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An Introduction to Clinical Neurology by Alan Guberman, M.D. , 1994


Spasticity is a special type of increased tone that always indicates an abnormality in the cortiospinal tracts. Its main characteristic is a velocity-dependent increase in tone accompanied by a "clasp-knife" reflex, or a sudden give or release of tone at a certain point following a gradual increase in tone starting from the onset of the movement. Spasticity is best felt in the upper extremity by grasping the patients hand in a "hand-shake" position and quickly supinating the forearm, whereupon the catch and give phenomenon can be detected. To test spasticity in the lower extremities, the patient is placed supine and the examiner clasps his or her hands behind the patients knee and quickly lifts the leg to produce hip and knee flexion. In a relaxed patient with spasticity, the knee will remain extended, the heel will come off the bed and the knee with flex only gradually as the clasp-knife reflex comes into play. Spasticity is also found in association with other evidence of an upper motor neuron lesion, such as hyperreflexia, clonus, and a Babinski sign.

Upper and Lower Motor Neuron Lesions: Spasticity

Spasticity is another feature of chronic upper motor neuron involvement, and is best seen in the context of spinal cord lesions. IT is a special type of increased muscle tone that exists during passive movement but not at rest. It is also velocity dependent and associated with the clasp-knife phenomenon, which is a sudden release of muscle tone occurring after gradual increase of tone with muscle stretch, and likely stems from the sudden inhibition of alpha motor neurons as inhibitory input from Golgi tendon organs comes into play with stretch.

The mechanism of spasticity is poorly understood but probably relates to increased excitability of alpha motor neurons due to a reduction in the inhibitory input from the descending corticospinal tract. Afferent segmental input to alpha motor neurons is particularly influenced by gamma aminobutyric (GA-BA)-ergic interneurons operating under the controld of presynaptic inhibition. Mechanisms that have been postulated to account for spasticity include a reduction in segmental GA-Baergic input, denervation hypersensitivity, or the sprouting of segmental axons to replace the lost suprasegmental inputs to motor neurons. Spasticity may be regarded as a "positive" phenomenon, unlike weakness, which is a "negative" consequence of upper motor neuron lesions. After an acute lesion in upper motor neurons, there is often a variable period of "shock" with muscle flaccidity before spasticity develops. The return of some movement often parallels the development of spasticity.

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