Muscle tone munish G B PANT DELHI

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MUSCLE TONE

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Muscle tone munish G B PANT DELHI

  1. 1. MUSCLE TONE Munish Kumar
  2. 2. Muscle Tone • The word TONUS was first used to designate the state of contraction of resting muscle by Muller in 1838. • Vulpian defined Tone as a state of permanent muscular tension. • Muscle tone is usually described as the resistance of a limb to passive movement (Foster 1892).
  3. 3. Neurophysiology of Muscle Tone • In a normally relaxed individual , the only resistance felt on moving the limb at a joint is that due to the mechanical properties of the limb ,its joints , ligaments and muscles.
  4. 4. Neurophysiology of Muscle Tone Control of Muscle tone Spinal control Supra spinal control
  5. 5. Spinal control of muscle tone • Stretch reflex of Sherrington is the basic mechanism of tonic activity. • Muscle spindle and alpha and gamma motoneurons are mainly implicated.
  6. 6. Muscle spindle • Muscle spindle is a fusiform structure laying between and parallel to the muscle fibres and sharing their tendinous attachement.
  7. 7. Muscle spindle • It consisting of about 4 to 12 intrafusal fibres, which have a smaller diameter than the extrafusal fibres. • Intrafusal fibres are of two types : Nuclear bag fibres and Nuclear chain fibres. • Serve to monitor both the length of the muscle and the velocity of its contraction
  8. 8. Nuclear bag fibers • These bulge out at the middle, where they are the most elastic . • A large diameter myelinated sensory nerve fibre (Ia) ends at nuclear bag. • Motor fibres ( γ efferents) which subserve contraction of of its striated portion. • This is the dynamic component of the stretch reflex
  9. 9. Golgi Tendon Organ • Net like collection of knobby nerve endings among the fascicles of a tendon. • Stimulated by passive stretch & active contraction of muscle. • Signals the tension and provides negative feedback control of muscle contraction and regulates muscle force rather than length.
  10. 10. Afferent and efferent pathways Afferent pathway • Ia from nuclear bag fibre passes via dorsal horn to synapse with α-motoneurons • II from muscle spindle synapse with interneurons • Ib from golgi tendon organ ends in nucleus dorsalis and synapse with interneurons. Efferent pathway • α-motoneurons runs from cell body in ant. horn to extrafusal muscle fibre. • γ- motoneurons runs from cell body in ant. horn to intrafusal muscle spindle.
  11. 11. Tone - Mechanism • γ- motoneurons activity causes the intrafusal fibre to contract this streches the primary sensory ending, thus increasing afferent discharge causing depolarisation of αmotoneurons supplying the extrafusal muscle, thereby increasing muscle tone.
  12. 12. Supra-spinal control The efferent fibres to the muscle spindle, γmotoneurones, receive input form higher centres via : • Facilitatory fibres and • Inhibitory fibres
  13. 13. Supra-spinal control In human spastic paretic syndrome, the three important pathways are – corticospinal, reticulospinal, and vestibulospinal.
  14. 14. Medial and lateral descending brain stem pathways involved in motor control Medial pathways (reticulospinal, vestibulospinal, and tectospinal) terminate in ventromedial area of spinal gray matter and control axial and proximal muscles Lateral pathway (rubrospinal) terminates in dorsolateral area of spinal gray matter and controls distal muscles.
  15. 15. Inhibitory Supraspinal Pathways 1. Corticospinal pathway –  Isolated pyramidal lesions have not produced spasticity in conditions such as destruction of motor cortex (area 4), unilateral lesion in cerebral peduncle, lesions in basis pontis and medullary pyramid (Bucy et al., 1964; Brooks, 1986). Instead of spasticity these lesions produced weakness, hypotonia, and hyporeflexia.  Spasticity however may be caused if the lesions include the premotor and supplementary motor areas.  Lesions in the anterior limb of internal capsule and not in the posterior limb produce spasticity as fibers from supplementary motor area pass through anterior limb.
  16. 16. Inhibitory Supraspinal Pathways 2. Corticoreticular pathways and dorsal (lateral) reticulospinal tract –  Medullary reticular formation is active as a powerful inhibitory center to regulate muscle tone (stretch reflex) and the cortical motor areas control tone through this center.  Lesions of supplementory motor area or internal capsule reduces control over medullary center to produce hypertonicity.  Flexor spams and Clasp-knife phenomenon are due to damage to dorsal reticulospinal pathway (Fisher and Curry 1965).
  17. 17. Excitatory Supraspinal pathways 1. Medial (ventral) Reticulospinal Tract –  Through this tract reticular formation exerts facilitatory influence on spasticity.  Origin mainly from pontine tegmentum.  More important than vestibulospinal system in maintaining spastic extensor tone. 2. Vestibulospinal pathway:  Vestibulospinal tract (VST) is a descending motor tract originating from lateral vestibular (Deiter‟s) nucleus and is virtually uncrossed.  This excitatory pathway helps to maintain posture and to support against gravity and so control extensors rather than flexors. This pathway is important in maintaining decerebrate rigidity but has lesser role in human spasticity (Fries et al., 1993).  The cerebellum through its connections with the vestibular nuclei and reticular formation may indirectly modulate muscle stretch reflexes and tone.
  18. 18. Inhibitory excitatory
  19. 19. Decerebration • A complete transection of the brain stem between the superior and inferior colliculi permits the brain stem pathways to function independent of their input from higher brain structures. This is called a midcollicular decerebration. (A)
  20. 20. Decerebration • This lesion interrupts all input from the cortex (corticospinal and corticobulbar tracts) and red nucleus (rubrospinal tract), primarily to distal muscles of the extremities. • The excitatory and inhibitory reticulospinal pathways (primarily to postural extensor muscles) remain intact. • The excitatory reticulospinal pathway leads to hyperactivity in extensor muscles in all four extremities which is called decerebrate rigidity.
  21. 21. Decortication • Removal of the cerebral cortex (D) produces decorticate rigidity. • The flexion can be explained by rubrospinal excitation of flexor muscles in the upper extremities. • The hyperextension of lower extremities is due to the same changes that occur after midcollicular decerebration.
  22. 22. Disorders of muscle tone • Abnormalities of the tone :  Hypertonia – Pyramidal hypertonia (Spasticity) Extrapyramidal hypertonia (Rigidity)  Hypotonia
  23. 23. Pyramidal hypertonia (Spasticity) • Spasticity – a motor disorder characterized by velocity- dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. • Pyramidal hypertonia is most pronounced in the muscle groups most used in voluntary movements.
  24. 24. Spasticity • Physiologic evidence suggests that interruption of reticulospinal projections is important in the genesis of spasticity. • In spinal cord lesions, bilateral damage to the pyramidal and reticulospinal pathways can produce severe spasticity and flexor spasms, reflecting increased tone in flexor muscle groups and weakness of extensor muscles.
  25. 25. Spasticity - EDX • There will be increased H reflexes, identified with an increase of maximum amplitude H reflex compared to the M wave – H/M ratio. • Increased F wave amplitude.
  26. 26. Spasticity – The Mechanism 1. α- motoneuron excitability- enhanced H:M ratio and F-wave amplitude suggest enhanced excitability of α- motoneuron. 2. γ- motoneuron excitability – causes increased spindle sensitivity to stretch, augmenting the Ia afferent response to stretch, and exaggerates the stretch reflex.
  27. 27. Spasticity – the mechanism 3. Recurrent inhibition –recurrent collateral axons from motoneurons activate Renshaw cell, which inhibit αmotoneurons. Changes in recurrent inhibition plays a role in the pathophysiology of spasticity. 4. Reciprocal inhibition-During active contraction, it is necessary to inhibit MNs supplying the antagonist muscle(s),at the same rate ( Sherrington’s law of reciprocal innervation). This is to prevent their reflex contraction in response to stretch. 5. Presynaptic inhibition
  28. 28. Clinical correlation In cortical and internal capsular lesions, the controlling drive on the inhibitory center in the medullary brain stem is lost and so in absence of inhibitory influence of lateral RST originating from this center, facilitatory action of ventral RST becomes unopposed. This results in spastic hemiplegia with antigravity posturing, but flexor spams are unusual.
  29. 29. Clinical correlation - Spinal lesions 1. Incomplete (partial) myelopathy involving lateral funiculus may affect CST only to produce paresis, hypotonia, hyporeflexia, and loss of reflexes. (Peterson et al., 1975) If lateral RST is involved in addition, unopposed ventral RST activity then results in hyper-reflexia and spasticity (similar to cortical or capsular lesions).
  30. 30. Clinical correlation - Spinal lesions 2. Severe myelopathy with involvement of all the four descending pathways produces less marked spasticity compared to isolated lateral cord lesion because of lack of unopposed excitatory influences of ventral RST. Neuroplasticity of the spinal cord in the form of receptor supersensitivity of neurons to a loss of synaptic input and sprouting of axon terminals are also responsible for hypertonicity in complete myelopathy with delayed reorganization after a variable period of spinal shock
  31. 31. Clonus • Clonus is the phenomenon of involuntary rhythmic contractions in response to sudden sustained stretch. • A sudden stretch activates muscle spindles, resulting in the stretch reflex. • Tension produced by the muscle contraction activates the Golgi tendon organs, which in turn activate an „inverse stretch reflex‟, relaxing the muscle. • If the stretch is sustained, the muscle spindles are again activated, causing a cycle of alternating contractions and relaxations.
  32. 32. Spinal shock • In 1750, Whytt first described the phenomenon of spinal shock as a loss of sensation accompanied by motor paralysis with gradual recovery of reflexes. • There are four phases of spinal shock.
  33. 33. Proposed mechanisms for the four phases of spinal shock (Ditunno et al.) Phase Time Physical exam finding Possible neuronal mechanisms Lost norml supraspinal excitation Increased spinal inhibition 1 0-1d Areflexia/Hyporeflexia Reduced neuronal metabolism Denervation supersensitivity 2 1-3d Initial reflex return NMDA receptor upregulation 3 1-4w Hyperreflexia (initial) Axon-supported synapse growth Hyperreflexia, 4 1-12m Soma-supported synapse growth Spasticity
  34. 34. Cerebellum and muscle tone • The cerebellum does not seem to have a direct effect on muscle tone determining spinal reflex pathways as there is no direct descending cerebellospinal tract. • The cerebellum mainly influences muscle tone through its connections with the vestibular and brain stem reticular nuclei. • Pure cerebellar lesions classically produce hypotonia.
  35. 35. Cerebellum and muscle tone • Gamma motor neurons selectively depressed • Alpha motor neurons can respond to inflow from spindles to produce tendon jerk. • Associated corticospinal tract involvement produces varying degrees of spasticity as seen in spinocerebellar ataxia (SCA).
  36. 36. Extrapyramidal hypertonia (Rigidity) • Rigidity is characterized by an increase in muscle tone causing resistance to externally imposed joint movements. • It does not depend on imposed speed and can be elicited at very low speeds of passive movement. • It is felt in both agonist and antagonist muscles and in movements in both directions.
  37. 37. Extrapyramidal hypertonia (Rigidity) • 'Cogwheel' rigidity and 'leadpipe' rigidity are two types. • 'Leadpipe' rigidity results when an increase in muscle tone causes a sustained resistance to passive movement throughout the whole range of motion, with no fluctuations. • 'Cogwheel' rigidity occus in association with tremor which presents as a jerky resistance to passive movement as muscles tense and relax. • Basal ganglia structures are clearly implicated in pathophysiology of rigidity.
  38. 38. Extrapyramidal hypertonia (Rigidity) Nurophysiology 1. Reflex origin of rigidity  Enhanced tonic reflex activity ( a stimulus produces a prolonged discharge of motor neurons causing sustained muscle contraction).  The phasic stretch reflex (monosynaptic) is not responsible for rigidity. 2. Segmental and supraspinal influences  α- motoneurons and possibly cortical excitability is enhanced in rigidity.  Recurrent Renshaw cell inhibition is normal.
  39. 39. Extrapyramidal hypertonia (Rigidity)  It has been suggested that the distribution of higher facilitatory influence between flexor and extensor motoneurons may be unequal in pyramidal and approximately equal in extrapyramidal type. 3. Inadequate voluntary relaxation.
  40. 40. Dystonia • Characterized by abnormal muscle spasm producing distorted motor control and undesired postures. • A principle finding is the loss of cortical inhibition. • Failure of “surround inhibition”. Brain activates a specific movement and simultaneously inhibits unwanted movements.
  41. 41. Hypotonia • Hypotonia may affect a muscle‟s resistance to passive movement and/or its extensibility. • Aetiological types of hypotonia : 1. Nerve trunk and root lesion 2. A lesion of anterior horn 3. Cerebellar lesions 4. Cerebral lesions
  42. 42. Hypotonia - causes Congenital Genetic Developmental Acquired Genetic Infectious Neuromuscular Jn
  43. 43. Clinical Examination  Tone is difficult to assess.  The determination of tone is subjective and prone to interexaminer variability.  The most important part of the examination of tone is determination of the resistance of relaxed muscles to passive manipulation as well as the extensibility, flexibility, and range of motion.  The examination of tone needs a relaxed & cooperative patient
  44. 44. Methods • Inspection : Attitude of the limb at rest. • Palpation : Feel of the muscle – normal, firm or flabby. • Range of movement at the joints. • Passive movement - first slowly and through complete range of motion and then at varying speeds. • Shake the distal part of the limb. • Brace a limb and suddenly remove support. • Bilateral examination of homologous parts helps compare for differences in tone on the two sides of the body.
  45. 45. Specific Maneuvers • The Babinski Tonus Test • The Head Dropping Test • Wartenberg‟s Pendulum Test • The Shoulder Shaking Test • The Arm Dropping Test ( Bechterew‟s Sign in spasticity)
  46. 46. Specific Maneuvers 1. The Babinski Tonus Test  The arms are abducted at the shoulders, and the forearms are passively flexed at the elbows.  With hypotonicity there is increased flexibility and mobility, and the elbows can be bent to an angle more acute than normal.  With hypertonicity there is reduced flexibility and passive flexion cannot be carried out beyond an obtuse angle. 2. The Head-Dropping Test  The patient lies supine without a pillow, completely relaxed, eyes closed and attention diverted.  The examiner places one hand under the patient's occiput and with the other hand briskly raises the head, and then allows it to drop. Normally the head drops rapidly into the examiner's protecting hand, but in patients with extrapyramidal rigidity there is delayed, slow, gentle dropping of the head because of rigidity.
  47. 47. Specific Maneuvers 3. Pendulousness of the Legs  The patient sits on the edge of a table, relaxed with legs hanging freely.  The examiner either extends both legs to the same horizontal level and then releases them (Wartenberg's pendulum test), or gives both legs a brisk, equal backward push.  If the patient is completely relaxed and cooperative, there will normally be a swinging of the legs that progressively diminishes in range and usually disappears after six or seven oscillations.  In spasticity, there may be little or no decrease in swing time, but the movements are jerky and irregular, the forward movement may be greater and more brisk than the backward, and the movement may assume a zigzag pattern.  In hypotonia, the response is increased in range and prolonged beyond the normal.
  48. 48. Specific Maneuvers 4. The Shoulder-Shaking Test  The examiner places her hands on the patient's shoulders and shakes them briskly back and forth, observing the reciprocal motion of the arms.  With extrapyramidal disease, there will be a decreased range of arm swing on the affected side.  With hypotonia, especially that associated with cerebellar disease, the excursions of the arm swing will be greater than normal 5. The Arm-Dropping Test  The patient's arms are briskly raised to shoulder level, and then dropped. In spasticity, there is a delay in the downward movement of the affected arm, causing it to hang up briefly on the affected side (Bechterew's or Bekhterew's sign).  With hypotonicity the dropping is more abrupt than normal.
  49. 49. Source • Handbook of clinical neurology. Vinken and Bruyn. • Ganong’s textbook of physiology. • DeJong’s The neurological examination. • Mukherjee A. Spasticity mechanisms – for the clinician.Frontiers in neurology.2010;1:149-54. • Ditunno JF. Spinal shock revisited: a four-phase model. Spinal Cord (2004) 42, 383–395. • Robert A. Davidoff, MD. Skeletal muscle tone. Neurology 1992;42:951-963. • Victor G. Postural Muscle Tone in the Body Axis of Healthy Humans. J Neurophysiol 96: 2678–2687, 2006

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