timing) • Muscle strength is diminished somewhat (gait changes include wide base stance, truncal tremor, irregularly placed steps, excessive leg lift)

2. Irregular Trajectories During Reaching

3. Inability to Keep Rhythm

4. Long Delay and Slow Movement Initiation

5. Clinical Signs of Cerebellar Disorders • Abnormalities of stance and gait • Titubation (rhythmic tremor of the body or head [rocking or rotational movement] a few times per second) • Rotated or tilted postures of the head • Disturbances of extraocular movements (nystagmus, impaired tracking, impaired VOR) • Decomposition of movement • Dysmetria • Dysdiadochokinesis and dysrhythmokinesis

6. Postural Sway in Ataxia

7. Excessive Postural Reactions to Perturbations

8. Lack of Adaptation to Prismatic Glasses

9. Problems With Control of Interaction Torques

10. Clinical Signs of Cerebellar Disorders • Ataxia (problems with movement initiation, termination, velocity control, etc.) • Check and rebound (effects of sudden tap or release) • Tremor (static and kinetic [intentional]) • Ataxic dysarthria (ataxia of speech) • Muscle tone abnormalities (a combination of hypotonia and cerebellar rigidity)

11. Causes of Cerebellar Disorders • Ischemia • Demyelination • Tumor • Degeneration (OPCA)

12. Cerebellar Disorders: Injury to Vermis (Fastigial N.) • Receives input mostly from the periphery and the brain stem; little input from the cortex • Directs output mostly to the brain stem and the spinal cord; little output to the cortex • Affects control of posture and balance • Can induce gait and truncal ataxia; movements of the extremities may be spared

13. Cerebellar Disorders: Injury to Paravermal Area (Interpositus N.) • Receives input from the periphery, the brain stem, and the cortex (particularly the motor cortex) • Directs output to the brain stem and the cortex • Affects motor cortex activity prior to movement initiation • No distinguishing symptoms because lesions are rarely restricted to this area

14. Cerebellar Disorders: Injury to Lateral Zone (Dentate N.) • Receives input mostly from the cortex; little from the periphery • Directs output mostly to the cortex and the brain stem • Affects voluntary movement of the extremities • Movements show ataxia and tremor

15. Drug treatment is limited at best (5-HTP, clonazepam, vitamin E, etc.) • Should be considered within normal functions of the cerebellum: • Control of posture and movement • Motor learning • Cognitive functions Treatment of Cerebellar Disorders

16. Joint angle EMG flexor EMG extensor Time Cerebellar Lesions: EMG Patterns After a cerebellar lesion, a perturbation of a joint may lead to an alternating EMG pattern in the joint flexors and extensors, leading to a joint oscillation. (Dashed lines: before the lesion; solid lines: after the lesion.)

17. Cerebellar Lesions: Problems With EMG Patterns • Prolonged agonist and delayed antagonist burst • Problems with antagonist EMG modulation (turning off) during rhythmic tasks • A decrease in gamma activity? However, cerebellar disorders are even worse in deafferented animals where the gamma system cannot do much.

18. Cerebellar Cognitive Affective Syndrome • Particularly prominent in patients with lesions of the posterior lobe and the vermis • Impairment of: • Planning • Verbal fluency • Abstract reasoning • Working memory • Spatial cognition (including visuospatial organization and memory) • Personality (disinhibited and inappropriate behavior) • Language (agrammatism, dysprosodia)