Clasp-knife response

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.

Cause

Although seemingly a stretch reflex when flexing a joint, force from the muscle during the attempt to flex a joint is actually thought to be caused by the tendon reflex of the antagonistic muscle of that joint, which is an extensor muscle that becomes stretched.[1] In upper motor neuron lesions, muscle tonus may increase and resistance of muscle to stretch increases. However, if sufficient force is applied, limb resistance suddenly decreases.[1]

Mechanism

This reflex is observed in patients with upper motor neuron lesions. It is frequently attributed to the action of the golgi tendon organ, likely because of early studies showing that tendon organs are activated by strong muscle stretch and inhibit motoroneurons of the stretched muscle. It was thought that this was a protective reflex, preventing application of so much force that muscles become damaged. More recent work strongly suggests that tendon organs are not involved in the clasp knife reflex, but that other sensory receptors in muscles are responsible.[2]

Example

Passive flexion of elbow meets immediate resistance due to stretch reflex in the triceps muscle. Further stretch activates inverse stretch reflex. The resistance to flexion suddenly collapses, and the elbow flexes. Continued passive flexion stretches the muscle and the sequence may be repeated.

             As the muscle tone is more, resistance against flexion of the limb is more.However, when flexion is continued,further stretch of triceps muscle activates inverse stretch reflex that relaxes the muscle due to autogenic inhibition

See also

References

  1. ^ a b "Spinal Relexes". Musom.marshall.edu. Archived from the original on 3 March 2016. Retrieved 23 February 2015.
  2. ^ Neural mechanisms underlying the clasp-knife reflex in the cat. I. Characteristics of the reflex. Cleland CL, Rymer WZ. J Neurophysiol. 1990 Oct;64(4):1303-18. Spasticity, decerebrate rigidity and the clasp-knife phenomenon: an experimental study in the cat. Burke D, Knowles L, Andrews C, Ashby P. Brain. 1972;95(1):31-48.

External links

Brown-Séquard syndrome

Brown-Séquard syndrome (also known as Brown-Séquard's hemiplegia, Brown-Séquard's paralysis, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis, or spinal hemiparaplegia) is caused by damage to one half of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion. It is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850.

Golgi tendon reflex

The Golgi tendon reflex is a normal component of the reflex arc of the peripheral nervous system. In a Golgi tendon reflex, skeletal muscle contraction causes the antagonist muscle to simultaneously lengthen and relax. This reflex is also called the inverse myotatic reflex, because it is the inverse of the stretch reflex. Though muscle tension is increasing during the contraction, alpha motor neurons in the spinal cord supplying the muscle are inhibited. However, antagonistic muscles are activated.

Hypertonia

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 and/or physical therapy.

Muscle tone

In physiology, medicine, and anatomy, muscle tone (residual muscle tension or tonus) is the continuous and passive partial contraction of the muscles, or the muscle's resistance to passive stretch during resting state. It helps to maintain posture and declines during REM sleep.

Stretch reflex

The stretch reflex (myotatic reflex) is a muscle contraction in response to stretching within the muscle. It is a monosynaptic reflex which provides automatic regulation of skeletal muscle length.

When a muscle lengthens, the muscle spindle is stretched and its nerve activity increases. This increases alpha motor neuron activity, causing the muscle fibers to contract and thus resist the stretching. A secondary set of neurons also causes the opposing muscle to relax. The reflex functions to maintain the muscle at a constant length.

Gamma motoneurons regulate how sensitive the stretch reflex is by tightening or relaxing the fibers within the spindle. There are several theories as to what may trigger gamma motoneurons to increase the reflex's sensitivity. For example, alpha-gamma co-activation might keep the spindles taut when a muscle is contracted, preserving stretch reflex sensitivity even as the muscle fibers become shorter. Otherwise the spindles would become slack and the reflex would cease to function.

This reflex has the shortest latency of all spinal reflexes including the Golgi tendon reflex and reflexes mediated by pain and cutaneous receptors.

Upper motor neuron lesion

An upper motor neuron lesion (also known as pyramidal insufficiency) 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).Upper motor neuron lesions occur in the brain or the spinal cord as the result of stroke, multiple sclerosis, traumatic brain injury and cerebral palsy.

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