SPASTICITY

1. CURRENT TRENDS IN THE MANAGEMENT OF SPASTICITY IN HEMIPLEGIC PATIENT. A SEMINAR PRESENTATION BY ELOCHUKWU, PEACE UJUAKU (BMR)PT

2. INTRODUCTION 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. Spasticity is a feature of altered skeletal muscle performance in muscle tone involving hypertonia ; It is also referred to as an unusual "tightness", stiffness, and/or "pull" of muscles. The word spasm comes from the Greek word, σπασμός ( spasmos ), meaning to ‘pull or drag’.

3. Spasticity is a physiological consequence of an insult to the brain or spinal cord, that can lead to life-threatening, disabling and costly consequences (Ward 2008) It is characterised by muscle over activity which, if left untreated, may lead to muscle and soft tissue contracture. Clinically, spasticity is defined as velocity dependent resistance to stretch, where a lack of inhibition results in excessive contraction of the muscles, ultimately leading to hyperflexia (overly flexed joints).

4. It mostly occurs in disorders of the central nervous system (CNS) -seen in persons who have had damage to their central nervous system. That means damage to the spinal cord or brain. Damage to the muscles themselves or to the peripheral nerves in the limbs does not produce spasticity. In fact, peripheral nerve damage produces the opposite of spasticity, a condition known as 'flaccidity' which means loose, flabby muscles. When damage to the central nervous system produces spasticity, it also produces weakness, loss of dexterity or other trouble controlling the muscles. These are called paresis or palsy; they produce almost all the handicap or functional deficit.

5. Classification: Spasticity is frequently classified by its presentation and divided into: Generalised Regional and Focal

6. EPIDEMIOLOGY There are varied figures for prevalence of spasticity in different conditions ( Sommerfeld et al. 2004, Pfister et al. 2003). This may be due to the presence of many patients with mild spasticity for whom little or no treatment is required for their condition. An early brain injury study in the UK estimates that 16% and 18% of first time stroke sufferers and patients following traumatic brain injury respectively require spasticity treatment ( Verplancke et al. 2005).

7. In a Swedish study ( Lundstrom et al. 2008), the observed prevalence of any spasticity one year after first ever stroke was 17% and of disabling spasticity was 4% and An American study showed a prevalence of 35% among adults living in a developmental centre. Among all ages, the estimated annual incidence of ischaemic and haemorrhagic stroke is 183 per 100,000 in the US. ( Hirtz et al, 2007)

8. PATHOPHYSIOLOGY The pathophysiology is obscure, findings on examination are inconsistent, and treatment is not always successful, hence spasticity is managed and not treated. Understanding the physiology of normal movement may help the physician in the understanding of pathophysiology of spasticity . Physiology of movement Afferent input from the internal organs, the musculoskeletal Afferent input from the internal organs, the musculoskeletal system , and the skin converge on the medulla spinalis , activates the stretch reflex, both directly and through neural pathways regulating muscle contraction i.e the interneuron, and this results in a reflex motor response. The same afferent information goes to the cerebellum and the somato -sensory cortex . It is processed in those centers as well as in the basal ganglia. The resulting motor response is relayed to the lower motor neuron through the pyramidal and extrapyramidal system tracts.

9. The pyramidal tracts go directly to the lower motor neuron whereas the extrapyramidal tracts end at the interneuron. The cerebellum, basal ganglia, and extrapyramidal system nuclei modify the motor response as it goes to the medulla spinalis . In this way all motor output is influenced by the incoming sensory input and converges on the lower motor neuron. The interneurons in the medulla spinalis regulate the activity of the motor neuron.

10. Spasticity arises from prolonged dis inhibition of spinal reflexes as a result of UMN lesion. These spinal reflexes include stretch, flexor and extensor reflexes and are under supraspinal control by inhibitory and excitatory descending pathways. Stretch reflexes are proprioceptive reflexes, and are either phasic or tonic. The tonic stretch reflex arises from a sustained muscle stretch and is the cause of spasticity ( Sheean 2002). Damage to pyramidal tracts alone does not result in spasticity. It occurs only when the lesion involves pre-motor and supplementary motor areas.

11. The motor cortex is responsible for planning voluntary movement. The nerve impulse arising from the cerebral motor cortex is also sent to the basal ganglia and the extrapyramidal system nuclei. The basal ganglia correct the timing of movement. The corticospinal tracts carry movement order to the lower motor neuron. The The extrapyramidal system corrects the force of contraction of the muscles involved. The cerebellum coordinates the speed and direction of movement Muscle spindles in the contracting muscle, golgi tendon organs in the tendons and mechanoceptors in the joints send information on the degree of contraction to the medulla spinalis , cerebellum and the somatosensory cortex. The lower motor neuron sends contraction impulse to the muscle through the peripheral nerve. This is the final common pathway from the nervous system to the muscle The interneurons send inhibitory or excitatory impulses to the lower motor neuron and regulate its activity These corrective impulses from the extrapyramidal system are sent to the interneurons in the medulla spinalis

12. Upper Extremity Spasticity

13. Lower Extremity Spasticity

14. SYMPTOMS Spasticity can range from mild muscle stiffness to severe, painful and uncontrollable muscle spasms. It is associated with both positive and negative components of upper motor neuron syndromes. Positive components include muscle overactivity , flexor and extensor spasm, hyperreflexia , athetosis , spastic dystonia , clonus , and an extensor plantar response. Common negative symptoms comprise weakness/ paralysis, early hypotonia , fatigue and loss of dexterity.  

15. Spasticity can be distinguished from rigidity by its dependence on the speed of muscle stretch and characteristic distribution in antigravity muscle groups.   Spasticity does not always cause harm and can occasionally assist in the rehabilitation process by enabling a patient to stand when their limb weakness would not otherwise allow it.

16. Clinical and functional problems associated with severe Spasticity Physical : Non- specific pain · Discomfort · Painful muscle spasm · Difficulties with activities of daily living. e.g. washing, dressing, eating, toileting, maintaining hygiene, sexual activity · Problems with posture and mobility · Physical deformity and long term contracture · Pressure ulcers Emotional/Social:   · Emotional e.g. low mood, distorted self image, impaired motivation · Impact on fulfilment of life roles as a partner or a parent · Sleep disturbance – due to pain and discomfort · Vocational- impact on employment or education · Social isolation – due to restricted mobility    

17. Vicious cycle of spasticity

18. Complications of spasticity Spasticity is in itself can be disabling and, if left untreated or sub-optimally treated, may lead to consequences, such as: Muscle contractures (leading to abnormal body segment loading and sensory change), limb deformity and altered body mechanics, altered body image, the need for special wheelchairs and seating and pressure-relieving equipment, loading on pressure points, pressure sores, difficulty in the management of pressure sores, pain from muscle spasms, degenerative joint disease, loss of function, and mood problems and inability to participate in rehabilitation.

19. Treatment of spasticity Assessment of spasticity: Before any intervention is undertaken to modulate hyper tonicity or spasticity, it is important to attempt to assess the severity of spasticity. Many grading scales are used to quantify spasticity. These address the degree of muscle tone, the frequency of spontaneous spasms and the extent of hyper reflexia . Goniometry, Ashworth scale, Tardieu Scales, Goal attainment scale are only a few of these scales. One of the most widely used scales is the modified Ashworth scale.  

20. Ashworth scale This scale is based on the assessment of resistance to stretch when a limb is passively moved. It was originally validated for patients with multiple sclerosis and was validated by Ashworth (1964). Its reliability is questioned by the subjectivity required by the observer to carry out the test and by the fact that it measures multiple aspects of limb stretch. However, it is in general use and has good inter-and intra- rater reliability (Ashworth 1964). The original Ashworth scale is only validated for measuring spasticity in the lower limb (Lee et al. 1989). In addition, it does not distinguish between increased neurogenic muscle tone and mechanical limb stiffness. Despite this, it has nonetheless become the measure against which all other measures are compared. The major modification (Modified Ashworth Scale) was proposed to differentiate between mild and moderate spasticity, as discrepancies appeared in clinical judgement at the lower end of the original scale. Bohannon validated the scale in elbow flexion in post-stroke patients and attempts have been made to widen the validity (Bohannon and Smith 1987). A grade 1+ was added and the top of the scale was reduced from 5 to 4.

21. Score Ashworth (Ashworth 1964) Modified Ashworth (Bohannon and Smith 1987) O No increase in tone No increase in tone 1 Slight increase in tone giving a catch when the limb is moved in flexion/ extension Slight increase in tone giving a catch, release and minimal resistance at the end of range of motion (ROM) when the limb is moved in flexion/extension 1+ Slight increase in tone giving a catch, release and minimal resistance throughout the remainder (less than half) of ROM 2 More marked increase in tone, but the limb is easily moved through its full ROM More marked increased in tone through most of the ROM, but limb is easily moved 3 Considerable increase in tone – passive movement difficult and ROM decreased Considerable increase in tone – passive movement difficult 4 Limb rigid in flexion and extension Limb rigid in flexion and extension

22. Tardieu scale The angle at the point of resistance is noted by stretching a limb passively. This is performed during as slow a movement as possible (V1), under gravitational pull (V2) and at a fast rate (V3). The examiner will feel a catch in a muscle under the influence of an overactive stretch reflex. Five levels have been described at the point of this catch to capture the quality of the muscular reaction. In essence the scale assesses dynamic and static muscle length as well as joint range of motion. The inter and intra- rater reliability is generally good ( Gracies 2001), but the technique does require training to achieve this.

23. Stretch Velocity V1 Slow as possible V2 Speed of limb falling under gravity V3 Fast as possible Y Angle (Dynamic Range of Motion) R2 Slow Velocity: Passive joint range of motion or muscle length R1 Fast Velocity: Movement through full range of motion

24. Quality of Muscle Reaction Course of Passive Movement 0 No resistance 1 Slight resistance 2 Clear catch at precise angle, then release 3 Fatiguable clonus at precise angle 4 Unfatiguable clonus at precise angle 5 Rigid limb & joint

25. Wartenberg Pendulum Test In this, the leg moves under gravity and the observer measures the pendular activity of a spastic limb as it relaxes. It is best carried out on the lower limb, for it is not so reliable for other limb segments. Other methods for evaluating or assessing spasticity include muscle grading, deep tendon reflexes and Range of Motion measuring, bilateral adductor tone score, visual analogue scale, spasm frequency score, torque devices and electrophysiological studies (including dynamic multichannel EMG, tonic vibratory reflexes and electrical tests related to the H reflex and F wave). Most of these methods are time consuming, expensive, require specialised equipment and are used mainly in research

26. M anagement of Spasticity It is also important to remember that not every “tight” muscle is spastic. The clinically detectable increase in muscle tone may be due to spasticity, rigidity or a fixed muscle contracture. The key to successful spasticity management is education of the patient and carers with both verbal and written information. This allows them to understand, appreciate and be fully involved in the management plan. All patients with spasticity should be followed up by a coordinated multidisciplinary team, which allows more timely intervention and close monitor of the progress. This helps to deliver a more consistent approach to the individual over time.

27. The first step in the management of spasticity is to identify the key aims and realistic goals of therapy. Understanding the underlying pathology and possible prognosis is helpful in planning these goals . Other key points to consider are:  ·          Identification and management of any trigger or aggravating factors- Initial assessment should exclude any co -morbidity that may worsen spasticity such as pressure sores, chronic pain, infection (commonly urinary tract infection), constipation etc.   Instigation of an effective and realistic physical therapy programme including attention to posture and positioning should also be noted.  

28. General aims of management 1. Improve function- mobility , dexterity etc 2. Symptom relief such as ·   Relief of pain -prevent deformity e g muscle shortening, ·  -decrease spasms 3.  Correcting postural body image 4.  Decrease carer burden- Care and hygiene, positioning, dressing 5.  Optimise service responses- facilitate other therapy, delay/prevent surgery  

29. General Management of spasticity This includes the medical and pharmacological management of spasticity and they are as follows: A) Pharmacological: 1. The oral agents: Although different categories of drugs are available, those most commonly used to treat spasticity are baclofen , tizanidine , dantrolene , diazepam, gabapentin , botulinum toxin injection etc Botulinum toxin is the most widely used treatment for focal spasticity in conjunction with physiotherapy.  

30. 2. Nerve block: Peripheral nerve blockade/ Regional blocks/ Neurolytic blockade are another therapeutic possibility in the treatment of spasticity. This can be done with the help of fluoroscopy or nerve stimulation. Chemical neurolysis by phenol/ alcohol is irreversible and can be used at several sites. Blocks are applied most often to 4 peripheral sites: the pectoral nerve loop, median, obturator , and tibial nerves. The main indication is debilitating or painful spasticity. Peripheral blocks with local anaesthetics are used as tests to mimic the effects of motor blocks and determine their potential adverse effects. Peripheral neurolytic blocks are easy to perform, effective, and inexpensive.  

31. 3. Surgical technique: Most surgical procedures are irreversible. This means that realistic goal setting between the health care provider, family and patient is critical. Neurosurgical techniques have been proven useful in conditions like cerebral palsy .

32. Physiotherapy Management Basic goals of management of spasticity: When treating a patient who shows spasticity it is necessary to carry out three important aims: Inhibit excessive tone as far as possible Give the patient a sensation of normal position and normal movement with the contra-lateral limb Facilitate normal movement patterns in the affected limbs

33. A. Body positioning: In cases of spasticity it is important to facilitate the patient’s ability to inhibit the undesirable activity of the released reflex mechanisms. The position adopted by the patient is important since the head and neck position can elicit strong postural reflex mechanisms. Avoiding these head and neck positions can facilitate the inhibition of the more likely reflexes and if positions have to be adopted, then help in preventing the rest of the body from going into the reflex pattern thus elicited may be required by the patient. As patient develops control in the suppression of the effect of the reflex activities then he can be gradually be introduced to the use of positions which make suppression of reflex activity more difficult.

34. Side lying position well supported by pillows is very convenient since it avoids stimulation of the tonic labyrinthine reflex . Also, as head and trunk are in alignment, the stimulation of the asymmetrical tonic neck reflexes makes a good resting position for the patient with spasticity and also is convenient for the application of rhythmical trunk rotations of both passive and assisted active form which further helps in reduction of tone. Side lying is not always desirable because of respiratory problems in the older patient or because of the need to obtain a greater range of movement. Other attitudes are often very satisfactory such as crook lying or even with the knees as high on the chest as possible. These two positions are helpful if there is flexor spasticity.

35. B. Rotatory movements: Trunk rotation produces lower limb to extend, abduct and externally rotate. Limb rotations are also very effective in helping to give a more normal control of muscle tone to the patient. C. Pressure under surface of the foot: If the pressure is applied to the ball of the foot it may well stimulate an extensor reflex in which a pathological pattern of extension, adduction, and medial rotation of hip is produced together with plantar flexion of the foot, which is undesirable in case of spasticity. If pressure is applied under the heel of the foot then a more useful contraction of muscle is likely to occur giving a suitable supporting pattern, normal movements patterns & avoidance of triggering factors .

36. Movement of a normal nature does appear in itself to reduce excessive tone and consequently this should be encouraged in the patient. However, care must be taken if conscious volitional movement is demanded. Due to reflex release, some motor neurone pools are already in an excitatory state and any volitional effort is likely to act as a triggering mechanism to those motor neurone pools giving associated muscle contraction in the spastic pattern. Such patients should not be encouraged to make strong volitional effort since this is inclined to facilitate the production of spastic patterning. Other factors such as quick movements, abruptly performed, noisy surroundings, anxiety, excitement, over exertion should also be avoided as it may increase spasticity.

37. D. Slow-sustained stretching: Stretching forms the basis of spasticity treatment. Stretching helps to maintain the full range of motion of a joint, and helps prevent contracture, or permanent muscle shortening . It activates muscle spindles, golgi tendon organs which are sensitive to length changes. It inhibits or dampens muscle contraction and tone due largely to peripheral reflex effects .

38. This method does have its dangers since, if stretching is forced against severe spasticity, the hyperexcitable stretch reflex reacts even more strongly and damage to the periosteum of bone may occur where excessive tension has been applied by the tendons of the stretched muscles. - Techniques used are - Manual contacts - Inhibitory casting or splinting - Reflex-inhibiting patterns - Mechanical low-load weights

39. E. Prolonged cold application: Application of cold packs to spastic muscles (usually for 10 minutes or longer) may improve muscle tone. While the effect doesn't last long, it may be used to improve function for a short period of time, or to ease pain. It activates thermoreceptors . It decreases neural, muscle spindle firing and provides inhibition of muscle tone. Techniques used - Immersion in cold water ice chips - Ice towel wraps - Ice packs - Ice massage - Ice application with exercises

40. F. Neutral warmth: Retention of body heat stimulates thermoreceptors , autonomic nervous system mainly parasympathetics , which produces generalized inhibition of tone, calming effect, relaxation and decreases pain. It should be applied for about 10 to 20 minutes. Overheating should be avoided as it might increase arousal or tone. Techniques used - Wrapping body or body parts: towel wraps - Application of snug fitting clothing (gloves, socks, tights) or air splints - Tepid baths

41. G. Relaxed passive movements: Rhythmical, slowly performed passive movements through normal patterns may also be helpful and in the more moderate cases patients may subconsciously join in and by his own activity a reduction in spasticity may occur. H. Deep Rhythmical Massage (Tendon Rolling): Deep rhythmical massage with pressure over the muscle insertions can be given to reduce spasticity. I. Biofeedback: Biofeedback is the use of an electrical monitor that creates a signal—usually a sound—as a spastic muscle relaxes. In this way, the person with spasticity may be able to train himself to reduce muscle tone consciously.

42. J. Inhibitory Pressure (Weight-Bearing): Prolonged pressure to long tendons inhibits the hypertonicity of a muscle. It activates muscle receptors (muscle spindles, golgi tendon organ) and tactile receptors. Firm pressure can be applied manually or by body weight. Weight bearing postures are used to provide inhibitory pressure, such as - Quadruped or kneeling postures can be used to promote inhibition of quadriceps and long finger flexors. - Sitting, with hands open, elbow extended, and upper extremity supporting body weight can be used to promote inhibition of long finger flexors.

43. K. Functional Electrical Stimulation : Electrical stimulation may be used to stimulate a weak muscle to oppose the activity of a stronger, spastic one. It improves standing, walking, and exercise training as well as decreases upper extremity contractures. Appears to improve motor activity in agonistic muscles and reduce tone in antagonistic muscles. Therapeutic effect may last for less than 1 hour after stimulation has been stopped, probably because of neurotransmitter modulation within reflex arc.

44. L. Tone Reducing Orthosis : These are plastic AFO’s in which foot plate and broad upright are designed to modify reflex hypertonicity by applying constant pressure to the plantarflexors and invertors. They control the tendency of the foot to assume an equino-varus posture. Foot plate may be modified which maintains the toes in an extended or hyperextended position, thus assisting individual to walk with better foot and knee control.

45. M. Slow Maintained Vestibular Stimulation: Low-intensity vestibular stimulation such as slow rocking produces generalized inhibition of tone. It facilitates primarily otolith organs (tonic receptors); less effects on semicircular canals ( phasic receptors). Slow, repetitive rocking movements; assisted rocking in a weight-bearing position, for example, rocking with equipments: - Rocking chair - Swiss ball - Equilibrium board - Slow rolling movements

46. N. Proprioceptive Neuromuscular Techniques : Techniques used - Rhythmic Initiation – Voluntary relaxation followed by passive movements through increments in range, followed by active movements progressing to resisted movements using tracking resistance to isotonic contractions. - Rhythmic Rotation – Voluntary relaxation combined with slow, passive, rhythmic rotation of the body or body part around a longitudinal axis, followed by passive movement into the antagonist range. - Contract Relax Active Contraction – Isotonic movement in rotation is performed followed by isometric hold of the range limiting muscles in the antagonist pattern against slowly increasing resistance followed by voluntary relaxation and active movement into the new range of the agonist pattern.

47. THANK YOU AND MERRY CHRISTMAS IN ADVANCE

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