August 2, 2011

THE ROLE OF SPINDLE AND GOLGI TENDON ORGAN

Posted in physiotherapy tagged at 2:56 am by Edwin

SKELETAL MUSCLE ACTIVATION, α & γ CO-ACTIVATION

Sensory Mechanism To Muscle Activation

Introduction

Neural control skeletal muscle are control by motor neuron which lie beneth in spinal cord and axons in motor nerves. They get sensory feedback from muscles and tendon to work. The proprioceptors are sensors that provide information to muscles and tendons about joint angle, muscle length and tension, which is integrated to give information about the position of limb.

Muscle spindle is types of proprioceptor that provide information about changes in muscle length and for a finer limb control (if there’s more spindles). Therefore muscle spindles has significant role to provide proprioceptive feedback for the movement, position and extension of muscles. Meanwhile golgi tendon organ is types of propriocetor that give information about changes in muscle tension (monitorize tension of the muscle).Golgi tendon organ located in muscle tendon, has a simple anatomy, sensitive to tension in tendon, and signal force produced from muscle. Muscle spindles are small sensory reseptors that are enclose within a capsule in belly of the muscle. Its contain specialized muscle cells and sensory and motor nerve ending.

Muscle spindles convey information to the central nervous system via sensory neuron. The respones of muscle spindles to changes in length also play an important role in regulating the contraction of muscle.

Muscle spindles are encapsulated by connective tissue, and are aligned parallel is extrafusal muscle fibers (all the remaining regular skeletal muscle cells in the muscle). Within a muscle spindle there are several small, specialized muscle fibers known as intrafusal fibers (Muscle cells inside the muscle spindle). Intrafusal muscle fibers are innervated and activated by efferent neuron known as gamma motor neurons. Axons of gamma motor neurons terminate in muscle spindles, and then gamma motor neurons make synapses at both of the ends of the intrafusal muscle fibers and regulate the sensitivity of the sensory afferents which are located in the non-contractile central region.

The role of gamma motor neurons is to maintain and enhance muscle spindles sensitivity, regardless of muscle length. Gamma motor neurons also tighten the spindles and maintain muscle tone. Gamma motor neurons also regulate the gain of the stretch reflex by adjusting the level of tension in the intrafusal muscle fibers of the muscle spindle. The function of the gamma motor neurons is not to supplement the force of muscle contraction provided by the extrafusal fibers, but to modify the sensitivity of the muscle spindle sensory afferents to stretch.

While intrafusal motor neurons is innervated by gamma motor neuron, the efferents that innervate extrafusal fibers are known as alpha motor neurons. The connection between the alpha motor neurons and extrafusal muscle fiber is called as a neuromuscular junction.

Anatomically extrafusal fiber is more bigger and numerous than intrafusal fiber its due to muscle contraction. The contraction muscle is promoted by alpha motor neuron. Therefore, the main job or role of alpha motor neuron is to contracting the muscle.

An alpha motor neuron and the muscle fibers it innervates is a motor unit. This motor unit contains the cell bodies of all the alpha motor neurons involved in contracting a single muscle. Alpha motor neuron lies beneath in brainstem and spinal cord.

Most of alpha motor neurons lies in the spinal cord due to brainstem only innervated muscle in the head and neck only, meanwhile alpha motor neurons that innervated by spinal cord are the remaining the rest of the body. In spinal cord, alpha motor neurons located in the grey matter that forms the ventral horn. These alpha motor neurons provide the motor component of the spinal nerves that innervate muscles of the body.

Alpha motor neurons pathways is not cross section, therefore it means the stimulus from one side of brainstem or spinal cord innervate muscle in the same side of body. Like another neurons, alpha motor neuron have both afferent (incoming input) and efferent (outgoing input) connections.

Alpha motor neuron recieve input from many sources, including upper motor neuron, sensory neurons and interneurons. Upper motor neurons send input to alpha motor neurons via several pathways, including corticospinal tracts and rubrospinal tracts. These tracts are commonly encountered in studies of upper motor neurons and lower motor neurons connectivity in the control of voluntary movements. The sensory input to alpha motor neurons is extensive and has its origin in golgi tendon organs, muscle spindles and other sensory neurons in the periphery. These connections provide the structure for the neural circuits that lie beneath reflexes.

The most extensive input to alpha motor neurons is from interneurons, which are the most nemurous type of neuron in the spinal cord. Among their roles, interneurons synapse on alpha motor neurons to create more complex reflex circuitry.

In the meantime the output of alpha motor neurons (Efferent) send fibers that mainly synapses on extrafusal muscle fiber. Other fibers from alpha motor neurons synapse on Renshaw cells, which role is inhibitory interneurons that synapse on the alpha motor neuron and limit its activity in order to prevent muscle damage. This afferent and efferent connectivity is required to achieve coordinated muscle activity.

The effects of damage or injury in alpha motor neurons is paralysis. It happened due to the alpha motor neurons provide the only voluntary innervation to extrafusal muscle fibers. Losing of alpha motor neurons effectively severs the connection between the brainstem and spinal cord and the muscle they innervate. Without this connection voluntary and involuntary ( reflex) muscle control is impossible.

Voluntary muscle control is lost because alpha motor neurons relay voluntary signals from upper motor neurons to muscle fibers. Meanwhile loss of involuntary control results from interruption of reflex circuits.

A consequence of reflex interruption is that muscle tone is reduced, resulting in flaccid paresis. Another consequences is the depression of deep tendon reflexes, which causing hyporeflexia. Muscle weakness and muscle atrophy also consequences of alpha motor neuron lesion as well. Its due to muscle size and strength are related to the extent of their use, denervated muscles are prone to atrophy.

A secondary cause of muscle atrophy is that denervated muscles are no longer supplied with alpha motor neuron that suppose to innervate them. In condition muscle has contraction actively (produced by activating alpha motor neurons only) the intrafusal muscle fibers go slack and both sensory neurons ( I and II) stop discharging or decrease firing, and it’s not very useful. Mean while if gamma motor neurons (motor neurons that innervate only muscle spindles) are activated at the same time as alpha motor neurons, the intrafusal fiber will takes up slack and the muscle spindles becomes taut, and it will adjust muscle spindle sensitivity to muscle length. its due to intrafusal muscle fibers are in paralel with extrafusal muscle fibers. This active muscle contraction mechanism called as alpha – gamma coactivation (Extrafusal fibers have been stimulated to contract by alpha motor neurons activation (produces the force for movements), the gamma motor neuron is simultaneously excited). In alpha-gamma coactivation, the gamma motor neurons stimulates contraction in the two ends of the intrafusal fiber, readjusting its length and keeping the central of the intrafusal fiber taut, which is necessary to keep the muscle spindle afferent responsive. Thus alpha-gamma coactivation forms a mechanism for telling the diffrence between desired position or movement (set by gamma activity) and actual position or movement, if you move your arm or leg with regular muscle cell and spindle muscle cells contracting at the same rate, you can tell if you encounter an obstacle or pertubration it depends on your environment.

The golgi organ or golgi tendon organ is a proprioceptive sensory receptor organ that is located at the insertion of skeletal muscle fibers into the tendons of skeletal muscle. The Golgi tendon organ is an elongated encapsulated structure where the extrafusal muscle fibers are attached to the collagen fibers of the organ. The golgi tendon organ provides the sensory component of the golgi tendon reflex.

The sensory dendrites of the golgi tendon organ afferent are interwoven with collagen fibrils in the tendon. Each golgii tendon organ is innervated bay a single myelinated axon, that becomes unmyelinated after it penetrates the tendon organ. There is no efferent connection from the CNS to the tendon organ. When the muscle contracts, the collagen fibrils are pulled tight, and this actives golgi tendon organ afferent, changes in muscle tension will provide different degree of pull on the tendon so that the golgi tendon organ provides information about muscle tension. So when we think that muscle which stretch would also pull on the tendons and stimulate the golgi tendon organ afferent, unfortunately it false, the truth is when we stretch the muscle , most of the force is absorbed by the muscle itself, so a muscle contraction is a much better stimulus for the golgi tendon organ.

In stroke condition theres many circumstances that happend with muscle activation. Its resulting from a lesion of the upper motor neurone in terms of an interference of normal postural control. In this circumstances we are dealing with abnormal condition of motor patterns of coordination in which the patterns of normal and abnormal postural control against gravity. Sherington (1947) states that normal movements need a background of normal tonus. It has to be of moderete intensity, not to high as to interfere movement, but high enough to make movement against gravity possible. Therefore the role of muscles spindle and golgi tendon organ in active muscle activation has significant role in interfere normal movement.

The abnormal types of postural tone and the stereotyped total motor patterns we see in our patients are the result of disinhibition (release of lower patterns of activity from higher inhibitory control). Its has shown that spasticity is due to a release of a facilitory centre within the reticular substance of the brain stem acting on the gamma motor neurons system from higher inhibitory control. Flaccidity, on the other hand, is due to excessive inhibition of gamma activity from the cerebellum with lack of postural tone against gravity (Magoun and Rhines (1946, 1948)).

The brain damaged patient suffer from a lack of inhibitory contol over his movements. This shows itself in the release of tonic reflex activity. As a result of his brain damage, is more or less dominated by his released abnormal reflex activity which interferes with normal activity. This lack of inhibitory will result or affect the patient so that the tonus will increase and it will come spasticity. Spasticity are seen to be lengthening and shorthening reactions, thie view has been supported by the discovery of the dual innervation of muscle; alpha motor system and gamma motor system.

Spasticity is now considered to be due to the release of the gamma motor neurons system and very rarely the alpha motor neurons system, from higher inhibitory control. Spasticity often associated with exaggerated tendon jerks, and is often accomponied by abnormal cutaneus and autonomic reflexes, muscle weakness, lack of dexterity, and co-contraction of agonist and antagonist muscles. Beside the importance role of inhibition in muscle activation there is one more that interfere normal motor activity, its reciprocal innervation.

Resiprocal innervation provides for the control of agonist and antagonist muscles. Reciprocal innervations describe skeletal muscles as existing in antagonistic pairs, with contraction of one muscle producing force opposite to those generated by contraction of the other. In order to reach optimum efficiency, contraction of opposing muscles must be inhibited while muscles with the desired action are excited.the reciprocal innervation occurs so that the contraction of a muscle results in the simultaneous relaxation of its corresponding antagonist.

Based on all explanation above muscle spindles and golgi tendon organ are often work together to make muscle activation. Muscle spindles work to make tension and contraction meanwhile golgi tendon organ make an inhibition to muscle contraction so that the muscle can adjust with the stimulus and adapted with the environment. Thus, both types of proprioceptor have complementary function in informing the CNS bout the mechanical status of the muscle at any given point or period of time. The golgi tendon organ provides afferent input regarding muscle tension. It also enables the organism to compensate for muscle fatigue by adjusting the motor effort apllied. The spindle is important for psture, since the length of the muscle will vary with the angle of the joint it is acting on, thus enabling the CNS to be aware to relative limb segment position. Meanwhile the difference between the nature of the response of the spindles and tendon organs can be explained in terms of the diffrent anatomical arrengement of the two proprioceptors. Spindles are arranged in paralel with extrafusal muscle fiber. Whereas tendon organs arearranged in series with the extrafusal fibers. Also, the collagen fibers of the tendon organ are less elastic than the intrafusal fiber spindles. Therfore the muscle fibers take up most of the stretch exerted. On the other hand, when the muscle fibers contract, they pull on the tendons directly. In case stroke patient which have spasticity in their limb, the work of muscle spindle that involve alpha motor neurons and gamma motor neurons and so golgi tendon organ are not activated meaningfully. So that there must be a stimulus in movement in affected limb. The movement must be selective and each movement facilitated must be recognize by muscle spindle and golgi tendon organ.

References

Adult in hemiplegia Wikipedia Encyclopedia

Selzer. Michael E, Clarke. Stephanie, Cohen. Leonardo ; Textbook of Neural Repair and Rehabilitation, Volume II Medical Neurorehabilitation, 2006, Cambridge University

Latash. Mark L, Lesstiene. Francis,Motor Control and Learning, 2006, Springer Montgomery.

Patricia, Connolly. Barbara, Clinical Applications for Motor Control, 2003, Slack Incorporated

1 Comment »

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