Spasticity

definition, clinical features, pathophysiology, assessment, treatment

1. topic ------ goniometer SPASTICITY PRATIGYA DEUJA

2. DEFINITION Spasticity is defined as velocity dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitabilty of the stretch reflex i.e , the faster the passive movements of the limb through it’s range, the greater the increase in muscle tone. Increased resistance to passive movements in one direction. It is an upper motor lesion. It is noted in cases like; SCI, multiple sclerosis,, traumatic brain injury, amyotrophic lateral sclerosis, cp, spinal cord tumors.

3. CLASSIFICATION ACCORDING TO SEVERITY MILD SPASTICITY: Clonus or mild increase in tone. No or minimal loss of range. Mild spasms; generally not problematic or affecting function but annoying or inconvenient

4. CLASSIFICATION cont.. 2. MODERATE SPASTICITY: Loss of range of movement and possible contracture. Walking is often effortful, may require aid or wheelchair. Difficulty releasing grip or in hand hygiene. Minor adaptations required for position in lying; t-roll, wedge, pillows, lumbar roll.

5. CLASSIFICATION cont… 3. SEVERE SPASTICITY: Marked increase in tone. Loss of range and probable contracture. Often hoisted for transfers. Difficult positioning despite complex seating systems. Often reliant on a catheter and regular enemas.

6. CLINICAL FEATURES Increasing tightness Worsening spasm Physical activities like; walking, transferring are affected Functional activities like picking, grasping are affected

7. PHYSICAL EXAMINATION Positive signs: Negative signs: Hyperreflexia Babinski responses clonus Fatigue Reduced motor control Loss of coordination Muscle weakness

8. PATHOPHYSIOLOGY Spasticity resulted from a loss of descending, facilitatory inhibitory influences that act on Ia interneuron inhibition. Reciprocal inhibition mediated through Ia interneuron requires facilitation from higher centers. With injury to CNS the interneuron is unable to shut off antagonist muscle firing with resultant increased velocity dependent resistance to movement.

9. PATHOPHYSIOLOGY The combination of both decrease inhibition, increased depolarization state of cell membrane, decrease action potential threshold for nerve signal conduction thus increase activity of structures innervated by the affected nerves. Recent studies suggest that intrinsic changes in the motor neurone develop over time following a lesion. These result in abnormally long plateau like potentials that prolong motor neurone discharge and thus muscle contraction in response to synaptic inputs.

10. ASSESSMENT Patient history DTR Range of motion Test for clonus Functional observation Aggravating factors Modified Ashworth scale

11. MODIFIED ASHWORTH ScALE 0 – No increase in muscle tone 1 – Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end range of motion when the part is moved in flexion or extension/ abduction or adduction 1+ - Slight increase in muscle tone, manifested by a catch, followed by a minimal resistance throughout the remainder (less than half) of the range of motion

12. MODIFIED ASHWORTH ScALE 2 – More marked increase in muscle tone through most of the range of motion, but the affected part is easily moved. 3 – Considerable increase in muscle tone, passive movement is difficult 4 – Affected part is rigid in flexion or extension / abduction or adduction

13. PHARMACOLOGICAL MANAGEMENT Baclofen Tizanidine Dentrolene Phenol block Botulinum toxin

14. SURGICAL MANAGEMENT Baclofen pump Tendon lengthening Tendon transfer Osteotomy Arthodesis

15. PHYSIOTHERAPY MANAGEMENT Positioning Ultrasound: 10 minutes/session : Continuous mode for 5 weeks : frequency : 1 mhz : intensity : 1.5 w/cm2 Cryotherapay : 20 minutes Thermotherapy : 20 minutes, prior to stretching Hydrotherapy Proprioceptive neuromuscular facilitation

16. PHYSIOTHERAPY MANAGEMENT Massage Passive movements Weight bearing through affected extremity Rood’s technique Yoga Relaxation techniques