WHOM is doing the same research in stroke? With NO leadership nothing will ever be done on spasticity.
Of course the infamous Dr. William M. Landau thinks spasticity is not worth treating.
Do you believe in the do nothingism of Dr. William M. Landau on spasticity?
His statement from here:
Spasticity After Stroke: Why Bother? Aug. 2004
Wonder if he will be singing the same tune after he becomes the 1 in 4 per WHO that has a stroke, will he be satisfied with not getting recovered due to his spasticity?
The latest here:
Evidence of treating spasticity before it develops: a systematic review of spasticity outcomes in acute spinal cord injury interventional trials
Abstract
Introduction:
Spasticity is a common consequence of spinal cord injury (SCI), estimated to affect up to 93% of people living with SCI in the community. Problematic spasticity affects around 35% people with SCI spasticity. The early period after injury is believed to be the most opportune time for neural plasticity after SCI. We hypothesize that clinical interventions in the early period could reduce the incidence of spasticity. To address this, we evaluated the spasticity outcomes of clinical trials with interventions early after SCI.Methods: We performed a systematic review of the literature between January 2000 and May 2021 to identify control trials, in humans and animals, that were performed early after SCI that included measures of spasticity in accordance with PRISMA guidelines.Results: Our search yielded 1,463 records of which we reviewed 852 abstracts and included 8 human trial peer-reviewed publications and 9 animal studies. The 9 animal trials largely supported the hypothesis that early intervention can reduce spasticity, including evidence from electrophysiological, behavioral, and histologic measures. Of the 8 human trials, only one study measured spasticity as a primary outcome with a sample size sufficient to test the hypothesis. In this study, neuromodulation of the spinal cord using electric stimulation of the common peroneal nerve reduced spasticity in the lower extremities compared to controls.
Conclusion:
Given the prevalence of problematic spasticity, there is surprisingly little research being performed in the early period of SCI that includes spasticity measures, and even fewer studies that directly address spasticity. More research on the potential for early interventions to mitigate spasticity is needed.
Introduction
Spasticity is a common consequence of spinal cord injury (SCI) and is estimated to affect around 65% of patients with SCI discharged from acute rehabilitation and up to 93% of people living in the community.1,2 Spasticity has been defined as a sensorimotor control disorder resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activations of muscles, and resulting in a number of impairments including hyperreflexia, hypertonia, dyssynergia, and clonus, to name a few.3 Problematic spasticity, defined as one that either limits function and/or requires antispasticity medications, has been estimated to affect around 35% of people living with SCI in the chronic stage, with 11–14% considered as moderate to severe problematic spasticity.1,4,5
Spasticity after an acute SCI develops gradually. There is usually an initial phase of areflexia following an acute SCI with flaccid tone below the level of injury.6 This period is known as spinal shock.6,7 This phase may last from days to weeks and sometimes even months.6,7 As a patient starts emerging from spinal shock, various reflexes return.6,7 Incomplete injuries with spared sensation and motor activity below the level of injury are prone to develop severe spasticity.1 Following the return of reflexes, various pathophysiological changes result in hyperreflexia, spasms, and clonus.8 In a recent retrospective study, emergence of spasticity in the first month after SCI was found to be associated with significantly decreased mobility and function.9 Poorly treated spasticity interferes with activities of daily living, transfers, gait, and quality of sleep and can cause joint contractures, skin breakdown, and ultimately decreases the potential of neurologic recovery.2,7
Despite the potentially negative impact of spasticity, clinicians are left to treat spasticity after it has developed, rather than implementing preventive strategies. Although there are anecdotal spasticity management successes, overall treatment options are suboptimal based on systematic reviews. Beginning with physiotherapy and pharmacologic interventions, as is often the initial treatment, there is no high-quality evidence to support either to decrease spasticity.10,11 Next steps in management often involve chemodenervation for treatment of limb spasticity, which has shown some evidence for reduction of spasticity, without improvement in function.12 Intrathecal baclofen showed a significant effect in reducing spasticity and improving activity performance, but there are risks of surgical complications, infections, pump failure, and life-threatening mismanagement.11,13 Even some of the latest advances, like robot-assisted gait training in SCI, have not shown clinically meaningful reductions in spasticity in a meta-analysis.14 Finally, barriers to treatment exist, including inadequate funding, lack of access to providers skilled at managing spasticity, and limited access to treatment options such as intrathecal baclofen pumps, alcohol/ phenol neurolysis, and botulinum toxin injections.15 Thus, treatment of spasticity after it has developed has not been an overall successful approach.
The objective of this systematic review is to identify control trials, in humans and animals, that were performed during the acute phase of SCI that may have an impact on mitigating the development of spasticity in SCI.
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