Muscle tone

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Muscle tone physiology and clinical approach 2013

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  • MUSCLE TONE - SPINAL REFELXESMuscles are always at least partially contracted. Even seemingly relaxed muscles possess a small degree of tension called resting muscle tonus or tone. This tone is ultimately controlled by impulses from the brain, though special receptors in the muscles themselves are also instrumental in its regulation. The brain relies on input from these receptors as well as those in tendons and joints to give it the information it needs to direct smooth and coordinated muscle movements. They constantly supply the brain with necessary information concerning the ever-changing tone in muscles as well as the present position of muscles at any time during a movement.Many aspects of posture and movement depend on appropriately controlled and subsequently monitored tone in the large postural muscles. Here, we will examine how muscle tone is regulated both by the brain and spinal cord and how the brain is kept informed of the ever-changing status of this tone. A second objective will be to examine spinal reflexes. It is easy for the beginner to treat reflexes lightly, associating them only with visible activities such as the knee jerk. In fact, the vast majority of reflex actions are unseen and unnoticed and yet are vitally important to normal function. Reflexes operating though the spinal cord are responsible for the smooth functioning of the gastrointestinal tract and bladder as well as all of the skilled movements of the trunk and limbs and the often-taken-for-granted activities of standing erect, walking, and running.
  • Sensation of resistance felt by the clinician as he manipulate a joint through a range of movement with subject attempting to relax. The resistance is determined partly by mechanical factors (joint, ligament and visco elastic properties of muscles) and partly by reflex muscle contraction.Muscles are always at least partially contracted. Even seemingly relaxed muscles possess a small degree of tension called resting muscle tonus or tone. This tone is ultimately controlled by impulses from the brain, though special receptors in the muscles themselves are also instrumental in its regulation. The brain relies on input from these receptors as well as those in tendons and joints to give it the information it needs to direct smooth and coordinated muscle movements. They constantly supply the brain with necessary information concerning the ever-changing tone in muscles as well as the present position of muscles at any time during a movement.OVERVIEW OF MUSCLE TONEThe muscle tone exhibited by otherwise relaxed muscles is necessary for these muscles to produce effective movements. If muscles relaxed completely (no resting tone), they would overlengthen, and too much time would be required to take up slack when a contraction was called for. On the other hand, too much tone would not allow for sufficient rest and recovery.The principal regulator of muscle tone is the small stretch-sensitive intramuscular unit called the muscle spindle. Muscle spindles are encapsulated units within the belly of a muscle that lie parallel to the muscle fibers, stretching when the muscle is stretched and shortening when the muscle contracts. Thus they are uniquely situated to detect slight changes in muscle tone. When stretched, muscle spindles become activated, causing an increase in the impulse firing rate of afferent nerve fibers from the spindles to the spinal cord. Some of these spindle afferents synapse on second-order neurons which conduct the stretch information up the spinal cord to the cerebellum and even the cerebral cortex. Since the firing rate of these neurons varies with the degree and velocity of stretch, the CNS is continually informed of the ever-changing status of muscle tone and movement.Other spindle afferents directly excite large alpha motor neurons innervating skeletal muscle fibers. This reflex activation causes contraction (and short­ening) of the muscle via the simple myotatic or stretch reflex. This reflex functions as a servo-mechanism to maintain muscle tone at a preset level. If tone in a particular muscle decreases, allowing the muscle to lengthen, the spindles become stretched and trigger increased impulse firing in the spindle afferents, thereby increasing the firing rate of the alpha motor neurons to that same muscle and causing it to contract. The stretch sensitivity of the spindles can be adjusted by action of the small gamma motor neurons in the anterior horn (lamina IX) of the spinal cord. This is an important capability, allowing the CNS to keep the spindles "in tune" with the muscles. These and other functions of the muscle spindles, as well as the tension-sensitive organs in tendons, will be discussed.
  • Comparison of the force and fatigability of the three different types of motor units. In each case. The response reflects stimulation of a single motor neuron. (A) Change in tension in response to single motor neuron action potentials. (B) Tension in response to repetitive stimulation of the motor neurons (C) Response to repeated stimulation at a level that evokes maximum tension. The y axis represents the force generated by each stimulus
  • Box 36-1 Muscle SpindlesMuscle spindles are small encapsulated sensory receptors that have a spindle-like or fusiform shape and are located within the fleshy part of the muscle. Their main function is to signal changes in the length of the muscle within which they reside. Changes in the length of muscles are closely associated with changes in the angles of the joints that the muscles cross. Thus, muscle spindles can be used by the central nervous system to sense relative positions of the body segments.Each spindle has three main components: (1) a group of specialized intrafusalmuscle fibers whose central regions are noncontractile; (2) large-diameter myelinated sensory endings that originate from the central regions of the intrafusal fibers; and (3) small-diameter myelinated motor endings that innervate the polar contractile regions of the intrafusal fibers (Figure 36-3A). When the intrafusal fibers are stretched, often referred to as “loading the spindle,” the sensory endings are also stretched and increase their firing rate. Because muscle spindles are arranged in parallel with the extrafusal muscle fibers that make up the main body of the muscle, the intrafusal fibers change in length as the whole muscle changes. Thus, when a muscle is stretched, the activity in the sensory endings of muscle spindles is increased. When a muscle shortens, the spindle is unloaded and the activity decreases.The motor innervation of the intrafusal muscle fibers comes from small-diameter motor neurons, called gamma motor neurons to distinguish them from the large-diameter alpha motor neurons that innervate the extrafusal muscle fibers. Contraction of the intrafusal muscle fibers does not contribute to the force of muscle contraction. Rather, activation of gamma motor neurons causes shortening of the polar regions of the intrafusal fibers. This in turn stretches the noncontractile central region from both ends, leading to an increase in firing rate of the sensory endings or to a greater likelihood that stretch of the muscle will cause the sensory ending to fire. Thus, the gamma motor neurons provide a mechanism for adjusting the sensitivity of the muscle spindles.The structure and functional behavior of muscle spindles is considerably more complicated than this simple description implies. When a muscle is stretched, there are two phases of the change in length: a dynamic phase, the period during which length is changing, and a static or steady-state phase, when the muscle has stabilized at a new length. Structural specializations within each component of the muscle spindles allow spindle afferents to signal aspects of each phase separately.There are two types of intrafusal muscle fibers: nuclear bag fibers and nuclear chain fibers. The bag fibers can be divided into two groups, dynamic and static. A typical spindle has 2 or 3 bag fibers and a variable number of chain fibers, usually about 5. Furthermore, there are two types of sensory fiber endings: a single primary ending and a variable number of secondary endings (up to 8). The primary (Ia fiber) ending spirals around the central region of all the intrafusal muscle fibers (Figure 36-3B). The secondary (group II fiber) endings are located adjacent to the central regions of the static bag and chain fibers. The gamma motor neurons can also be divided into two classes, dynamic and static. Dynamic gamma motor neurons innervate the dynamic bag fibers, while the static gamma motor neurons innervate the static bag and the chain fibers.This duality of structure is reflected in a duality of function. The steady-state or tonic discharge of both primary and secondary sensory endings signals the steady-state length of the muscle. The primary endings are, in addition, highly sensitive to the velocity of stretch, allowing them to provide information about the speed of movements. Because they are highly sensitive to small changes, primary endings provide quick information about unexpected changes in length, useful for generating quick corrective reactions.Increases in activity of dynamic gamma motor neurons increase the dynamic sensitivity of the primary endings but have no influence on the secondary endings. Increases in activity of static gamma motor neurons increase the tonic level of activity in both primary and secondary endings, decrease the dynamic sensitivity of primary endings, and can prevent the silencing of primary activity when a muscle is released from stretch (Figure 36-3C). Thus, the central nervous system can independently adjust the dynamic and static sensitivity of the sensory fibers from muscle spindles.Box 36-2 Selective Activation of Sensory Fibers from MuscleSensory fibers are classified according to their diameter. Axons with larger diameters conduct action potentials more rapidly. Because each class of receptors gives rise to afferent fibers with diameters within a restricted range, this method of classification distinguishes to some extent the fibers that arise from the different groups of sensory receptors. The main groups of sensory fibers from muscle are listed in Table 36-1 (see Chapter 24 for the classification of sensory fibers from skin and joints).The organization of reflex pathways in the spinal cord has been established primarily by electrically stimulating the sensory fibers and recording evoked responses in different classes of neurons in the spinal cord. This method of activation has three advantages over natural stimulation. The timing of afferent input can be precisely established, the central responses evoked by different classes of sensory fibers can be assessed by grading the strength of the electrical stimulus, and certain classes of receptors can be activated in isolation (impossible in natural conditions).The strength of electrical stimuli required to activate a sensory fiber is measured relative to the strength required to activate the largest afferent fibers since the largest fibers have the lowest threshold for electrical activation. Thus group I fibers are usually activated over the range of one to two times the threshold of the largest afferents (with Ia fibers having, on average, a slightly lower threshold than Ib fibers). Most group II fibers are activated over the range of 2-5 times the threshold, while the small group III and IV fibers require stimulus strengths in the range of 10-50 times the threshold for activation.Reciprocal innervation of opposing muscles is not the only useful mode of coordination. Sometimes it is advantageous to contract the prime mover and the antagonist at the same time. Such co-contraction has the effect of stiffening the joint and is most useful when precision and joint stabilization are critical. An example of this phenomenon is the co-contraction of flexor and extensor muscles of the elbow immediately before catching a ball. The Ia inhibitory interneurons receive both excitatory and inhibitory signals from all of the major descending pathways (Figure 36-5A). By changing the balance of excitatory and inhibitory inputs onto these interneurons, supraspinal centers can reduce reciprocal inhibition and enable co-contraction, thus controlling the relative amount of joint stiffness to meet the requirements of the motor act.The activity of spinal motor neurons is also regulated by another important class of inhibitory interneurons, the Renshaw cells (Figure 36-5B). Renshaw cells are excited by collaterals of the axons of motor neurons, and they make inhibitory synaptic connections to several populations of motor neurons, including the same motor neurons that excite them, and to the Ia inhibitory interneurons. The connections of Renshaw cells to motor neurons form a negative feedback system that may help stabilize the firing rate of the motor neurons, while the connections to the Ia inhibitory interneurons may regulate the strength of reciprocal inhibition to antagonistic motor neurons. In addition, Renshaw cells receive significant synaptic input from descending pathways and distribute inhibition to task-related groups of motor neurons and Iainterneurons. Thus, it is likely that they contribute to establishing the pattern of transmission in divergent group Ia pathways according to the motor task.K.Kenal
  • Static and dynamic response of muscle spindle affrentsStatic response is the discharge at any constant length of the muscle. The greater the muscle length greater is the stretch in the spindle and the higher is the static response of the spindle affrents. Both the primary (Iα) and secondary II spindle affrents gives static or length sensitive responses.The dynamic response of a spindle affrents refer to the discharge during stretch of the muscle. If the spindle affrents gives greater response during a fast stretch than it dose during a slow stretch (velocity different but distance of stretch same) it is said to poses a dynamic response component. Only the primary spindle affrents gives a dynamic or velocity sensitive response.
  • Static and Dynamic fusimotor neuronsDynamic fusimotor fiber increase the dynamic response of the primary spindle affrents (Iα) and have little or no effect on secondary.Static fusimotor fibers increases the static response of both the primary and secondary spindle affrents. However the effect of static fusimotor fiber on primary spindle affrents is less marked than their effect on the secondary.Static fusimotor fiber terminate as trail endings (mostly present in nuclear chain fibers). Experiment using depletion of muscle glycogen as an index of muscle fiber activity have shown that repetitive stimulation of the static fusimotor fiber result primarily in chain fiber glycogen depletion.Dynamic fusimotor stimulation produces mostly bag fiber glycogen depletion.Recent evidence suggest (cat) that there are two types of bag fibers static (γ) and dynamic (γ) bag fibers.
  • Spinal ReflexOne may divide the somatic reflex activity of spinal cord into a number of individual reflexes and consider each as a separate functional entity. The normal animal dose not use any one of these reflexes to the exclusion of all others. The interdependency of spinal reflexes has two morphologic and physiologic determinate.There is overlap of neuronal circuits, both in the periphery, where two reflexes may share the same affrent receptor population and in the spinal cord where the same interneuronal circuits and or motor neuron may serve more than one reflex.The end product of any single spinal reflex muscle contraction, itself initiates other reflexes by virtue of the stimulation of numerous muscle and joint receptors during the reflex movement. One should keep in mind this overlap and co-participation of the spinal reflexes when studying the motor behavior of the intact animal.Spinal reflexes are studied in spinal or decerebrate cat. With regard to central synaptic organization reflexes may be characterized by their central delay and their duration of discharge. Central delay of a spinal reflex at a given spinal cord segment is the time elapsed between entry of affrent activity into the segment and exit of efferent activity from the segment.Proprioceptive reflex (Stretch reflex Ia reflex)Stretch of muscle -> stretches muscle spindle -> affrent Ia stimulate ->monosynaptic stimulation of α motor neuron.Phasic response/tonic response depending upon type of stimuli , tendon jerk, muscle toneInhibition of antagonistic muscle disynaptic (Glycine) Group Ia affrent facilitate homonymous and synergistic muscle monosynaptically and partial synergist disynaptically.Extensor muscle exhibits more powerful stretch reflex a given degree of tension and better maintained Flexion muscle are more phasic exhibiting low stretch sensitivity and poorly maintained.Function maintain extensor posture
  • Exteroceptive reflex – (flexion reflex) Withdrawal reflexStimulus: Pain, deep pressure, electrical stimuliAfferent Aδ, C fiberReflex: PolysynapticIrradiation: depending on severity of stimulusResponse: facilitation of flexor muscle and inhibition of extensor muscle in the stimulated limb for long time or prolonged after dischargeLocal sign – reflex response localized to the part stimulated.
  • Crossed extensor reflexExtension of the contralateral limb on painful stimulation to support the bodyLong latency and prolonged after dischargeSmooth response, slow onset and prolonged after discharge is also due to reflex, stretch reflex of contralateral extensor muscle concomitant participation in the maneuver. Contralateral dorsal root section eliminate afferent feedback from muscle leads to a staccato like reflex with abrupt onset and cessation of movement.Both flexor reflex and crossed extensor response are controlled from the brainstem by the dorsal reticulospinal system noradrenergic reticulospinal tract which inhibit transmission in the same flexor reflex affrent (FRA) pathway. This is required to prevent spinal and supraspinal locomotor mechanism to use part of FRA pathway for the alternating flexion and extension pattern of walking undisturbed by irrelevant flow of cutaneous information.
  • Arising from the flower spray or secondary ending in the muscle spindle, do not segregate according to homonymous synergist and antagonist muscle. In the spinal animal these fiber act through polysynaptic pathway to produce a generalized facilitation of flexor muscle and inhibition of extensor muscle irrespective of the muscle from which the group II fiber arises. The flexor facilitation and extensor inhibition is widespread. It extends through out a given limb and sometime radiate to the contralateral limbs, where the reflex signs are inverted. In decerebrate animal group II afferent induce ipsilateral extensor facilitation and flexor inhibition.It constantly inform higher center of the length of the muscle (degree of stretch).More recently it has been shown that group II affrent fiber can monosynaptically excite motor neurons in a manner similar to a manner similar to a Ia afferent and may therefore contribute to the stretch reflex under certain circumstances.In summary group II fiber activity is a sign of muscle length which may be employed to facilitate flexor or extensor (and inhibit their antagonist) depending upon suprasegmental control of transmission in reflex pathway so that neuron system has the potential of adjusting posture appropriately for the movement under way at the time
  • Fusimotor Function in Motor ControlThe pattern of fusimotor reflex effect set up by stimulation of various peripheral afferent fibers is generally similar to the reflex effect seen for the skeleto-motor neuron.The fusimotor reflexes are characteristically polysynapticIt receive only weak reflex effect from muscle proprioceptorsCutaneous afferent fibers are very effective in provoking fusimotor excitationIt has lower threshold for reflex activityIn tonic muscle (soleus) the fusimotor neuron have higher tonic discharge rate than the skeletomotor neuronAmong phasic muscles where many skeletomotor neuron are silent the fusimotor neuron may sometime show level of activity
  • 1. During extrafusal muscle contraction they keep the muscle spindle receptors in tune, sending proprioceptive information centrally and thereby allowing CNS to judge. Whether or not the degree of muscle contraction is appropriate for the motor task.2. They permit the Ia afferent to continue their support of the skeletomoter neuron discharge during contraction by contraction by monosynaptic facilitation.
  • Golgi tendon is located near muscle tendon junction or in the tendonThe receptor consist of the end ramification of the group Ib fiber around several tendon fascicles. GTO is 700μ long and 200μ wide. The receptor is enclosed in a very delicate capsule which is divided into several longitudinal compartment by connective tissue strand derived from the capsule.Arranged in series with muscle.GTO signals muscle tension i.e. force exerted on the tendon are transmitted to muscle directly through the tendon organ.Muscle contraction or stretch stimulate the GTO.The relative effectiveness of stretch and contractile force as the adequate stimuli for the GTO has been a subject of much controversy in recent years.The earliest notion was that the GTO had a very high threshold to both stretch and contraction. This concept with the fact that in the spinal cord group Ib fiber from a muscle inhibit skeletomotor neuron innervating the same muscle, suggest that GTO participated in a safety reflex that inhibited muscle contraction whenever the stretch or contractile force become so great as to endanger the muscle itself.It is now known, however that the GTO and its reflex connection in the CNS do not merely as safety device rather they actually participate in the movement to movement feedback. GTO exhibits a lower threshold to muscle contraction than to a passive stretch of the muscle. This occur because the force of muscle contraction is transferred more efficiently to GTO than is the force of muscle stretch. During externally applied stretch the muscle fiber elongate and this absorb much of the stretch force whereas during isometric muscle contraction the tendon absorb the brunt of contractile force.GTO has both dynamic and static response and it cooperate with muscle spindle to send information to CNS. GTO are usually present at the same muscle fascicle tendon junction which contains muscle spindle.Function of the Golgi Tendon OrganThe sensitivity of the tendon organs is considerably less than that of the muscle spindles. As little as 1 or 2 g of tension is sufficient to increase the firing rate of the spindle afferents. On the other hand, the group Ib afferent fibers from the tendon organs don't register impulse conduction until the tension reaches as high as 100 g. When tension in the tendons begins to exceed this level, the tendon organs become sufficiently stimulated to produce impulse firing in the group Ib fibers. Like the spindle afferents, the group Ib fibers send collaterals into the nucleus dorsalis of lamina VII of the spinal cord gray matter. Subsequently, both ASCT and PSCT second-order neurons conduct information from the tendon organs to the cerebellum.If the tension developed in a strongly contracting muscle becomes excessive, it is not inconceivable that the tendon could pull free from the bone, certainly an undesirable situation. However, before this can happen the tendon organs become sufficiently stimulated to send large volleys of impulses into the cord to directly stimulate the alpha motor neurons to antagonistic muscles and inhibitory interneurons to homonymous alpha motor neurons. The resulting feed-forward inhibition to the strongly contracting muscle causes it to suddenly relax, relieving the strain on the tendon and preventing possible damage. This sudden relaxation of a muscle in the face of dangerously high tension is called the lengthening reaction or the "clasp-knife" reflex because of its similarity to the way a pocketknife suddenly snaps closed when the blade is moved to a certain critical position.It was originally thought that little if any information from the tendon organs or the muscle spindles reached the conscious level in humans. The vast majority of the signals from these receptors which ascend the cord were thought to be directed exclusively to the cerebellum for subconscious evaluation. However, recent evidence now indicates that input from muscle spindles, tendon organs, and joint receptors is also relayed to the cerebral cortex and is probably responsible for the conscious sensation associated with the position and movement of limbs.
  • Seen in pathologic state e.g. decerebrate rigidity – extensor rigidity. When on attempts to flex the rigidly extended limb it offer considerable resistance to the force flexion movement. If sufficient force is applied the limb begins to flex but develops greater resistance to further flexion and more force is required as the flexion movement progresses. At one point however extensor tone suddenly melts away and the limb collapse into the fully flexed position (lengthening reaction)This sudden disappearance of the extensor tone followed by collapse of the limb is attributed to the onset of Ib affrent discharge which reflexly inhibit its homonymous stretched muscle. In same instance it cause reflex contraction of antagonist muscle and may radiate into contralateral limb. But it facilitate extensor muscle and inhibit contralateral flexor muscle (Phillipon’s reflex).Normally detect more movement to movement state of affair in the periphery detecting change in muscle tension and perhaps muscle fatigue and for rapid movement tendon organ could contribute to the rapid alternate rhythmic alteration of flexion and extension.Ib fiber also alternate activity among different motor units during sustained muscular contraction. In the normal situation motor units are seen to come in and dropout during prolonged contraction this helps reduce overall muscle fatigue. The Ib fiber might contribute to dropping out by reflexly inhibiting those motor unit whose contraction excites the nearby tendon organs.
  • The vestibulospinal tract act with reticulospinal tract in the control of muscle tone potentiating the stretch reflex of antigravity muscle through monosynaptic connection with α and γ motor neuron as well as via interneuron.
  • Muscle tone

    1. 1. MUSCLE TONE Dr PS Deb MD, DM Director Neurology GNRC Hospital Assam, India
    2. 2. “Tonus is status of contraction of resting muscle” • Muller 1833 A state of partial contraction that is characteristic of normal muscle, is maintained at least in part by a continuous bombardment of motor impulses originating reflexively, and serves to maintain body posture.
    3. 3. Motor Unit Types Type A Type B Type C Size of M.Unit Large Small Intermediate Diameter of muscle fiber Small Intermediate Small Capillary Small Intermediate Large Mitochondrial ATPase Low Medium High Glycogen content High Medium Low Contraction Speed Fast Slow Intermediate Maximum Tetanic tension High Low Intermediate Fatigability Low Very high High Post tetanic potentiation of twitch contraction Poor Good Good Post tetanic repetitive activity Absent Present Absent Electric stimulation of peripheral nerve, motor cortex Fascilitatio n Inhibition Distribution Flexor Extensor, Antigravity
    4. 4. MUSCLE SPINDLE
    5. 5. MUSCLE SPINDLE: STRETCH RECEPTOR
    6. 6. THE INFLUENCE OF AFFERENT ACTIVITY O N MOTOR BEHAVIOR
    7. 7. STATIC AND DYNAMIC RESPONSE OF MUSCLE SPINDLE AFFRENTS  Static response is the discharge at any constant length of the muscle. The greater the muscle length greater is the stretch in the spindle and the higher is the static response of the spindle affrents. Both the primary (Iα) and secondary II spindle affrents gives static or length sensitive responses.  The dynamic response of a spindle affrents refer to the discharge during stretch of the muscle. If the spindle affrents gives greater response during a fast stretch than it dose during a slow stretch (velocity different but distance of stretch same) it is said to poses a dynamic response component. Only the primary spindle affrents gives a dynamic or velocity sensitive response.
    8. 8. STATIC AND DYNAMIC FUSIMOTOR NEURONS  Dynamic fusimotor fiber increase the dynamic response of the primary spindle affrents (Iα) and have little or no effect on secondary.  Static fusimotor fibers increases the static response of both the primary and secondary spindle affrents. However the effect of static fusimotor fiber on primary spindle affrents is less marked than their effect on the secondary.  Static fusimotor fiber terminate as trail endings (mostly present in nuclear chain fibers).  Experiment using depletion of muscle glycogen as an index of muscle fiber activity have shown that repetitive stimulation of the static fusimotor fiber result primarily in chain fiber glycogen depletion.  Dynamic fusimotor stimulation produces mostly bag fiber glycogen depletion.
    9. 9. STRETCH REFLEX
    10. 10. POLYSYNAPTIC REFLEX
    11. 11. ALPHA AND GAMMA MOTOR NEURONS ARE COACTIVATED DURING VOLUNTARY MOVEMENTS
    12. 12. WITHDRAWAL REFLEX
    13. 13. POLYSYNAPTIC WITHDRAWAL REFLEX
    14. 14. WITHDRAWAL AND CROSSED EXTENSOR REFLEX
    15. 15. GROUP II FIBER REFLEX (MASS REFLEX)  In spinal animal group II fiber from muscle spindle causes polysynaptic generalized facilitation of flexor muscle and inhibition of extensor muscle  Sometime it radiate to the contralateral limbs
    16. 16. FUSIMOTOR FUNCTION IN MOTOR CONTROL  The fusimotor reflexes are characteristically polysynaptic  It receive only weak reflex effect from muscle proprioceptors  Cutaneous afferent fibers are very effective in provoking fusimotor excitation  It has lower threshold for reflex activity  In tonic muscle (soleus) the fusimotor neuron have higher tonic discharge rate than the skeletomotor neuron  Among phasic muscles where many skeletomotor neuron are silent the fusimotor neuron may sometime show level of activity
    17. 17. COMPENSATORY MECHANISM FOR FUSIMOTOR  During extrafusal muscle contraction they keep the muscle spindle receptors in tune, sending proprioceptive information centrally and thereby allowing CNS to judge. Whether or not the degree of muscle contraction is appropriate for the motor task.  They permit the Ia afferent to continue their support of the skeletomoter neuron discharge during contraction by contraction by monosynaptic facilitation.
    18. 18. GOLGI TENDON ORGAN
    19. 19. GOLGI TENDON ORGAN
    20. 20. CEREBELLAR AWARENESS OF MUSCLE TONE  After MS stimulation (stretch) APs are conducted along the afferent fiber (Ia)  It enters into the spinal cord and divides into several collaterals.  Some of these collaterals synapse on the cell bodies of neurons which ascend to the cerebellum (anterior and posterior spinocerebellar tracts).  Thus, at all times the cerebellum is aware of the state of stretch in muscles, in other words the TONE of muscles.
    21. 21. CEREBELLAR CONTROL OF MUSCLE TONE  Golgi tendon organs detects tension in the tendon.  Afferent neurons conduct action potentials to the spinal cord.  Afferent neurons synapse with inhibitory (inter) association neurons (secretes GABA) which in turn synapse with alpha motor neurons.  Inhibition of the alpha motor neurons causes muscle relaxation, relieving the tension in the muscle.
    22. 22. CLASP KNIFE REFLEX  Seen in decerebrate rigidity  On stretching the muscle beyond a point causes Ib affrent inhibitory discharge from GTO which reflexly inhibits homonymous stretched muscle
    23. 23. EXTRAPYRAMIDAL PATHWAY  Vestibulospinal tract  Reticulospinal tract  Rubrospinal tract  Tectospinal tract
    24. 24. VESTIBULOSPINAL TRACT  Origen: Lateral vestibular nucleus  Course: Un-corssed  Termination: Periphery of the ant white column of spinal cord  Affrent: Neck proprioceptive affrent, Labrynth  Effect: Fasilitation of α γ motor neuron and stretch reflex.  Produces decerebrate rigidity, abolished by damage to lateral vestibular nucleus
    25. 25. RETICULOSPINAL TRACT (INHIBITORY)  A. Noradrinergic RST arise at Locus Ceruleus  B. Serotonergic RST arise near median raphe  Pathway ?  Function: Replal short latency flexor affrent, transient excitation of flexor and inhibition of extensor by asynchronus activity in flexon lasting 200-300 μ sec. accompanied by compansatory prolonged inhibition of extensors  Helps in locomotion
    26. 26. DORSAL RETICULOSPINAL SYSTEM  Arises from pontomedulary reticular formation and traverses the dorsolateral funiculus of spinal cord  Suppress Ib disynaptic inhibition and first interneuron of FRA pathway  Lesion of this tract in decerebrate cat produce spasticity and transform the reflex effect of group II affrent fibers from one of potentiating to one of inhibiting the stretch reflex of extensor muscle as the muscle is progressively lengthened  Release of FRA -> flexor spam in paraplegia
    27. 27. INHIBITORY RETICULOSPINAL TRACT  Origin: Ventromedian medulla  Course: Crossed and Uncrossed ant to lateral corticospinal tract in man  Driven by motor cortex by descending tract to medulla  Inhibits transmission of Ia affrent fiber (suppressing stretch reflex) as well as other terminal synapsing on motor neuron  Break reflex standing to walking  Lesion: Hypereflexia and Hypertonia
    28. 28. FASCILITATORY RETICULOSPINAL TRACT  Origin: Pontine and medullary reticuar formation  Course: Near sulcomarginal region near vestibulospinal tract  Facilitate flexion of upper limb and extension of lower limb -> Reflex standing
    29. 29. OTHER TRACT  Rubrospinal Tract: Facilitatory like pyramidal not seen in man  Tectospinal tract: Like vestibulospinal system help rotatory movement of head and trunk in response to visual stimuli  Pyramidal tract: Promote extension of upper limb and flexion of lower limb through α + γ motor neuron
    30. 30. ANTICIPATORY MAINTENANCE OF BODY POSTURE  At the onset of a tone, the subject pulls on a handle, contrcting the biceps muscle. Contraction of the gastronemius muscle precedes that of the biceps to ensure postural stability
    31. 31. SPASTICITY  Traditional conecept - Muscle hypertonia: velocity dependent resistance to stretch -Exaggerated reflexes(Ashworth’s Scale)  New concept - Loss of longer latency reflexes(spinal) - Decrease of muscle activity during function - Change in non-neural factors as a result of the decrease of supraspinal control - Biomechanical changes in both passive and active muscles (Dietz 2003)
    32. 32. DEFINITIONS OF SPASTICITY  The increase of stretch reflexes is not the only reason for established spasticity.  Factors which can lead to a mechanical resistant in movement are the reduced elasticity of the tendons and the biomechanical changes of musclefibres. -Dietz 1992
    33. 33.  Neural Mechanisms - Weakness and decreased skills (Astereognosia) - Changes in anticipatory contrast - Hyperexitability of motorneurons - Muscle hypertonicity (Hyporeflexia of tendon)  Non-neural Mechanisms - Biomechanical changes in muscle - Thixotrophia (Stiffness of myosin cross links)
    34. 34. CENTRAL LOSS OF FORCE PRODUCTION  Loss of central command to generate and sustain force  No loss of contractile capacity : not the same as peripheral weakness, Myopathy or general weakness -sahrmann 2002
    35. 35. MUSCLE ACTIVATION DEFICITS  Delayed initiation and termination of muscle contraction. (chae 2002)  Altered sequence of muscle firing (Dewald 2001)  Excessive activation/cocontraction:too many muscles with inappropriate force (sarmann 1977)
    36. 36. SENSORY DEFICITS  Deficits in awareness, processing and interpretation and kinesthetic memory - Fewer attempts at spontaneous movements - Altered sence of “weight”of a limb - Altered sence of timing and speed - Difficulty replaying movements in their imagination and recognizing them in facilitation - Contributes to development of pain
    37. 37. CLINICAL IMPLICTIONS  Non-neural components can be as singnificant in hypotonicity as hypertonicity.  The non-neural effects can also add to the neural mechanism  Limitation of range prevents movement and the static state further interferes with modulation of tonus
    38. 38. CLINICAL HYPERTONICITY MUSCLE ACTIVATION DEFICITS  Clinical Significance: - Do not treat the hypertonicity, treat the underlying cause >Central loss of force production is unique - Basic trunk-limb(girdle)movement patterns - Spasticity is different from clinical hypertonicity >Intralimb movement sequences * Muscle activation deficits result in disruption of voluntary movement * Prevent persistent posturing
    39. 39. THANKS

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