Clonus

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Clonus
Specialty Neurology
Ankle clonus

Clonus is a set of involuntary and rhythmic muscular contractions and relaxations. Clonus is a sign of certain neurological conditions, particularly associated with upper motor neuron lesions involving descending motor pathways, and in many cases is accompanied by spasticity (another form of hyperexcitability). [1] 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, and may last a few seconds to several minutes depending on the patient’s condition. [1]

Contents

Signs

Clonus is most commonly found at the ankle, specifically with a dorsiflexion/plantarflexion movement (up and down). [2] Some case studies have also reported clonus in the finger, toe, and laterally in the ankle (as opposed to the typical up and down motion). [3] [4]

Cause

Clonus is typically seen in people with cerebral palsy, stroke, multiple sclerosis, spinal cord damage and hepatic encephalopathy. [2] It can occur in epilepsy as part of a generalized tonic–clonic seizure, and in pregnant women presenting with severe pre-eclampsia and eclampsia. [5] It can also be an adverse drug reaction, such as after ingestion of potent serotonergic drugs, where clonus 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. [1] In order for self re-excitation to exist, both an increase in motor neuron excitability and nerve signal delay are required. [1] 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). [1] This lack of inhibition biases neurons to a net excitatory state, therefore increasing total signal conduction. [1] 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. Frequency of clonus beats have been found to be directly proportional to the length of the reflex 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. [1] It is thought that the stretch reflex pathway may be stimulated first, and through its events, cause a decreased synaptic current threshold. [1] 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.[ citation needed ] Clonus can also be tested in the knees by rapidly pushing the patella (knee cap), towards the toes.

Voluntary Induction in Healthy People

Gregory Bateson described the induction of clonus in healthy people: [6]

Balance is a partly involuntary and unconscious business, dependent on "spinal reflexes." When provided with appropriate context, these reflexes go into oscillation that is called "clonus," a phenomenon that is familiar to everybody and which is easily produced. (While sitting, place the leg with thigh horizontal and foot supported on the floor. Move the foot inward toward you so that the heel is off the floor and the ball of the foot supports the weight of the leg. When the weights and angles are correctly adjusted, an oscillation will start in the muscle of the calf with a frequency of about six to eight per second and an amplitude of about half an inch at the knee. This oscillation is called clonus in neurophysiology and is a recurrent series of patellar reflexes, generated in a feedback circuit. The effect of each contraction is fed back as a modification of tension to the calf muscle. This change of tension triggers the next patellar reflex.)

— Gregory Bateson, A Sacred Unity, p. 85

In the text, Bateson goes on to describe induction of clonus as a key element of Balinese ritual.

See also

Related Research Articles

In neuroscience, an F wave is one of several motor responses which may follow the direct motor response (M) evoked by electrical stimulation of peripheral motor or mixed nerves. F-waves are the second of two late voltage changes observed after stimulation is applied to the skin surface above the distal region of a nerve, in addition to the H-reflex which is a muscle reaction in response to electrical stimulation of innervating sensory fibers. Traversal of F-waves along the entire length of peripheral nerves between the spinal cord and muscle, allows for assessment of motor nerve conduction between distal stimulation sites in the arm and leg, and related motoneurons (MN's) in the cervical and lumbosacral cord. F-waves are able to assess both afferent and efferent loops of the alpha motor neuron in its entirety. As such, various properties of F-wave motor nerve conduction are analyzed in nerve conduction studies (NCS), and often used to assess polyneuropathies, resulting from states of neuronal demyelination and loss of peripheral axonal integrity.

<span class="mw-page-title-main">Human leg</span> Lower extremity or limb of the human body (foot, lower leg, thigh and hip)

The human leg is the entire lower limb of the human body, including the foot, thigh or sometimes even the hip or buttock region. The major bones of the leg are the femur, tibia, and adjacent fibula. The thigh is between the hip and knee, while the calf (rear) and shin (front) are between the knee and foot.

Spasticity is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.

<span class="mw-page-title-main">Tetraplegia</span> Paralysis of all four limbs and torso

Tetraplegia, also known as quadriplegia, is defined as the dysfunction or loss of motor and/or sensory function in the cervical area of the spinal cord. A loss of motor function can present as either weakness or paralysis leading to partial or total loss of function in the arms, legs, trunk, and pelvis; paraplegia is similar but affects the thoracic, lumbar, and sacral segments of the spinal cord and arm function is spared. The paralysis may be flaccid or spastic. A loss of sensory function can present as an impairment or complete inability to sense light touch, pressure, heat, pinprick/pain, and proprioception. In these types of spinal cord injury, it is common to have a loss of both sensation and motor control.

The ankle jerk reflex, also known as the Achilles reflex, occurs when the Achilles tendon is tapped while the foot is dorsiflexed. It is a type of stretch reflex that tests the function of the gastrocnemius muscle and the nerve that supplies it. A positive result would be the jerking of the foot towards its plantar surface. Being a deep tendon reflex, it is monosynaptic. It is also a stretch reflex. These are monosynaptic spinal segmental reflexes. When they are intact, integrity of the following is confirmed: cutaneous innervation, motor supply, and cortical input to the corresponding spinal segment.

<span class="mw-page-title-main">Patellar reflex</span> Monosynaptic reflex

The patellar reflex, also called the knee reflex or knee-jerk, is a stretch reflex which tests the L2, L3, and L4 segments of the spinal cord. Many animals, most significantly humans, have been seen to have the patellar reflex, including dogs, cats, horses, and other mammalian species.

<span class="mw-page-title-main">Upper motor neuron lesion</span> Medical condition

An upper motor neuron lesion Is an injury or abnormality that occurs in the neural pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves. Conversely, a lower motor neuron lesion affects nerve fibers traveling from the anterior horn of the spinal cord or the cranial motor nuclei to the relevant muscle(s).

<span class="mw-page-title-main">Upper motor neuron</span> Neurons in the brain that carry signals to lower motor neurons

Upper motor neurons (UMNs) is a term introduced by William Gowers in 1886. They are found in the cerebral cortex and brainstem and carry information down to activate interneurons and lower motor neurons, which in turn directly signal muscles to contract or relax. UMNs represent the major origin point for voluntary somatic movement.

<span class="mw-page-title-main">Gamma motor neuron</span>

A gamma motor neuron, also called gamma motoneuron, or fusimotor neuron, is a type of lower motor neuron that takes part in the process of muscle contraction, and represents about 30% of (Aγ) fibers going to the muscle. Like alpha motor neurons, their cell bodies are located in the anterior grey column of the spinal cord. They receive input from the reticular formation of the pons in the brainstem. Their axons are smaller than those of the alpha motor neurons, with a diameter of only 5 μm. Unlike the alpha motor neurons, gamma motor neurons do not directly adjust the lengthening or shortening of muscles. However, their role is important in keeping muscle spindles taut, thereby allowing the continued firing of alpha neurons, leading to muscle contraction. These neurons also play a role in adjusting the sensitivity of muscle spindles.

<span class="mw-page-title-main">Gastrocnemius muscle</span> Calf muscle

The gastrocnemius muscle is a superficial two-headed muscle that is in the back part of the lower leg of humans. It is located superficial to the soleus in the posterior (back) compartment of the leg. It runs from its two heads just above the knee to the heel, extending across a total of three joints.

<span class="mw-page-title-main">Plantaris muscle</span> One of the superficial muscles of the superficial posterior compartment of the leg,

The plantaris is one of the superficial muscles of the superficial posterior compartment of the leg, one of the fascial compartments of the leg.

Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions. Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition. These consequences result in abnormally increased muscle tone of symptomatic muscles. Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug or physical therapy.

<span class="mw-page-title-main">Foot drop</span> Gait abnormality

Foot drop is a gait abnormality in which the dropping of the forefoot happens due to weakness, irritation or damage to the deep fibular nerve, including the sciatic nerve, or paralysis of the muscles in the anterior portion of the lower leg. It is usually a symptom of a greater problem, not a disease in itself. Foot drop is characterized by inability or impaired ability to raise the toes or raise the foot from the ankle (dorsiflexion). Foot drop may be temporary or permanent, depending on the extent of muscle weakness or paralysis and it can occur in one or both feet. In walking, the raised leg is slightly bent at the knee to prevent the foot from dragging along the ground.

<span class="mw-page-title-main">Vestibulospinal tract</span> Neural tract in the central nervous system

The vestibulospinal tract is a neural tract in the central nervous system. Specifically, it is a component of the extrapyramidal system and is classified as a component of the medial pathway. Like other descending motor pathways, the vestibulospinal fibers of the tract relay information from nuclei to motor neurons. The vestibular nuclei receive information through the vestibulocochlear nerve about changes in the orientation of the head. The nuclei relay motor commands through the vestibulospinal tract. The function of these motor commands is to alter muscle tone, extend, and change the position of the limbs and head with the goal of supporting posture and maintaining balance of the body and head.

<span class="mw-page-title-main">Stretch reflex</span> Muscle contraction in response to stretching

The stretch reflex, or more accurately "muscle stretch reflex", is a muscle contraction in response to stretching a muscle. The function of the reflex is generally thought be maintaining the muscle at a constant length but the response is often coordinated across multiple muscles and even joints. The term deep tendon reflex is often wrongfully used by many health workers and students to refer to this reflex. "Tendons have little to do with the response, other than being responsible for mechanically transmitting the sudden stretch from the reflex hammer to the muscle spindle. In addition, some muscles with stretch reflexes have no tendons ".

The triceps reflex, a deep tendon reflex, is a reflex that elicits involuntary contraction of the triceps brachii muscle. It is sensed and transmitted by the radial nerve. The reflex is tested as part of the neurological examination to assess the sensory and motor pathways within the C7 and C8 spinal nerves.

Clasp-knife response refers to a Golgi tendon reflex with a rapid decrease in resistance when attempting to flex a joint, usually during a neurological examination. It is one of the characteristic responses of an upper motor neuron lesion. It gets its name from the resemblance between the motion of the limb and the sudden closing of a claspknife after sufficient pressure is applied.

The Golgi tendon reflex (also called inverse stretch reflex, autogenic inhibition, tendon reflex) is an inhibitory effect on the muscle resulting from the muscle tension stimulating Golgi tendon organs (GTO) of the muscle, and hence it is self-induced. The reflex arc is a negative feedback mechanism preventing too much tension on the muscle and tendon. When the tension is extreme, the inhibition can be so great it overcomes the excitatory effects on the muscle's alpha motoneurons causing the muscle to suddenly relax. This reflex is also called the inverse myotatic reflex, because it is the inverse of the stretch reflex.

Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion.

<span class="mw-page-title-main">Cutaneous reflex in human locomotion</span>

Cutaneous, superficial, or skin reflexes, are activated by skin receptors and play a valuable role in locomotion, providing quick responses to unexpected environmental challenges. They have been shown to be important in responses to obstacles or stumbling, in preparing for visually challenging terrain, and for assistance in making adjustments when instability is introduced. In addition to the role in normal locomotion, cutaneous reflexes are being studied for their potential in enhancing rehabilitation therapy (physiotherapy) for people with gait abnormalities.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Hilder, Joseph M.; Zev W. Rymer (September 1999). "A Stimulation Study of Reflex Instability in Spasticity: Origins of Clonus". IEEE Transactions on Rehabilitation Engineering. 7 (3): 327–340. doi:10.1109/86.788469. PMID   10498378.
  2. 1 2 3 4 5 Douglas, Wallace M.; Bruce H Ross; Christine K. Thomas (Aug 25, 2005). "Motor unit behaviour during clonus". Journal of Applied Physiology. 99 (6): 2166–2172. CiteSeerX   10.1.1.501.9581 . doi:10.1152/japplphysiol.00649.2005. PMID   16099891. S2CID   8598394.
  3. 1 2 3 Weisenburg, Theodore H (November 1903). "Triceps, Biceps and Finger Clonus". Journal of Nervous and Mental Disease. 30 (11): 681–683. doi:10.1097/00005053-190311000-00003. S2CID   143749312.
  4. ↑ Mitchell, John K. (May 1902). "Two unusual forms of clonus: toe clonus and lateral ankle clonus". Journal of Nervous and Mental Disease. 29 (5): 260–261. doi:10.1097/00005053-190205000-00002. S2CID   145648718.
  5. ↑ Anthony, J; Damasceno, A; Ojjii, D (2016-05-18). "Hypertensive disorders of pregnancy: what the physician needs to know". Cardiovascular Journal of Africa. 27 (2): 104–110. doi:10.5830/CVJA-2016-051. PMC   4928160 . PMID   27213858.
  6. ↑ Bateson, Gregory (1991). A Sacred Unity: Further Steps To An Ecology of Mind (1st ed.). New York: Cornelia & Michael Bessie. p. 85. ISBN   0-06-250100-3.
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