Clonus is an involuntary, rhythmic muscular contraction and relaxation caused by lesions in motor pathways from the brain. It causes large repetitive motions, usually initiated by a reflex, and can last from seconds to minutes. Clonus is most commonly seen at the ankle and is associated with conditions like cerebral palsy, stroke, and spinal cord injuries that damage motor control. It occurs due to hyperactive stretch reflexes in the affected muscles from increased motor neuron excitability and nerve signaling delays within long reflex pathways. While clonus often co-exists with spasticity, not all patients with spasticity exhibit clonus.
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Clonus
1. Time is a sort of river of passing events, and strong is its current; no sooner is a thing brought to
sight than it is swept by and another takes its place, and this too will be swept away
-Marcus Aurelius
Clonus
(from the Greek for "violent, confused motion") is a series of involuntary, rhythmic, muscular
contractions and relaxations.
a/w UMN lesions involving descending motor pathways
accompanied by spasticity
Unlike small, spontaneous twitches known as fasciculations (usually caused by lower motor neuron
pathology), clonus causes large motions that are usually initiated by a reflex.
Studies have shown clonus beat frequency to range from three to eight Hz on average
may last a few seconds to several minutes depending on the patient’s condition.[1]
Signs and symptoms
Clonus is most commonly found at the ankle, specifically with a dorsiflexion/plantarflexion
movement
Ankle (medial gastrocnemius)[2]
Patella (knee cap)
Triceps surae[2][3]
Biceps brachii[3]
Cause
Clonus is typically seen in people with cerebral palsy, stroke, multiple sclerosis, spinal cord
damage and hepatic encephalopathy
Clonus has also appeared after ingesting potent serotonergic drugs, where ingestion strongly
predicts imminent serotonin toxicity (serotonin syndrome).
Mechanism
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.[1] Long delays are
primarily due to long reflex pathways, which are common in distal joints and muscles.[1] This
may therefore explain why clonus is typically found in distal structures like the ankle G
Frequency of clonus beats have been found to be directly proportional to the length of the reflex
- Created with love
by Dr. Eashan Srivastava
2. Time is a sort of river of passing events, and strong is its current; no sooner is a thing brought to
sight than it is swept by and another takes its place, and this too will be swept away
-Marcus Aurelius
pathway it is found in.[1]
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.[1]
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.[1] This
theory is still being investigated.[1]
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.[1] Some consider clonus as simply an extended outcome
of spasticity.[1] Although closely linked, clonus is not seen in all patients with spasticity.[1]
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.[1] 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.[1] Clonus is commonly seen in the ankle but
may exist in other distal structures as well.[2]
Diagnosis
Clonus at the ankle is tested by rapidly flexing the foot into dorsiflexion (upward), inducing a
stretch to the gastrocnemius muscle.[1] Subsequent beating of the foot will result, however only
a sustained clonus (5 beats or more) is considered abnormal. Clonus can also be tested in the
knees by rapidly pushing the patella (knee cap), towards the toes.
TREATMENT OF CLONUS
Clonus can be treated by using
● Baclofen
● applying cold
● botox or phenol injections
- Created with love
by Dr. Eashan Srivastava
3. Time is a sort of river of passing events, and strong is its current; no sooner is a thing brought to
sight than it is swept by and another takes its place, and this too will be swept away
-Marcus Aurelius
● Tizanidine selectively blocks group II pathways, which have a role in spasticity but has
no effect on clonus
- Created with love
by Dr. Eashan Srivastava