1. 1. By :-Heena Moderator :-Dr.Dinesh Sir
2. 2. Contain Introduction Normal physiology Pathophysiology Assessment
3. 3. Introduction Spasticity is a motor disorder that is characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper excitability of the stretch reflex, as one component of the upper motor neuron syndrome. American Academy of Neurology (1990)
4. 4. Why spasticity is important???? Because it often causes disability and impairs functions of our patient. So based on that we plan treatment.
5. 5. Normal physiology Function of muscle spindle 1. It is receptor organ for stretch reflex 2. It is play important role in maintaining the muscle tone.
6. 6. Muscle spindle
7. 7. Innervation of the Spindles
8. 8. Pathophysiology Immediately after scl, there are depressed spinal reflexes during the state of spinal shock, followed by development of hyperreflexia and spasticity over the following weeks to month.
9. 9. The pathophysiology of spasticity is not completely understood; however, it is believed to arise primarily from loss of the effect of numerous descending inhibitory pathways. These include reciprocal 1a interneuronal inhibition, presynaptic inhibition, renshaw-mediated recurrent inhibition, group II afferent inhibition, and the Golgi tendon organs.
10. 10. Axonal collateral sprouting and denervation super sensitivity are change that may also play a role in the development of spasticity. T
11. 11. Let see normal physiology along with pathophysiology
12. 12. The Monosynaptic (Stretch) Reflex Change in muscle length can evoke a stretch reflex. Two type Nuclear bag fibers Nuclear chain fibers Group la and 2 fibers
13. 13. Reciprocal inhibition The la fibers also synapse on interneurons that inhibit antagonist muscle groups, thereby preventing contraction of antagonist muscle during activation of agonist muscle groups; this inhibitory pathway is referred to as reciprocal la inhibition and can be altered after SCI.
14. 14. Clinically, reciprocal inhibition can be grossly observed by eliciting monosynaptic muscle stretch reflexs: when tendon tapped, a stretch is applied to the target muscle, which is transmitted to the spinal cord through the la affrent fibers.
15. 15. This reciprocal la inhibition after SCI may result in simultaneous coactivation of agonist and antagonist muscle groups, as is often seen in patients with spasticity.
16. 16. Recurrent inhibition is mediated by Renshaw cells, which are inhibitory interneurons located in the ventral horn of spinal cord. Axon collaterals from alpha motor neurons synapse on and activate the Renshwa cells,which in turn project inhibitory impulses back to these motor neurons as well as to la inhibitory interneurons.
17. 17. Renshaw activity decreases the activity of the motor neurons that were previously active and also inhibits la inhibitory internurons. The level of recurrent inhibition has been explored in patient with UMN lesions, and these individuals have been noted to maintain normal recurrent inhibition during voluntary movement; this may contribute to impaired motor function in these patients.
18. 18. There is evidence for increased recurrent inhibition in the SCI population, which increases inhibition to the la interneurons. This ultimately allows for cocontraction of agonist and antagonist muscle groups due to the decreased la interneuron activity.
19. 19. Reduction in presynaptic inhibition of afferent is another potential contributor to the Pathophysiology of spasticity in SCI. reciprocal inhibition was described by Sherrington in 1906, and this process is responsible for relaxation of an antagonist muscle during contraction of agonist.
20. 20. in absence of reciprocal inhibition, cocontraction of agonist and antagonist muscle groups is seen simultaneously, interfering with intentional voluntary movement. GABA mediates spinal inhibition both presynaptically and postsynapticaly. presynaptic inhibition of Ia afferent occurs when the inhibitory aminiacid GABA binds to receptors on the la terminals, which subsequently increases the amount of input required to activate the alpha motor neurons.
21. 21. The decreased excitatory input to the alpha motor neurons in turn depresses the monosynaptic stretch reflex. Postsynaptic activation of GABA-A receptor can decrease the activity of motor neurons and interneurons .afterSCI, the decrease in presynaptic inhibition ultimately result in increased activity of the alpha motor neuron; this may contribute to the hyper reflexiya and spasticity seen in these individuals .it is possible to modulate the presynaptic inhibition in individuals with SCI with the use of GABA-Eergic medications including baclofen and diazepam.
22. 22. GOLGI TENDON ORGAN Sensitive to intramuscular tension and innervated by 1b sensory afferents. 1 or 2 g of tension is sufficient to increase the firing rate of the spindle afferents. But tendon organs don't register impulse conduction until the tension reaches as high as 100 g.
23. 23. GOLGI TENDON ORGAN
24. 24. If tension is generated beyond capacity there is sudden relaxation to prevent possible damage to tendon. . 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.
25. 25. Nonreciprocal lb inhibition is another mechanism that may play a role in development of spasticity of supraspinal origin but does not appear to be involved in spasticity related to SCI, Golgi tendon organs, which are contraction sensitive receptors, have group I afferents and lb inhibitory interneurons that projects to the spinal cord and are involved in preventing antagonist muscles from firing while the agonist is firing.
26. 26. There is evidence for replacement of lb inhibition with facilitation in hemiplegic individual with supraspinal lesions, leading to simultaneous cofiring of agonist and antagonist muscle groups: however, studies in individuals with SCI have shown that lb inhibition is unaltered.
27. 27. Two additional mechanisms that play role in the development of spasticity after SCI are axonal sprouting and denervation supersensitivity . Ditunno et al describe the transmition from spinal shock immediately after SCI the development of spasticity and hyperreflexia 1 to12 months later. in their proposed 4-phase model of spinal shock.
28. 28. There is observation of areflexia or hyporeflexia , as well as paralysis and muscle flaccidity for initial 0 to 24 hours postinjury. These findings are due to loss of excitatory input from supraspinal pathways, including vestibulospinal and reticulospinal pathways, among others.
29. 29. Loss of descending inhibitory input to spinal inhibitiory interneurons may cause further hyporeflexia. In the second phase of spinal shock, there is return of the H reflex 1 to 3 days after injury, although muscle stretch reflexs are still absent. This likely due to denervation supersensitivity, which causes increased neuronal firing in response to neurotransmitters and has been reported to occur in the brain and spinal cord .
30. 30. The denervation supersensitivity may be due to decreased reuptake of excitatory neurotransmitters, up-regulation of receptors on the postsynaptic membrane, or alteration of degragation and synthesis of receptors.
31. 31. Phase 3 and 4 of Ditunnos model describe early hyperreflexia and later development of spasticity in patient with SCI. the proposed physiologic mechanism for both phases is axonal regrowth .
32. 32. new synapse are formed by spinal afferents and interneurons as well as spared supraspinal descending pathways. Axonal sprouting of spared descending motor tracts may result in motor recovery, whereas axonal sprouting of the neurons involved in segmental reflexes may produce less desirable effects, such as the development of hyperreflexia and spasticity.
33. 33. Intrinsic changes within muscle may also play role in the development of increased muscle tone. These mechanical changes may include loss of sarcomeres, increased stiffness of muscle fibers, altered muscle fiber size and distribution of fiber types, and changes in collagen tissue and tendons.
34. 34. The work of Kamper et al in stroke patients demosttrated that muscle fiber played some part in phenomenon of spasticity as decresing the initial length of tested spastic metacarpophalangeal fibers reduced muscle stiffness suggesting that the biomechanical quality of muscle fibers play some part in the development of spasticity.
35. 35. These changes in spastic muscle may be a result of the development of subclinical contracture rather than true reflex hyperexitibility or be an intrinsic property of the changes in biomechanical property of the muscle.
36. 36. A strong, painful, or potentially damaging stimulus delivered to cutaneous or joint receptors can reflexly cause a sudden bodily withdrawal away from the stimulus. Stepping on a tack is a good example of this reflex in action. The person will typically flex (withdraw) the stimulated foot and leg while extending the other leg in order to propel the body away from the tack.. At the same time, inhibitory interneurons ipsilaterally inhibit extenders of the stimulated limb while contralaterally inhibiting flexors of the opposite limb.
37. 37. This is a polysynaptic, bilateral reflex incorporating both excitatory and inhibitory interneurons. Delivery of the stimulus to the receptors in a limb increases the firing rate of pain-carrying group III and IV afferents into the posterior horn. where they synapse with interneurons. Excitatory interneurons ipsilaterally stimulate alpha motor neurons to the flexors in that limb while contralaterally stimulating extenders in the opposite limb - thus the term flexor-crossed-extensor reflex
38. 38. This reflex is often intersegmental. This should not be surprising when one considers that many muscles are involved in such movements. In the cat, for example, a painful stimulus delivered to one hind leg will not only reflexly withdraw that leg, but will extend to both hind legs and forelegs on the opposite side as well. This means that the group III and IV afferents not only stimulated interneurons at the same segmental level at which they entered the cord, but activated synapses at higher and lower cord levels as well. The ascending and descending collaterals travel in the fasciculus proprius (ground bundles) of the white matter. The fibers in these tracts carry intersegmental connections.
39. 39. Flexor and cross extensor reflex
40. 40. Assessment In this we divide it in three category: Physiological measures Measures of voluntary activity Functional measures
41. 41. Measure of physiological activity Measure utilizing nerve conduction Tendon reflex Measure passive activity Ashworth scale Tardieu scale Range of motion Stiffness and muscle tone Stretch and stretch reflexes Pendulum test model Reflex threshold angle
42. 42. Measures of voluntary activity Isolated time movement tests Performance based measures Padobarography Detection of movement Gait Balance Body segment analysis
43. 43. Functional mesures Visual analoge scale and likert scale Timed ambulation tests Functional performance mesures The pediatric evaluation of disability inventory Qality of life mesures 36 item short from healthy survey Satsfaction with life scale Euro QOL
44. 44. Modified Asworth scale
45. 45. TARDIEU SCALE This scale quantifies muscle spasticity by assessing the response of the muscle to stretch applied at specified velocities. Grading is always performed at the same time of day, in a constant position of the body for a given limb. For each muscle group, reaction to stretch is rated at a specified stretch velocity with 2 parameters x and y.
46. 46. Velocity to stretch (V) Quality of muscle reaction (X) V1 As slow as possible V2 Speed of the limb segment falling V3 As fast as possible (> natural drop) with no clear catch at a precise angle V1 is used to measure the passive range of Motion. (PROM). Only V2 and V3 are used followed by release to rate spasticity ) 0 No resistance throughout passive movement 1 Slight resistance throughout, 2 Clear catch at a precise angle, Motion. (PROM). 3 Fatigable clonus (10secs) occurring at a precise angle 5. Joint Immobile Angle of muscle reaction (Y)
47. 47. Angle of muscle reaction (Y) Measure relative to the position of minimal stretch of the muscle (corresponding at angle) Spasticity Angle R1 Angle of catch seen at Velocity V2 or V3 R2 Full range of motion achieved when muscle is at rest and tested v1 velocity
48. 48. Testing Positions Upper Limb To be tested in a sitting position, elbow flexed by 90 at the recommended joint positions and velocities. Shoulder Horizontal Adductors V3 Vertical Adductors V3 Internal Rotators V3 Elbow Flexors V2 Shoulder adducted Extensors V3 Shoulder abducted Pronators V3 Shoulder adducted Supinators V3 Shoulder adducted Wrist Flexors V3 Extensors V3 Fingers Angle PII of digit III- MCP Palmar Interossei V3 Wrist resting position + FDS
49. 49. Lower Limb To be tested in supine position, at recommended joint positions and velocities Hip Extensors V3 Knee extended Adductors V3 Knee extended External Rotators V3 Knee flexed by 90 Internal Rotators V3 Knee flexed by 90 Knee Extensors V2 Hip flexed by 30 Flexors V3 Hip flexed Ankle Plantarflexors V3 Knee flexed by 30
50. 50. Spasm frequency scale: Most commonly used Penn Spasm frequency scale It is modified by Priebe at al
51. 51. Spinal cord assessment tool for spasticity Develop by Benz et al measure spasticity in spinal cord injury. Flexor spasm and clonus score of it correlate with PSFS. Not widely used.
52. 52. Spinal Cord Injury Spasticity Evaluation Total (SCI- SET) Patient reported impact of spasticity measure.
53. 53. References:- Rehabilitation medicine: principles and practice third addition edited by joel A.DeLisa Neurological rehabilitation , third addition Darcy ann Umphred Spasticity diagnosis and its manegment Ditunno et al describe the transmition from spinal shock immediately after SCI the development of spasticity Kamper et al in stroke patients demosttrated that muscle fiber played some part in phenomenon of spasticity
54. 54. Elovic EP, simone lk ,zaftonte r outcome and assessment for spasticity in patient with traumatic brain injury:the state of the art j head truama rehabili 2004. Lieber rl ,steinman s brash ia et al. structural and functional changes in spastic skeletal muscle .muscle nerve 2004 . RymerWZ powers rk pathophysiology of muscular hypertoniyain spasticity neurosurg art rev.