UMN: UPPER MOTOR NEURON
SPASM: SUPPORT PROGRAMME FOR ASSEMBLY OF DATABASE FOR SPASTICITY MEASUREMENT
CNS: CENTRAL NERVOUS SYSTEM
PMS: PASSIVE MUSCLE STRETCHING
TS: TRICEPS SURAE
TA: TIBIALIS ANTERIOR
ROM: RANGE OF MOTION
Spasticity is a major disabling symptom that most commonly arises after stroke, multiple sclerosis, spinal cord injury, some traumatic brain injuries and other central nervous system (CNS) lesion (Dietz and Sinkjaer 2007). Lesion of the cortico-fugal pathway along with the pyramidal tracts, at any level, like cortex, brainstem, internal capsule or spinal cord results in spasticity (Carr et al. 1995). The term spasticity was derived from the Greek word ‘
’ meaning ‘to pull or to tug’ (Ghai et al. 2013). The definition of spasticity that has been formerly cited is that of Lance in 1980: ‘Spasticity is motor disorder characterised 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 neurone (UMN) syndrome.’(Brown 1994). Though this definition is useful for diagnosis, yet for the purpose of understanding and managing the effects of inappropriate muscle actions after stroke, it is too restrictive (Bhakta 2000). Recently SPASM (Support Programme for Assembly of database for Spasticity Measurement) redefined spasticity as “disordered sensori-motor control, resulting from an UMN lesion, presenting as intermittent or sustained involuntary activation of muscles” (Mirbagheri et al. 2009). For the purpose of study the clinicians have divided the UMN syndrome into ‘positive’ and ‘negative’ effects. The characteristics of the negative features are loss of dexterity, weakness and easy fatigability on the other hand spasticity, increased tendon reflexes, extensor and flexor spasm, clonus etc are the features of positive UMN syndrome. The later definition of spasticity includes all the characteristics of positive UMN syndrome excluding its negative features and the biomechanical changes in the joints and soft tissues (Mirbagheri et al. 2009). The negative features of UMN syndrome are regarded to be more disabling than the positive features (Carr et al. 1995) but recent studies have showed that spasticity adds on to the impairment of function and to limitation of activity for the affected person (Bovend’Eerdt et al. 2008).
The core feature of spasticity is increase in stretch reflex, manifested as hypertonus. Muscle tone is defined as the tension of a muscle due to involuntary contractions of its motor units; it is determined both by the passive elasticity of muscular tissues, the viscoelastic properties of the fibrillary proteins contained within each muscle fibre and by the active (though not continuous) contraction of muscle in response to the reaction of the nervous system (Grabowski and Tortora, 2003). Alternately active and inactive motor units help in maintaining normal tone in a muscle. Any imbalance in the input from central motor pathways like the cortico-reticulo-spinal and other descending pathways to the inter-neuronal circuit of spinal cord results in alteration in the involuntary contraction in a muscle. The main tract restricting the spinal reflex activity is the dorsal reticulospinal tract that runs along the lateral spino thalamic tract. It arises from the ventero medial reticular formation which has less facilitatorty control over the cortical motor areas, thereby augmenting the inhibitory drive. The main excitatory pathway also arising in the brainstem is the medial reticulo spinal tract. Damage to these tracts give rise to a net loss of inhibitory control leading to increased alpha motor neurone excitability at the segmental cord level and subsequent increase in muscle tone. Several studies also claim that peripheral neural changes also contribute to the increased muscle tone. Muscle tone has two components, neural involving CNS and musculoskeletal, where muscles are involved (Barnes, M. P. et al. 2003). Both the components help in maintaining normal muscle tone. Normal tone is the slight amount of constant tension in the healthy muscles offering small resistance to displacement (Barnes, Michael P. and Johnson 2008). There is change in mechanical, visco-elastic properties of muscle fibres as a result of paresis and immobilisation after an UMN lesion.
Activation of actin and myosin cross bridges also increases muscle tone (Lee et al, 2005). CNS and neural pathways maintain tone by overlapping actin and myosin filaments on muscle contraction. Insufficient contraction results in decreased muscle tone due to insufficient development of tension (Grabowski and Tortora 2003). Through the phasic and tonic stretch reflexes the muscle spindle plays an important role in regulating the muscle tone (Cameron-Tucker 1983). These muscle spindles can be adjusted in terms of their response to stretching.
Spasticity is generated due to the over activity of the alpha motor neurons. Over activity occurs when the monosynaptic input via Ia afferent fibres and polysynaptic afferent input via the Golgi tendon organs and cutaneous receptors loose descending inhibition from the cerebral cortex and basal ganglia, which is relayed through the dorsal and medial reticulospinal and vestibulospinal tracts. Spinal inter-neurons are responsible for presynaptic and reciprocal inhibition of Ia fibres. Due to the loss of this inhibition inappropriate muscle co-contraction occur disabling voluntary limb movement (Bhakta 2000).
The course of development of both cerebral and spinal spasticity after an insult is slow in humans, except for the cases of high brain stem lesion like traumatic brain injury where the increase in the tone is immediate (Carr et al. 1995). The time gap between the injury and appearance of spasticity may vary from days to months, depending upon the level of lesion (Ghai et al. 2013).
The effect of spasticity ranges from mild muscle stiffness to severe, very painful and uncontrollable muscle spasm. If left untreated spasticity gives rise to many problems like pain, spasm, contracture and deformity leading to a loss of mobility and dexterity, problem in self hygiene, inability to wear orthotics hence resulting in decreased functioning, participation and low self esteem (Ghai et al. 2013). A multidisciplinary approach is required for the effective management of spasticity taking into consideration other variables that might affect treatment outcome. Aim of treatment should include prevention of abnormal limb or trunk posture and facilitation of movement in the context of functional activities (Bhakta 2000).
Secondary to the neural changes there are dramatic changes of the structural and mechanical properties of the spastic muscle. A review conducted by Jared et al. concluded that the following changes occur in a spastic muscle: a) alteration of the size of muscle fibre and the type of fibre distribution; b) morphologically and biomechanically measured there is proliferation of extracellular matrix material; c) increased stiffness in the spastic cell muscle; d) compared to the normal muscle there is inferior mechanical properties of extra cellular matrix in the spastic muscle (Foran et al. 2005).
As a management of spasticity the researchers have tried to alter the motor neuron excitability by many interventions like electrical stimulation (Bajd et al. 1985), pressure (Leone and Kukulka 1988), muscle tapping (Belanger et al. 1989), vibration (Gillies et al. 1969), cooling (Bell and Lehmann 1987), massage (Sullivan et al. 1991) and stretch (Kunkel et al. 1993, Avela et al. 1999). Among all of these, stretching has been intensively used as it is safe, economical and convenient (Tsai, KUEN-HORNG et al. 2001).
Stretching is the process of applying tension to the soft tissue structures like muscle, tendon, and vascular, dermal, connective, neural tissues for elongation. Stretching can be applied mechanically (example- with dynamometer or an intelligent feedback control device) offering well controlled intervention and manually, which is difficult to standardise but represents clinical practice better. Stretching changes the viscoelastic, structural and excitatory property of the muscle. (Nielsen et al. 2007). However many neural as well as non neural property of stretching remains unclear. Stretching aims on decreasing muscle tone, maintain or increase soft tissue extensibility leading to improvement in function (Barnes, Michael P. and Johnson 2008). Lots of variation can be done while implementing stretching as an intervention. The amount of tension, the duration of the stretch, the velocity of stretch, the number of repetition can all be varied.
A study was done by Harvey et al. in the year 2000 on the “
Effects Of Four Weeks Of Daily Stretching On Ankle Mobility In Patients With Spinal Cord Injuries”.
14 recently injured subjects with paraplegia and quadriplegia were taken from two spinal injury units in Sydney, Australia. Their ankle was stretched into dorsiflexion, continuously for 30 minutes with a torque of 7.5 Nm for every weekday, for 4 consecutive weeks. The main outcome measure was measuring the torque angle in knee flexed and extended position. Measurements were taken pre-test and post test. Post test measurements were also taken thrice I,e, during the study (2nd week), just after the study (4th week) and one week after the study (5th week). Intervention was given by a custom made stretching device that is able to give ankle stretch. The baselines of all the subjects were same. The result showed that even after stretching for a longer time than usual there was no significant difference in the post test value in any of the three parameters from pre test. Hence the study concluded that there is no significant change in ankle mobility after 30 minutes of stretching for 4 weeks in SCI patients. The strength of the study is good, with random allocation, blinding of assessor, similar baseline of all the subjects but the intervention device needed to be more standardised. The study has a score of 8 on PEDro scale of assessment.
A study by Tsai et al. 2001 examined the effect of a single session of prolonged muscle stretch (PMS) on the spastic muscle. 17 spastic hemiplegic patients were selected for the study and as an intervention PMS was given on the triceps surae (TS) muscles by standing on the tilt table with feet dorsiflexed for 30 minutes. Here the outcome measures were Modified Ashworth scale of the TS, the H/M ratio of TS and the F/M ratio of tibialis anterior (TA) and passive range of motion (ROM) of ankle dorsiflexion,. The measurements were taken pre test, post test and 45 minutes after the test. ROM was measured with a goniometer and electromiograph was used to perform nerve stimulation and reflex recording. The results showed non-significant difference in the Modified Ashworth scale, significant change in the ROM of ankle dorsiflexion, F/M ratio and H/M ratio. There was increase in the passive ROM of the ankle dorsiflexion post treatment compared to pre treatment, additionally PMS reduced motor neuron excitability of the TS and increased that of TA in the post treatment. There was no significant difference of result with in immediate post test and 45 minutes after post test. The study was well written but the sample size was too small. The age of the effected patients varied from 33 till 79 years which is a very wide range and the acuteness of the patients varied from 4.5 months post attack to 79.6 months post attack. These factors may cause a problem while generalising the results and the amount of stiffness may vary with the duration of illness.
Bressel and McNair (2002) did a study to compare prolonged static stretch with cyclic stretching on ankle joint stiffness, torque relaxation and gait in stroke patients. 10 community dwelling people were randomly allocated into two groups; one of the groups received single session of static stretch and the other cyclic stretch of the calf muscle for 30 minutes. There was a washout period for one week and then the group interventions were exchanged. The interventions were given by an isokinetic dynamometer that measured the torques and the angles also. Before and after treatment the time taken to walk 10 m was taken and stiffness of the ankle joint was calculated from the slope of the torque and angle curves before and immediately after the treatments. Over the 30 minutes stretch the percentage of the decrease in peak passive torque was the torque relaxation achieved. Results showed that there was significant decrease in ankle stiffness in both the intervention but there was not much significant difference between the post test values of the two interventions. The amount of torque relaxation was 53% greater in static stretching than that of cyclic stretching. And the 10 m walk duration did not have any significant difference pre and post test. The sample size of the study was very small to generalise the results and the wash over period between the two sessions were of just one week. Since the prolonged effect of the stretching is unknown hence it can’t be commented that whether there was any residual effect of the previous session that may have affected the results of the second session. Nowhere in the study blinding was done hence there may be a chance of being bias from the assessor. The baselines of both the groups were not similar.
A study by Yeh et al. (2005) compared the effectiveness of constant-torque prolonged muscle stretching (PMS) treatment in subjects with ankle hypertonia. The study design was a pre and post test analysis. 30 subjects suffering from hemiplegia and calf muscle hypertonia were given stretching device using a motor driven stretching device for 30 minutes in constant torque or constant angle mode. The main outcome measures were Modified Ashworth scale, passive range of motion and viscoelastic property of the planter flexors were measured pre and post treatment. Result showed significant improvement in all the measures, but the in the viscoelastic component the constant torque showed more evident changes compared to the constant angle measure. This study proved that there is significant reduction in spasticity after a single session of PMS. The methodology of the study was appropriate and the analysis of the data leading to the result was done well. the study also mention about the future scope of study by changing the mode of stretch from constant to intermittent. Neither the subjects, nor the assessor was blinded in the study, so the question of bias remains.
A systemic review done by Bovend’Eerdt et al. (2008) was the first review done on the effects of stretching in spasticity. Studies were taken from databases like Medline, Cochrane library, CINHAL, Web of Science, PEDro and Alied and Complementary medicine for review. 10 RCTs and 11 clinical trials were assessed. Randomised control trails were assessed on PEDro scale for methodologic quality and the other clinical trials were assessed using data extraction form containing 13 items from CASP guidelines and CONSORT statement. The methodological qualities of the RCTs were low and there was a huge diversity on the methodology, intervention, population etc. Both manual and mechanical stretching was given. The review concludes as there is not much evidence on the basis of which the review can say if stretching on spasticity has its clinical benefit.
A recent study by Gao et al. (2011) aims to investigate the changes occurring in biomechanical properties of the calf muscle–tendon unit after controlled ankle stretching in stroke survivors. Comparison was done between 10 stroke patients with ankle spasticity/contracture in one group and ten healthy subjects in the control group. 60 minute ankle stretching was given as an intervention to both the groups. Joint biomechanical properties like resistance torque, index of hysteresis and stiffness were evaluated pre- and post-intervention. Length of Achilles tendon was measured with ultrasonography. The force output of the triceps surae muscles was given in torque–angle relationship, by stimulating the calf muscles at a definite intensity across different ankle positions. The device used for intervention was an ankle stretching device with intelligent control (the velocity of stretching was inversely proportional to the joint resistance torque) was used. Pre test the stroke survivors showed significantly higher resistance torques and joint stiffness, which were to a large extent reduced after the stretching intervention, especially in dorsiflexion. Stretching also significantly improved the force production of the impaired calf muscles in stroke population under matched stimulations, along with the ankle ROM. The study interpreted that at the joint level, repeated stretching leads to increased passive ROM and decreased joint stiffness; at the muscle–tendon level, calf muscle force output improved. The study provided evidence of improvement in muscle tendon properties through stretching intervention. Apart from the small sample size the study was well written and the methodology was well described.
Spasticity is a disabling and often painful condition that occur secondary to the UMN lesion that leads to hypertonicity, exaggerated reflexes, weakness of muscle and loss of dexterity. Spasticity has both neural and non neural components. Stretching is a very commonly used intervention used in clinical physiotherapy. But stretching and spasticity together is a very complicated concept. From the articles reviewed one can conclude that stretching does have a positive effect on spasticity, but its effect on the neural component of spasticity alone is yet not proved. In this study the stretching that has been described are mechanical stretches, but there are various other form of stretches given through splinting, plaster cast, weights which could not be discussed because of their low level of evidence. Many studies could not be included because there stretching was combined with strengthening, stimulation, passive motion etc. Even among the articles taken in this study there is heterogeneity in methodology of stretching, its duration, the type of stretch and even the outcome measures used. Inspite of being a component in the definition none of the articles investigated spasticity by using different velocities of displacement. Due to so much of diversity it is tough to comment on which mode of stretching is most beneficial for spasticity. To come down to a conclusion, future studies are needed to be done to find a standardised protocol of stretching for spasticity. In the future studies the outcome measure should be chosen carefully and intervention should be planed keeping the aim of the study in mind.
The studies taken in this review shows a great diversity in respect to methodology, intervention, population and outcome measures. Though from the reviewed articles it can be said that stretching is effective for spasticity but there is need of good quality of studies to decide on a stretching protocol, its long term and short term effects and to come down to a conclusion as to which type of stretching is most effective in spasticity .
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