Introduction

Sherrington (1906) called the cerebellum the ‘head ganglion of the proprioceptive system’. When it is damaged, movement deficits result. In humans, certain characteristic abnormalities arise, including locomotor ataxia, intention tremor and hypermetria. Hypotonia, or generalized weakness, may also result. Holmes (1922, 1939) provided a detailed and definitive description of these symptoms in his studies of soldiers wounded in World War I. He concluded that cerebellar lesions led to abnormalities in the rate, regularity and force of voluntary movement. But there were reasons to doubt that the cerebellum is the primary generator of motor commands: several months after a cerebellar lesion, the accuracy of movement in humans can sometimes return to near-normal. Shortly after complete cerebellar ablation, animals can still initiate voluntary movements and perform goal-directed activities, albeit inaccurately (Mackay & Murphy, 1979). It has therefore been posited that the cerebellum provides adjustment and co-ordination of CNS centres and pathways which are the primary generators of motor commands (Luciani, 1915; Holmes, 1917; Lorento de Nó, 1924; Rosenblueth, Wiener & Bigelow, 1943). MacKay & Murphy (1979) coined the term ‘accessory gain adjustment’ to describe this role.

Gain control of proprioception

Gamma efferent nerve fibres control muscle spindle sensitivity by activating the small intrafusal muscle fibres within spindles (review: Matthews, 1972). By the early 1950s it was clear that spindle responses to stretch could be greatly modulated by γ action.