Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,685 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
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.
Tuesday, July 14, 2026
CT vs MRI: Assessing Stroke and Dementia Risk in White Matter Disease
Monday, June 29, 2026
Modified small vessel disease score as the top predictor of stroke outcome after thrombectomy: a CT-based machine learning study
Why are your predicting failure to recover RATHER THAN DELIVERING RECOVERY?
Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!
You're all fired! You need to create EXACT RECOVERY PROTOCOLS!
Prediction crapola like this does nothing to get survivors recovered! Your comeuppance when you have a stroke and don't recover will be a bitter pill for you to swallow.
Modified small vessel disease score as the top predictor of stroke outcome after thrombectomy: a CT-based machine learning study
Thiago Oscar Goulart 1† *
Rui Kleber do Vale Martins-Filho 2
Millene Rodrigues Camilo 2
Daniel Giansante Abud 2
Octávio Marques Pontes-Neto 2
1. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, United States
2. Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil
Abstract
Background:
Mechanical thrombectomy (MT) improves outcomes in ischemic stroke (IS) due to large vessel occlusion (LVO), but ~50% of patients fail to achieve functional independence.
Objectives:
We investigated whether cerebral small vessel disease (cSVD), assessed by the modified Small Vessel Disease (mSVD) score and Brain Frailty Score (BFS), outperforms individual CT markers in predicting 90-day outcomes after MT.
Design:
Prospective cohort with retrospective analysis.
Methods:
We included 351 patients with anterior circulation LVO treated with MT. Admission CT was used to score cSVD markers (leukoaraiosis, atrophy, lacunes) and compute mSVD and BFS. Eight logistic regression models and a Random Forest algorithm were used to predict poor outcome [modified Rankin Scale (mRS) 3–6]. Model performance was evaluated using AUC-ROC and compared via DeLong tests.
Results:
Poor outcomes were associated with older age, higher NIHSS, systolic blood pressure, glycemia, and more severe leukoaraiosis and atrophy. Severe mSVD (score = 3) independently predicted poor outcomes (OR = 3.267; CI: 1.731–6.168; p = 0.009). mSVD outperformed BFS and individual CT markers (AUC = 0.904 vs. 0.889/0.898; DeLong p < 0.05) and ranked as the top predictor in Random Forest (importance = 42.05). Treatment efficacy declined with increasing mSVD: the probability of a favorable outcome was 15.53% and poor outcome was 84.47% for mSVD = 3, compared to 89.23% and 10.77%, respectively, for mSVD = 0. A secondary model incorporating 24h NIHSS and hemorrhagic transformation improved discrimination (AUC = 0.954), but mSVD remained a key independent predictor.
Conclusions:
In this prospective study in a middle-income country, mSVD score was the strongest predictor of post-thrombectomy outcome, outperforming BFS and isolated imaging markers. While cSVD does not contraindicate MT, it reflects reduced cerebrovascular resilience. Integrating mSVD into baseline CT evaluation may enhance risk stratification and treatment guidance.
More at link.
Wednesday, June 24, 2026
Passive sensing of gait and medication-related fluctuations in Parkinson’s disease
Is your doctor competent enough to IMMEDIATELY get this for creating AN EXACT DAMAGE DIAGNOSIS to be followed by AN EXACT REHAB PROTOCOL FOR COMPLETE RECOVERY OF WALKING? Oh NO, your doctor is fucking incompetent;
KNOWS NOTHING AND DOES NOTHING!
Passive sensing of gait and medication-related fluctuations in Parkinson’s disease
- Juyoung Jenna Yun,
- Charalambos Hadjipanayi,
- Arya Jahangiri,
- Alan Bannon,
- Timothy G. Constandinou &
- Shlomi Haar
We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.
Abstract
Background
Gait impairment is a hallmark symptom of Parkinson’s Disease (PD). Traditional clinical assessments cannot capture real-world motor fluctuations, as they are sparsely performed. We validated the use of nearables, passive sensing technologies, including Kinect RGB-D cameras and ultra-wideband (UWB) radar, for continuous, objective assessment of gait fluctuations in PD within a home-like setting.
Methods
Fifteen PD patients with mild symptoms and fourteen age- and sex-matched healthy controls (HC) performed 4-metre walking tasks in a living lab facility. Patients repeated the task during “ON” and “OFF” states of their daily medication cycle. Gait features, including stride length, stride time, and gait speed, were extracted from Kinect, radar, and a ground-truth smart floor. Data were analysed to assess inter-sensor agreements and group-level differences.
Results
Stride time demonstrated the highest agreement between devices (r = 0.903), while stride length was weaker (r = 0.779). Nevertheless, stride length from both Kinect and radar distinguished PD OFF from HC (camera q = 0.020; radar q = 0.005), and radar additionally differentiated ON from OFF (q = 0.020). Neither device differentiated PD ON from HC, indicating medication reduced observable gait differences.
Conclusions
Although some spatial metrics show device discrepancies, both systems demonstrate sensitivity to gait patterns and medication-dependent changes, supporting their use for longitudinal, real-world monitoring of motor symptoms.
Sunday, May 10, 2026
How Chronic Stress Accelerates Aging (and How to Slow the Process) by Super Age
All stroke patients are under massive stress because your incompetent? doctor doesn't have 100% RECOVERY PROTOCOLS. Your doctor has known since medical school that stroke recovery is a complete shitshow and done nothing to fix that!
How Chronic Stress Accelerates Aging (and How to Slow the Process)
Saturday, May 9, 2026
FDA-Listed Interactive Devices for Home Movement Rehabilitation After Stroke: A Mixed-Methods Study of Availability, User Needs, Information Gaps, and an Accompanying Dataset
Does your competent? doctor know of all 57 of these and determined the best ones for your recovery? Oh NO, knows nothing and has done nothing! WOW! You picked a winner!
Here you are :
- AI-Enabled Medical Devices: The FDA's AI-Enabled Medical Devices List includes over 1,450 devices as of March 2026, mostly authorized via 510(k) clearance. These are heavily focused on radiology and cardiology.
- Sensor-Based Digital Health Technology: The Medical Devices that Incorporate Sensor-based Digital Health Technology list includes wearable, sensor-based devices that monitor physiological signals.
- AR/VR Medical Devices: The Augmented Reality and Virtual Reality in Medical Devices list tracks devices using these technologies for therapy and diagnostics.
- Breakthrough Devices Program: The Breakthrough Devices Program - FDA list features innovative devices that receive expedited development and review. [1, 2, 3, 4, 5, 6]
FDA-Listed Interactive Devices for Home Movement Rehabilitation After Stroke: A Mixed-Methods Study of Availability, User Needs, Information Gaps, and an Accompanying Dataset
,
,
,
Abstract
Friday, May 1, 2026
New-Onset Constipation May Shape Stroke Recovery
Your competent? doctor has been working on this problem for almost a decade, right?
OH NO! Knows nothing AND does nothing!
And your board of directors is so incompetent they can't recognize incompetence in their hospital!
The incidence of constipation for stroke was 48%. June 2017
NO PROTOCOLS THAT WILL CURE IT.
In my non-medical opinion, full physical recovery should lessen this problem immensely!
New-Onset Constipation May Shape Stroke Recovery
New-Onset Constipation After Stroke
NEW-ONSET constipation after stroke was common and independently linked to poorer discharge outcomes in acute rehabilitation.
Constipation may be an underrecognized complication in acute stroke care, with new data showing high rates of poststroke constipation and a measurable association with rehabilitation outcomes. In a cross sectional study of 600 patients with acute stroke, investigators examined the incidence, contributing factors, and discharge impact of constipation developing after stroke in patients with no previous history of the condition.
Among all participants, 126 patients, or 21%, had a history of constipation. Poststroke constipation was identified in 278 patients, representing 46.3% of the cohort. New-onset constipation after stroke occurred in 184 patients, accounting for 38.8% of those without prior constipation.
Risk Factors for New-Onset Constipation
Several clinical and functional factors were associated with new-onset constipation after stroke. Hemorrhagic stroke, posterior circulation stroke, diabetes, use of osmotic diuretics, antacids, bedpan use, difficulty falling asleep, depression, and higher admission NIHSS scores were all identified as significant risk factors.
The findings suggest that bowel dysfunction after stroke may reflect more than immobility or routine medication exposure. Sleep disruption and depression appeared to contribute to constipation risk, pointing to the need for broader assessment during the acute stage of stroke rehabilitation.
Impact on Stroke Rehabilitation
New-onset constipation was independently associated with poor discharge outcome after adjustment for confounders, with the strongest signal seen among patients with moderate stroke severity. This association reinforces the importance of early recognition, particularly in patients whose rehabilitation trajectory may be vulnerable to preventable complications.
(WRONG, WRONG, WRONG! Survivors don't want it identified, you blithering idiots; they want it cured! And you're too stupid to deliver what is needed!)
For clinicians, the results support routine screening for constipation risk in patients with stroke, including review of medication exposure, toileting method, neurologic severity, sleep quality, mood symptoms, and metabolic comorbidities. Identifying patients at risk may help optimize rehabilitation protocols and reduce barriers to recovery during the acute phase.
(But you completely missed marijuana! Why?
Marijuana use linked with decreased constipation)
While the study design does not establish causality, the high incidence of new-onset constipation after stroke and its association with discharge outcome highlight a clinically relevant target for early supportive care.
Reference
Lv Z et al. New-onset constipation at acute stage after stroke: incidence, risk factors, and impact on stroke rehabilitation. Frontiers in Neurology. 2026;17:1721157.
Tuesday, April 7, 2026
Linking eye movements, pupil responses, and brain networks in early cognitive decline
Will your competent? doctor put this into a testing protocol, so if problems are found, that EXACT DEMENTIA PREVENTION PROTOCOL WILL BE USED?
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
24 Accesses
7 Altmetric
1 Mention
Abstract
Background
Early detection of Alzheimer’s disease (AD) requires biomarkers sensitive to pre-neurodegenerative dysfunction. Task-evoked ocular responses index arousal‑based gain and the stability of executive timing, but their relationship to brain structure, especially within AD‑signature cortex; regions that thin early in AD, remains poorly characterized. We tested whether ocular metrics map onto cortical thickness and subcortical volumes, and whether brain–ocular coupling differs between cognitively normal (CN) adults and those with mild cognitive impairment (MCI).
Methods
Participants with MCI (n = 212) and CN controls (n = 516) completed an interleaved prosaccade–antisaccade task; binocular pupil diameter and eye movements were time‑locked to cue and target onsets to derive pupil amplitude/variability and saccade metrics. Region‑wise linear mixed‑effects models quantified brain–ocular coupling to cortical thickness and subcortical volumes and tested group (CN vs. MCI) differences in coupling slopes.
Results
Diagnosis‑independent analyses showed that saccade latency variability (Latency SD) and pupil amplitude/variability exhibited robust region‑dependent coupling across cortical and subcortical volumes, whereas mean saccadic latency and pupil timing measures displayed no reliable spatial pattern.
Diagnostic effects were modest and spatially selective but directionally opposite across modalities. For saccades, CN displayed positive thickness–variability slopes in frontal, cingulate, and insular cortices whereas MCI showed negative or near‑zero slopes. In the AD‑signature cortex, this inversionn CN(+)/MCI(−/0) was localized specifically to the supramarginal gyrus (Δβ≈–0.026). Subcortical volumes showed no significant diagnostic differences. For pupils, MCI showed more positive pupil–thickness coupling than CN within global cortex, most prominently in temporal, parietal, and insular regions, and within AD‑signature cortex this selective increase localized to medial temporal cortex (Δβ = 0.042) and to supramarginal gyrus (Δβ = 0.030); subcortical diagnostic differences were not significant after correction.
Conclusions
Task‑evoked ocular signals yield two complementary, region‑specific readouts of early Alzheimer‑relevant dysfunction. Pupil amplitude and variability reflect the strength of phasic, arousal‑linked responses arising from coordinated brainstem control hubs and show selective increases in MCI within medial temporal and temporoparietal regions that are vulnerable early in Alzheimer’s disease. Saccadic latency variability indexes loss of timing stability, revealing a thickness–stability inversion—positive in controls, absent or negative in MCI—that localizes to supramarginal gyrus within attention and executive‑control networks. Effects are modest and spatially circumscribed, positioning ocular measures as scalable, adjunct biomarkers of prodromal disease.