The stretch reflex is the contraction of a muscle that occurs in response to its stretch. It is not controlled by higher functioning centre i.e. the brain, and is a monosynaptic response that is transmitted to the spinal cord. Our body needs to be able to respond without our cortical input. In this article we will discuss the stretch reflex, the anatomy that underpins it, as well as the clinical relevance.
- Clinical testing of reflexes
- Clinical points
- Related diagrams and images
Reflexes are automatic, subconscious responses to changes within or outside the body. They function to maintain the homeostasis (autonomic reflexes), which include breathing, blood pressure regulation and heartbeat. We also have reflexes that carry out automatic things we don’t need to think about to perform e.g. swallowing, sneezing, coughing and vomiting. We require reflexes to maintain our posture and trunkal balance. These are known as spinal reflexes. Finally we have brainstem reflexes, e.g. the eye movement reflexes.
The stretch reflex is also referred to as the deep tendon reflex or myotatic reflex. It is a simple pre-programmed response by the human body in response to the muscle being passively stretched e.g. by a tendon hammer, or a sudden change in the ground surface. The stretch reflex can be activated by external forces such as a load placed on the muscle or internal forces i.e. the motor neurons being stimulated from within. An example of the former is someone holding a plate, and someone serving them some food. An example of the latter is shivering that occurs when the person is cold, and is instigated by the internal neurons of the muscle.
MicroanatomyEmbedded within a muscle are the muscle spindles. Muscle spindles are composed of a few intrafusal fibres (nuclear bag and nuclear chain are the subtypes), which in fact lack the contractile proteins of normal muscle (actin and myosin), they are non contractile, and they serve as receptive surfaces. Two types of afferent nerve endings penetrate muscle spindles, these are primary sensory fibres of type Ia and secondary sensory fibres of type II. The gamma efferent fibres innervate these regions. It is worth remembering, that the contractile skeletal muscle fibres are ‘extrafusal’ and are thus innervated by the alpha efferent nerves.
The static component of the stretch reflex is in place as long as the muscle is stretched. The dynamic phase occurs only when the muscle is stretched e.g. when the tendon is struck with a tendon hammer. When the muscle is stretched, they send an impulse via the sensory neurons to the relevant spinal cord segment. The nerve synapses with a second nerve within the spinal cord, with the alpha motor neuron to contract. This impulse does not need to travel to the brain, and therefore simply travels from the muscle spindles to the spinal cord, and back to the muscle. The entire reflex process takes place over a few milliseconds.
There is a second set of motoneurons called Golgi tendon organs. Golgi tendon organs are sensory receptor organs present where the muscle is connected to the tendon, and which regulate the tension within the muscle. Alpha gamma coactivation maintains the tension in the muscle spindles when a muscle is in a state of contraction.
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Evolutionarily, the stretch reflex was designed as a protective measure for the muscles, in order to prevent tearing that can occur due to vigorous movement. Once the muscle spindle is stretched, the impulse is sent back to the muscle very quickly, and protects it from being pulled forcefully or beyond its normal range of motion. When a reflex takes place, all of the synergistic muscles (those that cause the same movement) also contract while antagonistic muscles are inhibited. The decrease in the simultaneous contraction of the opposing muscles reduces the likelihood of injury.
When a stretch reflex is activated, it not only causes contraction of the synergistic muscles, but also caused relaxation i.e. has an inhibitory effect on the antagonist muscles. Once a stretch reflex occurs, the impulse is sent from the stretched muscle spindle, to the alpha motor neuron. The alpha motor neuron is split. Hence it is able to cause contraction in the synergistic group, and relaxation in the antagonistic group. If the antagonistic group did not relax, both groups of muscles would contract, resulting in no corrective movement.
The stretch reflex is an example of a circuit that skips the brain, and follows the simple neural loop connecting the muscle to the spinal cord and back. This enables a rapid response. This particular response is crucial. For example, if the muscle is working against a load and shortening during contraction and a subsequent extra load is added, the muscle is able to recognize the stretch immediately and can compensate with a stronger contraction. This also protects the inhibited antagonist muscles from being injured from excessive stretching.
The first major function of the stretch reflex is muscle protection. When a muscle length increases, the muscle spindle within that muscle stretches, and its nerve activity will increase. Resulting from this is increased alpha motor neuron activity. These neurons will cause the muscle to contract, and therefore reduce the stretching of the muscle. The whole system functions as an autonomic regulation of muscle length.
Posture is also a very important consequence of the stretch reflex. It is relevant, as leaning to one side will result in the muscle spindles of the leg and spinal muscles of the opposite side being stretched. This is quickly countered by the stretch reflex, which will keep us upright. Another example is if we encounter a sudden change in the ground we are standing/walking on. If we are to prevent ourselves falling from the force of gravity, we will require rapid correction, mediated by the stretch reflex. The motor neurons travel from the spinal cord itself, and return to the muscle in a loop of neural circuitry. When we make conscious movements, we send impulses from our brains down our spinal cords, and then back to the brain for cerebral processing.
Clinical testing of reflexes
- Mandibular division of the Trigeminal nerve): It is a stretch reflex used to test the cranial nerve V. The mandible is struck just below the lower lips while the mouth is slightly open. This causes the masseter muscle to contract, and the jaw to shut. In a normal person, the reflex is small or absent. In a person with an upper motor neuron lesion, it may be brisk. Jaw jerk reflex (CN V-
- Biceps reflex C5/C6: This is performed by striking the biceps tendon within the cubital fossa. This will cause elbow flexion.
- Brachioradialis reflex C6: This is performed by striking the brachioradialis tendon at the wrist, just before it inserts into the radial styloid process. This will cause supination of the forearm.
- Extensor digitorum reflex C6/C7: This reflex can be elicited by striking the extensor digitorum muscle when the fingers are flexed or half flexed. Extension of the fingers should result.
- Triceps reflex–C7-8: This three-headed muscle causes elbow extension. Its tendon is located just superior to the olecranon process of the elbow.
- Patellar reflex L2-4 (knee-jerk): This is very commonly performed by doctors who wish to test the integrity of the peripheral nerves, and the reflex arc components. The patient is asked to completely relax their leg, and a tendon hammer is used to tap on the patellar tendon. The striking of the tendon will cause a slight stretch, which will result in stretch, and contraction of the quadriceps femoris muscle . The patient should give a small kicking motion caused by knee extension.
- Ankle jerk reflex S1-2: This test will assess the integrity of the sciatic nerve mainly. It is an ankle plantar flexor, and therefore will cause the patient to point their toes, when its tendon (Achilles tendon) is struck.
Nervous system lesions
Lesions of the nervous system can be divided into either upper or lower (some disease processed can affect both). Causes of upper motor neuron damage include:
- increased tone
- clasp-knife spasticity
- lead-pipe rigidity
- leg weakness
- double vision
- gaze palsy
- dementia in its late stages
'Charcot Marie Tooth' disease
This is a disease caused by degeneration of the peripheral motor and sensory neurons i.e. a lower motor neuron disease. It is associated with diminished reflexes. Symptoms usually begin in adulthood, but may begin in childhood. They include:
- muscle weaknes
- reduced muscle tone
- loss of sensation.
This is the archetypal upper motor neuron lesion and the one that presents most often clinically. The underlying cause is the disturbance of blood flow to a region of the brain (similar to a myocardial infarction). The precise mechanism is either ischaemic (commonly from an atherotic embolus) or haemmorhagic (commonly from a perforating vessel of the brain e.g. the middle cerebral artery). Symptoms will vary according the anatomical site. Reflexes are brisk.