To provide a systematic overview of interventions for stroke related visual impairments.
[Helping Others Understand is an open-ended, intermittent series designed to support stroke survivors and family caregivers with helping friends and family better understand the nuances, complications and realistic expectations for common post-stroke conditions. If there is a specific post-stroke condition you’d like to see us address in future issues, we invite you to let us know: firstname.lastname@example.org.]
Stroke is unpredictable both in its arrival and in the consequences it leaves, but one common stroke deficit is fatigue. Some studies indicate that as many as 70 percent of survivors experience fatigue at some time following their stroke. Unlike exertional fatigue that we feel after working in the yard, post-stroke fatigue occurs from doing typical everyday tasks or sometimes from not doing anything. “It is a fatigue associated with the nervous system, which is quite difficult to understand,” said Jade Bender-Burnett, P.T., D.P.T., N.C.S., a neurological physical therapist in Falls Church, Virginia. “It’s very frustrating to the person who’s living with it because, unlike exertional fatigue, post-stroke fatigue doesn’t always resolve after you take a break, or get some rest.”
That has been Roman Nemec’s experience since surviving an ischemic stroke 11 years ago. It doesn’t seem to matter how much sleep he gets, “I walk around tired all the time, even after 9-10 hours of sleep,” he said from his home in Georgia.
This can be difficult for friends and family members to get their heads around because they have not likely experienced this kind of brain fatigue. Bender-Burnett has asked her clients who were marathoners prior to their stroke to compare the fatigue one feels following a marathon to post-stroke fatigue: “They said the fatigue you feel after damage to the brain is unlike any fatigue they’ve ever felt,” she said.
While there is no standardized scale for post-stroke fatigue, Bender-Burnett says that therapists distinguish between two types of fatigue. “Objective fatigue occurs when we can see physical, mental or cognitive changes,” she said. “With subjective fatigue we don’t see any changes, but the survivor will tell you that they’re feeling extremely weary and have no energy.”
For some this goes on for a few months after their stroke, for others, like Roman, it is persistent. Fatigue may be a side effect of medication. “Post-stroke fatigue is very individualized,” Bender-Burnett said. “One of the most frustrating parts of post-stroke fatigue is that it’s so unpredictable. Today, getting up, brushing your teeth and putting on your clothes may be fine, but tomorrow you may not be able to complete the morning routine without a rest break. That unpredictability is very frustrating for people and makes reintegration into daily life difficult.”
Post-stroke fatigue often changes over time. People report more and greater fatigue in the first six months. It’s episodic at first and seems to come out of nowhere: “They may be functioning well, and then all of a sudden they hit a wall,” she said. “It seems that as they get farther along in recovery, those hit-the-wall episodes decrease, and the lingering effect is ‘I just don’t have the energy to do all the things on my plate.’”
Life consequences span the spectrum from nuisance to career-ending. It can impact a survivor’s ability to function in unpredictable ways: As they tire, they may become clumsy or their speech may be affected. Their ability to understand, comprehend or recall may be compromised. Some people get irritable, while others experience increased emotional lability (crying or laughing with no apparent trigger). Bender-Burnett has worked with people who have made remarkable recoveries but were not able to return to work because of post-stroke fatigue.
Just as the consequences are individualized, so are the responses. If your energy is better in the morning, then take advantage of that. For mental fatigue, the most effective response is to sit quietly with low sensory stimulation, not necessarily take a nap. Some survivors may require regular and scheduled rest breaks or even a nap; that does not work for Roman: “I just live through it,” he said. “There are worse things than being tired. I feel good; I can get around; I can talk. Life is good compared to what it could be. Being tired all the time is not a big problem.”
Rhonda Hand, whose significant other, Tarvin, is a survivor, said: “In our household the fatigue issue is factored in before any event or activity and recuperation time after an event or activity. We just block off rest time like another activity; if we don’t, everything shuts down, including speech. Over the years, we have become much more proactive in scheduling appointments with anybody. There is nothing before 8 a.m. That’s when deep sleep is happening.”
Knowing your limits — and quitting before you hit them — is key to living with post-stroke fatigue. Survivors with fatigue have limited energy reserves, and if they get depleted, they take longer to replenish. “You don’t want push to the point just before you’re exhausted, you want to end on a high note, leaving some reserves,” Bender-Burnett said.
“We’re still learning about post-stroke fatigue from the healthcare perspective, and so I think it’s important that we all be willing to recognize it and have open communication about it,” Bender-Burnett said. “I urge family members and friends to come from a position of compassion and understanding rather than expectation that everything should be better, because, much like depression, others can’t always see it but, if you’re feeling it, it can be quite limiting.”
The Stroke Connection team knows that it can sometimes be hard for family and friends to understand how profoundly post-stroke fatigue may be impacting a survivor. We encourage you to share this article with the people in your life — and, for those pressed for time, we’ve created a quick-reference sheet that you can print or share via email or socia
Transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (TDCS) are two types of non-invasive transcranial brain stimulation (TBS). They are useful tools for stroke research and may be potential adjunct therapies for functional recovery. However, stroke often causes large cerebral lesions, which are commonly accompanied by a secondary enlargement of the ventricles and atrophy. These structural alterations substantially change the conductivity distribution inside the head, which may have potentially important consequences for both brain stimulation methods. We therefore aimed to characterize the impact of these changes on the spatial distribution of the electric field generated by both TBS methods. In addition to confirming the safety of TBS in the presence of large stroke-related structural changes, our aim was to clarify whether targeted stimulation is still possible. Realistic head models containing large cortical and subcortical stroke lesions in the right parietal cortex were created using MR images of two patients. For TMS, the electric field of a double coil was simulated using the finite-element method. Systematic variations of the coil position relative to the lesion were tested. For TDCS, the finite-element method was used to simulate a standard approach with two electrode pads, and the position of one electrode was systematically varied. For both TMS and TDCS, the lesion caused electric field “hot spots” in the cortex. However, these maxima were not substantially stronger than those seen in a healthy control. The electric field pattern induced by TMS was not substantially changed by the lesions. However, the average field strength generated by TDCS was substantially decreased. This effect occurred for both head models and even when both electrodes were distant to the lesion, caused by increased current shunting through the lesion and enlarged ventricles. Judging from the similar peak field strengths compared to the healthy control, both TBS methods are safe in patients with large brain lesions (in practice, however, additional factors such as potentially lowered thresholds for seizure-induction have to be considered). Focused stimulation by TMS seems to be possible, but standard tDCS protocols appear to be less efficient than they are in healthy subjects, strongly suggesting that tDCS studies in this population might benefit from individualized treatment planning based on realistic field calculations.
Transcranial brain stimulation (TBS) methods are useful tools to induce and to quantify neural plasticity, and as such are increasingly being used in stroke research and as potential adjunct therapies in stroke rehabilitation. The cerebral lesions caused by stroke result in persisting physical or cognitive impairments in around 50% of all survivors (Di Carlo, 2008; Leys et al., 2005 ; Young and Forster, 2007), meaning that new therapies are urgently needed. Transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (TDCS) are two TBS approaches which are being increasingly utilised in stroke research. Single-pulse TMS combined with electromyography (EMG) or electroencephalography (EEG) can be used to assess cortical excitability, for example to index the functional state of the perilesional tissue. The neuromodulatory effects of repetitive TMS protocols (rTMS) may, in association with neuro-rehabilitative treatments, enhance motor recovery (Liew et al., 2014). Similar results have been demonstrated for TDCS. For example, anodal TDCS of the hand area in the primary motor cortex has been shown to improve motor performance of the affected hand (Allman et al., 2016; Hummel et al., 2005 ; Stagg et al., 2012) and anodal TDCS applied over the left frontal cortex enhanced naming accuracy in patients with aphasia (Baker et al., 2010). However, not all studies report a clear-cut positive impact of TBS on the stroke symptoms. Rather, the observed effects are often weak and not consistent across patients, demonstrating the need for a better understanding of the underlying biophysical and physiological mechanisms.
Compared with healthy subjects, several factors might contribute to a change in the neuroplastic response to TBS protocols in stroke patients, including changes in the neural responsiveness to the applied electric fields, as well as differences in the underlying physiology and metabolism (Blicher et al., 2009; Blicher et al., 2015 ; O’Shea et al., 2014). When the lesions are large, they may also substantially alter the generated electric field pattern, meaning that the assumptions on spatial targeting as derived from biophysical modelling and physiological experiments in healthy subjects might no longer be valid. Stroke lesions are often accompanied by secondary macrostructural changes such as cortical atrophy and enlargement of the ventricles (e.g., Skriver et al., 1990), which may further contribute to changes in the field pattern. In addition, the safety of TBS in patients with large lesions needs to be further clarified, as it is possible that the lesions might cause stimulation “hot spots”. In chronic patients, the stroke cavity becomes filled with corticospinal fluid (CSF), which might cause shunting of current, funnelling the generated currents towards the surrounding brain tissue and potentially causing localized areas of dangerously high field strengths.
Here, using finite-element calculations and individual head models derived from structural MR images, we focused on the impact of a large cortical lesion in chronic stroke on the electric field pattern generated in the brain by TMS and TDCS, respectively. Firstly, we assessed the safety of the stimulation by comparing the achieved field strengths with those estimated for a healthy control. Secondly, we tested how reliably we can accurately target the perilesional tissue, often the desired target for TBS, as reorganisation here is thought to underpin functional recovery (Kwakkel et al., 2004). Finally, we were also interested to see whether any observed changes in the field pattern were specific to a patient with a cortical lesion (which is connected to the CSF layer underneath the skull), or whether similar effects might occur in case of large chronic subcortical lesion. We therefore additionally tested the field distribution in a head model of a patient with a subcortical lesion occurring at a similar position as the cortical lesion.
The aim of this study was to characterize the effect of a large chronic cortical stroke lesion on the electric field distribution generated by TBS, and to compare the effects of this lesion to that caused by a large chronic subcortical lesion. MR images of several patients were visually inspected to select two datasets, which had a cortical [P01] and subcortical lesion [P02], respectively, within the same gross anatomical regions.
Patient P01 was a 36 year old female with episodic migraine; she was admitted with left hemiparalysis, fascial palsy and a total NIHSS score of 16 due to a right ICI/MCI occlusion. She was treated with IV thrombolysis and thrombectomy and recanalization was achieved 5 h after symptom onset. One year post-stroke she still suffered from motor impairment (Wolf Motor Function Test [WMFT] score of 30) and was scanned as part of a clinical study investigating the effect of combining Constraint-Induced Movement Therapy and tDCS (Figlewski et al., 2017; Clinical trials NCT01983319, Regional Ethics approval: 1-10-72-268-13). The structural scans showed a cortical lesion in the right parietal lobe (Fig. 1A). The lesion volume, delineated manually with reference to T1- and T2-weighted imaging, was 26,415 mm3.
A) Coronal view of patient P01 with a cortical lesion in the right hemisphere. The top shows the T1-weighted MR image and the bottom the reconstructed head mesh. The view was chosen to include the lesion centre. The lesion is marked by red dashed circles. B) Corresponding view of patient P02 with a large subcortical lesion at a similar location in the right hemisphere. C) Corresponding view of the data set of the healthy control. D) The coil and electrode positions were systematically moved along two directions that were approximately perpendicular to each other. Five positions were manually placed every 2 cm in posterior – anterior direction symmetrically around the centre of the cortical lesion. The same was repeated along the lateral – medial direction. Both lines share the same centre position above the lesion, resulting in 9 positions in total. E) At each position, two coil orientations were tested which resulted in a current flow underneath the coil centre from anterior to posterior (top) and from lateral to medial, respectively (bottom). F) For each position of the yellow “stimulating” electrode, two positions of the blue return electrode were tested. First, the contralateral equivalent of the electrode position above the centre of the cortical lesion was used (top). In addition, a position on the contralateral forehead was tested (bottom).
To provide a systematic overview of interventions for stroke related visual impairments.
A systematic review of the literature was conducted including randomized controlled trials, controlled trials, cohort studies, observational studies, systematic reviews, and retrospective medical note reviews. All languages were included and translation obtained. This review covers adult participants (aged 18 years or over) diagnosed with a visual impairment as a direct cause of a stroke. Studies which included mixed populations were included if over 50% of the participants had a diagnosis of stroke and were discussed separately. We searched scholarly online resources and hand searched articles and registers of published, unpublished, and ongoing trials. Search terms included a variety of MESH terms and alternatives in relation to stroke and visual conditions. Article selection was performed by two authors independently. Data were extracted by one author and verified by a second. The quality of the evidence and risk of bias was assessed using appropriate tools dependant on the type of article.
Forty-nine articles (4142 subjects) were included in the review, including an overview of four Cochrane systematic reviews. Interventions appraised included those for visual field loss, ocular motility deficits, reduced central vision, and visual perceptual deficits.
Further high quality randomized controlled trials are required to determine the effectiveness of interventions for treating post-stroke visual impairments. For interventions which are used in practice but do not yet have an evidence base in the literature, it is imperative that these treatments be addressed and evaluated in future studies.
Visual impairments following stroke may include abnormalities of central and/or peripheral vision, eye movements and a variety of visual perception problems such as inattention and agnosia. The visual problems (types of visual impairment) can be complex including ocular as well as cortical damage (Jones & Shinton, 2006; Rowe et al., 2009a). Visual impairments can have wide reaching implications on daily living, independence, and quality of life. Links with depression have also been documented in the literature (Granger, Cotter, Hamilton, & Fiedler, 1993; Nelles et al., 2001; Ramrattan et al., 2001; Tsai et al., 2003; West et al., 2002). The estimation of the overall prevalence of visual impairment is approximately 60% at the acute stage following stroke (Ali et al., 2013; Barrett et al., 2007; Clisby, 1995; Freeman & Rudge, 1987; Isaeff, Wallar, & Duncan, 1974; Rowe et al., 2009b; Rowe et al., 2013). A review of the individual prevalence figures and the recovery rates for each of the possible post-stroke visual impairments has been reported elsewhere in the literature (Hepworth et al., 2016).
In order to treat and manage visual impairments caused by stroke it is important to establish the range and effectiveness of the available treatment options. The aim of this literature review is to provide a comprehensive synthesis of the evidence relating to treatment of visual problems after stroke.
Stroke instigates a dynamic process of repair and remodelling of remaining neural circuits, and this process is shaped by behavioural experiences. The onset of motor disability simultaneously creates a powerful incentive to develop new, compensatory ways of performing daily activities. Compensatory movement strategies that are developed in response to motor impairments can be a dominant force in shaping post-stroke neural remodelling responses and can have mixed effects on functional outcome. The possibility of selectively harnessing the effects of compensatory behaviour on neural reorganization is still an insufficiently explored route for optimizing functional outcome after stroke.
Figure 1: The motor cortex and its descending projection pathways are often affected by strokes that result in upper-extremity impairments.
a | Simplified illustrations of motor cortical regions of a human (left), and of motor cortical regions of a naive rat, derived using intracortical microstimulation (right), are shown. The colours show the cortical territories that are…
Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for post-stroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the key to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.
According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).
Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (4–7). Accumulated evidence from animal (8) and human studies (9–18) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (20–36), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (37, 38). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.
• Poststroke spasticity and motor recovery are mediated by different mechanisms
• Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)
• Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity
• Possible roles of RS hyperexcitability in motor recovery
• An example of spasticity reduction for facilitation of motor recovery
RGS is a highly innovative Virtual Reality (VR) tool for the rehabilitation of deficits that occur after brain lesions and has been successfully used for the rehabilitation of the upper extremities after stroke.
The RGS is based on the neurobiological considerations that plasticity of the brain remains throughout life and therefore can be utilized to achieve functional reorganization of the brain areas affected by stroke. This can be realized by means of activation of secondary motor areas such as the so called mirror neurons system.
RGS deploys a deficit oriented training approach. Specifically, while training with RGS the patient is playing individualized games where movement execution is combined with the observation of correlated actions performed by a virtual body. The system optimizes the user’s training by analyzing the qualitative and quantitative aspects of the user’s performance. This warranties a detailed assessment of the deficits of the patient and their recovery dynamics.
also see specs.upf.edu
Interhemispheric inhibition in the brain plays a dynamic role in the production of voluntary unimanual actions. In stroke, the interhemispheric imbalance model predicts the presence of asymmetry in interhemispheric inhibition, with excessive inhibition from the contralesional hemisphere limiting maximal recovery. Stimulation methods to reduce this asymmetry in the brain may be promising as a stroke therapy, however determining how to best measure and modulate interhemispheric inhibition and who is likely to benefit, remain important questions.
This review addresses current understanding of interhemispheric inhibition in the healthy and stroke lesioned brain. We present a review of studies that have measured interhemispheric inhibition using different paradigms in the clinic, as well as results from recent animal studies investigating stimulation methods to target abnormal inhibition after stroke.
The degree to which asymmetric interhemispheric inhibition impacts on stroke recovery is controversial, and we consider sources of variation between studies which may contribute to this debate. We suggest that interhemispheric inhibition is not static following stroke in terms of the movement phase in which it is aberrantly engaged. Instead it may be dynamically increased onto perilesional areas during early movement, thus impairing motor initiation. Hence, its effect on stroke recovery may differ between studies depending on the technique and movement phase of eliciting the measurement. Finally, we propose how modulating excitability in the brain through more specific targeting of neural elements underlying interhemispheric inhibition via stimulation type, location and intensity may raise the ceiling of recovery following stroke and enhance functional return.
Background: Eclectic treatment method is a flexible approach that uses techniques drawn from various schools of thought involving several treatment methods and allows the therapist to adapt to each client’s individual needs. Wider application for eclectic approach is however limited in stroke rehabilitation. Aim: The objective is to find out whether eclectic approach improves upper extremity (UE) functional recovery in acute stroke rehabilitation. Methodology: Twenty-five postacute unilateral supratentorial stroke subjects recruited from tertiary care hospitals recovered with Stage 2–5 in Brunnstorm stage of UE motor recovery (BRS-UE) underwent 45 min of eclectic approach for UE every day involving seven different treatment methods (5 min for each method) for 6 days consecutively. The outcome was UE subscale of the Fugl-Meyer Motor test (UE-FM), UE subscale of the Stroke Rehabilitation Assessment of Movement (UE-STREAM), Wolf Motor Function test (WMFT-FAS), and Stroke Impact Scale-16 (SIS-16) was collected at the end of the sixth session. Results: All the participants showed significant improvement in all the outcome measures. The Stage 2 and 3 subjects showed UE-STREAM (P = 0.007) WMFT-FAS (P < 0.001), SIS (P = 0.023) respectively and for Stage 4 and 5 the subjects have shown UE FM (P < 0.001), WMFT-FAS (P < 0.001), SIS (P = 0.004) with large magnitude of treatment effect for all stages of BRS-UE. Conclusion: Our study findings are in favor of integrating eclectic approach than single intervention/approach in clinical practice to improve the UE functional recovery for motor rehabilitation when the stroke occurs.
Globally, stroke is the third major cause of mortality and a major health issue in low- and middle-income countries like India.Eighty percent of stroke survivors experience motor impairments (hemiparesis) typically affecting movement of the face, arm, trunk, and leg of one side of the body often persistent and disabling them. These residual impairments limit their functional independence and predisposing them to restrict their participation in community and social roles.,
Upper limb hemiparesis is one of the primary impairments following the stroke. It is often reported to be incomplete in functional recovery and to restore the motor skills. The studies on recovery of voluntary arm movements have also shown that 5–20% of stroke survivors achieved complete functional recovery and 30–60% of paretic arm can never have complete recovery during the first 6 months after the stroke., Common upper extremity (UE) impairments after the stroke include paresis, loss of fractionated movement, abnormal muscle tone and/or changes in somatosensation, shoulder pain, and subluxation which prevents the functional use of the arm, bimanual tasks and also for fine motor skills., Post stroke, persistent arm motor impairment (a period of 1 year or above) can be associated with anxiety and poorer perception of health-related quality of life and subjective well-being.,
One of the primary aims of the stroke rehabilitation is to improve the arm functions and to regain the gross and fine motor skills. Currently, the existing rehabilitation protocols that are designed to improve UE functions include the various treatment methods/interventions such as Roods, Brunnstorm, proprioceptive neuromuscular facilitation, neuro-developmental therapy techniques, repetitive/task-specific training, strength training, sensorimotor interventions, constraint-induced movement therapy, virtual reality, spasticity treatment, electromyographic/biofeedback, transcutaneous electrical nerve stimulation, neuromuscular electrical stimulation, functional electric stimulation, motor imagery, mirror therapy, and bilateral arm training. However, recent systematic reviews have concluded that there is insufficient evidence observed for any intervention or approach that can currently be used in routine practice to improve the paretic upper limb functions.
An eclectic therapy is a therapeutic approach that incorporates a variety of therapeutic principles and philosophies to create the ideal treatment program to meet the specific needs of the patient or client. The intervention of an eclectic approach is based on the stable principles of the classic traditional methods but is open to refining and can be used in conjunction with the elements of other various new methods, thus providing a framework for designing an optimal neurorehabilitation protocol., The studies have shown that the eclectic approach is suitable for a diverse and complex set of patients.,, However, wider application of eclectic approach in stroke rehabilitation is limited in literature.
BACKGROUND: Post-stroke fatigue (PSF) is a common and distressing problem after stroke. The best ways to prevent or treat PSF are uncertain. Several different interventions can be argued to have a rational basis. OBJECTIVES: To determine whether, among people with stroke, any intervention reduces the proportion of people with fatigue, fatigue severity, or both; and to determine the effect of intervention on health-related quality of life, disability, dependency and death, and whether such intervention is cost effective.
To compare amount of activity of virtual reality (VR) and conventional task-oriented training (CT).
Source: Upper Limb Virtual Reality Training Provides Increased Activity Compared With Conventional Training for Severely Affected Subacute Patients After Stroke – Archives of Physical Medicine and Rehabilitation