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
central nervous system (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 clonus is typically found in
distal structures like the ankle.
Frequency of clonus beats have been found to be directly proportional to the length of the reflex pathway it is found in.
Central oscillator Clonus, 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 clonus. 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 clonus. 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.
Clonus and spasticity Clonus tends to co-exist with
spasticity in many cases of
stroke and
spinal cord injury likely due to their common physiological origins. Some consider clonus as simply an extended outcome of spasticity. Although closely linked, clonus is not seen in all patients with spasticity. Clonus 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 clonus. Clonus 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. Clonus is commonly seen in the ankle but may exist in other distal structures as well. == Diagnosis ==