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The Adverse Effect of Spasticity on 3-Month Poststroke Outcome Using a Population-Based Model

DOI: 10.1155/2014/696089

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Several devices and medications have been used to address poststroke spasticity. Yet, spasticity’s impact on outcomes remains controversial. Using data from a cohort of 460 ischemic stroke patients, we previously published a validated multivariable regression model for predicting 3-month modified Rankin Score (mRS) as an indicator of functional outcome. Here, we tested whether including spasticity improved model fit and estimated the effect spasticity had on the outcome. Spasticity was defined by a positive response to the question “Did you have spasticity following your stroke?” on direct interview at 3 months from stroke onset. Patients who had expired by 90 days or did not have spasticity data available were excluded. Spasticity affected the 3-month functional status ( , to 0.645) after accounting for age, diabetes, leukoaraiosis, and retrospective NIHSS. Using spasticity as a covariable, the model’s changed from 0.599 to 0.622. In our model, the presence of spasticity in the cohort was associated with a worsened 3-month mRS by an average of 0.4 after adjusting for known covariables. This significant adverse effect on functional outcomes adds predictive value beyond previously established factors. 1. Introduction Spasticity is defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. The definition, however, fails to describe the complex etiologies of spasticity, especially after a stroke. It can be due to a loss of upper motor neuron function, changes in the properties of the muscle membranes, augmentation of prior reflexes, or a combination of the above. Equally unclear is spasticity’s effect on poststroke recovery. There are some reports which suggest adverse effects on recovery. In a longitudinal study of 95 subjects, Sommerfeld et al. found that, at 3-month poststroke, patients without spasticity had statistically significant better motor and activity scores than patients with spasticity [1]. However, there are others who argue that spasticity’s effects are being overstated, specifically by mentioning the absence of evidence to suggest that treatment of spasticity improves stroke recovery [2]. In fact multiple medications and treatments of spasticity have been developed and are used routinely in the clinical setting for poststroke spasticity. The literature describes improvements in passive function only and reduction in disability after botulinum toxin administration to spastic muscles [3–5]. In their approval of


[1]  D. K. Sommerfeld, E. U. Eek, A. Svensson, L. W. Holmqvist, and M. H. Von Arbin, “Spasticity after Stroke: its Occurrence and Association with Motor Impairments and Activity Limitations,” Stroke, vol. 35, no. 1, pp. 134–139, 2004.
[2]  W. M. Landau, “Clinical Neuromythology XIV. There you go again: the steadfast fad of fixing spasticity,” Neurology, vol. 45, pp. 2295–2296, 1995.
[3]  A. Welmer, M. von Arbin, L. W. Holmqvist, and D. K. Sommerfeld, “Spasticity and its association with functioning and health-related quality of life 18 months after stroke,” Cerebrovascular Diseases, vol. 21, no. 4, pp. 247–253, 2006.
[4]  B. B. Bhakta, J. A. Cozens, M. A. Chamberlain, and J. M. Bamford, “Impact of botulinum toxin type A on disability and carer burden due to arm spasticity after stroke: a randomised double blind placebo controlled trial,” Journal of Neurology, Neurosurgery & Psychiatry, vol. 69, no. 2, pp. 217–221, 2000.
[5]  A. Brashear, M. F. Gordon, E. Elovic, et al., “Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke,” The New England Journal of Medicine, vol. 347, no. 6, pp. 395–400, 2002.
[6]  FDA Approved Label,
[7]  B. Kissela, C. J. Lindsell, D. Kleindorfer et al., “Clinical prediction of functional outcome after ischemic stroke the surprising importance of periventricular white matter disease and race,” Stroke, vol. 40, no. 2, pp. 530–536, 2009.
[8]  J. Broderick, T. Brott, R. Kothari et al., “The Greater Cincinnati/Northern Kentucky Stroke Study: preliminary first-ever and total incidence rates of stroke among blacks,” Stroke, vol. 29, no. 2, pp. 415–421, 1998.
[9]  L. S. Williams, E. Y. Yilmaz, and A. M. Lopez-Yunez, “Retrospective assessment of initial stroke severity with the NIH stroke scale,” Stroke, vol. 31, no. 4, pp. 858–862, 2000.
[10]  B. Kissela, A. Schneider, D. Kleindorfer et al., “Stroke in a biracial population: the excess burden of stroke among blacks,” Stroke, vol. 35, no. 2, pp. 426–431, 2004.
[11]  C. L. Watkins, M. J. Leathley, J. M. Gregson, A. P. Moore, T. L. Smith, and A. K. Sharma, “Prevalence of spasticity post stroke,” Clinical Rehabilitation, vol. 16, no. 5, pp. 515–522, 2002.
[12]  M. J. Leathley, J. M. Gregson, A. P. Moore, T. L. Smith, A. K. Sharma, and C. L. Watkins, “Predicting spasticity after stroke in those surviving to 12 months,” Clinical Rehabilitation, vol. 18, no. 4, pp. 438–443, 2004.
[13]  R. Moura, M. M. Fukujima, A. S. Aguiar, S. V. Fontes, R. F. B. Dauar, and G. F. do Prado, “Predictive factors for spasticity among ischemic stroke patients,” Arquivos de Neuro-Psiquiatria, vol. 67, no. 4, pp. 1029–1036, 2009.
[14]  P. P. Urban, T. Wolf, M. Uebele et al., “Occurence and clinical predictors of spasticity after ischemic stroke,” Stroke, vol. 41, no. 9, pp. 2016–2020, 2010.
[15]  A. K. Welmer, L. W. Holmqvist, and D. K. Sommerfeld, “Location and severity of spasticity in the first 1-2 weeks and at 3 and 18 months after stroke,” European Journal of Neurology, vol. 17, no. 5, pp. 720–725, 2010.
[16]  E. Lundstr?m, A. Terént, and J. Borg, “Prevalence of disabling spasticity 1 year after first-ever stroke,” European Journal of Neurology, vol. 15, pp. 533–539, 2008.


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