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.

Showing posts with label correlation. Show all posts
Showing posts with label correlation. Show all posts

Tuesday, December 30, 2025

Daytime Naps May Increase Risk for Stroke

 Correlation! Solve the causation problem; NAPS ARE NOT THE PROBLEM! What is causing the naps? 

Daytime Naps May Increase Risk for Stroke

Stroke risk was highest in individuals who took unplanned naps longer than 60 minutes and lowest in those who took planned short naps, indicating that both duration and intention modify vascular risk.

Longer daytime naps are associated with a progressively higher risk for stroke, according to findings published in Sleep Medicine Reviews.

Researchers conducted a systematic review and meta-analysis to assess the relationship between daytime napping and stroke risk. The analysis included 13 quantitative studies, encompassing 15,855 individuals with stroke and 595,520 control individuals. An additional 7 studies were utilized for qualitative review.

Across studies, napping duration was associated with increasing stroke risk. Compared with no napping, naps lasting 1 to 30 minutes were associated with a modestly higher risk for stroke (odds ratio [OR], 1.27; 95% CI, 0.98-1.64), while naps longer than 90 minutes showed the strongest association (OR, 1.79; 95% CI, 1.37-2.35).

When grouped more broadly, naps lasting 60 minutes or less were associated with an OR of 1.27 (95% CI, 1.06-1.51), whereas naps exceeding 60 minutes were linked to a substantially higher risk (OR, 1.86; 95% CI, 1.53-2.27), indicating a progressively increasing association with longer nap duration.

 

The extensive amount of clinical material collected suggests that naps, especially those longer than 60 or 90 min, are risk factors for stroke.

Nap intention also appeared to modify risk. Planned naps lasting 60 minutes or less were associated with a lower risk for stroke (OR, 0.82; 95% CI, 0.70-0.96). In contrast, unplanned naps of similar duration were linked to increased risk (OR, 1.37; 95% CI, 1.10-1.70). Both planned and unplanned naps lasting longer than 60 minutes were associated with elevated risk, with the strongest association observed for unplanned long naps (OR, 2.88; 95% CI, 2.05-4.04), compared with planned long naps (OR, 1.78; 95% CI, 1.14-2.26).

Daytime napping was also associated with increased risk across stroke subtypes. The association was strongest for ischemic stroke (OR, 1.48; 95% CI, 1.05-2.09), followed by hemorrhagic stroke (OR, 1.45; 95% CI, 1.09-1.94), and subarachnoid hemorrhage (OR, 1.44; 95% CI, 1.08–1.92).

Studies that classified napping as present vs absent also showed higher odds of total stroke among individuals who napped (OR, 1.44; 95% CI, 1.27-1.67).

Although differences in study design prevented pooled meta-analysis of nap frequency, several large prospective studies suggested that napping more than twice per week was associated with increased stroke risk, with particularly strong associations among individuals who napped 6 to 7 times per week.

Study limitations included substantial heterogeneity across studies, reliance on self-reported nap characteristics, inconsistent adjustment for confounding variables, and limited availability of detailed sleep-quality measures.

“The extensive amount of clinical material collected suggests that naps, especially those longer than 60 or 90 min, are risk factors for stroke. However, the cause of napping warrants further research and currently appears to be related to night sleep disturbances,” the study authors concluded.

Monday, October 13, 2025

Correlating the triglyceride glucose index with short-term neurological and functional prognosis following intravenous thrombolysis in acute ischemic stroke patients

You described a correlation, but NOTHING HERE will help get survivors recovered! The whole fucking point of stroke research is to get survivors recovered, and this completely FAILED! You're fired!

 Correlating the triglyceride glucose index with short-term neurological and functional prognosis following intravenous thrombolysis in acute ischemic stroke patients


Defeng HuaDefeng Hua1Zhen Guo
Zhen Guo2*
  • 1Department of Neurology, Weifang People’s Hospital, Weifang, China
  • 2Department of Clinical Laboratory, Weifang People’s Hospital, Weifang, China

Objective: To assess the correlation between the triglyceride glucose (TyG) index and short-term neurological and functional outcomes in patients with acute ischemic stroke (AIS) post-intravenous thrombolysis (IVT).

Methods: This prospective observational study included AIS patients treated with IVT within 4.5 h from symptom onset. The TyG index was calculated using fasting triglyceride and glucose levels. Neurological improvement was evaluated by a reduction in National Institutes of Health Stroke Scale (NIHSS) scores, and functional outcome by modified Rankin Scale (mRS) at discharge. Statistical analysis included correlation and regression analyses.

Results: Among 150 AIS patients, the TyG index significantly correlated with both NIHSS (rho = 0.45, p < 0.01) and mRS (rho = 0.38, p < 0.01) scores at discharge. A higher TyG index was associated with neurological non-improvement (OR = 2.11, p = 0.002) and poor functional outcomes (OR = 1.89, p = 0.005) after adjustment for confounders.

Conclusion: The TyG index is significantly associated with short-term outcomes in AIS patients post-IVT, suggesting its potential as a prognostic marker for stroke severity and recovery. Future studies with larger cohorts are needed to confirm these findings.


Tuesday, June 10, 2025

Correlation between neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) and adverse prognosis in patients who achieve complete recanalization after thrombectomy for acute large vessel occlusion stroke

 

USELESS! Correlations give us NOTHING ON HOW TO RECOVER FROM THIS! You're fired!

Correlation between neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) and adverse prognosis in patients who achieve complete recanalization after thrombectomy for acute large vessel occlusion stroke

Shunchao CiShunchao Ci1Di LiDi Li2Feng WangFeng Wang3Ke LiKe Li3Lin Yin
Lin Yin1*
  • 1Department of Neurology, The Second Hospital of Dalian Medical University, Dalian, China
  • 2Department of Neurological Intervention and Neurological Intensive Care, Central Hospital of Dalian University of Technology, Dalian, China
  • 3Department of Interventional Therapy, The First Hospital of Dalian Medical University, Dalian, China

Background: The neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) has emerged as a novel inflammatory marker with prognostic significance. This study aims to explore the association between NHR and adverse prognosis in patients with acute large vessel occlusion (LVO) stroke who achieved complete recanalization after mechanical thrombectomy (MT).

Methods: This retrospective study analyzed acute ischemic stroke (AIS) patients with LVO who underwent MT at three stroke centers in Dalian, China, between January 2016 and November 2023. Complete recanalization was defined as achieving a modified Thrombolysis in Cerebral Infarction (mTICI) grade 3. Blood parameters were assessed within 24 h after MT. We compared intergroup differences based on NHR tertiles and employed the multivariate logistic regression analysis to assess the relationship between NHR and adverse outcomes.

Results: This study included 348 AIS patients with LVO, of whom 215 (61.8%) had adverse clinical outcomes at 90 days. The multivariate logistic regression analysis revealed a significant association between an elevated NHR and 90-day adverse outcomes (OR 2.311, 95% CI 1.248–4.278, p = 0.008). A restricted cubic spline curve demonstrated a linear dose–response relationship between NHR and adverse outcomes, with a p-value of 0.348 for non-linearity.

Conclusion: Our findings revealed that an elevated NHR could increase the risk of adverse prognosis following complete recanalization after MT in acute LVO stroke patients, which indicated that NHR could serve as a potential inflammatory marker for identifying high risk patients.

Introduction

Mechanical thrombectomy (MT) has been established as an effective treatment for acute ischemic stroke (AIS) caused by large vessel occlusion (LVO) (1). Successful recanalization is typically defined as achieving modified Thrombolysis in Cerebral Infarction (mTICI) grade 2b-3 (2). Previous studies have demonstrated that successful recanalization can be achieved in over 83% of patients after MT (3, 4). Despite successful recanalization, nearly half of the patients still exhibit unfavorable clinical outcomes at 90 days, a phenomenon termed futile recanalization (5–7). Current studies on futile recanalization primarily focus on patients who achieve successful recanalization (mTICI 2b-3) after MT; however, the understanding of potential factors associated with poor outcomes in patients who achieve complete recanalization (mTICI 3) remains limited. A systematic review and meta-analysis indicated that mTICI 3 is associated with better outcomes and safety compared to mTICI 2b, and the recanalization grade represents the most important modifiable predictor of patient prognosis (8). VanHorn et al. found that patients with complete recanalization still had a high proportion of adverse outcomes (9). Therefore, actively exploring the factors associated with futile recanalization in patients with mTICI grade 3 may help optimize patient management and improve clinical outcomes.

The inflammatory immune response plays a crucial role in the pathophysiology, treatment outcomes, and prognosis of ischemic stroke (10). Among leukocytes, neutrophils are the first immune cells to increase in circulation shortly after the onset of ischemic stroke (11). Neutrophils in the blood infiltrate ischemic or infarcted tissue through the compromised blood–brain barrier (BBB) and release inflammatory mediators, thereby increasing the risk of BBB disruption, reperfusion injury, hemorrhagic transformation, and malignant brain edema (12). High-density lipoprotein cholesterol (HDL-C) regulates macrophages and adipocytes via cholesterol transporters, exerting anti-inflammatory (13) and anti-atherosclerosis effects (14). As a potential inflammatory marker, the neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) has demonstrated certain prognostic value. This blood indicator is inexpensive and readily available. Huang et al. found that an elevated NHR is a potential predictor of long-term mortality and recurrence rates in elderly patients with acute myocardial infarction (15). A previous study indicated that NHR may be associated with an increased risk of adverse short-term outcomes following intravenous thrombolysis in AIS patients (16). However, its correlation with futile recanalization at mTICI3 remains unclear. This study aimed to investigate the relationship between NHR and adverse prognosis in LVO patients who achieved complete recanalization after MT.

More at link.

Friday, November 8, 2024

Early imaging correlates of subsequent motor recovery after stroke

 Well, lesion volume from the initial CT or MRI scan completely misses the continuing death of neurons from the 5 causes of the neuronal cascade of death in the first week thus killing off millions to billions of neurons!

Does anyone in stroke actually think?

Early imaging correlates of subsequent motor recovery after stroke

Randolph S Marshall, MS, MD, Eric Zarahn, PhD, Leeor Alon, MS, Brandon Minzer, MS, Ronald M Lazar, PhD, and John W Krakauer, MD Department of Neurology, Columbia University Medical Center, New York 

INTRODUCTION 


There is unexplained variability in the extent to which patients recover after stroke, particularly from the reference point of the first few days after onset. Among studies tracking motor impairment and recovery, only 30–50% of the variance of recovery is explained by the most commonly reported predictors --lesion volume and initial stroke severity 1 , 2. We hypothesized that functional imaging early after stroke could provide information over and above initial severity and lesion volume about the degree of subsequent recovery. Several prior functional imaging studies have reported altered brain activation patterns in patients at various stages of motor recovery after stroke3 – 6. These studies describe brain activation related to concurrent recovered performance at the time of scanning that differs to varying degrees from what is seen in age-matched controls. In this study we used functional imaging to ask a specific and unique question about motor recovery after stroke: can functional imaging in the early period after stroke detect brain activation related to subsequent recovered performance? Should such activation be identified then it could serve as a physiological target for intervention (e.g. non-invasive brain stimulation) in this early time period. To investigate whether brain activation early after stroke can be correlated with subsequent recovery, we scanned patients approximately 48 hours after stroke using fMRI, and defined recovery as the change in motor impairment from the time of scanning to a follow up point 3 months later. We used 3 different statistical tests: 1) a multivariate test, which is most sensitive to spatially diffuse activation, 2) voxel-wise statistical parametric mapping (SPM), which is most sensitive to focal activation, and 3) primary motor cortex (M1) region of interest (ROI) analysis, which is most sensitive to average activation within this region. The ROI analysis was chosen to test existing hypotheses implicating M1 and the corticospinal tract in recovery.7 – 9 All tests controlled for lesion volume and initial stroke severity, as well as other established clinical variables. METHODS Subjects We recruited stroke patients from a large screening data base of all patients with the diagnosis of ischemic stroke admitted to Columbia University Medical Center between December, 2004 and April, 2007 (n=993), part of Columbia’s Specialized Program of Translational Research in Acute Stroke (SPOTRIAS), an NINDS-funded national network to investigate new pathophysiologic, diagnostic and clinical approaches in acute stroke. Thirty-three consecutive patients with first ever ischemic stroke and hemiparesis able to undergo fMRI within 48 hours of stroke onset were recruited. Five patients were eligible but refused the fMRI scan. Three underwent the fMRI, but did not complete the 3-month clinical follow up (1 developed dementia, 1 left the country, 1 was incarcerated). Two patients had recurrent stroke prior to the 3-month follow-up and were excluded from analysis. The final sample size of 23 was considered adequate for a functional imaging study of this type. Patients with aphasia or hemineglect alone were not included in this analysis. See Table 1 for more demographic and clinical details. All patients except for 4 underwent a single session of fMRI scanning at our target of 24–48 hours after stroke onset (the remaining 4 patients had their scans between 49 and 96 hours due to scheduling delays; mean time to scan=47.8±21.6h, median=46h). Exclusion criteria also included seizure at stroke onset, moderate to severe aphasia or other cognitive impairment that precluded training on the fMRI task, or any contraindication to MRI. None of the patients had neglect or apraxia on examination. Patients did not smoke on the day of scanning (they were inpatients); caffeine intake was not recorded. The strict eligibility criteria permitted us to control for unwanted variables while preserving the wide spectrum of initial motor severity that would contribute to the correlation analysis. Total lesion volumes were estimated by summing the volumes of the DWI lesion in each slice (length by width by slice thickness measured with the measurement tool in the PACS system software) in which the DWI was positive. Recovery measure Motor impairment was measured with the upper limb Fugl-Meyer assessment (FM)11, which has a maximum score of 66, and is valid and highly reliable over a wide spectrum of severities.12 – 16 FM was assessed on the day of scanning (FM initial ) and again at 3 months (FM 3 months ). Recovery (ΔFM) was defined as ΔFM = FM 3 months − FM initial . Our decision to use a change score as our measure of recovery was based on the idea that the degree of change, rather than the final level achieved, would better reflect a biological recovery process 17. In addition to the FM we also measured hand dynamometry at baseline on the day of scanning (DYN initial ). The reason for doing so was that hand dynamometry score should presumably correlate with the degree of difficulty subjects would have to perform the fMRI hand closure task. DYN initial was taken as an average of 3 measurements of maximal grip force. fMRI data acquisition Patients underwent gradient echo-echoplanar fMRI (GE 1.5 T, 64 × 64 matrix, FOV = 19 cm, 21 slices, slice thickness/skip = 4.5 mm/0 mm, TR = 4000 ms, TE = 52 ms, flip angle = 60°) while performing the repetitive hand closure task described below. One session (40 volumes) was performed per hand. The order in which the hands (affected/unaffected) were tested was counterbalanced across patients except for those with complete plegia (see below). Motor task used during fMRI The task was a simple repetitive hand closure in synchrony with a 1 Hz metronome click, following a block design: 20-second rest epochs alternating with 20-second task epochs (4 cycles total per hand). The instruction was: ”Close your hand gently in rhythm with the click you hear. Start and stop when you hear the instructions through the headphones.” The metronome click was played continuously via MRI-compatible headphones in the scanner. Marshall et al. Page 2 Ann Neurol. Author manuscript; available in PMC 2010 May 1. NIH-PA Author Manuscript NIH-PA Author Manuscript

Tuesday, July 30, 2024

Motor recovery after stroke: Lessons from functional brain imaging

You described a correlation, but NOTHING HERE will help get survivors recovered! The whole fucking point of stroke research is to get survivors recovered, and this completely FAILED! You're fired!

Motor recovery after stroke: Lessons from functional brain imaging


Pages 453-458 | Published online: 19 Jul 2013
 

 

Abstract

Several theories have been proposed to explain recovery from stroke. Functional brain imaging offers an opportunity to evaluate these theories and visualize recovery after stroke(But it doesn't provide recovery, soes it?). Functional brain imaging has proven to be an effective tool to map brain areas activated during a specific task. This paradigm can extend our understanding of the mechanisms of motor recovery after stroke. Functional brain imaging tools such as functional MRI, PET, transcranial Doppler ultrasonography, and transcranial magnetic stimulation can be used to evaluate motor activation after stroke. Functional imaging is proving useful in identifying areas, pathways and mechanisms involved in motor recovery after stroke. Studies have shown changes in motor organization with rehabilitation. Functional brain imaging may assist in the selection of rehabilitation methods that best foster recovery. [Neurol Res 2002; 24: 453-458]

Sunday, February 25, 2024

Neuroimaging correlates of post-stroke fatigue: A systematic review and meta-analysis

The point is to solve the fatigue problem! HOW EXACTLY ARE YOU GOING TO ACCOMPLISH THAT? 

Survivors don't want correlates that do nothing to get fatigue cured. They want to have fatigue cured! GET THERE!

 

Neuroimaging correlates of post-stroke fatigue: A systematic review and meta-analysis

Abstract

Background:

Fatigue is a common and disabling symptom following stroke, but its underlying mechanisms are unknown. Associations with a number of imaging features have been proposed.

Aims:

We aimed to assess whether neuroimaging parameters could better inform our understanding of possible causes of post-stroke fatigue (PSF) through systematic review and meta-analysis.

Methods:

Using a predefined protocol registered with PROSPERO (ID: CRD42022303168), we searched EMBASE, MEDLINE, PubMed, and PsycInfo for studies assessing PSF and computerized tomography (CT), magnetic resonance (MR), positron emission tomography (PET) imaging, or diffusion tensor imaging (DTI). We extracted neuroimaging parameters and narratively analyzed study results to assess any association with PSF. Where there were 3+ similar studies, we carried out a meta-analysis using inverse-variance random-effects model to estimate the total association of each neuroimaging parameter on PSF. The risk of bias was assessed using the Newcastle and Ottawa Scale.

Results:

We identified 46 studies (N = 6543); in many studies, associations with fatigue were secondary or subanalyses (28.3%). Imaging parameters were assessed across eight variables: lesion lateralization, lesion location, lesion volume, brain atrophy, infarct number, cerebral microbleeds, white matter hyperintensities (WMHs), and network measures. Most variables showed no conclusive evidence for any association with fatigue. Meta-analysis, where possible, showed no association of the following with PSF; left lesion lateralization (OR: 0.88, 95% CI (0.64, 1. 22) (p = 0.45)), infratentorial lesion location (OR: 1.83, 95% CI (0.63, 5.32) (p = 0.27)), and WMH (OR: 1.21, 95% CI (0.84, 1.75) (p = 0.29)). Many studies assessed lesion location with mixed findings; only one used voxel-symptom lesion-mapping (VSLM). Some small studies suggested an association between altered functional brain networks, namely frontal, fronto-striato-thalamic, and sensory processing networks, with PSF.

Conclusion:

There was little evidence for the association between any neuroimaging parameters and PSF. Future studies should utilize advanced imaging techniques to fully understand the role of lesion location in PSF, while the role of altered brain networks in mediating PSF merits further research.

Tuesday, April 4, 2023

Fatal Post COVID mRNA-Vaccine Associated Cerebral Ischemia

 For you doomsayers out there cherry picking one case out of billions to justify not taking a lifesaving vaccine.

Fatal Post COVID mRNA-Vaccine Associated Cerebral Ischemia

Abstract

Background

Venous thromboses have been linked to several COVID-19 vaccines, but there is limited information on the Moderna vaccine’s effect on the risk of arterial thrombosis. Here we describe a case of post-Moderna COVID-19 vaccination arterial infarct with vaccine-associated diffuse cortical edema that was complicated by refractory intracranial hypertension.

Case Summary

24 hrs after receiving her first dose of the Moderna COVID-19 vaccine, a 30-year-old female developed severe headache. Three weeks later she was admitted with subacute headache and confusion. Imaging initially showed scattered cortical thrombosis with an elevated opening pressure on lumbar puncture. An external ventricular drain was placed, but she continued to have elevated intracranial pressure. Ultimately, she required a hemicraniectomy, but intractable cerebral edema resulted in her death. Pathology was consistent with thrombosis and associated inflammatory response.

Conclusion

Though correlational,(Meaning not proven) her medical team surmised that the mRNA vaccine may have contributed to this presentation. The side effects of COVID-19 infection and vaccination are still incompletely understood. Though complications are rare, clinicians should be aware of presentations like this one.

Thursday, December 15, 2022

Fatal Post COVID mRNA-Vaccine Associated Cerebral Ischemia

FYI, just correlation not proven cause and effect.

Fatal Post COVID mRNA-Vaccine Associated Cerebral Ischemia

Abstract

Background

Venous thromboses have been linked to several COVID-19 vaccines, but there is limited information on the Moderna vaccine’s effect on the risk of arterial thrombosis. Here we describe a case of post-Moderna COVID-19 vaccination arterial infarct with vaccine-associated diffuse cortical edema that was complicated by refractory intracranial hypertension.

Case Summary

24 hrs after receiving her first dose of the Moderna COVID-19 vaccine, a 30-year-old female developed severe headache. Three weeks later she was admitted with subacute headache and confusion. Imaging initially showed scattered cortical thrombosis with an elevated opening pressure on lumbar puncture. An external ventricular drain was placed, but she continued to have elevated intracranial pressure. Ultimately, she required a hemicraniectomy, but intractable cerebral edema resulted in her death. Pathology was consistent with thrombosis and associated inflammatory response.

Conclusion

Though correlational, her medical team surmised that the mRNA vaccine may have contributed to this presentation. The side effects of COVID-19 infection and vaccination are still incompletely understood. Though complications are rare, clinicians should be aware of presentations like this one.

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Saturday, August 6, 2022

Frequent Napping Linked To Higher Risk Of Stroke, High Blood Pressure

You'll have to ask your doctor what should be the length of your daytime naps so you can set the timer appropriately. I can't see the cause and effect here, just correlation.

 

Frequent Napping Linked To Higher Risk Of Stroke, High Blood Pressure

 

Are you a frequent napper? A new study has found that frequent napping could be a risk factor for stroke and high blood pressure.

Several studies in the past pointed out that napping helped reduce daytime sleepiness and boost learning and performance. It also improved alertness and reaction time, per some findings.

But a new study published in Hypertension, a journal produced by the American Heart Association, found a link between frequent napping and stroke and high blood pressure.

The researchers combined observational analyses with Mendelian randomization and used genetic markers to determine whether a risk factor can contribute to a particular disease. They also analyzed data from the U.K. Biobank, which recorded genetic and health data from more than 500,000 participants ages 40-69 living in the United Kingdom between 2006 and 2010. Those who already had a stroke or suffered hypertension when the study began were excluded from the results.

The researchers found that participants who napped in the daytime more frequently increased their hypertension risk by 12%, stroke risk by 24%, and the risk of ischemic stroke (the most common type of stroke caused by a blood clot preventing blood and oxygen from reaching an area of the brain) by 20%. Meanwhile, those who sometimes napped increased hypertension risk by 7%, stroke risk by 12%, and the risk of ischemic stroke by 9%.

Participants younger than 60 who frequently napped also had an increased chance of developing hypertension than those who didn’t take naps. Meanwhile, the percentage dropped to 10% in participants older than 60 who usually napped.

All the participants who napped in the daytime were mostly male, non-European, less educated, had a lower income, and had a higher body mass index and waist-hip ratio.

The study authors were aware of the limitations of their study since only the frequency and not the length of naps was considered. Additionally, the participants in the U.K. Biobank were a fairly homogenous group.

According to Dr. E. Wang, an author of the study and professor and chair of the department of anesthesiology at Xiangya Hospital Central South University, the participants were “predominantly middle-aged Europeans who might not be generalizable to other racial groups.”

Lastly, the researchers pointed out that daytime napping, in general, was not the problem since it also has some benefits.

Monday, August 30, 2021

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.

 
 

Friday, January 29, 2021

Correlation between ASPECTS and Core Volume on CT Perfusion: Impact of Time since Stroke Onset and Presence of Large-Vessel Occlusion

 So you found a correlation. WHAT THE HELL ARE YOU GOING TO DO ABOUT IT TO GET TO 100% RECOVERY? If nothing, then get the hell out of stroke.

Correlation between ASPECTS and Core Volume on CT Perfusion: Impact of Time since Stroke Onset and Presence of Large-Vessel Occlusion

S. Nannoni, F. Ricciardi, D. Strambo, G. Sirimarco, M. Wintermark, V. Dunet and P. Michel

Abstract

BACKGROUND AND PURPOSE: Both ASPECTS and core volume on CTP are used to estimate infarct volume in acute ischemic stroke. To evaluate the potential role of ASPECTS for acute endovascular treatment decisions, we studied the correlation between ASPECTS and CTP core, depending on the timing and the presence of large-vessel occlusion.

MATERIALS AND METHODS: We retrospectively reviewed all MCA acute ischemic strokes with standardized reconstructions of CTP maps entered in the Acute STroke Registry and Analysis of Lausanne (ASTRAL) registry. Correlation between ASPECTS and CTP core was determined for early (<6 hours) versus late (6–24 hours) times from stroke onset and in the presence versus absence of large-vessel occlusion. We used correlation coefficients and adjusted multiple linear regression models.

RESULTS: We included 1046 patients with a median age of 71.4 years (interquartile range, IQR = 59.8–79.4 years), an NIHSS score of 12 (IQR, 6–18), an ASPECTS of 9 (IQR, 7–10), and a CTP core of 13.6 mL (IQR, 0.6–52.8 mL). The overall correlation between ASPECTS and CTP core was moderate (ρ = –0.49, P < .01) but significantly stronger in the late-versus-early window (ρ = –0.56 and ρ = –0.48, respectively; P = .05) and in the presence versus absence of large-vessel occlusion (ρ = –0.40 and ρ = –0.20, respectively; P < .01). In the regression model, the independent association between ASPECTS and CTP core was confirmed and was twice as strong in late-arriving patients with large-vessel occlusion (β = –0.21 per 10 mL; 95% CI, −0.27 to –0.15; P < .01) than in the overall population (β = –0.10; 95% CI, −0.14 to –0.07; P < .01).

CONCLUSIONS: In a large cohort of patients with acute ischemic stroke, we found a moderate correlation between ASPECTS and CTP core. However, this was stronger in patients with large-vessel occlusion and longer delay from stroke onset. Our results could support the use of ASPECTS as a surrogate marker of CTP core in late-arriving patients with acute ischemic stroke with large-vessel occlusion.