Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, February 29, 2024

Bridging the Gap: Innovative Rehabilitation for Stroke Survivors

You tell us NOTHING about how EXACTLY to get recovered. I'd fire all of you!

Treatment and Outcomes of Cervical Artery Dissection in Adults: A Scientific Statement From the American Heart Association

 I can't see anything here that even remotely looks like a protocol on how to handle these dissections. So completely useless! If we had survivors in charge we would get protocols out of stroke research that gets survivors recovered!

Treatment and Outcomes of Cervical Artery Dissection in Adults: A Scientific Statement From the American Heart Association

Originally publishedhttps://doi.org/10.1161/STR.0000000000000457Stroke. 2024;55:e91–e106

Abstract

Cervical artery dissection is an important cause of stroke, particularly in young adults. Data conflict on the diagnostic evaluation and treatment of patients with suspected cervical artery dissection, leading to variability in practice. We aim to provide an overview of cervical artery dissection in the setting of minor or no reported mechanical trigger with a focus on summarizing the available evidence and providing suggestions on the diagnostic evaluation, treatment approaches, and outcomes. Writing group members drafted their sections using a literature search focused on publications between January 1, 1990, and December 31, 2022, and included randomized controlled trials, prospective and retrospective observational studies, meta-analyses, opinion papers, case series, and case reports. The writing group chair and vice chair compiled the manuscript and obtained writing group members’ approval. Cervical artery dissection occurs as a result of the interplay among risk factors, minor trauma, anatomic and congenital abnormalities, and genetic predisposition. The diagnosis can be challenging both clinically and radiologically. In patients with acute ischemic stroke attributable to cervical artery dissection, acute treatment strategies such as thrombolysis and mechanical thrombectomy are reasonable in otherwise eligible patients. We suggest that the antithrombotic therapy choice be individualized and continued for at least 3 to 6 months. The risk of recurrent dissection is low, and preventive measures may be considered early after the diagnosis and continued in high-risk patients. Ongoing longitudinal and population-based observational studies are needed to close the present gaps on preferred antithrombotic regimens considering clinical and radiographic prognosticators of cervical artery dissection.

Cervical artery (internal carotid or vertebral artery) dissection can occur in the absence of major trauma.1 It is usually attributable to an intimal tear or rupture of the vasa vasorum. This can lead to an intraluminal thrombus, vascular stenosis, occlusion, or dissecting aneurysm formation. Cervical artery dissections can present with local signs and symptoms (eg, pain or cranial nerve compression) or cerebral or spinal cord ischemia.1

Cervical artery dissection is an important cause of stroke and stroke-related disability in young adults.2 Despite high-quality studies, data conflict on the diagnostic evaluation, treatment, and outcomes of patients with suspected non–major trauma–associated cervical artery dissection with or without cerebral ischemia.2 Conflicting evidence has led to clinical equipoise and variability in practice across clinicians.3

In this scientific statement, we aim to provide an overview of non–major trauma–associated cervical artery dissection, hereafter referred to as cervical artery dissection, with a focus on summarizing the available evidence on the diagnostic evaluation, treatment approaches, and outcomes.

METHODS

A multidisciplinary team of 11 writing group members from neurology, neuroradiology, neurosurgery, emergency medicine, and interventional neurology were identified to cover the sections. Each writing group member wrote and reviewed at least 1 section. In this scoping review, authors performed a literature search using key words relevant to each section, and the search results were reviewed for relevant publications. The literature search focused on publications between January 1, 1990, and December 31, 2022, and included randomized controlled trials, prospective and retrospective observational studies, meta-analyses, opinion papers, case series, and case reports. Apart from meeting presentations for clinical trials, meeting abstracts were not included.

Using the information from relevant publications, the writing group members drafted their sections. Once the sections were complete, the writing group chair and vice chair compiled the manuscript and circulated it to the writing group members for review and feedback. Multiple drafts were circulated among writing group members until a consensus was achieved. A summary of suggestions to clinicians pertinent to each section is provided in the Table.

Section Summary of suggestions

Table. Summary of Conclusions From Each Section

EpidemiologyCervical artery dissection is a common cause of stroke in younger adults and caused by the interplay between comorbidities, genetic or congenital factors, anatomic factors, and environmental triggers.
Clinical diagnosisIt is reasonable to perform urgent cervical vascular imaging with CTA or MRI with MRA in patients with headache or neck pain associated with symptoms of ischemia or a partial Horner syndrome and considered in those with new or worsening headache or neck pain, especially when there is a history of minor cervical trauma or other risk factors for cervical artery dissection.
Imaging tools for diagnosisIn patients with suspected cervical artery dissection, an MRA or CTA is a reasonable test to consider. In patients with negative CTA and continued clinical concern for cervical artery dissection, MRA with fat-suppressed images may be considered, given the high sensitivity to visualize a mural hematoma. DSA should be avoided as a first-line diagnostic tool but may be considered in patients with clinical concern and negative MRA and CTA. Ultrasound might be useful for follow-up assessments of arterial remodeling.
Imaging diagnostic challengesImaging signs of dissection include a tapering stenosis or occlusion, intramural hematoma, dissecting aneurysm, double lumen, and dissection flap. It is crucial to carefully review the cervical vascular imaging studies of patients with ≥1 signs of dissection present and to recognize dissection mimics such as carotid artery web, fenestrated artery, pseudo-occlusion, and imaging artifacts.
Role of genetic testingIt is reasonable to screen patients with cervical artery dissection for clinical signs of monogenic connective tissue disorders (eg, recurrent dissection, family history, physical examination) and to perform appropriate genetic counseling and testing based on the previously discussed screening tools. Routine genetic testing in the absence of signs or symptoms of monogenic connective tissue disorder is not suggested because of its increased cost and low yield but may be considered in patients with recurrent dissection.
Diagnostic testing after dissection diagnosisIn patients with cervical artery dissection, it is reasonable to screen for cerebral aneurysm and aortic root dilation. In those with hypertension or evidence of fibromuscular dysplasia, screening for renal artery stenosis with a renovascular Doppler is reasonable.
Timing and predictors of ischemic strokeThe early ischemic stroke risk supports the timely recognition, diagnosis, and initiation of optimal antithrombotic treatment for cervical artery dissection. Clinicians can use demographics, clinical characteristics, and imaging findings to predict which patients are at higher risk of developing an ischemic stroke after cervical artery dissection.
IVTIn the absence of data suggesting safety concerns and given the proven efficacy of IVT in otherwise eligible patients with acute ischemic stroke, it is reasonable to consider IVT for patients with acute ischemic stroke with cervical artery dissection if they meet other standard criteria, as recommended by current guidelines. For patients with intracranial extension of the dissection, the risks and benefits of IVT are not well established.
Mechanical thrombectomyIt is reasonable to perform mechanical thrombectomy in otherwise eligible patients with a large-vessel occlusion in the setting of cervical artery dissection.
Antithrombotic treatmentBecause most ischemic events occur within the first several days after diagnosis, optimizing antithrombotic treatment (when safe) early is of paramount importance. In addition, it is reasonable that clinicians start immediate antithrombotic treatment if deemed safe. Parenteral followed by oral anticoagulation may be considered in particular in patients at low risk of intracranial hemorrhage (small infarct size, no intradural extension, and no intracranial hemorrhage) but at high risk for ischemic stroke (eg, intraluminal thrombus, occlusive dissection). Although the evidence for use in cervical artery dissection is weak, a short course of dual antiplatelet therapy with a loading dose (followed by single antiplatelet agent) might be preferred over monotherapy when deemed safe, particularly in patients who would have qualified for the dual antiplatelet trials for early prevention after minor stroke/TIA. Otherwise, antiplatelet monotherapy could be used. In the absence of a general superiority of any antithrombotic regimen, it is reasonable that clinicians individualize treatment on the basis of the risk of ischemic stroke and ICH, as well as a shared decision-making process with their patients.
Antithrombotic treatment durationIt is reasonable that the duration of antithrombotic therapy in patients with cervical artery dissection be 3–6 mo. Decisions to extend antithrombotic therapy past the 6-mo mark may be considered in the context of an individual’s overall vascular risk factor profile and in the context of neuroimaging features as remodeling occurs.
Subacute stentingPatients with cervical artery dissection with significant stenosis causing distal hemodynamic compromise AND recurrent ischemic stroke despite optimal medical treatment AND who can withstand surgery may be considered for stenting as a measure for secondary stroke prevention.
Risk and predictors of recurrent dissectionThe risk of recurrent cervical artery dissection is 1%–2% per y but is particularly increased in the first few months after the initial cervical artery dissection. Younger age and fibromuscular dysplasia are risk factors for dissection recurrence.
Precautions to reduce the risk of dissection recurrenceBecause the risk of recurrent or worsening dissection is highest in the first few months after the initial dissection, it is reasonable that all patients with cervical artery dissection avoid activities that increase the risk of cervical injury for 1–6 mo from diagnosis and until healing of the index dissection. Furthermore, although there are no proven precautions to reduce the long-term risk of recurrent dissection, it is reasonable for health care clinicians to suggest that patients with cervical artery dissection who are at high risk for recurrent cervical dissection (eg, known connective disorder, recurrent dissection) avoid such activities lifelong.
Radiological recanalization of the dissectionRecanalization of cervical artery dissections occurs mostly in the first 12 mo after diagnosis. Cervical artery–dissecting aneurysms infrequently increase in size, become symptomatic, and require treatment. Recanalization and development or resolution of cervical artery–dissecting aneurysms do not seem to be affected by antithrombotic treatment regimens.

CTA indicates computed tomography angiography; DSA, digital subtraction angiography; ICH, intracranial hemorrhage; IVT, intravenous thrombolysis; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; and TIA, transient ischemic stroke.

EPIDEMIOLOGY/RISK FACTORS

Cervical artery dissection contributes to 2% of all ischemic strokes4 but up to 25% of ischemic stroke in adults <50 years of age.5,6 Prior studies reported an incidence rate of 2.6 to 3.0 per 100 000 people4,7,8 but the true incidence is likely higher,9 partly because some patients with dissection may not seek medical attention because of self-limited or minor symptoms.

The mean age at diagnosis is 45 years.7 Although the proportion of dissection-related stroke is higher in younger patients, the absolute prevalence of dissection-related ischemic strokes increases with age.10 The incidence is slightly higher in men,11 but the age at onset and the peak age prevalence of dissection-related stroke are lower in women (30–49 years) compared with men (50–89 years).10,11

The pathogenesis of cervical artery dissection is multifactorial and involves the interplay of comorbidities, environmental triggers, genetic or congenital factors, including connective tissue disorders, and anatomic factors such as elongated styloid process (>30 mm; Eagle syndrome) or increased vascular tortuosity (Figure S1).1,12–14 Furthermore, risk factors may differ according to dissection location; recent systemic infection is more common in carotid artery dissection, and history of minor trauma is more common in vertebral artery dissection.15

CHALLENGES IN DIAGNOSIS

Clinical Diagnostic Challenges

Because of the often nonspecific nature of symptoms (eg, headache, neck pain, dizziness, and tinnitus), diagnosis of cervical artery dissection is challenging, especially in the absence of ischemic or localizing symptoms. In a statewide study of claims data, 3.1% of patients with cervical artery dissection were previously seen in the emergency department for possible related symptoms in the 14 days preceding diagnosis16; younger and female patients were more likely to have a probable missed diagnosis.16

Evaluation for suspected cervical artery dissection should include a detailed symptom history, questions about minor trauma, and a detailed neurological examination. Common initial symptoms of cervical artery dissection include facial pain, headache (≈65%), and neck pain (≈50%),15 which tend to precede cerebrovascular ischemic symptoms17,18; thus, early diagnosis and treatment could reduce the risk of cerebrovascular ischemia. Isolated pain (without cerebral ischemia) occurs in 8% to 12% of diagnosed cases.19,20 For internal carotid dissections, pain is often facial, frontal, or temporal, whereas vertebral artery dissections generally cause pain in the cervical or occipital area.17,21 In carotid dissection, pain may also be associated with a (partial) Horner syndrome (≈25%7) and cranial nerve palsies (≈12%),22 and both carotid and vertebral dissection can be associated with pulsatile tinnitus (≈8%).17,23,24 In fact, a partial Horner syndrome in a patient with new or worsening headache may suggest a carotid dissection diagnosis. Headache characteristics are not specific but can rarely be acute and of thunderclap nature.

Diagnostic Imaging Tools and Their Yield

The diagnostic modalities for cervical artery dissection are magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA), computed tomography angiography (CTA), ultrasound, and conventional digital subtraction angiography (DSA). Historically, DSA has been considered the reference imaging technique to demonstrate the lumen content and can delineate the presence of an intimal flap, double lumen, and dissecting aneurysm.25 DSA, however, provides limited information on the arterial wall (ie, intramural hematoma). Moreover, DSA carries periprocedural risks (≈0.5% iatrogenic dissection26 and 0.15% stroke).27

CTA is an effective noninvasive alternative to DSA that can display luminal contour alterations with rapid acquisition time, ready availability, and high spatial resolution; disadvantages include the exposure to radiation and iodinated contrast, and for intramural hematoma, CTA may show an eccentric or crescent-shaped vessel wall thickening or the rind sign in vertebral dissection28 (Figure 1), but these findings are neither sensitive nor specific to cervical artery dissection. A false-positive CTA can be due to streak artifact mimicking a double lumen and pulsation artifact mimicking an intramural hematoma. A false-negative CTA could be seen in the setting of a non–flow-limiting nondominant vertebral artery dissection but most commonly is due to failure of attributing an abnormality to dissection.29

Figure 1.

Figure 1. Imaging signs suggestive of dissection diagnosis. A, Double lumen. B, Tapered or flame-shaped occlusion at typical dissection site. C, Intimal flap. D, Pseudoaneurysm. E, Intramural hematoma on fat-suppressed T1. F, Carotid imaging duplex mural hematoma (white arrows) as hypoechogenic structure compromising the arterial blood flow in the vertebral artery (V3 segment). G, Axial source image from computed tomography angiography (CTA) neck in a patient with complete occlusion of the left internal carotid artery (ICA) related to a dissection, showing the ring sign, with enhancement of the carotid wall and fresh nonenhancing thrombus within the carotid lumen. This sign is nonspecific for ICA dissection but points to a recent rather than a chronic occlusion. H, Axial source image from CTA neck in a patient with left vertebral artery dissection, with thrombus surrounding the hypoplastic but apparently normal lumen vertebral artery, known as the suboccipital rind sign, involving the atlanto-occipital (V3) segment.

MRA may be superior to CTA for the identification of the intramural hematoma when the appropriate protocol including axial fat-suppressed T1-weighted images is used. Limitations of MRA include the cost, availability, patient-related restrictions (eg, pacemakers and claustrophobia), and diagnostic limitations of time-of-flight MRA of the neck (eg, signal loss due to turbulence or vessel turn, susceptibility to artifact, and flow reversal artifact). False-positive MRA can be due to a hyperintense signal in the setting of turbulent flow and adjacent structures simulating a periarterial double-lumen sign. False-negative MRA can be related to the absence of hyperintense signal of the intramural hematoma in the hyperacute setting.29

Overall, both MRA and CTA have good sensitivity and specificity for diagnosis of cervical arterial dissection. MRA has high sensitivity in diagnosing carotid dissection (95%), but its sensitivity is lower for vertebral artery dissection (60%) compared with DSA.30 This is not the case with CTA, which has been shown to have similar sensitivity and specificity compared with DSA in diagnosing vertebral artery dissection.25

Ultrasound with color Doppler is noninvasive but is operator dependent and is of poor diagnostic utility,31 especially when the dissection is high cervical. Ultrasound may be helpful in rare cases with hyperacute dissection where the intramural hematoma can be visualized on ultrasound but not MRA (Figure 1). Ultrasound generally requires confirmation by CTA or MRA. Ultrasound has been shown to be useful for follow-up assessments within the first 4 weeks, when arterial remodeling is most prevalent.32

Image

More at link.


Higher hourly heat exposure tied to acute ischemic stroke risk

 FYI.

Higher hourly heat exposure tied to acute ischemic stroke risk

Key takeaways:

  • Higher hourly heat exposure conferred elevated risk for acute ischemic stroke.
  • The findings could help in developing public policies to combat the risks of climate change.

High hourly heat exposure was associated with elevated risk for acute ischemic stroke, researchers reported in JAMA Network Open.

“A nationwide case-crossover investigation based on individual acute ischemic stroke onset time is imperative to quantify the association between acute ischemic stroke onset and hourly ambient heat exposure,” Xinlei Zhu, MS, from the School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and National Health Commission Key Lab of Health Technology Assessment, Fudan University, Shanghai, and colleagues wrote. “As one of the world’s largest middle-income countries, China has the highest stroke burden and is among the most vulnerable to global climate change. Accordingly, in the present time-stratified case-crossover analysis, we aimed to evaluate the association between hourly high ambient temperature and the onset of acute ischemic stroke using a nationwide registry of acute ischemic stroke. Additionally, we assessed possible association modifiers, such as geographic region, smoking, alcohol drinking, sex, age and history of other disease.”

City on a hot day
Higher hourly heat exposure conferred elevated risk for acute ischemic stroke. Image: Adobe Stock

The analysis involved 82,455 patients with acute ischemic stroke (mean age, 66 years; 63% men) included in a national registry of more than 200 stroke centers in China who were hospitalized in the warm seasons from 2019 to 2021.

The researchers found that a monotonically increasing risk for acute ischemic stroke onset was associated with higher temperatures, and that the excess acute ischemic stroke risk occurred immediately at lag 0 hours and persisted for 10 hours.

Compared with the reference temperature of 12.1°C, the cumulative OR over lag of 0 to 10 hours of acute ischemic stroke onset for extremely high temperatures (33.3°C) was 1.88 (95% CI, 1.65-2.13), Zhu and colleagues wrote.

The exposure-response curve was steeper in Northern institutions (OR = 1.8; 95% CI, 1.53-2.11) compared with Southern institutions (OR = 1.57; 95% CI, 1.31-1.87; P for z score = .27), according to the researchers.

The ORs were greater among men than women and for those with a history of dyslipidemia or atrial fibrillation compared with those without a history, but the differences were not significant, Zhu and colleagues wrote.

The study “presents robust evidence of high temperature as an important factor in increased risk of acute ischemic stroke onset,” the researchers wrote. “The results add valuable insights to the adverse cardiovascular outcome of climate warming and may benefit the formulation of public health strategies to reduce cerebrovascular risk associated with high ambient temperature under global warming. Additionally, the findings underscore the ongoing need for public health agencies to advocate for interventions that mitigate heat exposure and bolster cooling measures, particularly among populations at high risk for acute ischemic stroke.”

Quantitative Evaluation of Motion Compensation in Post-stroke Rehabilitation Training Based on Muscle Synergy

 If anything here gets survivors recovered it  is well hidden and thus useless for survivors.

Quantitative Evaluation of Motion Compensation in Post-stroke Rehabilitation Training Based on Muscle Synergy

  • 1School of Electrical and Information Engineering, Zhengzhou University, China
  • 2Zhengzhou University, China
  • 3The Rehabilitation Department, Fifth Affiliated Hospital of Zhengzhou University, China

The final, formatted version of the article will be published soon.

Stroke is the second leading cause of death globally and a primary factor contributing to disability. Unilateral limb motor impairment caused by stroke is the most common scenario. The bilateral movement pattern plays a crucial role in assisting stroke survivors on the affected side to relearn lost skills. However, motion compensation often lead to decreased coordination between the limbs on both sides. Furthermore, muscle fatigue resulting from imbalanced force exertion on both sides of the limbs can also impact the rehabilitation outcomes.In this study, an assessment method based on muscle synergy indicators was proposed to objectively quantify the impact of motion compensation issues on rehabilitation outcomes.Muscle synergy describes the body's neuromuscular control mechanism, representing the coordinated activation of multiple muscles during movement. 8 post-stroke hemiplegia patients and 8 healthy subjects participated in this study. During hand-cycling tasks with different resistance levels, surface electromyography signals were synchronously collected from these participants before and after fatigue. Additionally, a simulated compensation experiment was set up for healthy participants to mimic various hemiparetic states observed in patients.: Synergy symmetry and synergy fusion were chosen as potential indicators for assessing motion compensation. The experimental results indicate significant differences in synergy symmetry and fusion levels between the healthy control group and the patient group (p ≤ 0.05), as well as between the healthy control group and the compensation group. Moreover, the analysis across different resistance levels showed no significant variations in the assessed indicators (p > 0.05), suggesting the utility of synergy symmetry and fusion indicators for the quantitative evaluation of compensation behaviors. Although muscle fatigue did not significantly alter the symmetry and fusion levels of bilateral synergies (p > 0.05), it did reduce the synergy repeatability across adjacent movement cycles, compromising movement stability and hindering patient recovery. Based on synergy symmetry and fusion indicators, the degree of bilateral motion compensation in patients can be quantitatively assessed, providing personalized recommendations for rehabilitation training and enhancing its effectiveness.

Keywords: Rehabilitation training, motion compensation, surface electromyography, Muscle Synergy, Quantitative assessment

Received: 23 Jan 2024; Accepted: 20 Feb 2024.

Copyright: © 2024 Liu, Li, Zhang, Huo and Dong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

Wednesday, February 28, 2024

Implementing ward-based practice books to increase the amount of practice completed during inpatient stroke rehabilitation: a mixed-methods process evaluation

You don't understand ONE GODDAMN THING ABOUT SURVIVOR MOTIVATION, DO YOU? You create 100% recovery protocols and your survivor will be motivated to do the millions of reps needed because they are looking forward to 100% recovery. GET THERE! 

The problem is stroke researchers are not motivated to solve stroke. What the fuck is your solution to that failure? We still don't know how to motivate stroke medical 'professionals' to solve stroke to 100% recovery!

 Implementing ward-based practice books to increase the amount of practice completed during inpatient stroke rehabilitation: a mixed-methods process evaluation

To cite this article: Claire Stewart, Emma Power, Annie McCluskey, Suzanne Kuys & Meryl
Lovarini (22 Feb 2024): Implementing ward-based practice books to increase the amount
of practice completed during inpatient stroke rehabilitation: a mixed-methods process
evaluation, Disability and Rehabilitation, DOI: 10.1080/09638288.2024.2315502
To link to this article: https://doi.org/10.1080/09638288.2024.2315502
Claire Stewarta, Emma Powerb,c, Annie McCluskeyc,d, Suzanne Kuyse and Meryl Lovarinic
aaustralasian Rehabilitation outcomes Centre, University of Wollongong, Wollongong, australia; bthe University of technology sydney, Graduate
school of health, sydney, australia; csydney school of health sciences, the University of sydney, sydney, australia; dthe strokeed Collaboration,
sydney, australia; eschool of allied health, australian Catholic University, banyo, australia

ABSTRACT

Purpose: Stroke survivors must complete large amounts of practice to achieve functional improvements
but spend many hours inactive during their rehabilitation. We conducted a mixed methods process
evaluation exploring factors affecting the success of a 6-month behaviour change intervention to
increase use of ward-based practice books.
Methods: Audits of the presence, quality and use of ward based-practice books were conducted,
alongside focus groups with staff (n = 19), and interviews with stroke survivors (n = 3) and family
members (n = 4). Quantitative data were analysed descriptively. Focus group and interview transcripts
were analysed using qualitative analysis.
Results: Personal (patient-related) factors (including severe weakness, cognitive and communication
deficits of stroke survivors), staff coaching skills, understanding and beliefs about their role, affected
practice book use. Staff turnover, nursing shift work and a lack of action planning reduced success of
the behaviour change intervention.
Conclusions: Staff with the necessary skills and understanding of their role in implementing ward practice
overcame personal (patient-related) factors and assisted stroke survivors to successfully practice on the ward.
To improve success of the intervention, repeated training of new staff is required. In addition to audit and
feedback, team action planning is needed around the presence, quality, and use of ward practice books.
h IMPLICATIONS FOR REHABILITATION
• Ward-based practice books are one evidence-based strategy that can be used by rehabilitation
teams to increase the amount of practice completed by stroke survivors during inpatient rehabilitation.
• Stroke survivors’ personal factors (including severe weakness, cognitive and communication deficits),
staff beliefs about their role and coaching skills, affected stroke survivors ability to practice on the
ward using practice books.
• Staff with the necessary skills, understanding and belief about their role in implementing ward
practice can overcome personal (patient related) factors (such as severe weakness) and assist stroke
survivors to successfully practice on the ward.
• To increase the success of ward practice, repeated booster training of staff is required along with audit
and feedback and team action planning on the presence, quality, and use of ward practice books

Posttraumatic Stress Disorder Is Associated With Elevated Risk of Incident Stroke and Transient Ischemic Attack in Women Veterans

Since there is a 23% chance of stroke survivors getting PTSD what is your doctor doing to reduce that further risk of stroke due to PTSD? How EXACTLY  is your doctor preventing PTSD from stroke? And then treating it?

Maybe these?

Microbiome and Diet Could Mitigate PTSD Symptoms October 2023 

Psychoactive Ibogaine and Magnesium Show Promise for PTSD January 2024

Harnessing Psilocybin to Treat PTSD

Treating PTSD With Ecstasy? You Might Have Some Questions. May 2018

Ecstasy Was Just Labelled a 'Breakthrough Therapy' For PTSD by The FDA August 2017

 

Posttraumatic Stress Disorder Is Associated With Elevated Risk of Incident Stroke and Transient Ischemic Attack in Women Veterans

Originally publishedhttps://doi.org/10.1161/JAHA.123.033032Journal of the American Heart Association. 2024;0:e033032

Abstract

Background

Posttraumatic stress disorder (PTSD) has been associated with ischemic heart disease in women veterans, but evidence for associations with other cardiovascular disorders remains limited in this population. This retrospective longitudinal cohort study evaluated the association of PTSD with incident stroke/transient ischemic attack (TIA) in women veterans.

Methods and Results

Veterans Health Administration electronic health records were used to identify women veterans aged ≥18 years engaged with Veterans Health Administration health care from January 1, 2000 to December 31, 2019. We identified women veterans with and without PTSD without a history of stroke or TIA at start of follow‐up. Propensity score matching was used to match groups on age, race or ethnicity, traditional cardiovascular risk factors, female‐specific risk factors, a range of mental and physical health conditions, and number of prior health care visits. PTSD, stroke, TIA, and risk factors used in propensity score matching were based on diagnostic codes. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% CIs for associations of PTSD with an incident stroke/TIA composite. Subanalyses considered stroke and TIA separately, plus age‐ and race‐ or ethnicity‐stratified analyses were carried out.

The analytic sample included 208 092 women veterans (104 046 with and 104 046 without PTSD). PTSD was associated with a greater rate of developing stroke/TIA (HR, 1.33 [95% CI, 1.25–1.42], P<0.001). This elevated risk was especially pronounced in women <50 years old and in Hispanic/Latina women.

Conclusions

Findings indicate a strong association of PTSD with incident stroke/TIA in women veterans. Research is needed to determine whether addressing PTSD and its downstream consequences can offset this risk.

Outcomes and Predictors of Seizure Recurrence in Post-Stroke Epilepsy, A Retrospective Hospital-based Study

 Predicting post stroke epilepsy rather than preventing it is the HEIGHT OF STUPIDITY! And you're still employed in stroke? Look how long we've known of the problem.

Just maybe you want your doctor to try these solutions.


Cannabidiol May Reduce Seizures by Half in Hard-to-treat Epilepsy

Or maybe the nasal spray referred to in here:

Preventing Seizure-Caused Damage to the Brain

The answers are out there, does your doctor know about them? 

Mozart may reduce seizure frequency in people with epilepsy

 

A dietary supplement dampens the brain hyperexcitability seen in seizures or epilepsy

 The latest here:

Outcomes and Predictors of Seizure Recurrence in Post-Stroke Epilepsy, A Retrospective Hospital-based Study

, , , , , , , , , , , , ,
https://doi.org/10.1016/j.clineuro.2024.108208Get rights and content

Highlights

  • •

    Recurrence in Post-Stroke seizure (PSS) is associated with significant functional decline in stroke patients.

  • •

    Choice of anti-seizure medications (ASMs) may influence the morbidity and mortality.

  • •

    Future research is needed to explore the effects of ASMs on PSS pathophysiology.

Abstract

Background

The occurrence of seizures following a stroke is a well-recognized complication associated with a significant increase in morbidity and mortality. Despite the numerous studies examining outcomes and risk factors related to post-stroke seizures (PSS), there remains a lack of clarity(And you incompetently didn't create a protocol on how to prevent this problem?)  regarding the clinical characteristics, treatment, and PSS recurrence (PSSR) rates in patients experiencing their initial episode of PSS.

Purpose

This study aimed to determine the risk factors for developing recurrent seizures after first PSS and their effects on functional outcomes and mortality.

Methods

All patients underwent an electroencephalography (EEG) and were monitored for a minimum of 24 months following the first PSS. The primary endpoint was the recurrence of seizures. Predictive factors for PSSR were determined by using the Cox-proportional hazards model, and the cumulative latency of recurrence at 90, 180, 360, and 720 days was estimated using Kaplan-Meier analysis.

Results

Seizure recurred in 36.8% (39/106). Significant association of PSSR was noted with female gender, use of older anti-seizure medications (ASMs) (p<0.001), EEG findings as focal slow wave activity (p<0.001), Ictal epileptiform abnormalities (p=0.015), status epilepticus (p=0.015), and with severe disability (p=0.008). However, multivariate cox-proportional hazards model showed significant association of female gender (HR=3.28; 95% CI: 1.42-7.58; p=0.006). Hazard ratio (HR) was increased with older ASMs use, focal aware seizure types, Ictal EAs, and periodic discharges on EEG; though, statistically significant.

Conclusion

Factors such as the type of ASMs, EEG findings, and seizure type were significantly linked to PSSR. Female gender was the only independent predictor established. Additionally, significant functional decline was reported with recurrence.

More at link.

Case report: Intrathecal baclofen therapy improved gait pattern in a stroke patient with spastic dystonia

'Improved' may be good enough for you but definitely not for your survivor!  Survivors want 100% recovery! When the hell are you going to deliver that?


Case report: Intrathecal baclofen therapy improved gait pattern in a stroke patient with spastic dystonia

  • 1Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea
  • 2Department of Neurosurgery and Brain Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea
  • 3Graduate Program of Biomedical Engineering, Yonsei University College of Medicine, Seoul, Republic of Korea
  • 4Brain Korea 21 FOUR Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea
  • 5Rehabilitation Institute of Neuromuscular Disease, Yonsei University College of Medicine, Seoul, Republic of Korea

Background: Intrathecal baclofen (ITB) therapy, a viable alternative for unsuitable candidates of conventional spasticity medications, is a preferred method of administration over the oral route. Owing to its enhanced bioavailability, ITB ensures a more effective delivery at the target site.

Objective: There is a lack of conclusive evidence regarding the use of ITB treatment in managing ambulatory patients with spastic dystonia. Before ITB pump implantation, patients commonly undergo an ITB bolus injection trial to rule out potential adverse reactions and verify the therapeutic effects on hypertonic issues. In this report, we highlight a case of spastic dystonia, particularly focusing on an ambulatory patient who demonstrated significant improvement in both the modified Ashworth scale (MAS) score and gait pattern following the ITB injection trial.

Case report: This case report outlines the medical history of a 67-year-old male diagnosed with left-side hemiplegia and spastic dystonia, resulting from his second episode of intracranial hemorrhage in the right thalamus. An ITB injection trial was initiated because the patient was not suitable for continued botulinum toxin injections and oral medications. This was due to the persistent occurrence of spastic dystonia in both the upper and lower extremities. The patient underwent a four-day ITB injection trial with progressively increasing doses, resulting in improved MAS scores and gait parameters, including cadence, step length, step time, stride length, and stride time were increased. Particularly, kinematic gait analysis demonstrates a substantial improvement of increased knee flexion in the swing phase in stiff knee gait pattern. These findings indicated a gradual reduction in spasticity-related symptoms, signifying the positive effect of the ITB injection trial. The patient eventually received an ITB pump implantation.

Conclusion: In this post-stroke patient with spastic dystonia, ITB therapy has demonstrated effective and substantial management of spasticity, along with improvement in gait patterns.

Introduction

Spasticity is defined as velocity-dependent hypertonia and tendon jerk hyperreflexia, resulting from stretch reflex excitability (1, 2). In contrast, dystonia involves involuntary muscle contractions, often leading to abnormal posturing and twisting movements (3). There are different types of dystonia, including focal dystonia such as blepharospasm, oromandibular dystonia, spasmodic dysphonia, torticollis, and writer’s cramp (4, 5). Generalized dystonia involves the leg, trunk, and at least one other body part (6). Spastic dystonia, which is a specific aspect of the upper motor neuron syndrome, is characterized by involuntary tonic contractions caused by the inability to relax the muscles (1). Spastic overactivity, a prevalent subtype of muscle hypertonia is frequently observed in patients with spinal or cerebral dysfunction. The term “spastic overactivity,” frequently employed to describe stretch-sensitive muscle overactivity, poses difficulties in precisely defining this intricate condition, as it includes spasms, involuntary motions, and undesired muscle activity (7).

The primary treatment for muscle overactivity and generalized dystonia typically involves oral medications, including baclofen, benzodiazepines, anticholinergics, antispasmodics, and levodopa (8, 9). Baclofen, an agonist for gamma-aminobutyric acid (GABA) B receptors, inhibits mono- and polysynaptic reflexes in the central and peripheral nervous systems, contributing to its therapeutic effect in reducing spasticity (10). Previous research explored the effectiveness of oral baclofen in managing poststroke spasticity, focusing on ankle stiffness and clonus during passive stretch, and identified factors influencing responsiveness (2). Nevertheless, oral baclofen may not always be effective for all patients due to the low concentration of baclofen in the cerebrospinal fluid (2). These non-responders exhibited a positive effect at higher cerebrospinal fluid levels achievable through intrathecal baclofen injection (2). Benzodiazepines demonstrate limited effectiveness, with approximately 16 to 23% showing a good clinical response (11). Trihexyphenidyl, a widely used agent, is a muscarinic acetylcholine receptor antagonist with a notably variable therapeutic dosage. While children may effectively respond to doses as low as 4 mg/day, adults are less likely to tolerate increasing dosages when necessary as they tend to be more sensitive to side effects such as memory loss, confusion, restlessness, insomnia, and nightmares (11). Intramuscular botulinum toxin injections can be beneficial in reducing focal spasticity in specific muscle groups (12, 13). Adverse effects, including dry mouth, fatigue, and flu-like symptoms, may occur when the drug spreads to unintended muscles and organs during botulinum toxin therapy (13). In some cases, these manifestations can escalate to systemic botulism signs. Although recent studies support the safety of botulinum toxin high-dose therapy, official documents recommend maximum botulinum toxin doses of onabotulinumtoxinA (Botox®, Allergan, Irvine, CA, USA) 400 units for upper limb or lower limb spasticity (14, 15). In the 1980s, intrathecal baclofen (ITB) therapy emerged as potentially effective next-in-line management for severe spasticity unresponsive to oral medications (9, 16–18), delivering concentrated drug doses directly into the intrathecal space to minimize systemic toxicity (19). Given the delicate nature of baclofen therapy and its potential complications, ITB bolus injections are administered to rule out adverse reactions and ensure the drug’s therapeutic effect on hypertonia before ITB pump implantation (9). ITB therapy offers reversible treatment of spasticity and effective modulation of muscle tone to reduce severe spasticity, for it was approved for the management of spasticity (20, 21). However, current literature highlights the necessity for additional research on the effectiveness of ITB treatment for mixed hypertonia, including spastic dystonia (21). In particular, additional research dedicated to ambulatory patient is essential.

Evaluating the effectiveness of treatment is crucial in managing spastic overactivity, and commonly employed methods include high-speed passive muscle stretching assessments like the modified Ashworth scale (MAS) and the modified Tardieu scale. However, these evaluations solely gauge resistance to passive movement and lack insight into muscle dynamics during dynamic tasks like gait (22). These scales also rely on subjective interpretation by clinicians, making it challenging to differentiate specific types of spastic hyperactivity, such as spasticity, spastic dystonia, and spastic co-contraction. Therefore, surface electromyography or gait analysis reflecting muscle activity during dynamic tasks has recently been used to classify spastic overactivity in detail (23, 24). Gait analysis, in particular, assesses muscle hyperactivity during functional tasks, allowing for a comprehensive understanding of specific movement patterns and continuous monitoring of various gait factors (23). Moreover, a transient decrease in spastic dystonia following ITB therapy can induce changes in gait pattern that are not easily discernible through casual observation. In such cases, gait analysis offers precise and objective measurements, detecting even subtle modifications in ambulatory performance (25).

Herein, we report an ambulatory patient with spastic dystonia demonstrating significant improvement in both the MAS score and gait pattern following the ITB bolus injection trial. The objective of this case study is to enhance comprehension of the response of adult spastic dystonia patients to ITB bolus injections and identify prospective recipients who may experience improved gait after ITB pump implantation. This study also represents the first stage in assessing whether the walking performance observed during the ITB bolus injection trial, evaluated through computerized gait analysis, is associated with changes following ITB pump implantation.

More at link.