A physiological approach to motor disorders.
Spasticity in man is presented as a disinhibition of spinal cord mechanisms, the responses to stretch depending on the interaction of the reflex effects of group Ia with those of group II afferent fibres. The reflex responses to muscle stretch and shortening in Parkinson's disease do not depend on an abnormality of spinal reflex mechanisms. The superimposition of physiological tremor or alternating tremor in rigidity produces the classical cog-wheel sensation. The phase lead of the action tonic stretch reflex was found to be reduced in patients with athetosis and cerebellar disease, thus diminishing damping of unwanted movements. The more complex transmission characteristics of the action tonic stretch reflex of normal man are absent in patients with spasticity and cerebellar lesions, presumably due to interference with long-loop pathways. In normal subjects gain of the reflex loop increases with voluntary contraction but in spasticity gain remains high irrespective of contraction level.
D001264:Athetosis / Q000503:physiopathology; D002526:Cerebellar Diseases / Q000503:physiopathology; D006801:Humans; D009069:Movement Disorders / Q000503:physiopathology*; D009119:Muscle Contraction; D009127:Muscle Rigidity / Q000503:physiopathology; D009128:Muscle Spasticity / Q000503:physiopathology; D009470:Muscle Spindles / Q000503:physiopathology; D010300:Parkinson Disease / Q000503:physiopathology; D012026:Reflex, Stretch; D013116:Spinal Cord / Q000503:physiopathology