Definitions and Pathophysiology of Spasticity

1. Definitions and Pathophysiology of Spasticity

2. Definition of Spasticity �Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.� -- Lance, 1980 Tonic Stretch Reflex Tonic muscle response to vibratory stretch Tonic response to a phasic stimulus Thus spasticity = velocity-dependent increase of muscle response to phasic stretch, routinely tested by tendon taps or passive mobilization

3. What is spasticity Velocity dependent tonic stretch reflex Resulting from abnormal processing of propioceptive input In response to stretching the muscle Other influences Nociceptive Loss of reciprocal inhibition

4. Terminology Spasticity Motor disorder Velocity-dependent increase in stretch reflexes One component of the upper motor neuron (UMN) syndrome UMN Syndrome Positive symptoms Increased tone Clonus Released flexor reflexes Negative symptoms Loss of dexterity Weakness We will be focusing on the management of spasticity, which is one component of upper motoneuron (UMN) syndrome.We will be focusing on the management of spasticity, which is one component of upper motoneuron (UMN) syndrome.

5. Upper Motor Neurone Syndrome Spastic Dystonia Spastic Paresis Symptoms Positive Negative

6. Features of Spasticity Positive Symptoms Muscle Tone Tendon Jerks Repetitive Stretch Reflexes - Clonus Extensor St. Reflexes Released Flexor Reflexes - Babinski, Mass synergy pattern Negative Symptoms Paresis Fine Control Dexterity Fatiguability Early Hypotonia

7. Etiologies Cerebral palsy Stroke Multiple sclerosis Traumatic brain injury Spinal cord injury Anoxia Neurodegenerative disease This slide shows some important etiologies of spastic disorders. These disorders are all characterized by spasticity as one of their features.This slide shows some important etiologies of spastic disorders. These disorders are all characterized by spasticity as one of their features.

8. Vicious cycle Spasticity Shortened muscle Greater activity More spasticity Spasticity is relieved by stretching Clasp knife

9. Pathophysiology Spinal Reflexes - Afferent Drive Efferent Reflexes - Non-Afferent Drive Disordered Control of Vol. Movement

10. Pathophysiology

11. Pathophysiology: Normal tone is a balance of inhibitory and excitatory control In spasticity, normal inhibitory control is lost/diminished

12. Spasticity

13. Pathophysiology of Spasticity Not completely understood, despite considerable investigation Interruption of descending inhibitory pathways Rearrangement of spinal circuitry

14. Pathophysiology of Spasticity: Established Mechanisms Alterations within the reflex arc Change in muscle active properties (increased ratio torque/EMG) Change in muscle passive properties (decreased extensibility) Decreased pre-synaptic inhibition, at least in paraplegics Increased fusimotor activity and increased excitability of the alpha motor neuron have not been established

15. Pathophysiology of Spasticity: Established Mechanisms, cont�d Mechanisms affecting the reflex arc Decreased reciprocal Ia inhibition on extensors Decreased non-reciprocal Ib inhibition Decreased inhibition from flexor reflex afferents It has been established that in spastic disorders, there is a decreased reciprocal Ia inhibition on the extensor muscles, which could explain overactivity in these muscles in the lower limbs. There is also decreased nonreciprocal Ib inhibition that could participate in the mechanism of co-contraction. Finally, there is decreased inhibition from flexor reflex afferents that could also participate in the hyperexcitability of the stretch reflex arch.It has been established that in spastic disorders, there is a decreased reciprocal Ia inhibition on the extensor muscles, which could explain overactivity in these muscles in the lower limbs. There is also decreased nonreciprocal Ib inhibition that could participate in the mechanism of co-contraction. Finally, there is decreased inhibition from flexor reflex afferents that could also participate in the hyperexcitability of the stretch reflex arch.

16. Phenomena Commonly Associated with Spasticity Abnormal cutaneous reflexes (Babinski sign) Spastic dystonia muscle contraction present at rest, dependent on tonic stretch significant contribution to deformity Spastic co-contraction abnormal antagonist contraction present during voluntary agonist effort, dependent on tonic stretch on antagonist Extra-segmental co-contraction abnormal contraction distant from the muscles involved in a voluntary effort The phenomena commonly associated with spasticity are abnormal and exaggerated cutaneous and nociceptive responses, such as the elevation of the great toe when rubbing the external edge of the sole of the foot. Spastic dystonia is a very important form of overactivity. Defined by the presence of abnormal muscle contraction as the patient is at rest, this abnormal contraction is influenced by the degree of tonic stretch imposed on the muscle. Spastic dystonia may be the main factor of deformities and muscle shortening and finally, disfigurement. Pathological antagonistic co-contraction, or �spastic co-contraction,� is an abnormal contraction occurring in an antagonist muscle, when the agonist is involved in a voluntary effort. It has been established that these co-contractions are aggravated when the antagonist muscle is under tonic stretch. Spastic dystonia and spastic co-contraction are two different types of muscle overactivity -- one present at rest and one present during voluntary effort -- that both are influenced by the degree of recruitment of stretch receptors. Extra-segmental co-contractions are those abnormal contractions occurring at distance from the muscles involved in voluntary efforts: for example, contraction of the plantar flexors when the patient tries to elevate his paretic arm. The phenomena commonly associated with spasticity are abnormal and exaggerated cutaneous and nociceptive responses, such as the elevation of the great toe when rubbing the external edge of the sole of the foot. Spastic dystonia is a very important form of overactivity. Defined by the presence of abnormal muscle contraction as the patient is at rest, this abnormal contraction is influenced by the degree of tonic stretch imposed on the muscle. Spastic dystonia may be the main factor of deformities and muscle shortening and finally, disfigurement. Pathological antagonistic co-contraction, or �spastic co-contraction,� is an abnormal contraction occurring in an antagonist muscle, when the agonist is involved in a voluntary effort. It has been established that these co-contractions are aggravated when the antagonist muscle is under tonic stretch. Spastic dystonia and spastic co-contraction are two different types of muscle overactivity -- one present at rest and one present during voluntary effort -- that both are influenced by the degree of recruitment of stretch receptors. Extra-segmental co-contractions are those abnormal contractions occurring at distance from the muscles involved in voluntary efforts: for example, contraction of the plantar flexors when the patient tries to elevate his paretic arm.

17. Phenomena Commonly Associated with Spasticity, cont�d Other types of muscle overactivity (present with yawning, breathing etc.) Muscle shortening consequence of both immobilization and muscle overactivity Motor weakness significant source of disability There are several other types of muscle overactivity associated with spasticity, for example, contraction of the elbow and forearm flexors during yawning, or of the plantar flexors during yawning and heavy breathing. Muscle shortening is a consequence of both immobilization and muscle overactivity. Motor weakness accounts for a part of the functional impairment in these patients.There are several other types of muscle overactivity associated with spasticity, for example, contraction of the elbow and forearm flexors during yawning, or of the plantar flexors during yawning and heavy breathing. Muscle shortening is a consequence of both immobilization and muscle overactivity. Motor weakness accounts for a part of the functional impairment in these patients.

18. Disabling Phenomena Associated with Spasticity Muscle shortening, motor weakness, and stretch-dependent muscle overactivity (spastic co-contraction and spastic dystonia) are probably the most disabling features in spastic patients. ? Three logical solutions in therapy: muscle lengthening, motor training, and local muscle relaxation In summary, muscle shortening, motor weakness, and stretch-dependent forms of muscle overactivity, with in particular spastic co-contraction and spastic dystonia, are probably the most disabling features in spastic patients. In therapy, there will be three logical solutions: muscle lengthening to address the contractures, motor training to address the lack of motor power in those muscles that are mostly weak and hypoactive, and local muscle weakening in those muscles where overactivity is disabling. In summary, muscle shortening, motor weakness, and stretch-dependent forms of muscle overactivity, with in particular spastic co-contraction and spastic dystonia, are probably the most disabling features in spastic patients. In therapy, there will be three logical solutions: muscle lengthening to address the contractures, motor training to address the lack of motor power in those muscles that are mostly weak and hypoactive, and local muscle weakening in those muscles where overactivity is disabling.

19. Pathophysiology of Impairment After a Central Nervous System Lesion