Stretch hyperreflexia of triceps surae muscles in the conscious cat after dorsolateral spinal lesions.

Resistive force and electromyograms from triceps surae muscles were measured during dorsiflexion of both ankles of awake cats before and after interruption of one dorsolateral funiculus (DLF). DLF lesions produced ipsilateral increases in dynamic and static reflex force that persisted over 66 weeks. The increase in dynamic reflex force was velocity sensitive, as demonstrated by a greater effect for 60 degrees /sec than for 10 degrees /sec dorsiflexion. Also, the lesions increased dynamic force to a greater extent than static force (increased dynamic index). Background force (recorded immediately before each reflex response) was elevated ipsilaterally. However, increases in reflex force were observed when preoperative and postoperative background forces were matched within 10% and were associated with equivalent resting levels of electromyographic (EMG) activity. Resistive reflex force was significantly correlated with EMG responses to dorsiflexion and was not determined by nonreflexive mechanical stiffness of the muscles. Contralateral background and reflex force and associated EMG activity were decreased slightly, comparing preoperative and postoperative records. Clinical testing revealed ipsilateral postoperative increases in extensor tone, increased resistance to hindlimb flexion, hypermetria during positive support responses, and appearance of the Babinski reflex. However, the most reliable tests of DLF lesion effects were the quantitative measures of dynamic and static reflex amplitude. The enhancement of stretch reflexes is suggestive of spasticity. However, hyperactive stretch reflexes, hypertonicity, and the Babinski reflex were observed soon after interruption of the ipsilateral DLF, in contrast to a gradual development of positive signs that is characteristic of a more broadly defined spastic syndrome from large spinal lesions. Also, other signs that often are included in the spastic syndrome, including clonus, increased flexor reflex activity, and flexor spasms, did not result from DLF lesions. Thus, unilateral DLF lesions provide a model of spasticity but produce only several components of a more inclusive spastic syndrome.