Hyperactive stretch reflexes The self re-excitation of hyperactive stretch reflexes theory involves a repetitive contract-relax cycle in the affected muscle, which creates oscillatory movements in the affected limb. In order for self re-excitation to exist, both an increase in motor neuron excitability and nerve signal delay are required. Increased motor neuron excitability is likely accomplished by alterations to the net inhibition of neurons occurring as a result of injury to the CNS (stroke/ spinal cord injury). This lack of inhibition biases neurons to a net excitatory state, therefore increasing total signal conduction. Signaling delay is present due to an increased nerve conduction time. Long delays are primarily due to long reflex pathways, which are common in distal joints and muscles. This may therefore explain why<unk>  is typically found in distal structures like the ankle G Frequency of<unk>  beats have been found to be directly proportional to the length of the reflex pathway it is found in. Central oscillator<unk> , with respect to the presence of a central oscillator, functions on the theory that when the central oscillator is turned on by a peripheral event, it will continue to rhythmically excite motor neurons; therefore creating<unk> . Although the two proposed mechanisms are very different in theory and are still debated, some studies now propose the potential of both mechanisms co-existing to create<unk> . It is thought that the stretch reflex pathway may be stimulated first, and through its events, cause a decreased synaptic current threshold. This decreased synaptic current threshold would enhance motor neuron excitability as nerve impulses would be more readily conducted, and thus turn on this central oscillator. This theory is still being investigated.<unk>  and spasticity<unk>  tends to co-exist with spasticity in many cases of stroke and spinal cord injury likely due to their common physiological origins. Some consider<unk>  as simply an extended outcome of spasticity. Although closely linked,<unk>  is not seen in all patients with spasticity.<unk>  tends to not be present with spasticity in patients with significantly increased muscle tone, as the muscles are constantly active and therefore not engaging in the characteristic on/off cycle of<unk> .<unk>  results due to an increased motor neuron excitation (decreased action potential threshold) and is common in muscles with long conduction delays, such as the long reflex tracts found in distal muscle groups.<unk>  is commonly seen in the ankle but may exist in other distal structures as well.
Clonus
Opsoclonus
Opisthotonus
Myoclonus
Paratonia
Stuttering
Catalepsy
Hyperkinesia