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.

Monday, August 30, 2021

Transcirculation Embolization to New Territory During Mechanical Thrombectomy for Acute Ischemic Stroke

 They don't say but I'm sure their definition of excellent is not what the survivor would say. Am I 100% recovered? Yes/No? Only yes can be defined as excellent.

Transcirculation Embolization to New Territory During Mechanical Thrombectomy for Acute Ischemic Stroke

First Published August 25, 2021 Case Report 

Embolization in new territories (ENT) is a known complication of mechanical thrombectomy with incidence dependent upon a variety of procedural factors. We present 2 cases of anterior circulation to posterior circulation ENT. These cases were managed with manual aspiration thrombectomy with excellent radiographic and clinical outcome. We present the available literature involving ENT along with our experience in management.

 

Self-Directed Exergaming for Stroke Upper Limb Impairment Increases Exercise Dose Compared to Standard Care

But what EXACTLY is your doctor doing to ensure you can do these extra exercxises? Like 100% recovery protocols? Oh s/he doesn't have any? Well then you are totally fucking screwed because your doctors are completely failing at their job.  The board of directors needs to be fired if that is the case. You can't let failure to continue forever in your hospital. Your children and grandchildren just might want better recovery than you did.

Oops, I'm not playing by the polite rules of Dale Carnegie,  'How to Win Friends and Influence People'. 

Telling stroke medical persons they know nothing about stroke is a no-no even if it is true. 

Politeness will never solve anything in stroke. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will try to ream me out for making them look bad by being truthful , I look forward to that day.

Self-Directed Exergaming for Stroke Upper Limb Impairment Increases Exercise Dose Compared to Standard Care

First Published August 27, 2021 Research Article 

Background

One of the strongest modifiable determinants of rehabilitation outcome is exercise dose. Technologies enabling self-directed exercise offer a pragmatic means to increase dose, but the extent to which they achieve this in unselected cohorts, under real-world constraints, is poorly understood. Objective. Here we quantify the exercise dose achieved by inpatient stroke survivors using an adapted upper limb (UL) exercise gaming (exergaming) device and compare this with conventional (supervised) therapy.  

Methods

Over 4 months, patients presenting with acute stroke and associated UL impairment were screened at a single stroke centre. Participants were trained in a single session and provided with the device for unsupervised use during their inpatient admission.  

Results

From 75 patients referred for inpatient UL therapy, we recruited 30 (40%), of whom 26 (35%) were able to use the device meaningfully with their affected UL. Over a median enrolment time of 8 days (IQR: 5–14), self-directed UL exercise duration using the device was 26 minutes per day (median; IQR: 16–31), in addition to 25 minutes daily conventional UL therapy (IQR: 12–34; same cohort plus standard care audit; joint n = 50); thereby doubling total exercise duration (51 minutes; IQR: 32–64) relative to standard care (Z = 4.0, P <.001). The device enabled 104 UL repetitions per day (IQR: 38–393), whereas conventional therapy achieved 15 UL repetitions per day (IQR: 11–23; Z = 4.3, P <.001).  

Conclusion. 

Self-directed adapted exergaming enabled participants in our stroke inpatient cohort to increase exercise duration 2-fold, and repetitions 8-fold, compared to standard care, without requiring additional professional supervision.

 

Statin Users See Good Changes in Atherosclerotic Plaques

More reasons for your stroke hospital to have a protocol on this. 

Statin Users See Good Changes in Atherosclerotic Plaques

Plaques undergo metamorphosis toward harder, denser composition

A computer rendering of atherosclerotic plaque buildup causing a blood clot in an artery.

While statin therapy didn't curb overall atherosclerotic plaque progression on serial coronary CT angiography, it was associated with plaques transforming to a lower-risk composition.

Statin use was associated with volume decreases in low-attenuation plaque and fibro-fatty plaque and greater progression of high-density calcium plaque and very dense 1K plaque. In contrast, untreated coronary lesions increased in volume over time for all calcified and noncalcified plaque types alike.

Coronary lesions without low-attenuation plaque or fibro-fatty plaque at baseline changed after statin therapy to include more dense calcium, reported Jeroen Bax, MD, PhD, of Leiden University Medical Center in The Netherlands, and collaborators of the PARADIGM study in JAMA Cardiology.

Moreover, increasing calcium density was associated with slower overall plaque progression -- a finding in line with prior work tying 1K plaque, with its very dense calcium, with a reduced risk of acute coronary syndrome.

"Atherosclerotic features associated with ruptured plaques are large necrotic cores with an inflamed and thin fibrous cap. However, plaque features hypothesized to contribute to plaque stability are small necrotic cores that have been replaced by sheets of calcification," Bax and colleagues wrote.

PARADIGM included 857 patients (mean age 62.1 years, 63.0% men) undergoing serial coronary CT angiography 2 or more years apart in 2013-2016, and was conducted at 13 sites in seven countries.

Images of 2,458 coronary lesions were assessed, over two-thirds of which were in patients treated with statins.

Plaque composition was categorized according to calcium content on CT angiography: low attenuation (-30 to 75 Hounsfield units [HU]), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1,000 HU), and 1K (>1,000 HU).

Based on study results, plaques with growing attenuation over 700 HU "may have protective implications, but this hypothesis requires further study," Bax and colleagues noted.

The observational study left room for unmeasured confounding. As such, the authors were unable to claim that statin use directly causes compositional plaque changes.

  • author['full_name']

    Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow

Disclosures

The study was supported by grants or gifts from the National Research Foundation of Korea, the Dalio Institute of Cardiovascular Imaging, and the Michael Wolk Heart Foundation.

Bax reported no disclosures. Co-authors reported ties to industry and other institutions.

 

Deintensification or No Statin Treatment Is Associated With Higher Mortality in Patients With Ischemic Stroke or Transient Ischemic Attack

Well shit, your doctor should have been prescribing statins way back in 2003 when only rats/mice were tested yet.  Does your hospital have a protocol on statins? If not your board of directors needs to be fired.

Statins.

tested in rats from 2003

http://Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke  

Simvastatin Attenuates Stroke-induced Splenic Atrophy and Lung Susceptibility to Spontaneous Bacterial Infection in Mice

Or,

Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons   October 2012

tested in humans, March, 2011

http://www.medwirenews.com/39/91658/Stroke/Acute_statin_therapy_improves_survival_after_ischemic_stroke.html

And now lost even to the Wayback Machine

So I think this below is the actual research;

Association Between Acute Statin Therapy, Survival, and Improved Functional Outcome After Ischemic Stroke April 2011

The latest here:

Deintensification or No Statin Treatment Is Associated With Higher Mortality in Patients With Ischemic Stroke or Transient Ischemic Attack

Originally publishedhttps://doi.org/10.1161/STROKEAHA.120.030089Stroke. 2021;52:2521–2529

Background and Purpose:

Practice guidelines recommend that most patients receive moderate- or high-potency statins after ischemic stroke or transient ischemic attack (TIA) of atherosclerotic origin. We tested the association of different patterns of potency for prescribed statin therapy—assessed before admission and at hospital discharge for ischemic stroke or TIA—on mortality in a large, nationwide sample of US Veterans.

Methods:

The study population included patients with an ischemic stroke or TIA occurring during 2011 at any of the 134 Veterans Health Administration facilities. We used electronic outpatient pharmacy files to identify statin dose at hospital admission and within 7 days after hospital discharge. We categorized statin dosing as low, moderate, or high potency; moderate or high potency was considered at goal. We created 6 mutually exclusive groups to reflect patterns of statin potency from hospital admission to discharge: goal to goal, low to goal, goal to low or goal to none (deintensification), none to none, none to low, and low to low. We used logistic regression to compare 30-day and 1-year mortality across statin potency groups.

Results:

The population included 9380 predominately White (71.1%) men (96.3%) who were hospitalized for stroke or TIA. In this sample, 34.1% of patients (n=3194) were discharged off a statin medication. Deintensification occurred in 14.0% of patients (n=1312) and none to none in 20.5% (n=1924). Deintensification and none to none were associated with a higher odds of mortality as compared with goal to goal (adjusted odds ratio 1-year mortality: deintensification versus goal to goal, 1.26 [95% CI, 1.02–1.57]; none to none versus goal to goal, 1.59 [95% CI, 1.30–1.93]). Adjustments for differences in baseline characteristics using propensity weighted scores demonstrated similar results.

Conclusions:

Underutilization of statins, including no treatment or underdosing after stroke (deintensification), was observed in approximately one-third of veterans with ischemic stroke or TIA and was associated with higher mortality when compared with patients who were at goal for statin prescription dosing.

Footnotes

The Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.120.030089.

For Sources of Funding and Disclosures, see page 2528.

Correspondence to: Jennifer L. Dearborn-Tomazos, MD, Department of Neurology, Beth Israel Deaconess Hospital, Harvard Medical School, 330 Brookline Ave, Palmer 127, Boston, MA 02215. Email
 

Predicting 90-Day Outcome After Thrombectomy: Baseline-Adjusted 24-Hour NIHSS Is More Powerful Than NIHSS Score Change

In what parallel universe do you live where you think that predicting failure to recover is of any interest or help to survivors? 

 

Predicting 90-Day Outcome After Thrombectomy: Baseline-Adjusted 24-Hour NIHSS Is More Powerful Than NIHSS Score Change

Originally publishedhttps://doi.org/10.1161/STROKEAHA.120.032487Stroke. 2021;52:2547–2553

Background and Purpose:

The National Institutes of Health Stroke Scale (NIHSS) measured at an early time point is an appealing surrogate marker for long-term functional outcome of stroke patients treated with endovascular therapy. However, definitions and analytical methods for an early NIHSS-based outcome measure that optimize power and precision in clinical studies are not well-established.

Methods:

In this post-hoc analysis of our prospective observational study that enrolled endovascular therapy-treated patients at 12 comprehensive stroke centers across the US, we compared the ability of 24-hour NIHSS, ΔNIHSS (baseline minus 24-hour NIHSS), and percentage change (NIHSS×100/baseline NIHSS), analyzed as continuous and dichotomous measures, to predict 90-day modified Rankin Scale (mRS) using logistic regression (adjusted for age, baseline NIHSS, glucose, hypertension, Alberta Stroke Program Early CT Score, time to recanalization, recanalization status, and intravenous thrombolysis) and Spearman ρ.

Results:

Of 485 patients in the BEST (Blood Pressure After Endovascular Stroke Therapy) cohort, 446 (92%) with 90-day follow-up data were included. An absolute 24-hour NIHSS, adjusted for baseline in multivariable modeling, had the highest predictive power of all definitions evaluated (aR2 0.368 and adjusted odds ratio 0.79 [0.75–0.84], P<0.001 for mRS score 0–2; aR2 0.444 and adjusted odds ratio 0.84 [0.8–0.86] for ordinal mRS). For predicting mRS score of 0–2 with a cut point, the second most efficient approach, the optimal threshold for 24-hour NIHSS score was ≤7 (sensitivity 80.1%, specificity 80.4%; adjusted odds ratio 12.5 [7.14–20], P<0.001), followed by percent change in NIHSS (sensitivity 79%, specificity 58.5%; adjusted odds ratio 4.55 [2.85–7.69], P<0.001).

Conclusions:

Twenty-four–hour NIHSS, adjusted for baseline, was the strongest predictor of both dichotomous and ordinal 90-day mRS outcomes for endovascular therapy-treated patients. A dichotomous 24-hour NIHSS score of ≤7 was the second-best predictor. Although ΔNIHSS, continuous and dichotomized at ≥4, predicted 90-day outcomes, absolute 24-hour NIHSS definitions performed better.

Footnotes

This manuscript was sent to Ajay K. Wakhloo, Guest Editor, for review by expert referees, editorial decision, and final disposition.

The Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.120.032487.

 
 

World Stroke Day Campaign 2021 Launch

I most certainly am not going to waste 65 minutes of my time listening to the wrong focus on solving stroke. 

World Stroke Day Campaign 2021 Launch

World Stroke Day Campaign 2021 Launch

01:05:00

Aug 25, 2021 02:46 PM

 

 

Access to Mechanical Thrombectomy for Ischemic Stroke in the United States

All the more reason to have stroke protocols to 100% recovery for any situation. If we had any leadership at all in stroke we would solve this problem. But since we don't, 1/6 of the United States is screwed if they have a stroke and almost all of third world countries.  This meme from World Stroke Day a few years ago was a complete lie.

The whole problem is the stroke world thinks nothing needs to be done as proven by this meme on World Stroke Day a few years ago. Whomever approved that is a complete blithering idiot.

Access to Mechanical Thrombectomy for Ischemic Stroke in the United States

 
Originally publishedhttps://doi.org/10.1161/STROKEAHA.120.033485Stroke. 2021;52:2554–2561

Background and Purpose:

Mechanical thrombectomy helps prevent disability in patients with acute ischemic stroke involving occlusion of a large cerebral vessel. Thrombectomy requires procedural expertise and not all hospitals have the staff to perform this intervention. Few population-wide data exist regarding access to mechanical thrombectomy.

Methods:

We examined access to thrombectomy for ischemic stroke using discharge data from calendar years 2016 to 2018 from all nonfederal emergency departments and acute care hospitals across 11 US states encompassing 80 million residents. Facilities were classified as hubs if they performed mechanical thrombectomy, gateways if they transferred patients who ultimately underwent mechanical thrombectomy, and gaps otherwise. We used standard descriptive statistics and unadjusted logistic regression models in our primary analyses.

Results:

Among 205 681 patients with ischemic stroke, 100 139 (48.7% [95% CI, 48.5%–48.9%]) initially received care at a thrombectomy hub, 72 534 (35.3% [95% CI, 35.1%–35.5%]) at a thrombectomy gateway, and 33 008 (16.0% [95% CI, 15.9%–16.2%]) at a thrombectomy gap. Patients who initially received care at thrombectomy gateways were substantially less likely to ultimately undergo thrombectomy than patients who initially received care at thrombectomy hubs (odds ratio, 0.27 [95% CI, 0.25–0.28]). Rural patients had particularly limited access: 27.7% (95% CI, 26.9%–28.6%) of such patients initially received care at hubs versus 69.5% (95% CI, 69.1%–69.9%) of urban patients. For 93.8% (95% CI, 93.6%–94.0%) of patients with stroke at gateways, their initial facility was capable of delivering intravenous thrombolysis, compared with 76.3% (95% CI, 75.8%–76.7%) of patients at gaps. Our findings were unchanged in models adjusted for demographics and comorbidities and persisted across multiple sensitivity analyses, including analyses adjusting for estimated stroke severity.

Conclusions:

We found that a substantial proportion of patients with ischemic stroke across the United States lacked access to thrombectomy even after accounting for interhospital transfers. US systems of stroke care require further development to optimize thrombectomy access.

Vaccine Effect or Functional Neurological Disorder?

 The real takeaway is that the problems associated with this are treatable while COVID-19 can still cause you massive problems. Get vaccinated.

Current Concepts in Diagnosis and Treatment of Functional Neurological Disorders

 

"Correlation does not imply causation,"

The latest here:

Vaccine Effect or Functional Neurological Disorder?

— COVID vaccination may trigger FND, much like other stressors

A glitch/distortion of a computer rendering of a brain

COVID-19 vaccination can be one of a number of events that may trigger functional neurological disorder (FND), experts said.

Two cases of young women manifesting FND after COVID-19 vaccination were reported by Alfonso Fasano, MD, PhD, of the University of Toronto, and Antonio Daniele, MD, PhD, of Università Cattolica del Sacro Cuore in Rome, in a letter to the Journal of Neurology, Neurosurgery, and Psychiatry.

Two other published reports showed probable FND precipitated by COVID-19 vaccine administration, highlighting that FND should be considered when assessing post-vaccine neurologic symptoms, wrote Matthew Butler, MD, of Kings College London in England, and co-authors in the Journal of Neuropsychiatry and Clinical Neuroscience.

FND involves a disruption in normal brain mechanisms for controlling the body. It can be triggered by physical or emotional events including head injury, medical or surgical procedures, or vaccinations. People with FND may present with a range of neurological symptoms such as seizures, sensory abnormalities, gait or balance disturbance, or weakness. FND is distinct from feigning because patients perceive their symptoms as involuntary. Once it is recognized and diagnosed, FND can be treated.

"We strongly encourage clinicians to be aware of the possibility for FND in response to SARS-CoV-2 vaccinations," Butler told MedPage Today. "FND can be a serious and debilitating condition; however, it does not implicate any vaccine constituents and should not hamper ongoing vaccination efforts."

"Making clinicians aware of this can benefit people with FND reactions to vaccines, as well as maintaining public confidence in the vaccine," Butler added. "Rigorous causality assessments should occur when FND reactions are suspected."

"Among the various adverse events which might be observed after COVID-19 vaccination, the occurrence of functional -- once called psychogenic -- neurological disorders might be a challenging issue for healthcare providers, media, and public opinion with a negative impact on vaccination campaigns," noted Fasano and Daniele.

"In our view, FND following COVID-19 vaccination will not be a rare phenomenon and will be widely covered by the media, being interpreted as a direct consequence of the vaccine, as already seen in the past," they wrote.

The first case from Fasano and Daniele involved a woman who presented with a short episode of generalized psychogenic non-epileptic seizures 20 minutes after receiving her second dose of the Pfizer-BioNTech vaccine. The event was followed by different episodes that included an inability to move her whole body. No postictal period followed these episodes, some of which were captured by video-electroencephalography and did not show any epileptic activity.

The second patient had persistent dizziness and reported loss of tactile sensitivity in her right arm and leg about 2 weeks after receiving the AstraZeneca vaccine. Her brain CT scan was unremarkable, and neurological examination did not show objective loss of tactile or pain sensitivity.

"In both patients, neurological symptoms were characterized by a sudden onset and overt inconsistency, as typically observed in patients with FND," Fasano and Daniele wrote.

The cases reported by Butler and colleagues involved previously healthy women, both in their 30s. One had probable FND after her first dose of the Pfizer-BioNTech vaccine; the other, after her first Moderna shot.

"The close development of functional motor symptoms after the vaccine does not implicate the vaccine as the cause of those symptoms," observed Alberto Espay, MD, MSc, of the University of Cincinnati, who was not involved with the case reports.

"Correlation does not imply causation," Espay told MedPage Today. "If neurological symptoms following vaccination are determined to be functional during a neurological exam, then the vaccination can only be considered a stressor or precipitant, much like any other stressor might, such as a motor vehicle accident or sleep deprivation."

Earlier this year, a group led by David Perez, MD, MMSc, of Massachusetts General Hospital in Boston, published a paper in JAMA Neurology that discussed videos that had emerged on Facebook, YouTube, and other channels showing people with severe neurological symptoms, such as convulsions and difficulty walking, after receiving a COVID-19 vaccine.

"The spread of these videos could fuel vaccine hesitancy by giving an overly simplistic impression of potential links between the vaccine and major neurological symptoms," Perez said in a statement. "Instead, these are symptoms of a real, brain-based disorder that sits at the intersection of neurology and psychiatry."

"It is recognized that physical events such as head injury, surgeries, or vaccinations in some individuals can precipitate the development of FND," Perez told MedPage Today. "In such instances, one of the important mechanisms is the attention drawn to the body."

Neurologists and other healthcare professionals have an obligation to explain FND to the public, he added.

While health experts have tried to stress that in most cases, there is no direct link between COVID-19 vaccines and various media-covered adverse events, more needs to be done, Fasano and Daniele noted.

This is especially true in light of misinformation and conspiracy beliefs about the COVID-19 pandemic, which are "now enriched by the theories of anti-vaccine movements," they wrote. "We suggest that the medical community should be more vocal in informing the media and public opinion about FND, thus making a further step towards the establishment of 'eHealth literacy.'"

Last Updated August 23, 2021
  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

The study by Fasano and Daniele was funded by the University of Toronto and the University Health Network Chair in Neuromodulation and Multidisciplinary Care.

Fasano and Daniele reported no competing interests.

Butler and co-authors reported relationships with the National Institutes of Health Research, the NIH National Institute of Neurological Disorders and Stroke, the United Kingdom Research and Innovation/Medical Research Council, and the European Union's Horizon 2020 research and innovation program ZikaPLAN.

 
 

Automated emergent large vessel occlusion detection by artificial intelligence improves stroke workflow in a hub and spoke stroke system of care

Flawed research. No measurement of 100% recovery. Until we get survivors in charge most stroke research will fail to be useful and what is needed.

 Automated emergent large vessel occlusion detection by artificial intelligence improves stroke workflow in a hub and spoke stroke system of care

  1. Lucas Elijovich1,2,
  2. David Dornbos III2,
  3. Christopher Nickele2,
  4. Andrei Alexandrov1,
  5. Violiza Inoa-Acosta1,2,
  6. Adam S Arthur2,
  7. Daniel Hoit2
  1. Correspondence to Dr Lucas Elijovich, Semmes-Murphey Neurologic and Spine Institute, Memphis, TN 38120, USA; lelijovich@semmes-murphey.com

Abstract

Background Emergent large vessel occlusion (ELVO) acute ischemic stroke is a time-sensitive disease.

Objective To describe our experience with artificial intelligence (AI) for automated ELVO detection and its impact on stroke workflow.

Methods We conducted a retrospective chart review of code stroke cases in which VizAI was used for automated ELVO detection. Patients with ELVO identified by VizAI were compared with patients with ELVO identified by usual care. Details of treatment, CT angiography (CTA) interpretation by blinded neuroradiologists, and stroke workflow metrics were collected. Univariate statistical comparisons and linear regression analysis were performed to quantify time savings for stroke metrics.

Results Six hundred and eighty consecutive code strokes were evaluated by AI; 104 patients were diagnosed with ELVO during the study period. Forty-five patients with ELVO were identified by AI and 59 by usual care. Sixty-nine mechanical thrombectomies were performed.

Median time from CTA to team notification was shorter for AI ELVOs (7 vs 26 min; p<0.001). Door to arterial puncture was faster for transfer patients with ELVO detected by AI versus usual care transfer patients (141 vs 185 min; p=0.027). AI yielded a time savings of 22 min for team notification and a 23 min reduction in door to arterial puncture for transfer patients.(But you don't even know how fast this has to be to get to 100% recovery. Without that knowledge you don't even know what goal to shoot for.)

Conclusions AI automated alerts can be incorporated into a comprehensive stroke center hub and spoke system of care. The use of AI to detect ELVO improves clinically meaningful stroke workflow metrics, resulting in faster treatment times for mechanical thrombectomy.

Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

View Full Text

Young Adult Survivors of Preterm Birth Are at Increased Risk of Stroke: The Missing Link

 Unless you can time travel back to your birth and prevent your preterm birth this gives no preventative measures on preventing these early strokes.

Young Adult Survivors of Preterm Birth Are at Increased Risk of Stroke: The Missing Link

Originally publishedhttps://doi.org/10.1161/STROKEAHA.121.035283Stroke. 2021;52:2618–2620

See related article, p 2609

Adult survivors of prematurity are at increased risk of hypertension, diabetes, lipid disorders, and ischemic heart disease.1–4 Crump et al5 used data from the Swedish Birth Register and Swedish Death Register to investigate stroke risk in premature infants. This national retrospective cohort study included 95% of all singleton births in Sweden from 1973 to 1994 who survived to 18 years of age, were still living in Sweden, and had gestational age information in the birth register for a total of 2 140 866 individuals. Participants were followed up for first-time stroke (identified via the International Classification of Disease codes) through 2015, allowing 28 million years of follow-up. People with stroke at <18 years of age were excluded, and thus ages at the time of stroke were 18 to 43 years for a total of 4861 strokes (0.2%). Cox regression was used to examine stroke risks associated with gestational age at birth. Participants were grouped as follows: early preterm (22–33 weeks), late preterm (34–36 weeks), early term (37–38 weeks), full term (39–41 weeks), which was the reference group, and post-term (42 weeks). In addition, the first 2 groups were combined to provide summary estimates for preterm birth (<37 weeks). Importantly, preterm infants were also compared with full-term siblings, in the 1.7 million with siblings, to reduce confounding familial, genetic, or environmental risk factors for stroke unrelated to preterm birth. Low gestational age (22–33 weeks) was the highest risk group for any stroke; adjusted hazard ratio (1.42 [95% CI, 1.11–1.81]) and estimates were similar for ischemic or hemorrhagic stroke. Of note, stroke risk increased by 3% for each week of lower gestation, that is, the greater the degree of prematurity, the greater the stroke risk. After comparison to full-term siblings, termed co-sibling analysis, the hazard ratios attenuated slightly but still suggested increased risk of stroke. The age of the study cohort ranged from 25 to 43 years at the time of the study. Thus, the current cohort reports on stroke risk in young adults rather than all adults. While this is a weakness in one sense, factors contributing to stroke risk in young adults are of high interest.The incidence of stroke is changing over time, but the changes vary by age. While the incidence is decreasing in people over 65 years of age, it is increasing in young adults.6 This increase in young adult stroke is occurring on the backdrop of improved outcomes and increased life expectancy in children with critical or chronic medical conditions such as prematurity.7 Crump et al highlighted the high incidence of known adult stroke risk factors and elevated stroke risk in adult survivors of preterm birth. However, the mechanisms that underpin these observations are not well understood. To date, multiple mechanisms have been proposed including arterial stiffness, impairment in arterial vasodilatation, and tissue developmental arrest. A plausible unifying process, and potentially the missing link that explains the association between prematurity and young adult stroke risk, is vascular endothelial dysfunction at the microcirculatory level of the tissue capillary bed. Acute and chronic disturbances in oxygenation, altered hemodynamics, inflammation, and infection activate signaling molecules such as bradykinin and vascular endothelial growth factor and the production of NO through numerous pathways. Sustained NO activation, reduced NO bioavailability, and overproduction of reactive oxygen signaling results in oxidative stress and the tipping of normal vascular endothelial function into that of dysfunction. This results in disrupted vascular homeostasis, abnormal vasomotor tone and vascular reactivity, vascular remodeling, and a prothrombotic state.8 Vascular endothelial dysfunction is shown to begin early in childhood and is recognized as an early pathophysiological process in atherogenesis—the subclinical precursor of arteriosclerosis or arterial stiffness.9 This may result in accelerated vascular aging, which then eventually contributes to increased ischemic risk.

The reported relationship between gestational age and stroke risk is also striking as it points to critical developmentally determined periods of vulnerability. This is in-keeping with theories of selective vulnerability whereby the brain injury mostly reflects the specific cell lines maturing at the time of injury.10 It is notable that collagen content within the vascular wall is known to increase between the 12th and 25th weeks of fetal life.11 From the 25th to 42nd week of gestation, there is an increase in elastin production triggered by the release of endothelial factors such as platelet-derived growth factor and insulin-like growth factors. This is a critical period of vascular remodeling in which the elastin/collagen ratio plays a major role in the development of arterial compliance. Much of this work has been in systemic arteries necessitating further studies within the blood vessels of the brain.11 However, these observations of a lower elastin/collagen ratio in preterm compared with term infants and arterial stiffness provide a likely pathological basis for the association between gestation and stroke risk.

A major strength of this work was the co-sibling analysis, which demonstrated that the increased risk in ischemic and hemorrhagic stroke was partially explained by familial (genetic or environmental) factors. Modifiable environmental and lifestyle factors such as smoking and exercise are known to be important for the maintenance of vascular health and are, therefore, tangible interventions that target many of the proposed mechanisms of ischemic injury in adults. Crump et al also highlight the importance and impact of maternal health on fetal health and future adult stroke risk. Many of these modifiable environmental and lifestyle factors relate to social determinants of health and are also associated with preterm birth.12

Noninvasive cranial ultrasound and novel applications of functional magnetic resonance imaging provide tools for future research in this field. Hemodynamic disturbance and abnormal oxygenation are known to cause microstructural alterations in white matter and the secretion of toxic factors that impair myelination.13 Of note, abnormalities commonly seen on brain magnetic resonance imaging of preterm infants are similar to those associated with vascular endothelial dysfunction in the brain. Magnetic resonance angiography assessment of vessel wall macrostructure that uses black-blood imaging techniques represents an area of major advancement in noncontrast-based vessel wall imaging in children and an additional modality for the measurement of macrostructural changes in the circulatory system.14,15 However, much more work must be done to understand the pathophysiology.

Weaknesses in this work are those inherent to large administrative data studies including lack of complete clinical records particularly those to assess later-in-life risk factors and reliance on the International Classification of Disease codes. Other weaknesses include that improvements in care over time may result in survivor bias for preterm infants surviving early in the study and that Sweden is a country with a fairly homogeneous population. Additional geographic, racial, and ethnic diversity is needed in future work.

We have made great strides in caring for premature infants such that survivors of prematurity from the 1970s may be different than those from the 1990s. Today our neonatal intensive care units save incredibly sick premature infants, thus it is not surprising that Crump et al found that associations between premature birth and stroke risk are slightly stronger in more recent births. Follow-up programs track these former premature infants throughout childhood, but this study suggests the need for attention to medical conditions and stroke and cardiovascular risk factors is lifelong. Overall, this work, in combination with additional discussed literature, suggests that illness early in life may lead to premature vascular aging, particularly if hemodynamics and oxygenation are altered.

Disclosures Dr Jordan has served as a consultant for bluebird bio and Global Blood Therapeutics. The other author reports no conflicts.

Footnotes

The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.

For Disclosures, see page 2619.

Correspondence to: Nomazulu Dlamini, MD, PhD, Division of Neurology, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario M5G 1X8, Canada. Email
 

Do somatosensory deficits predict efficacy of neurorehabilitation using neuromuscular electrical stimulation for moderate to severe motor paralysis of the upper limb in chronic stroke?

In what parallel universe do you live where you think that predicting failure to recover is of any interest to survivors?  Except maybe to fire you and get someone competent instead?

Do somatosensory deficits predict efficacy of neurorehabilitation using neuromuscular electrical stimulation for moderate to severe motor paralysis of the upper limb in chronic stroke?

First Published August 25, 2021 Research Article 

Various neurorehabilitation programs have been developed to promote recovery from motor impairment of upper extremities. However, the response of patients with chronic-phase stroke varies greatly. Prediction of the treatment response is important to provide appropriate and efficient rehabilitation. This study aimed to clarify whether clinical assessments, such as motor impairments and somatosensory deficits, before treatment could predict the treatment response in neurorehabilitation.

The data from patients who underwent neurorehabilitation using closed-loop electromyography (EMG)-controlled neuromuscular electrical stimulation were retrospectively analyzed. A total of 66 patients with chronic-phase stroke with moderate to severe paralysis were included. The changes from baseline in the Fugl-Meyer Assessment–Upper Extremity (FMA-UE) and the Motor Activity Log-14 (MAL-14) of amount of use (AOU) and quality of movement (QOM) were used to assess treatment response, and multivariate logistic regression analysis was performed using the extracted candidate predictors, such as baseline clinical assessments, to identify predictors of FMA-UE and MAL-14 improvement.

FMA-UE and MAL-14 scores improved significantly after the intervention (FMA-UE p < 0.01, AOU p < 0.01, QOM p < 0.01). On multivariate logistic regression analysis, tactile sensory (p = 0.043) and hand function (p = 0.030) were both identified as significant predictors of FMA-UE improvement, tactile sensory (p = 0.047) was a significant predictor of AOU improvement, and hand function (p = 0.026) was a significant predictor of QOM improvement. The regression equations explained 71.2% of the variance in the improvement of FMA-UE, 69.7% of AOU, and 69.7% of QOM.

Both motor and tactile sensory impairments predict improvement in motor function, tactile sensory impairment predicts improvement in the amount of paralytic hand use, and motor impairment predicts improvement in the quality of paralytic hand use following neurorehabilitation treatment in patients with moderate to severe paralysis in chronic-phase stroke. These findings may help select the appropriate treatment for patients with more severe paralysis and to maximize the treatment effect.

Motor impairment of the upper extremities is one of the major symptoms in patients with stroke. Motor impairment occurs in approximately 70% or more of patients,1,2 and various rehabilitation programs have been developed to promote recovery from motor impairment after stroke.3 In addition, with the recent development of neurorehabilitation, reports of interventions for residual motor paralysis in the chronic phase are increasing. However, the response to rehabilitation therapy of patients with chronic stroke varies greatly from patient to patient. Therefore, it is important to define an individualized rehabilitation treatment program according to the severity of stroke to provide appropriate and efficient rehabilitation. For this purpose, accurate prediction of the treatment response is necessary.

Somatosensory deficits, as well as motor impairments, are major symptoms in patients with stroke. Somatosensory deficits occur in more than 60% of patients4 and remain in about 40% of patients in the chronic phase.5 Along with motor impairments, somatosensory deficits affect motor functions and activities of daily living (ADLs), such as hand dexterity6,7 and grasping and manipulating objects.810 Although both motor and somatosensory functions are considered important predictors of motor function recovery in rehabilitation, many reports of patients with chronic stroke have focused only on motor function before intervention. In addition, reports using other clinical assessments, including of somatosensory deficits, are limited to mild to moderate paralysis.11 Thus, whether somatosensory impairment has an impact on the recovery of motor function in neurorehabilitation of patients with chronic stroke who have more severe paralysis remains unclear.

In addition to recovery of motor function, increasing the AOU and improving the quality of movement (QOM) of the paralyzed hand are also major goals of neurorehabilitation.12,13 It has been reported that baseline motor and somatosensory functions can both be used as predictors of the AOU and improvement in the QOM of the paralyzed hand by neurorehabilitation in subacute stroke patients.14 A report on chronic stroke patients also showed that both motor and somatosensory functions have a significant impact on prediction.15 However, similar to the recovery of motor function, reports on the AOU and QOM of the paralyzed hand are limited to mild to moderate paralysis.

This study aimed to determine the effects of clinical assessments of motor impairments and somatosensory deficits on the prediction of treatment response, such as recovery of motor impairments (increases in the amount of use and in the QOM of the paralyzed hand) in rehabilitation of patients with moderate to severe paralysis in chronic-phase stroke. We hypothesized that both pretreatment motor and somatosensory functions would be useful predictors of recovery of motor impairments (increased amount of use and improved QOM of the paralyzed hand).