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[WEB SITE] Traumatic Brain Injury Resource Guide – Neuroplasticity


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[BLOG POST] Neuroplasticity After Aquired Brain Injury

By Heidi Reyst, Ph.D., CBIST
Rainbow Rehabilitation Centers

Annually, 1.7 million people incur a traumatic brain injury (TBI); (Faul, Xu, Wald and Coronado; 2010) and over 795,000 people sustain a stroke in the U.S. alone (Roger et al., 2012). Collectively, nearly 2.5 million individuals sustain an acquired brain injury (ABI) annually. The annual incidence rate of TBI from 2002 to 2006 was 579 people per 100,000 (Faul, Xu, Wald and Coronado; 2010). The corresponding annual incidence rate for stroke was 189 persons per 100,000 based on a standardized sampling schema (Kleindorfer et al., 2010). Taken together, the annual incidence rate for TBI and Stroke combined is 768 persons per 100,000. Comparing this number to all cancers combined at 463 persons per 100,000 highlights the significant prevalence of acquired brain injury (Howlader, 2012). See Figure 1. In light of these numbers, it is critical that the processes underlying ABI injury as well as the processes modulating recovery are understood. Only then can treatment and rehabilitation be further refined to enhance recovery.


Figure 1. Number of persons affected per 100,000 (CDC)

Brain injury cascade

When a traumatic brain injury occurs, there are two distinct phases of injury. The first is the primary insult or injury, where the injury etiology is direct mechanical damage. The second is the secondary insult or injury, following mechanical damage, with the etiology being a cascade of pathophysiological processes. Because the “cure” for the primary phase is prevention, research has focused on improvement of the second phase processes in hopes for increasing outcomes post injury (Shlosberg, Benifla, Kaufer and Friedman, 2010). It is also important to note that depending on the mechanism of injury (for example closed versus penetrating injuries, etc.), the process can differ, as it can depending on other factors like age, location of primary injury etc. Figure 2 outlines the general process of the TBI cascade.


Figure 2. Injury cascade

Phase One

In the primary phase, injuries typically include direct tissue damage, impaired cerebral blood flow, and impaired metabolic activity, leading to edema formation and cytoarchitecture changes like membrane permeability (Werner and Engelhard, 2007). There are contact forces which cause contusion, hemorrhage and lacerations throughout, and inertial forces which cause shearing and/or compression of brain tissue (Werner and Engelhard, 2007). These forces cause multifocal injuries (usually termed diffuse axonal injury) affecting axons, blood vessels, junctions between white and gray matter, and other select focal areas like the corpus callosum and junctions between the frontal and parietal lobes (McAllister, 2011). As a result of direct damage, a cascade of pathological processes begins.

Phase Two

After the initial injury, neurons are disrupted resulting in depolarization and then a substantive release of excitatory neurotransmitters (McAllister, 2011; Werner & Engelhard, 2007). This results in release of Ca++ (calcium) and Na+ (sodium) ions, which lead to intracellular breakdowns. This sets in motion the release of caspases and calpains, both of which initiate processes leading to cell death. The release of calpains quickly leads to necrosis where cells die as a response to mechanical or hypoxic damage and metabolic failure. This leads to an inflammatory response with the cells being removed (Werner & Engelhard, 2007; McAllister, 2011). The release of caspases initiates the process of apoptosis (programmed cell death), which can take hours to weeks to progress. Apoptosis, contrary to necrosis, is an active process, whereby initially intact cells cause cell membrane disintegration, disruption of cell transport and ultimately cell death (McAllister, 2011).

Throughout the injury processes, there are other critical factors in the injury process affecting outcome. One is the breakdown of the blood brain barrier (BBB). There can be direct injury to the BBB in the primary phase and in injury to the endothelium of the BBB in the secondary phase. This increases permeability of the blood vessels and results in vascular pathology (Shlosberg, Benifla, Kaufer and Friedman, 2010). Breakdown of the BBB is implicated in the formation of edema (causing fluid accumulation within the brain), excitotoxicity, inflammation, and cell death. When the BBB breaks down, an inflammatory response begins, where injured tissue (and tissue adjacent to it) is eliminated, further impacting functional outcomes (Werner & Engelhard, 2007). While inflammation is generally thought to be primarily maladaptive, it is now known that a limited amount of inflammation plays an essential role for repair after injury (Ziebell and Morganti-Kossmann, 2010).

The processes after stroke are similar to those in TBI. For example, the pathophysiological cascade (secondary phase) after ischemic stroke includes loss of cell homeostasis, calcium ion release, neurotransmitter release, excitotoxicity, disruption of the BBB, reduced cerebral blood flow, inflammation, necrosis, and apoptosis. Thus, after acquired brain injury, both primary and secondary injuries can lead to significant deficits and functional problems for individuals. While researchers attempt to find treatments that ameliorate the secondary injury factors (e.g., progesterone, t-PA, etc.), the main recourse after brain injury is neuroplasticity.

Neuroplasticity and brain function after acquired brain injury

Probably the easiest way to conceptualize neuroplasticity after injury to the brain is to view it simply as re-learning (Plowman and Kleim, 2010; Warraich and Kleim, 2010). As Kleim (2011) noted, “the brain will rely on the same fundamental neurobiological process it used to acquire those behaviors initially. The basic rules governing how neural circuits adapt to encode new behaviors do not change after injury” (p. 522). For example, the changes seen in the motor cortex after brain injury in response to motor re-learning are the same motor changes seen in the motor cortex during development of those motor functions.

While we can view re-establishing function as a re-learning process, there are two conceptual differences when it occurs after a brain injury.

First, because neural circuits for a particular function were previously established during the brain’s neurodevelopmental process, it may be possible to take advantage of those learned behaviors should they persist in residual areas of the brain during the rehabilitation (Kleim, 2011). This presents as a potentially adaptive circumstance.

Second, a more maladaptive consequence which occurs post injury relates to the concept of learned non-use. Just as increasing dexterity of motor function leads to increased motor cortex representation of neural circuitry (and therefore improved function), non-use can lead to decreased motor cortex representation, and therefore decreased function (Plowman and Kleim, 2010). Post stroke, research indicates that learned non-use of a paretic limb, combined with an increased reliance on the unaffected limb can result in major brain reorganization.

Learned non-use

This occurs when, post stroke, a paretic limb is not used due to the infarct affecting the area of the primary motor area (M1) controlling that limb. Consequently, the individual relies heavily on the intact (unaffected) limb. Holding to the maxim of “use it or lose it,” in the acute phase after stroke, if the affected limb goes unused, the motor map size decreases (see previous article titled Neuroplasticity in the intact brain). At the same time, the unaffected limb is substantially utilized, and the motor map for that area increases in size. Thus, experience (or lack thereof) impacts the cortical representations of M1 during the stage of spontaneous recovery, but learned non-use in particular may also be implicated in a more nefarious manner, as it may be a contributing factor to interhemispheric imbalance (Takeuchi & Izumi, 2012).

Interhemispheric imbalance

Studies have found that in the affected hemisphere where the infarct or lesion occurred (termed the ipsilesional hemisphere) there is decreased excitability leading to a reduction in the likelihood of neurons generating an action potential (which is the precipitant in neuron-to-neuron ‘firing’). The overall result of decreased excitability is a reduction in neuronal communications within that hemisphere. On the contrary, in the unaffected hemisphere (termed the contralesional hemisphere) there is increased excitability. Studies have shown that the over-excitability of the unaffected hemisphere inhibits the excitability of the affected hemisphere, resulting in decreased motor functioning (Corti et al., 2011). Learned non-use has been theorized as a contributing factor in interhemispheric imbalance additionally by the attenuated neuronal activity in the affected hemisphere, coupled with the greatly increased use of the intact limb driving neuronal activity higher in the unaffected hemisphere (Takeuchi & Izumi, 2012). Credence is given to this idea, in that research has shown that if the unaffected hemisphere is artificially inhibited, this leads to excitability of the affected hemisphere, impacting motor movements positively (Pascual-Leone, Amedi, Fregni & Merabet, 2005).

As noted above, there is substantial biological change to the brain after focal injury (e.g., stroke) and diffuse injury (e.g., TBI). The effect of this biological change is profound. There can be damage to the tissue directly, due to the loss of oxygen resulting from a stroke, or due to inert forces like in a traumatic injury. In addition to these direct effects, additional, and potentially equally damaging biological changes occur at sites of the brain both distant and close to the lesioned areas. This includes the inflammatory process, attenuated blood flow, changes to metabolic processes, edema, and neuronal excitability (Kleim, 2011). These cascade processes result in disruption to intact areas of the brain particularly those areas with connectivity to the injured regions, and has been termed diaschisis.

Diaschisis is in essence a disturbance or loss of function in one part of the brain due to a localized injury in another part of the brain, and these areas can be of considerable distance from the lesioned area including the opposite hemisphere (Stein, 2012). One effect post stroke that affects function within the brain considerably is hyper-excitability in the opposite hemisphere. This, coupled with under-excitability in the damaged hemisphere results overall in a disrupted neural network (Pascual-Leone, Amedi, Fregni and Merabet, 2005). Research has shown that these changes can occur up to 12 months after the initial injury (Cramer and Riley, 2008). With the likelihood of widespread neural dysfunction after injury, what then are the mechanisms for recovery?

Mechanisms of recovery

After injury to the brain, there are two mechanisms whereby functional improvement may occur. These are recovery and compensation (Kleim, 2007). Using World Health Organization definitions,

Recovery relates to:

  1. Restoration of neural tissue initially perturbed after the injury (neural level)
  2. Restoration of movement exactly as it was performed prior (behavioral level)
  3. Restoration of activity exactly as it was performed prior (activity level)

Compensation refers to:

  1. Recruitment of new neural circuits (neural level)
  2. Training of new movement sequences (behavioral level)
  3. Training of activity in a new way after injury (activity level)

Recovery therefore relates to lost functions being restored, and compensation relates to the acquisition of new functions or behaviors to replace those lost after injury (Kleim, 2011). Research has shown that after a stroke, for motor deficits, notable recovery takes place within 30 days for mild, moderate, and moderate-severe severity with additional recovery up to 90 days for severe strokes (Duncan, P., Goldstein, L., Matchar, D., Divine, G. and Feussner, J., 1992). These times frames are similar with other areas of dysfunction where the final level of language function was achieved within six weeks post stroke for 95% of patients (with mild, moderate and severe aphasia; Pedersen, Jorgenson, Nakayama, Raaschou and Olsen, 1995). The level of recovery from spatial neglect was maximized within nine weeks (Hier, Mondlock and Caplan, 1983, cited in Cramer and Riley, 2008). With these types of findings, what is the neurobiological explanation of these changes early on post-injury?

Neurobiological plasticity changes during recovery

Figure 3 displays a model that incorporates a two-stage process of recovery, and within those two stages, provides the neural strategies utilized within the central nervous system.

The first stage is Spontaneous Recovery, and the second stage is Training Induced Recovery (Chen, Epstein and Stern, 2010). Depending on the stage of recovery, different neural mechanisms are at work to either initiate recovery strategies or in response to changes in experience in the form of training or rehabilitation. Each aspect of the model is described below.


Figure 3. Two-stage model of recovery with corresponding neurological strategies and recovery vs. compensation distinctions.

STAGE ONE: Spontaneous Recovery

With spontaneous recovery, even in the absence of training or rehabilitation, there is resolution of injury and functional change in close time proximity after injury which plateaus within three months for focal injury and six months for diffuse injury (Chen, Epstein and Stern, 2010). Within that time frame three processes have been theorized to explain this early recovery after injury when specific intervention has not ensued (Dancause and Nudo; 2011). They are:

  1. Diaschisis reversal
  2. Changes in kinematics.
  3. Cortical reorganization.

Diaschisis Reversal

Diaschisis as previously described begins to resolve, whereby the inflammatory process, blood flow changes, metabolic changes, edema, and neuronal excitability begin to subside (Warraich and Kleim, 2010). The result of diaschisis reversal is improved function due to intact brain areas that were previously disrupted now being restored. Restoration is therefore a crucial neural strategy after injury. From a purely neurobiological level, this may be thought of as the only true level of recovery in the strictest sense of the word, in that the same brain circuits are facilitating function post injury as they were pre injury. Restoration has been found in both cognitive (e.g., language and attention) and physical (e.g., motor movement) domains (Kleim, 2011).

Changes in Kinematics

The second aspect of early recovery relates to changes in kinematic (movement) patterns where compensatory patterns are utilized. The individual intrinsically begins to complete motor movements in a different manner, resulting in improved function, sometimes in drastically different ways than prior to injury. While these new movements likely contribute to functional improvement, these compensatory strategies have the potential to be maladaptive.

Cortical Reorganization

The third strategy identified as spontaneous recovery is that the nervous system undergoes within-area and between-area reorganization or rewiring. For example, many researchers have found elements of neuroplasticity near the infarct area after stroke, including cortical reorganization, neurogenesis, axonal sprouting, dendritic plasticity, new blood vessel formation (Kerr, Cheng and Jones, 2011), as well as excitability changes (Nudo, 2011). Chen, Epstein and Stern (2010) outlined neural shifts in recruitment of brain areas in the spontaneous recovery period. Soon after stroke, in homologus (similar) areas, the opposite side of the brain is recruited. Later on during spontaneous recovery, there is a shift in activation back to the injury side. An example would be if the left-sided language area (Broca’s area) was damaged, the right-sided equivalent Broca’s area would be recruited. After a period of time, it would then shift back to the left side.

Another key change in brain function relates to activation of learning networks in the early phase, where plasticity similar to when the brain was developing is induced. This includes motor control and task-learning networks (Chen, Epstein and Stern, 2010).

Overall, cortical reorganization during spontaneous recovery is thought to be compensatory as different circuits or networks of neurons are utilized post injury than those utilized pre injury. While spontaneous recovery occurs in the absence of rehabilitation, there is certainly the opportunity for overlap of training induced recovery while spontaneous recovery takes its course.

STAGE TWO: Training-induced recovery

Training in the form of rehabilitation can induce plasticity post injury, but is not necessarily time limited like spontaneous recovery processes demonstrate (Chen, Epstein and Stern, 2010). Recovery in this stage involves compensation, in that either new brain areas or neural networks are enlisted to complete previous functions. Through the process of training, neuroplasticity is induced. Chen, Epstein and Stern (2010) note that adaptive changes after injury are the outcome of new patterns of activation which include plasticity in areas surrounding the damaged cortex, reorganization of existing networks or recruitment of new cortical areas or networks.


During training-induced recovery, areas which did not make a significant contribution to that particular function pre-injury now contribute to function post-injury (Kleim, 2011). Often times this may be in the form of recruitment of neural areas from the undamaged hemisphere. From a physical perspective, this may include changes in motor maps where the non-injured hemisphere motor cortex can play a distinct role in producing motor movements in an impaired limb, which was previously controlled by the injured motor cortex. From a cognitive perspective, neural recruitment may entail the enlistment of the right side homologue (similar) to Broca’s area to improve language function if Broca’s area (left frontal lobe) is damaged. Rehabilitation to induce such changes may involve constraint induced manual therapy or completion of cognitive tasks while using complex hand movements in the opposite hemisphere which promotes a shift to the uninjured hemisphere.


Retraining involves the training of residual brain areas, resulting in reorganization within the cortex and compensation for lost function (Kleim, 2007). This often comes in the forms of reorganization within the damaged hemisphere. In the case of motor function, if tissue is lost which controlled finger movements, other cortical tissue nearby can reorganize to control that lost movement.

Ultimately, recruitment and retraining involve rewiring or reorganization of neural networks. What then are the properties of the brain which, after injury, provide the mechanisms for recovery? Two basic properties provide us the answer:

The first is that our brains have a tremendous amount of redundancy. There is internal redundancy in areas like the primary visual cortex, the somatosensory areas, the primary auditory cortex and the primary motor cortex (Warraich and Kleim, 2010). So within primary cortex areas there may be multiple areas that respond to the same or similar stimuli. External redundancy refers to similar functionality being processed across different areas of the brain (Warraich and Kleim, 2010). Both of these redundancies allow for better information integration, but they also provide a pathway to improved function after brain injury.

The second property relates to a concept discussed in the previous article; that of experience dependent plasticity. This is where changes in behavior or experience result in changes at a neurobiological level.

Neurobiological Changes after Acquired Brain Injury

After injury to the brain, the processes of neuroplasticity are thought to be the underpinnings of recovery (Carmichael, 2010). To begin, research has found a variety of neuroplastic changes which occur after injury, including:

  1. Increases or changes to synapses:
    • This includes synaptogenesis and synaptic plasticity (Chen, Epstein and Stern; 2010; Nudo, 2011)• Dendrite changes including increased arborization, dendritic growth and spine growth (Nudo, 2011)• Axonal changes including axonal sprouting (Nudo, 2011; Charmichael, 2010)
  2. Increased neuron growth:
    • Neurogenesis in specific brain areas like the hippocampus subgranular zone of the dentate gyrus and subventricular zone in some areas (Schoch, Madathil and Saatman, 2012), substantia nigra and perinfarcted areas (Font, Arboix & Krupinski, 2010).
  3. Angiogenesis
    • Angiogenesis is the process through which new blood vessels form from pre-existing vessels.
  4. Excitability changes:
    • Excitability refers to the ability of a neuron to generate action potentials, which is a short-term change in the electrical potential on the surface of a cell. It is an all or nothing proposition as it either fires or does not fire depending on the strength of the potential.

The first two items on the list above relate to increases in either the number of neurons (this occurs in a very limited sense) or the numbers of synapses or increased strength of existing synapses (this far more prevalent). These changes seen post injury mirror changes seen in the intact brain in the form of experience dependent learning. But instead of it being a learning process, it is a relearning process, aided substantially by rehabilitation.

With experience dependent learning, new synapses form (synaptogenesis) or strengthen through changes in dendrites (new dendritic spine formation), axonal sprouting and long term potentiation (synaptic plasticity). Both synaptogenesis and synaptic plasticity are the main underpinnings of cortical reorganization, recruitment and retraining as identified in Mechanisms of Recovery above. For a general overview of experience dependent learning see the side bar on page 35. For a detailed overview of both synaptogenesis and synaptic plasticity, see the previous article titled Neuroplasticity in the Intact Brain: Experience-Dependent Learning and Neurobiological Substrates.

The third and fourth items on the list relate to changes in excitability homeostasis within the brain (electrophysiological balance across the two hemispheres) and new blood vessel formation. These are described further in the next section.


Figure 4. Dendritic Arbor Expansion and Retraction.

Findings Related to Neurobiological Changes

Synaptic, Dendritic and Axonal Related Changes

Perederiy and Westbrook (2013) reported post injury that researchers found when an area of the brain stops receiving inputs from the body via afferent nerves, the dendritic arbor retracts (Figure 4). This results in the loss of synapses with other neurons. On the other hand they also reported that in areas of the brain not affected after injury, dendritic arbors increased (Figure 4). This former finding indicates a maladaptive response after injury, while the latter finding reflects the brain’s response post injury to increase synapses in intact areas, thereby providing cortical reorganization or rewiring, which is an adaptive response.

Axonal sprouting and reorganization occurs post injury. This sprouting has adaptive consequences in that increased axonal growth leads to greater levels of synapses allowing reinnervation (Perederiy & Westbrook, 2013). Re-innervation can then lead to adaptive changes. However, there are issues with axonal regeneration in that glial scars can prevent axons from reaching their target, and for patients with temporal lobe epilepsy, specific axonal sprouts can synapse onto granule cells which may relate to the recurrence of seizures (Perederiy & Westbrook, 2013).

Research has found that there may be changes within the damaged hemisphere. For example in motor areas, topographical map changes occur, where different areas controlling motor movements compensate for the damaged areas. The neurobiological foundation of motor map changes is synaptic change. This includes synaptogenesis where new synapses form through dendritic growth and axonal sprouting, and synaptic plasticity which strengthens existing synapses through the process of long-term potentiation (see previous article for a description).

Nudo, Wise, SiFuentes and Milliken (1996) mapped the motor areas of monkeys to determine the areas of the brain which controlled hand motor movements. After training on a skilled-hand task, infarcts were induced in the monkey’s mapped motor area. The monkeys were then retrained on the same skilled task. Initially, the monkeys demonstrated significant deficits on the skilled-hand task. After retraining, however, their skills substantially improved, and this related to significant changes to their motor maps. Specifically the hand and digit areas increased significantly during spontaneous recovery between the injured monkeys and a control group. In addition, for monkeys who received re-training, there was no loss of spared hand motor map in nearby intact areas, suggesting that therapy prevented further loss of hand areas representation.


Angiogenesis is the process through which new blood vessels form from pre-existing vessels. In ischemic stroke, which is loss of blood flow leading to neuronal death, increased vasculature relates to increase circulation (Font, Arboix, Krupinski, 2010). The benefit is return of blood flow to previously damaged areas, which is assists in establishing metabolic support (Krum, Mani, & Rosenstein, 2008).

In a review assessing research on neurovascular response after stroke, Arai, Jin, Navaratna & Lo (2009) examined the role of angiogenesis. The authors distinguish injury in the acute phase where neurovascular damage causes the primary disruption of the blood brain barrier. After stroke, it is now widely held that the penumbra (which is an area around the infarct affected by vascular compromise) is more than just dying cells – it may be a precursor of neuroplasticity. In the delayed phase after acute stroke, angiogenesis and neurogenesis, which are closely tied together, are primary responses post stroke. One cytokine of note relating to angiogenesis is vascular endothelial growth factor (VEGF), which in its endogenous form relates to brain neuroprotection. Krum, Mani and Rosenstein (2008), found that VEGF is an important factor in post-injury recovery. In particular, by blocking VEGF receptors, preventing them from upregulating, they found that vascular proliferation was decreased. By blocking VEGF, and showing a clear decrease in positive vascular changes, they were able to isolate its effect – vascular remodeling (i.e., angiogenesis).

Changes to Network Organization

While reorganization of neural networks has been found post injury, the amount of reorganization depends on the size of the injured area. For example, with areas of smaller damage, reorganization tends to occur close to the injury area. For larger areas of damage, reorganization or recruitment is more widespread to other areas of the brain (Chen, Epstein and Stern; 2010).

Schlaug, Marchina and Norton (2009), using melodic intonation therapy to treat aphasia found that after intensive treatment, significant white matter changes occurred. In particular, through use of diffusion tensor imaging (which detects functionality of white matter tracts) they found increases in the right arcuate fasiculus, which is a white matter tract connecting Wernicke’s area and Broca’s area. Key to this finding is that the right arcuate fasiculus is not typically well developed, indicating that the right hemisphere reorganized to improve function. Another important factor in this finding is that increases in the number of fibers in the arcuate fasiculus correlated with measurable improvement in conversational skills.

Activation and Excitatory Changes

After injury, changes in the excitability of the damaged and intact hemispheres can impact cortical functioning. Excitatory changes across hemispheres can occur quickly after brain injury, where cortical excitability in the affected areas is generally decreased. A model of interhemispheric rivalry has been suggested, where there are distinct differences in the excitability of analogous areas between hemispheres (e.g., motor areas). For example in the damaged hemisphere there is hyperpolarization (inhibition of neurons) and in the intact hemisphere there is depolarization (excitation of neurons; Bolognini, Pascual-Leone & Fregni, 2009). Calautti & Baron (2003) reported that in the chronic phase after stroke, researchers found that better recovery was found if activation of the affected-side is more predominant than the unaffected hemisphere over time. This shift of activation to the unaffected side is “the sign of a distressed system” (Cramer et al., 2011, p. 1593). So from a long term perspective if the damaged side was more involved in function, that related to better outcomes. However, if the patient had to rely on the unaffected side more for function, that related to poorer outcomes.

In a study on memory and attention deficits after damage to the prefrontal cortex (PFC) by Voytek, Davis, Yago, Barcelo, Vogel and Knight (2010) they found evidence that the PFC in the undamaged hemisphere compensates for the damaged PFC areas in the opposite hemisphere “on a trial by trial basis dependent on cognitive load” (p. 401). In other words, the undamaged hemisphere dynamically compensates for the damaged hemisphere depending on the level of challenge the damaged hemisphere must deal with. This demonstrates that the intact hemisphere can adapt rapidly and that it is not an all or nothing proposition, where function is relegated to either the intact or damaged hemisphere post injury.

Collectively, this research highlights processes post injury which are similar to those neuroplastic changes in the intact brain. Namely, that when experience in the form of changes to nerve inputs or motor outputs occurs, cortical changes like those of experience dependent learning occurs where synaptogenesis, synaptic plasticity, and axonal sprouting take place. Furthermore, after injury, through aspects of the injury cascade, certain adaptive processes initiate, resulting in changes like angiogenesis, and network reorganization changes. Neuroplasticity is a remarkable tool in our cortical toolbox. And, like many other adaptive tools, it too can have maladaptive consequences.

The maladaptive side of neuroplasticity

While there is huge upside to neuroplasticity, we cannot afford to overlook the downside. While beyond the scope of this article to go into any depth there are plenty of examples to point out that neuroplasticity has its dark side, too. Just a few examples include addictions to alcohol, elicit substances or prescription drugs, pornography addictions (Doidge, 2007), seizure disorders post injury (Cramer et al., 2011), phantom limb pain (Doidge, 2007), hand dystonias in musicians (Candia, Rosset-LLobet, Elbert and Pascual-Leone, 2005), learning and memory interference (Carmichael, 2010) and chronic pain (Cramer et al., 2011). Thus, while we search for adaptive examples of neuroplasticity and ways to promote it both in the intact brain and after injury, we must also seek to prevent these brain changes which can have profound impacts on function, not to mention societal implications.

Final thoughts


Figure 5. Synapses

In an article put together by 27 leading neuroscientists from the National Institutes of Health Blueprint for Neuroscience Research (Cramer et al., 2011), they noted that “[n]europlasticity occurs with many variations, in many forms, and in many contexts” (p. 1952). This reminds us that brain injury in all of its forms is quite heterogeneous. The host of variables which affect outcomes after acquired injury are vast and varied (e.g., age, lesion area, pre-injury characteristics, genetic profile, etc.).

Yet with all of this heterogeneity, there are similar neuroplastic processes after injury. Cramer et al. (2011) write that “common themes in plasticity that emerge across diverse central nervous system conditions include experience dependence, time sensitivity and the importance of motivation and attention” (p. 1952). Thus it is important that neuroscience and its practitioners continue to identify at the key factors which contribute to neuroplastic changes be it at the molecular, cellular, architectural, behavioral or network level.


As we better understand the neurobiological level of neuroplasticity, we can then begin to better understand how to harness treatments that enhance the recovery process and ultimately patient function. There is currently a tremendous amount of research addressing neuroplasticity at both a basic and applied level. Both are needed to continue to learn more about effective treatments. Some are pharmacologic and focus on drugs or molecules that may impact the secondary phase of injury, or that “prime” the central nervous system in preparation of traditional neurorehabilitation in the form of occupational therapy, physical therapy, and speech & language pathology. Such priming includes non-invasive brain stimulation (e.g., transcranial magnetic stimulation, transcranial direct simulation), deep brain stimulation, and neuropharmacology. Others focus on the timing of rehabilitation efforts, in order to maximize plastic states where the opportunity for recovery is at its highest. Still others focus on the principles of Hebbian learning wherein understanding how experience shapes the brain can best be utilized in any form of treatment.

In closing, neuroplasticity is not an idea, it is a state. This state exists from our earliest years of neurodevelopment (prenatal and postnatal), to our ongoing changing brains as a result of experience, to changes after injuries to our most precious resource, our brain. Our transformative experiences shape and mold our neurochemicals, axons, dendritic arbors and spines, motor maps, cortical networks—in other words, our very essence. And likewise, when our very essence is transformed via injury, the change to our networks and synapses then shape our experiences. How we can best reclaim those experiences by harnessing neuroplasticity is the focus of an article in the next issue of RainbowVisions® Magazine.

Overview of Experience-Dependent Learning

For neurons or networks of neurons to communicate they need to have extensive connections with one another (or, quite literally hundreds to thousands of connections for each neuron.) These extraordinarily complex connections require junctions or connections termed synapses.

For example, neuron A connects via its axon terminal to neuron B at its dendrite (see Figure 5). The space between the axon and dendrite is the synapse. In a basic sense, the greater the number of synapses, the greater and stronger the connections between neurons. Likewise, the more synapses, dendrites and axons that develop, the greater the opportunity to connect more neurons together and strengthen the existing connections.

As our experiences change, at a neurobiological level, we either increase or decrease the numbers of synapses, dendrites and axons. If we stop a function, we lose synapses, etc., and if we increase an activity we proliferate synapses, etc., resulting in experience-dependent learning.

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Source: Neuroplasticity After Aquired Brain Injury – Rainbow Rehabilitation Centers

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[BOOK] Chapter 9: Neuroscience-Based Rehabilitation for Stroke Patients

The Book: Neuroscience-Based Rehabilitation for Stroke Patients | InTechOpen, Published on: 2017-05-10. Authors: Takayuki Kodama and Hideki Nakano

Chapter 9: Neuroscience-Based Rehabilitation for Stroke Patients


Hitherto, physical therapy for rehabilitating patients with cerebral dysfunction has focused on acquiring and improving compensatory strategies by using the remaining functions; it has been presumed that once neural functions have been lost, they cannot be restored. However, neuroscience-based animal research and neuroimaging research since the 1980s have demonstrated that recovery arises from plastic changes in the central nervous system and reconstruction of neural networks; this research is ushering in a new age of neuroscience-based rehabilitation as a treatment for cerebral dysfunction (such as stroke). In this paper, in regard to mental practices using motor imagery and kinaesthetic illusion, we summarize basic discoveries and theories relating to motor function therapy based on neuroscientific theory; in particular, we outline a novel rehabilitation method using kinaesthetic illusion induced by vibrational stimulus, which the authors are currently attempting in stroke patients.

1. Introduction

Conventional physical therapy (PT) for the rehabilitation of patients with brain dysfunction focuses on the acquisition of function through alternative means by using and improving the patients’ existing functions, and it is based on the assumption that once a neutral function is lost, it can never be recovered [1]. However, animal neuroscience studies [24] that were conducted after the 1980s and neuroimaging studies [5, 6] have shown that recovery can occur as a result of plastic changes in the nervous system or reorganization of the neural network, and rehabilitation (neuroscience-based rehabilitation, NBR) after cerebral dysfunction (e.g. stroke) has reached a new era in treatment. These observations suggest that the plasticity that is observed in patients is related to the characteristic that the more the patient receives therapy in specific parts of their body, the more that the brain areas that control these parts will be functionally as well as anatomically extended.

Functional recovery originally referred to a patient’s recovery from limitations in their behavior, movements, and/or activity [7]. Therefore, the purpose of NBR is not only to induce the reorganization of brain functions through neural plasticity mechanisms but also recover comprehensive bodily motor functions and brain functions for autonomous and active social behavior. What type of treatment strategy is required so that patients feel positively engaged by it, gradually understand its effects, and work toward a goal? Previous studies have revealed important factors in the effects of NBR treatment, such as the amount of therapy [8, 9], rehabilitation implementation environment [10], and performance of neurocognitive rehabilitation [11] through mental practice techniques, such as motor imagery (MI) [12]. Among these factors, treatments involving MI are strongly recommended because MI contributes to the reorganization of neural functions. MI, which is an approach that is based on neuroscientific data and the motor learning theory, is defined as the capacity to internally mimic physical movements without any associated motor output [13]. The cognitive process that occurs during the imagination of movements involves various components, such as mutual understandings between oneself and others (environment), observations of movements, mental manipulations of objects, and psychological time and movement planning. Instead of repeating simple physical movements to receive feedback on outcome in the actual therapy, the practice of voluntary and skill-requiring movements that are geared toward task completion induces the functional recovery [14]. Thus, an important element of the patients’ engagement in the therapy is that it occurs in an active and top-down fashion through the use of MI. However, because MI has a task-specific nature, cognitive functions and memories of motor experiences that equip the patients to perform the task are required. Patients with neurofunctional states that make motor execution (ME) difficulty may suffer not only from impairments in motor-related brain areas but also from modifications in their intracerebral body representations (e.g. somatoparaphrenia) [15, 16]. In such cases, the exploitation of kinaesthetic illusions [1720], which can be induced in the brain by extraneous stimuli, such as vibratory stimulations, becomes important for inputting appropriate motor-sensory information into the brain in a passive and bottom-up fashion. Therefore, the implementation of a mental practice to determine the criteria for adequate treatment according to the states of the patient’s cognitive functions and motor functions is important in order to select and implement the best therapy. Thus, this paper summarizes the basic understanding and theories of mental practices that use MI or kinaesthetic illusion and discusses, in particular, research results concerning kinaesthetic illusions that are induced by vibratory stimulations, which we are currently attempting on stroke patients.

2. What is neuroscience-based rehabilitation?

NBR involves a series of processes that are selected for the intervention according to the current brain function theories that have been revealed by neuroscience and other similar studies and verification of its outcomes. For example, the selection of a NBR strategy for a stroke patient requires a combination of deep clinical reasoning, the experience of the therapist, and a vast understanding of the evidence obtained by studies from wide-ranging academic fields on the factors that support recovery mechanisms and produce particular outcomes. First, the neural basis of brain cell reorganization will be presented.

2.1. Neural basis of brain cell reorganization

The current understanding of neural reorganization after dysfunction is not that the neurons themselves recover after their axons are damaged but rather that damaged functional networks recover due to several processes that induce the recovery of motor and cognitive functions. Cajal [1], who was a proponent of neuron theory, stated that the central nervous system (brain and spinal cord) of adult mammals would not recover once it is damaged. However, studies that have been conducted since the 1980s and that have shown that alterations in the peripheral nervous system, such as denervation and amputation, change somatic sensations and the representations of body parts while they are in motion have revealed that the brain has plasticity. In 1998, Eriksson et al. [21] reported the new formation of neurons in the central nervous system of human beings. These findings raised the question of whether the plastic changes and functional reorganization that occur in subjects with cranial nerve disorders originate from an ischemic state, such as a cerebrovascular disturbance. The underlying mechanisms of the plasticity that occurs after a cortical deficit are thought to involve (i) the redundancy of neuronal connections in the central nervous system, (ii) morphological changes in the neurons, and (iii) changes in synaptic information transmission [22]. If neurons are damaged, astrocytes begin to divide due to the activity of microglia. These glial cells then reinforce the areas that have been damaged by brain lesions and release neurotrophic factors, such as nerve growth factor, to promote neuronal sprouting (it takes around two weeks for synapses to grow after nerve damage [23]). The sprouted neurons are then connected to an existing neural network, which forms a new network. In other words, if neurons are damaged, new neurons begin to reorganize themselves in order to compensate for it. Adequate NBR stimulates the neural network with the neurofunction that is most similar to the predamaged functional state of the neural network, even though the new network is not located in the damaged region. If strong inputs enter the network multiple times, the synaptic connections will be reinforced. However, plasticity will not be induced in synapses with little information (input specificity), and the synapses will be excluded from the network formation [24, 25].

These findings have been confirmed by several famous studies. Nudo et al. [8] caused artificial cerebral infarcts in monkeys in the region of the primary motor cortex (M1) that corresponds to fingers and then forced the monkeys to use fingers with motor deficits. Thus, they reported that the brain region that previously controlled the shoulders and elbows prior to the therapy then controlled the fingers and more distal body parts (Figure 1). Merzenich et al. [26] surgically sutured the fingers of monkeys and then compared the pre- and post-surgical somatotopies of Brodmann area (BA) 3b, which corresponds to the sensorimotor area (SMA). Microelectrodes were used to record the responses in BA3b to finger stimuli. The third and fourth fingers were then surgically sutured, and the responses were recorded again a month later. Thus, the boundary between the third and fourth fingers became unclear. In addition, the results of a study that was conducted in human beings suggested that the plasticity of brain cells depends on sensory input. The results of a magnetoencephalography study that compared the somatotopies of the first and fifth fingers of string players to normal controls showed that a broader cerebral cortical area was activated for string players compared to the controls [6].


Figure 1. Representation of the distal forelimb in cortical area 4 derived from pre- and post-training mapping procedures [8].

These findings suggest that the size of the intracerebral somatotopic representation, which is vital to ME, is determined by the degree of use of the region. If you try to induce plasticity in specific parts of the bodies of stroke patients, as mentioned above, the induction of neural plasticity in a pathway that allows highly efficient information processing by repeating movements in a pattern like the normal pattern should be possible, provided the patient has retained their motor functions to a certain degree. However, if a patient has the functional level of almost not able to perform movement or is only able to perform the movement in an abnormal pattern, the stimulation of the plasticity for the formation of a neural network that is required to be able to regain normal motor function may not be possible. Ward et al. [27] chronologically examined the relationships between motor function recovery scores and task-related brain activities for approximately 12 months after the onset of stroke with functional magnetic resonance imaging. They found a negative correlation between motor function recovery scores and a decline in the hyperactivity of brain areas in the damaged and undamaged hemispheres (M1, premotor cortex; PMC, supplementary motor cortex; SMC, cerebellum). These findings suggest that a better recovery of motor function is associated with better connectivity between the functional systems of multiple brain regions and that a continuous and long-term approach is required to study the changes in the morphologies and networks of neurons. Thus, a qualitative and continuous approach [28] is required in studies of the recovery of the entire neural system (e.g. transcortical network, M1-PMC neural network [29]) in order to be able to perform movement rather than merely establishing quantitative interventions of movement. Thus, next, we will discuss the current understanding of what is required in interventions for stroke patients.[…]

Continue —> Neuroscience-Based Rehabilitation for Stroke Patients | InTechOpen

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[ARTICLE] Neural Plasticity in Moderate to Severe Chronic Stroke Following a Device-Assisted Task-Specific Arm/Hand Intervention – Full Text

Currently, hand rehabilitation following stroke tends to focus on mildly impaired individuals, partially due to the inability for severely impaired subjects to sufficiently use the paretic hand. Device-assisted interventions offer a means to include this more severe population and show promising behavioral results. However, the ability for this population to demonstrate neural plasticity, a crucial factor in functional recovery following effective post-stroke interventions, remains unclear. This study aimed to investigate neural changes related to hand function induced by a device-assisted task-specific intervention in individuals with moderate to severe chronic stroke (upper extremity Fugl-Meyer < 30). We examined functional cortical reorganization related to paretic hand opening and gray matter (GM) structural changes using a multimodal imaging approach. Individuals demonstrated a shift in cortical activity related to hand opening from the contralesional to the ipsilesional hemisphere following the intervention. This was driven by decreased activity in contralesional primary sensorimotor cortex and increased activity in ipsilesional secondary motor cortex. Additionally, subjects displayed increased GM density in ipsilesional primary sensorimotor cortex and decreased GM density in contralesional primary sensorimotor cortex. These findings suggest that despite moderate to severe chronic impairments, post-stroke participants maintain ability to show cortical reorganization and GM structural changes following a device-assisted task-specific arm/hand intervention. These changes are similar as those reported in post-stroke individuals with mild impairment, suggesting that residual neural plasticity in more severely impaired individuals may have the potential to support improved hand function.


Nearly 800,000 people experience a new or recurrent stroke each year in the US (1). Popular therapies, such as constraint-induced movement therapy (CIMT), utilize intense task-specific practice of the affected limb to improve arm/hand function in acute and chronic stroke with mild impairments (2, 3). Neuroimaging results partially attribute the effectiveness of these arm/hand interventions to cortical reorganization in the ipsilesional hemisphere following training in acute and mild chronic stroke (4). Unfortunately, CIMT requires certain remaining functionality in the paretic hand to execute the tasks, and only about 10% of screened patients are eligible (5), thus disqualifying a large population of individuals with moderate to severe impairments. Recently, studies using device-assisted task-specific interventions specifically targeted toward moderate to severe chronic stroke reported positive clinical results (68). However, these studies primarily focus on clinical measures, but it is widely accepted that neural plasticity is a key factor for determining outcome (911). Consequently, it remains unclear whether moderate to severe chronic stroke [upper extremity Fugl-Meyer Assessment (UEFMA) < 30] maintains the ability to demonstrate neural changes following an arm/hand intervention.

Neural changes induced by task-specific training have been investigated widely using animal models (12). For instance, monkeys or rodents trained on a skilled reach-to-grasp task express enlarged representation of the digits of the hand or forelimb in primary motor cortex (M1) following training as measured by intracortical microstimulation (13, 14). Additionally, rapid local structural changes in the form of dendritic growth, axonal sprouting, myelination, and synaptogenesis occur (1518). Importantly, both cortical and structural reorganization corresponds to motor recovery following rehabilitative training in these animals (19, 20).

The functional neural mechanisms underlying effective task-specific arm/hand interventions in acute and chronic stroke subjects with mild impairments support those seen in the animal literature described above. Several variations of task-specific combined arm/hand interventions, including CIMT, bilateral task-specific training, and hand-specific robot-assisted practice, have shown cortical reorganization such as increased sensorimotor activity and enlarged motor maps in the ipsilesional hemisphere related to the paretic arm/hand (2124). These results suggest increased recruitment of residual resources from the ipsilesional hemisphere and/or decreased recruitment of contralesional resources following training. Although the evidence for a pattern of intervention-driven structural changes remains unclear in humans, several groups have shown increases in gray matter (GM) density in sensorimotor cortices (25), along with increases in fractional anisotropy in ipsilesional corticospinal tract (CST) (26) following task-specific training in acute and chronic stroke individuals with mild impairments.

The extensive nature of neural damage in moderate to severe chronic stroke may result in compensatory mechanisms, such as contralesional or secondary motor area recruitment (27). These individuals show increased contralesional activity when moving their paretic arm, which correlates with impairment (28, 29) and may be related to the extent of damage to the ipsilesional CST (30). This suggests that more impaired individuals may increasingly rely on contralesional corticobulbar tracts such as the corticoreticulospinal tract to activate the paretic limb (29). These tracts lack comparable resolution and innervation to the distal parts of the limb, thus sacrificing functionality at the paretic arm/hand (31). Since this population is largely ignored in current arm/hand interventions, it is unknown whether an arm/hand intervention for these more severely impaired post-stroke individuals will increase recruitment of residual ipsilesional corticospinal resources. These ipsilesional CSTs maintain the primary control of hand and finger extensor muscles (32) and are thus crucial for improved hand function. Task-specific training assisted by a device may reengage and strengthen residual ipsilesional corticospinal resources by training distal hand opening together with overall arm use.

The current study seeks to determine whether individuals with moderate to severe chronic stroke maintain the ability to show cortical reorganization and/or structural changes alongside behavioral improvement following a task-specific intervention. We hypothesize that following a device-assisted task-specific intervention, moderate to severe chronic stroke individuals will show similar functional and structural changes as observed in mildly impaired individuals, demonstrated by (i) a shift in cortical activity related to paretic hand opening from the contralesional hemisphere toward the ipsilesional hemisphere and (ii) an increase in GM density in sensorimotor cortices in the ipsilesional hemisphere.[…]

Continue —> Frontiers | Neural Plasticity in Moderate to Severe Chronic Stroke Following a Device-Assisted Task-Specific Arm/Hand Intervention | Neurology

Figure 5. Statistical maps of gray matter (GM) density changes across all patients. Significant increases (red/yellow) and decreases (Blue) in GM density are depicted on sagittal, coronal, and axial sections (left to right) on Montreal Neurological Institute T1 slices. Sections show the maximum effect on (A) ipsilesioned M1/S1, (B) contralesional M1/S1, and (C) ipsilesional thalamus. Les indicates the side of the lesioned hemisphere. Color maps indicate the t values at every voxel. A statistical threshold was set at p < 0.001 uncorrected.

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[VIDEO] Plasticity Brain Centers: Neuroplasticity. What Does the Term Mean? – YouTube

What is Neuroplasticity? Dr. Matthew Antonucci from Plasticity Brain Centers of Orlando, Florida gives us a breakdown of what the term really means.



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[Abstract] Neural Plasticity in Moderate to Severe Chronic Stroke Following a Device-Assisted Task-Specific Arm/Hand Intervention

Currently, hand rehabilitation following stroke tends to focus on mildly impaired individuals, partially due to the inability for severely impaired subjects to sufficiently use the paretic hand. Device-assisted interventions offer a means to include this more severe population, and show promising behavioral results. However, the ability for this population to demonstrate neural plasticity, a crucial factor in functional recovery following effective post-stroke interventions, remains unclear. This study aimed to investigate neural changes related to hand function induced by a device-assisted task-specific intervention in individuals with moderate to severe chronic stroke (upper extremity Fugl Meyer < 30). We examined functional cortical reorganization related to paretic hand opening and gray matter structural changes using a multi-modal imaging approach. Individuals demonstrated a shift in cortical activity related to hand opening from the contralesional to the ipsilesional hemisphere following the intervention. This was driven by decreased activity in contralesional primary sensorimotor cortex and increased activity in ipsilesional secondary motor cortex. Additionally, subjects displayed increased gray matter density in ipsilesional primary sensorimotor cortex and decreased gray matter density in contralesional primary sensorimotor cortex. These findings suggest that despite moderate to severe chronic impairments, post-stroke participants maintain ability to show cortical reorganization and gray matter structural changes following a device-assisted task-specific arm/hand intervention. These changes are similar as those reported in post-stroke individuals with mild impairment, suggesting that residual neural plasticity in more severely impaired individuals may have the potential to support improved hand function.

Source: Neural Plasticity in Moderate to Severe Chronic Stroke Following a Device-Assisted Task-Specific Arm/Hand Intervention

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[WEB SITE] Neuroplasticity after Stroke

Neuroplasticity after Stroke

Neuroplasticity after stroke is the #1 thing that every stroke survivor should know about.

If you want to maximize your recovery, then understanding and applying the concept of neuroplasticity to your regimen will help you harness your brain’s full healing potential.

It’s an inspiring phenomenon, so let’s get started.

What Is Neuroplasticity?

The word neuroplasticity is the combination of 2 words: neuron and plasticity. Neurons are the nerve cells in your brain, and plasticity refers to something that is capable of being molded or reorganized.

Therefore, neuroplasticity refers to the process of reorganizing the neurons in your brain. It’s the mechanism that your brain uses to heal from damage and rewire itself.

Rewiring Your Brain after Stroke

After a stroke, certain parts of the brain can become damaged (depending on what type of stroke and where it occurred) and the functions that were once stored in those parts of the brain become impaired. For example, if the part of your brain responsible for motor control on the right side of your body becomes damaged, it will make it hard to move your right arm.

That’s when neuroplasticity comes into play.

Neuroplasticity allows your brain to rewire functions that were once held in damaged areas of the brain over to new, healthy parts of the brain. So with our right arm example, a different, healthy area of your brain is capable of picking up the slack and taking on the task of moving your right arm.

There’s one important requisite for neuroplasticity to occur, however, and it’s repetition.

You need to utilize a high number of repetitions during your rehab exercises, otherewise it won’t work that well.

How to Make Neuroplasticity Work for You

To rewire your brain after stroke, think of it as paving new roads.

If you only put a little effort in, then the new pathways won’t be that strong and they will fade with time. However, if you put a lot of effort in, you can pave a strong, durable road that will last for a long time.

The same goes with your rehab exercises.

The more you practice and repeat an exercise over and over, the stronger those new pathways in your brain become.

Neuroplasticity is nothing without good reinforcement and diligence.

One Last Bit

To really maximize your brain’s healing, you should be aware of all the other elements that go into stroke recovery.

This guide covers all the bases, we hope you find it useful.

Did you know that your brain was capable of such magic?

How will you apply this concept to your rehabilitation?

Leave us a comment below and share your thoughts with us!

Source: Neuroplasticity after Stroke – Flint Rehab

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[WEB SITE] How to PERMANENTLY Treat Post Stroke Spasticity

The Complete Guide to Treating Post Stroke Spasticity – for Good!

The Complete Guide to Treating Post Stroke Spasticity – for Good!

Post stroke spasticity is the most common post stroke side effect, and it’s likely that you’ve never heard the whole truth about it.

Most likely, you were told that there’s something wrong with your muscles, and Botox can fix it.

While this is partially true, it omits more effective and permanent solutions to spasticity.

There is tons of hope for treating spasticity – even severe spasticity in paralyzed muscles.

Today, we’re sharing the most valuable way to fix this frustrating problem.

Spasticity as Brain-Muscle Miscommunication

Before, you’ve probably heard spasticity explained in relation to your muscles.

Spasticity causes your muscles to become tightened, so it’s natural to focus on your muscles as what needs to be fixed. But spasticity is actually caused by miscommunication between your brain and your muscles.

Normally your muscles are in constant communication with your brain about how much tension they’re feeling, and the brain has to constantly monitor this tension to prevent tearing. Your brain continuously sends out messages telling your muscles when to contract and relax.

When a stroke damages part of the brain responsible for muscle control, this communication is thrown off. The damaged part of your brain no longer receives the messages that your muscles are trying to send, and as a result, your brain no longer tells them when to contract or relax.

So, your muscles keep themselves in a constant state of contraction in order to protect themselves.

That’s the cause of spasticity from the muscular perspective.

However, there’s a second layer to spasticity that no one talks about. Spasticity is also caused by miscommunication from your spinal cord.

The OTHER Cause of Spasticity

While your muscles are always in communication with your brain, they’re also in communication with your spinal cord.

Usually the spinal cord takes the messages from your muscles and sends them up to the brain. But since the brain is no longer reading those messages, your affected muscles have no one to talk to.

So the spinal cord takes over.

But the spinal cord doesn’t know how to properly operate your muscles. It really only has one goal: to prevent your muscles from tearing. In order to do that, your spinal cord sends signals to keep your muscles in a constant state of contraction, which is what causes spasticity.

Your spinal cord only has the best intentions – to prevent your muscles from tearing – but it’s frustrating because now your muscles are painfully stiff.

Let’s look at some temporary and permanent treatment options to fix this issue and alleviate your spasticity.

How to Temporarily Treat Spasticity

There are temporary ways to treat spasticity, which includes locally administered or orally taken drugs.

Locally administered drugs are injected into the affected muscles and help reduce pain, increase movement, and curb potential bone and joint problems.

Orally taken drugs offer the same benefits, but they are not site-specific and will affect all the muscles in your body.

As with most drugs in Western society, they only treat the symptom, not the underlying cause. This means that drugs are only a short-term solution.

So how can you treat the underlying cause?

With the help of your good ol’ friend neuroplasticity.

How to Permanently Reduce Spasticity

Neuroplasticity is your long-term, permanent solution to overcoming spasticity.

When a stroke damages part of the brain responsible for motor function, it decreases the number of brain cells dedicated to moving your affected limbs.

Neuroplasticity comes into play by rewiring your brain and dedicating more brain cells to controlling your affected limbs.

In order for this rewiring to occur, you have to repeat your rehab exercises over and over. The more you repeat the movement, the better the spasticity will subside and movement will improve.

It’s like paving new roads. The more you reinforce those new roads, the stronger they’ll become.

Putting in hard work is essential.

5 Ways to Activate Neuroplasticity and Treat Spasticity

If spasticity is causing you pain, then using temporary solutions in the meantime can help alleviate the barriers keeping you from your rehab exercises.

Since rehab exercise is the only permanent solution to spasticity, getting yourself to participate is crucial.

Here are 5 ways to maximize your benefit from rehab exercise and reduce spasticity:

There’s one thing these methods all have in common: Repetition.

No matter which option you choose, be sure to create an at-home rehabilitation regimen that utilizes a high number of repetitions.

You’ll get better faster this way because it’s the only way to retrain your brain to relax your spastic muscles – permanently.

3 Ways to Treat Spasticity When You Can’t Move Your Muscles

Sometimes muscles become so stiff with spasticity that it feels like they’re paralyzed.

The following 3 methods can help reduce spasticity in paralyzed muscles:

Practice these methods repetitively and you can regain movement in paralyzed muscles.

Yes, it’s possible to regain movement in paralyzed muscles! Read a success story on that here.

Then, once you’ve regained some movement, you can use any of the previous 5 methods to keep improving.

Spasticity as a Surprising Sign of Recovery

And that’s a wrap!

You are now aware that spasticity is caused by miscommunication between your brain and your muscles…

And this should bring you tons hope that your spasticity is treatable because it means that your muscles are still trying to communicate with your brain!

Your body hasn’t given up, and neither should you.

There are tons of success stories of stroke survivors who regained way more movement than doctors ever thought possible. Don’t let someone else’s limiting beliefs limit your recovery.

Even if you have no movement in your spastic muscles, keep trying by focusing on high repetition and taking small steps.

Eventually, your spasticity will start to improve – for good.

Source: How to PERMANENTLY Treat Post Stroke Spasticity – Flint Rehab

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[ARTICLE] Update on cell therapy for stroke – Full Text


Ischaemic stroke remains a leading cause of death and disability. Current stroke treatment options aim to minimise the damage from a pending stroke during the acute stroke period using intravenous thrombolytics and endovascular thrombectomy; however, there are no currently approved treatment options for reversing neurological damage once a stroke is completed. Preclinical studies suggest that cell therapy may be safe and effective in improving functional outcomes. Several recent clinical trials have reported safety and some improvement in outcomes following cell therapy administration in ischaemic stroke, which are reviewed. Cell therapy may provide a promising new treatment for stroke reducing stroke-related disability. Further investigation is needed to determine specific effects of cell therapy and to optimise cell delivery methods, cell dosing, type of cells used, timing of delivery, infarct size and location of infarct that are likely to benefit from cell therapy.


Until recently, intravenous recombinant tissue plasminogen activator was the only proven effective treatment for acute stroke. Endovascular thrombectomy has now been added to our arsenal for acute stroke treatment following the publication of five randomised trials demonstrating highly significant treatment effects favouring endovascular therapy.1–6 Outcome data support advancements in acute stroke care and neurorehabilitation with a significant increase in stroke survivors over time.7 However, despite these advancements, stroke remains a leading cause of long-term disability.8 For patients with residual deficits after stroke, we have no currently approved therapy for restoring function.

Cell therapy is one approach to enhancing recovery after stroke. In animal models, delivery of several different types of stem cells reduce infarct size and improve functional outcomes.9 Clinical trials of cell therapy completed in the 2000s mostly treating small cohorts of patients with chronic stroke demonstrated adequate safety and a suggestion of efficacy with the use of cell therapy. Kondziolka and colleagues used N-Tera 2 cells derived from a lung metastasis of a human testicular germ cell tumour that when treated with retinoic acid generate postmitotic neurons that maintain a fetal neuronal phenotype indefinitely in vitro (LBS neurons). LBS neurons were stereotactically implanted around the stroke bed of chronic subcortical ischaemic stroke. This study demonstrated safety and feasibility of stereotactic cell implantation, although there was no significant improvement in functional outcomes.10 11 Using a similar stereotactic approach implanting cells into the basal ganglia, Savitz and colleagues transplanted LGE cells (fetal porcine striatum-derived cells, Genvec) in five patients. Two patients showed improvements, but two patients experienced adverse effects including delayed worsening of neurological symptoms and seizure resulting in early termination of the study.12 Bang and colleagues reported the safety and feasibility of intravenous infusion of autologous mesenchymal stem cells (MSCs) with no reported adverse effects in five patients treated with intravenous MSCs. Although they reported some initial motor improvements, at 12 months, there was no significant difference in motor scores.13 These early clinical trials mostly focused on chronic subcortical strokes, but more recent trials are now investigating cell therapy for treatment of both cortical and subcortical infarcts. This review discusses the considerations for design of cell therapy trials and summarises the results of more recent studies.

Continue —> Update on cell therapy for stroke | Stroke and Vascular Neurology

Table 1

Summary of recent human cell therapy trials for stroke

Clinical trial/sponsor Age Time after stroke Additional selection criteria Cell type Route Stroke location Patients (n) Safety results Efficacy results
MASTERS/Athersys 18–83 24–48 hours NIHSS 8–20, infarct 5-100cc, premorbid mRS 0–1 Multistem adult-derived stem cell product Intravenous Cortical 129 Similar SAE at 1 year 22(34%) versus 24 (39%) placebo,
Lower mortality—5 deaths (8%) versus 9deaths (15%) in placebo19
No effect on 90-day Global Stroke Recovery Assessment (mRS 0–2, NIHSS increase by 75%, Barthel Index >95) but trend towards improved outcome with earlier delivery of cells19
InveST/Department of Biotechnology, India 18–75 7–29 days NIHSS >7, GCS >8, BI <50, paretic arm or leg stable >48 hours Autologous marrow-derived stem cells Intravenous 120
(58 cell therapy)
61 AE (33%) and eight deaths versus 60 AEs (36%) and five deaths placebo22 No effect on 180-day Barthel Index Score, mRS shift or score >3, NIHSS, change of infarct volume22
RECOVER-Stroke/Aldagen 30–75 13–19 days NIHSS 7–22, mRS >3 ALDHbrautologous marrow-derived stem cells Intracarotid infusion distal to ophthalmic Anterior circulation ± subcortical 29 IA, 19 sham 12 SAE IA, 11 SAE sham; 0 cell-related SAE23 No difference in mRS, Barthel, NIHSS at 90 days or 1 year
PISCES-II/ReNeuron 40–89 2–13 months Paretic arm with NIHSS motor arm score 2–3 CTX0E03 DP allogeneic human fetal neural stem cells Stereotaxic infusion into ipsilateral putamen 21 Pending Pending
Sanbio 18–75 6–60 months NIHSS>7, mRS 3–4, stable symptoms>3 weeks SB623 allogeneic marrow-derived stem cells transiently transfected with plasmid encoding Notch122 Stereotaxic infusion peri-infarct Subcortical ± cortical component24 18 28 SAE, 0 cell-related SAE25 Improved ESS at 6 months (p<0.01) and 12 months (p<0.001)
Improved NIHSS at 6 months (p<0.01) and 12 months(p<0.001)
Improved Fugl-Meyer at 6 months (p<0.001) and 12 months(p<0.001)25
PISCES/ReNeuron >60, male only 6–60 months Persistent hemiparesis, Stable NIHSS over 4 weeks (Pt 2 CTX0E03 DP allogeneic human neural stem cells Stereotaxic infusion into putamen Subcortical 11 16 SAE (in nine patients), 0 cell-related SAE28 Improved NIHSS at 2 years (p=0.002), No change, Barthel Index, MMSE, Ashworth, mRS28 29
  • AE, Adverse Event; ARAT, Action Research Arm Test; BI, Barthel Index; DP, drug product; ESS, European Stroke Scale; IA, intra-arterially; MASTERS, Multistem Administration for Stroke Treatment and Enhanced Recovery Study; MMSE, Mini-Mental Status Examination; mRS, modified Rankin Score; NIHSS, National Institutes of Health Stroke Scale; PISCES, Pilot Investigation of Stem Cells in Stroke; SAE, Serious aAverse Events.

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[Abstract] Supporting Stroke Motor Recovery Through a Mobile Application: A Pilot Study


Neuroplasticity and motor learning are promoted with repetitive movement, appropriate challenge, and performance feedback. ARMStrokes, a smartphone application, incorporates these qualities to support motor recovery. Engaging exercises are easily accessible for improved compliance. In a multiple-case, mixed-methods pilot study, the potential of this technology for stroke motor recovery was examined. Exercises calibrated to the participant’s skill level targeted forearm, elbow, and shoulder motions for a 6-wk protocol. Visual, auditory, and vibration feedback promoted self-assessment. Pre- and posttest data from 6 chronic stroke survivors who used the app in different ways (i.e., to measure active or passive motion, to track endurance) demonstrated improvements in accuracy of movements, fatigue, range of motion, and performance of daily activities. Statistically significant changes were not obtained with this pilot study. Further study on the efficacy of this technology is supported.

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Source: Supporting Stroke Motor Recovery Through a Mobile Application: A Pilot Study | American Journal of Occupational Therapy

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