Cerebellar control of postural scaling and central set in stance

Fay Horak, H. C. Diener

Research output: Contribution to journalArticle

233 Citations (Scopus)

Abstract

1. The effects of cerebellar deficits in humans on scaling the magnitude of automatic postural responses based on sensory feedback and on predictive central set was investigated. Electromyographic (EMG) and surface reactive torques were compared in patients with anterior lobe cerebellar disorders and in normal healthy adults exposed to blocks of four velocities and five amplitudes of surface translations during stance. Correlations between the earliest postural responses (integrated EMG and initial rate of change of torque) and translation velocity provided a measure of postural magnitude scaling using sensory information from the current displacement. Correlations of responses with translation amplitude provided a measure of scaling dependent on predictive central set based on sequential experience with previous like displacements because the earliest postural responses occurred before completion of the displacements and because scaling to displacement amplitude disappeared when amplitudes were randomized in normal subjects. 2. Responses of cerebellar patients to forward body sway induced by backward surface displacements were hypermetric, that is, surface-reactive torque responses were two to three times larger than normal with longer muscle bursts resulting in overshooting of initial posture. Despite this postural hypermetria, the absolute and relative latencies of agonist muscle bursts at the ankle, knee, and hip were normal in cerebellar patients. 3. Although they were hypermetric, the earliest postural responses of cerebellar patients were scaled normally to platform displacement velocities using somatosensory feedback. Cerebellar patients, however, were unable to scale initial postural response magnitude to expected displacement amplitudes based on prior experience using central set. Randomization of displacement amplitudes eliminated the set effect of amplitude on initial responses in normal subjects, but responses to randomized and blocked trials were not different in cerebellar patients. 4. Cerebellar patients compensated for hypermetric responses and lack of anticipatory scaling of earliest gastrocnemius activity by scaling large, reciprocally activated tibialis and quadriceps antagonist activity with the displacement velocity and amplitude. Correlations between these antagonist EMG integrals and displacement amplitudes were preserved when amplitudes were randomized, suggesting that feedback-dependent and not set-dependent mechanisms were responsible for scaling of antagonists by cerebellar patients. Antagonist compensation for initial hypermetric responses also could be induced in normals when they overresponded to unexpectedly small amplitudes of surface displacements. 5. The major effects of anterior lobe cerebellar damage on human postural responses involves impairment of response magnitude based on predictive central set and not on use of velocity feedback or on the temporal synergic organization of multijoint postural coordination. Thus the anterior lobe of the cerebellum appears to play a critical role in modifying the magnitude of automatic postural responses to anticipated displacement conditions based on prior experience. This study suggests that the midline cerebellum tunes the magnitude of somatosensory loops for maintenance of stance posture by adjusting the threshold or bias, and not the slope or gain, of automatic postural responses.

Original languageEnglish (US)
Pages (from-to)479-493
Number of pages15
JournalJournal of Neurophysiology
Volume72
Issue number2
StatePublished - 1994
Externally publishedYes

Fingerprint

Torque
Posture
Cerebellum
Cerebellar Diseases
Muscles
Cerebellar Ataxia
Sensory Feedback
Random Allocation
Ankle
Hip
Knee
Maintenance

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

Cerebellar control of postural scaling and central set in stance. / Horak, Fay; Diener, H. C.

In: Journal of Neurophysiology, Vol. 72, No. 2, 1994, p. 479-493.

Research output: Contribution to journalArticle

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