Key points

■ In veterinary species, the extrapyramidal motor system is most important for gait and movement. Output from the motor cortex, through the pyramidal system, influences voluntary, skilled movement but has minimal influence on gait.

■ Alternation between extension and flexion is largely generated by spinal cord reflexes; such patterns are triggered and sustained by central pattern generators.

■ UMN tracts primarily responsible for the support phase are the vestibulospinal and pontine reticulospinal tracts facilitating extensor muscles. The flexor phase is controlled by the medullary reticulospinal and the rubrospinal tracts.

■ Some UMN nuclei in the brainstem work as locomotive trigger centres and stimulate or inhibit ambulation.

■ Forebrain lesions in non-primates can cause postural reaction deficits and mild motor signs.

■ Brainstem lesions can cause opisthotonus due to loss of cerebral inhibition of the UMN nuclei that facilitate extensor muscle activity. Or lesions may cause paresis due to loss of UMNs facilitating locomotory activity.

■ Cerebellar lesions can cause ataxia without paresis.

■ UMN and LMN lesions result in disparate types of paresis distinguishable by the Neuro ‘RAT’ - (reflexes, atrophy and tone). The signs are also determined by lesion location and severity, and the number of tracts that have been compromised.