Spasticity Following Stroke: a Literature Review

Spasticity Following Stroke a Literature ReviewABBREVIATIONSUMN UPPER MOTOR NEURONSPASM financing PROGRAMME FOR ASSEMBLY OF DATABASE FOR SPASTICITY MEASUREMENTCNS CENTRAL NERVOUS ar redactmentPMS PASSIVE MUSCLE STRETCHINGTS TRICEPS SURAETA TIBIALIS priorROM RANGE OF MOTIONINTRODUCTIONSpasticity is a major diverseness symptom that most commonly arises by and by stroke, multiple sclerosis, spinal anesthesia corduroy dishonor, some traumatic capitulum injuries and other central nervous frame (CNS) lesion (Dietz and Sinkjaer 2007). Lesion of the cortico-fugal pathway along with the pyramidal packets, at any level, like cortex, brainstem, inwrought capsule or spinal cord military issues in spasticity (Carr et al. 1995). The term spasticity was derived from the Grecian word spasticus 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 travel disorder characterised by a hurrying depe ndent increase in tonic str etcetera reflexes ( go throughbuilder-builder tone) with exaggerated muscularity jerks, resulting from hyper-excitability of the stretch reflex, as one component of the upper force back nerve celle (UMN) syndrome.(Brown 1994). though this definition is useful for diagnosis, yet for the purpose of understanding and managing the nucleuss of improper go through actions after stroke, it is too restrictive (Bhakta 2000). Recently SPASM (Support course for Assembly of selective informationbase for Spasticity Measurement) redefined spasticity as disordered sensori-motor adduce-so, resulting from an UMN lesion, presenting as intermit tent or uphold in spontaneous activation of go throughs (Mirbagheri et al. 2009). For the purpose of orbit the clinicians wear divided the UMN syndrome into domineering and negative mental pictures. The characteristics of the negative features atomic number 18 dismission of dexterity, weakness and easy fatigability on the other hand spasticity, change magnitude tendon reflexes, extensor and flexor spasm, clonus etc argon the features of absolute UMN syndrome. The later definition of spasticity includes all told 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) entirely recent studies have showed that spasticity adds on to the impairment of function and to demarcation line of activity for the affected person (BovendEerdt et al. 2008).The core feature of spasticity is increase in stretch reflex, manifested as hypertonus. Muscle tone is defined as the tautness of a ponderosity repayable to involuntary contractions of its motor units it is determined twain by the passive elasticity of muscular tissues, the viscoelastic properties of the fibrillary proteins cont ained within for each one muscle fibre and by the spry (though non 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 master(prenominal)taining 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 alte ration in the involuntary contraction in a muscle. The chief(prenominal) tract restricting the spinal reflex activity is the abaxial reticulospinal tract that runs along the lateral spino thalamic tract. It arises from the ventero medial reticular formation which has less facilitatorty reckon oer the cortical motor areas, in that respectby augmenting the inhibitory drive. The main excitatory pathway also arising in the brainstem is the medial reticulo spinal tract. handicap to these tracts give rise to a net loss of in hibitory simplicity leading to increase alpha motor neurone excitability at the segmental cord level and subsequent increase in muscle tone. some(prenominal) studies also cl admit that peripheral neuronic 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). two the components help in retaining normal muscle tone. habitual tone is the slight amount of constant tension in the goodish muscles offering small opposite 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. activating 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. short contraction results in decreased muscle tone due to lacking(p) development of tension (Grabowski and Tortora 2003). Through the phasic and tonic stretch reflexes the muscle spike plays an important role in regulating the muscle tone (Cameron-Tucker 1983). These muscle spindles can be adjusted in terms of their response to stretchiness.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 liberate 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. receivable to the loss of this inhibition inappropriate muscle co-contraction occur disabling voluntary limb movement (Bhakta 2000).The course of development of both(prenominal) cerebral and spinal spasticity af ter 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 in the midst of the injury and way of spasticity whitethorn 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 glide path is required for the stiff management of spasticity taking into consideration other variables that major power affect treatment outcome. Aim of treatment should include pr howevertion of irregular limb or trunk posture and fa cilitation of movement in the mise en scene of functional activities (Bhakta 2000).Secondary to the neural changes in that respect are dramatic changes of the morphological and mechanical properties of the spastic muscle. A review conducted by Jared et al. concluded that the pursuance changes occur in a spastic muscle a) alteration of the coat of muscle fibre and the type of fibre distribution b) morphologically and biomechanically calculated in that location is proliferation of extracellular matrix material c) increased stiffness in the spastic cell muscle d) compared to the normal muscle in that respect is low 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 comment (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, reach has been intensively utilise as it is safe, economical and convenient (Tsai, KUEN-HORNG et al. 2001). reach is the process of applying tension to the soft tissue structures like muscle, tendon, and vascular, dermal, connective, neural tissues for elongation. stint can be applied mechanically (example- with dynamometer or an wakeless feedback control contrivance) offering well controlled intervention and manually, which is difficult to standardise but represents clinical practice better. Stretching changes the viscoelastic, structural and excitatory airplane propeller of the muscle. (Nielsen et al. 2007). so far many neural as well as non neural berth of reaching 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 do fleck implementing stretching as an intervention. The amount of tension, the eon of the stretch, the velocity of stretch, the number of repeating can all be vary.LITERATURE REVIEWA demand was through by Harvey et al. in the year 2000 on the Effects Of intravenous feeding Weeks Of Daily Stretching On Ankle Mobility In Patients With Spinal corduroy Injuries. 14 recently injured subjects with paraplegia and quadriplegia were taken from two spinal injury units in Sydney, Australia. Their mortise joint was stretched into dorsiflexion, continuously for 30 proceedings with a tortuousness of 7.5 Nm for every calendar weekday, for 4 consecutive weeks. The main outcome bank none was measuring the crookedness angle in knee flexed and extended position. Measurements were taken pre- seek and post test. Post test notements were also taken thrice I,e, during the guide (2nd week), just after the scan (4th week) and one week after the study (5th week). I ntervention was apt(p) by a custom made stretching device that is able to give articulatio talocruralis stretch. The baselines of all the subjects were same. The result showed that even after stretching for a longer time than usual in that respect was no significant difference in the post test apprise in any of the three parameters from pre test. Hence the study concluded that there is no significant change in ankle mobility after 30 proceedings 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 academic 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) muscl es 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 human face 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 strain size was too smal l. The age of the effected patients varied from 33 till 79 years which is a very ample 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 quiet stretch with cyclic stretching on ankle joint stiffness, tortuosity relaxation and gait in stroke patients. 10 community ingleside 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 crookednesss and the angles also. originally and after treatment the time taken to walk 10 m was taken and stiffness of the ankle joint w as calculated from the slope of the crookedness 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 value 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 cant 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 d one hence there may be a chance of macrocosm bias from the assessor. The baselines of both the groups were not similar.A study by Yeh et al. (2005) compared the effectuality 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 employ 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 stud y was appropriate and the analysis of the data leading to the result was done well. the study also mention about the future compass 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 BovendEerdt 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, net 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 stretchin g was given. The review concludes as there is not much grounds 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 muscletendon 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 opposite torque, index of hysteresis and stiffness were evaluated pre- and post-intervention. Length of Achilles tendon was measured with ultrasonography. The force take of the triceps surae muscles was given in torqueangle relationship, by stimulating the calf muscles at a definite intensity across various ankle positions. The device used for intervention was an ankle stretching device wi th good 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 afflicted 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 muscletendon level, calf muscle force output improved. The study provided evidence of improvement in muscle tendon properties through stretching intervention. asunder from the small sample size the study was well written and the methodology was well described.DISCUSSIONSpasticity is a disabling and often painful set that occur secondary to the UMN lesion that leads to hypertonicit y, 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 in concert 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, poultice 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 rase 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.CONCLUSIONThe 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 .TOTAL WORD COUNT IS 2978.