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 NIHSS score. Show all posts
Showing posts with label NIHSS score. Show all posts

Tuesday, June 16, 2026

Impact of Intraoperative Oxygenation Practices on Patient Outcome

 It's in the stroke section of Medpage Today but nothing even remotely looks like something useful for oxygen delivery!

Maybe these, why isn't your incompetent doctor already delivering these to you?

cerebral blood flow (29 posts to July 2016)

Cerebral blood flow autoregulation (1 post to July 2021)

Cerebral Blood Flow Velocity (1 post to Febraury 2020)

cortical oxygenation (1 post to November 2020)

oxygen delivery (20 posts to January 2020)

oxygen uptake (5 posts to August 2013)

Normobaric oxygen (10 posts to January 2020)

  • brain blood flow (3 posts to April 2019)
  • Well, since this has been around for years why the hell doesn't someone actually do human testing and create protocols on stroke recovery?

    Earlier research on Metformin has this line: The drug, which is cheaply available for just $0.16 a day, works by boosting the number of oxygen molecules released into a cell, which in turn seems to benefit the robustness and longevity of the body’s basic building blocks. (This would seem to be much easier and faster than HBOT. I'm requesting this at my next stroke, my doctor won't know what hit her when I tell her how to treat me.)

  • If your doctor doesn't know about this s/he IS COMPLETELY FUCKING INCOMPETENT? And not creating protocols is even worse, allowing millions to billions of neurons to die because of lack of oxygen during the neuronal cascade of death!

    Impact of Intraoperative Oxygenation Practices on Patient Outcome

    ClinicalTrials.gov IDNCT07224243
    SponsorFrederic T Billings IV
    Information Provided byFrederic T Billings, MD
    Study Start (Actual)2025-12-01
    Primary Completion (Estimated) 2028-02
    Study Completion (Estimated)2028-04
    Enrollment (Estimated)54000
    Study TypeInterventional
    Last Update Posted2026-06-10

    Study Overview

    Brief Summary

    This multicenter, cluster-randomized, cluster-crossover clinical trial evaluates the impact of three intraoperative FiO2 (Fraction of Inspired Oxygen) oxygenation strategies-lower (FiO₂ 0.21-0.40), intermediate (FiO₂ 0.40-0.80), and higher (FiO₂ 0.80-1.00)-on postoperative organ injury and mortality in adult surgical patients. The trial aims to determine the optimal oxygenation strategy to improve perioperative outcomes.

    Tuesday, May 26, 2026

    Risk factors for early neurological deterioration in patients with acute ischaemic stroke and assessment of short-term prognosis

     Totally wrong objective; Survivors actually want early neurological deterioration prevented! 'Assessments' DO NOTHING TOWARDS RECOVERY! 

    Risk factors for early neurological deterioration in patients with acute ischaemic stroke and assessment of short-term prognosis


    • Department of Neurology, Sinopharm Tongmei General Hospital, Datong, Shanxi, China

    Abstract

    Objective: 

    To identify independent risk factors for early neurological deterioration (END) in patients with acute ischaemic stroke (AIS) and evaluate its impact on short-term clinical outcomes.

    Methods: 

    A total of 186 AIS patients admitted between January 2023 and January 2025 were retrospectively enrolled and divided into an END group (n = 62) and a non-END group (n = 124), based on a NIHSS score increase of ≥2 points within 72 h. Baseline characteristics, laboratory parameters, neuroimaging features, and treatment details were compared. Multivariable logistic regression identified independent risk factors for END and for unfavorable outcomes among END patients. Neurological function was assessed by serial NIHSS scores, and 3-month prognosis by the modified Rankin Scale (mRS).

    Results: 

    The END group showed significantly higher admission NIHSS score, fasting plasma glucose, glycated hemoglobin, homocysteine, high-sensitivity C-reactive protein (hs-CRP), D-dimer, and greater proportions of hypertension, diabetes mellitus, atrial fibrillation, large artery atherosclerosis, cardioembolic subtypes, and large infarction (all P < 0.05). Multivariable analysis identified higher admission NIHSS score, fasting plasma glucose, hs-CRP, D-dimer, atrial fibrillation history, and large infarction as independent risk factors for END. END patients had persistently elevated NIHSS scores, higher rates of unfavorable 3-month outcomes (mRS ≥3), longer hospital stays, and greater mortality (all P < 0.05). Among END patients, admission NIHSS ≥12, large infarction, and hs-CRP ≥15 mg/L independently predicted unfavorable outcomes.

    Conclusions: 

    Higher admission NIHSS score, fasting plasma glucose, hs-CRP, D-dimer, atrial fibrillation, and large infarction are independent risk factors for END in AIS. END is associated with worse neurological recovery, prolonged hospitalization, and higher 3-month mortality. Early identification of high-risk patients and targeted intervention are essential for improving outcomes.

    Monday, May 25, 2026

    Combination of flupentixol and melitracen tablets and rTMS improves post-stroke depression through neurovegetative symptoms changes: a retrospective analysis

     Preventing depression by having EXACT 100% RECOVERY PROTOCOLS makes much more sense that after the fact treatment! And your stroke medical 'professionals' are too stupid to understand that!

    Combination of flupentixol and melitracen tablets and rTMS improves post-stroke depression through neurovegetative symptoms changes: a retrospective analysis


    • 1. Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China

    • 2. First Clinical College of Xuzhou Medical University, Xuzhou, Jiangsu, China

    Abstract

    Background:

    Post-stroke depression (PSD) is one of the most common neuropsychiatric complications among stroke survivors, with a substantial impact on functional recovery and quality of life. This study aimed to investigate the effect of flupentixol and melitracen tablets combined with repetitive transcranial magnetic stimulation (rTMS) on patients with post-stroke depression (PSD) and analyze the differences in the key factors of the 17-item Hamilton Depression Scale (HAMD17) scores.

    Methods: 

    We conducted a retrospective analysis of 121 patients with PSD, including 57 patients who used the flupentixol and melitracen tablets alone and 64 patients who additionally received rTMS. General information was assessed. Follow-up indices after treatment included P300, National Institutes of Health Stroke Scale (NIHSS), HAMD17, and the Barthel Index (BI) and Pittsburgh Sleep Quality Index (PSQI) questionnaire. Observable mood (OM), cognitive symptoms (CS) and neurovegetative symptoms (NS), the three dimensions of HAMD17 was also analyzed. The concentrations of 5-hydroxytryptamine (5-HT), norepinephrine (NE), neuropeptide Y (NPY) and brain-derived neurotrophic factor (BDNF) in the serum were measured during all time points.

    Results: 

    There was significant difference in the amplitude and latency of P300 and NS after 2 weeks and 4 weeks treatment between the groups, while there was significant difference in the concentrations of 5-HT, NE, NPY, BDNF and the scores of NIHSS, HAMD17, BI, PSQI after 4 weeks treatment. The treatment outcomes at 4 weeks demonstrated statistically significant differences compared to those observed at 2 weeks both at control group and combination group. The results also indicated that the treatment in the combined group demonstrated superiority over that in the control group with respect to both onset time and therapeutic efficacy.

    Conclusion: 

    Combination of flupentixol and melitracen tablets and rTMS could significantly improve the depressive symptoms of patients with PSD, NS was the symptom dimension most closely related to the therapeutic response. More importantly, the P300 parameter might provide an early and objective indicator of the neurophysiological changes associated with the treatment.

    Tuesday, May 19, 2026

    Role of Hyperbaric Oxygen Therapy in Rehabilitation of Stroke Patients: A Randomized Controlled Pilot Study

     Why HBOT? There are much faster and easier ways to get extra oxygen to stroke patients. But I guess your incompetent? doctor doesn't know of them!

    Why do HBOT when there are vastly simpler, cheaper and less risky ways to increase oxygen uptake?

     I can't see any use for HBOT unless it's delivered in the first week and there are vastly easier options for delivering oxygen than that.

    Google this for risks: hyperbaric oxygen therapy deaths. 

    Here are 43 posts on HBOT for your edification

    Well, since this has been around for years why the hell doesn't someone actually do human testing and create protocols on stroke recovery?

    Earlier research has this line:The drug, which is cheaply available for just $0.16 a day, works by boosting the number of oxygen molecules released into a cell, which in turn seems to benefit the robustness and longevity of the body’s basic building blocks. (This would seem to be much easier and faster than HBOT. I'm requesting this at my next stroke, my doctor won't know what hit her when I tell her how to treat me.)

    If your doctor doesn't know about this s/he IS COMPLETELY FUCKING INCOMPETENT? And not creating protocols is even worse, allowing millions to billions of neurons to die because of lack of oxygen during the neuronal cascade of death!

     What other protocols is your doctor using to significantly improve oxygen delivery immediately post stroke? The first hours and days? NOTHING? Then you DON'T have a functioning stroke doctor, do you?

    Maybe these, why isn't your incompetent doctor already delivering these to you?

    cerebral blood flow (29 posts to July 2016)

    Cerebral blood flow autoregulation (1 post to July 2021)

    Cerebral Blood Flow Velocity (1 post to Febraury 2020)

    cortical oxygenation (1 post to November 2020)

    oxygen delivery (20 posts to January 2020)

    oxygen uptake (5 posts to August 2013)

    Normobaric oxygen (10 posts to January 2020)

  • brain blood flow (3 posts to April 2019)

  •  Oh, your incompetent doctor doesn't have any and doesn't fucking care about learning better ways to get you recovered! Well, fire them! 

    The latest here:

    Role of Hyperbaric Oxygen Therapy in Rehabilitation of Stroke Patients: A Randomized Controlled Pilot Study


    • Ramakant Yadav
    • Usha Shukla1
    • Urvashi Yadav1
    • Shipra Verma1,
    • Sushil Kumar Shukla2
    Annals of African Medicine Publish Ahead of Print, April 16, 2026. | DOI: 10.4103/aam.aam_804_25

    Background:

    Improvement in neurological function has been reported in stroke patients after hyperbaric oxygen therapy (HBOT) administration. Although the majority of spontaneous neurological recovery occurs within the first 90 days poststroke, HBOT may further augment this recovery process. This study aimed to evaluate the role of HBOT in improving neurological function and quality of life (QoL) in stroke patients.

    Materials and Methods:

    This randomized controlled pilot study involved 30 patients who experienced an ischemic stroke 3–6 months before enrollment, randomly assigned to two groups: Group H (n = 15), which received 24 sessions of HBOT along with conventional physiotherapy and Group C (n = 15), which received only conventional physiotherapy. The primary outcome was the change in motor function, assessed using the National Institutes of Health Stroke Scale (NIHSS). The secondary outcomes included the changes in cognitive function, evaluated with the Mini-Mental State Examination (MMSE), and QoL, measured using the Short Form-36 questionnaire.

    Results:

    Following HBOT, there was a significant improvement in the NIHSS score from a baseline of (7.27 ± 2.71) to (5.46 ± 2.47) and in the MMSE from a baseline of (24.8 ± 2.98) to (26.73 ± 1.90). Similar improvements were also observed in Group C after the intervention compared to baseline. Group H showed significant improvement in the SF-36 questionnaire except for bodily pain and vitality, while Group C showed no significant change.

    Conclusion:

    Although clinical improvement in motor and cognitive function was better after giving HBOT in the 3–6 months poststroke period, the between-group comparisons postintervention were not statistically significant.

    Thursday, December 4, 2025

    Health Rounds: Experimental drug shows promise for stroke patients who miss the current medical treatment window

    Will your incompetent? doctor DO NOTHING WITH THIS RESEARCH? Just like they know nothing about EXACT stroke recovery?


    Health Rounds: Experimental drug shows promise for stroke patients who miss the current medical treatment window

    (This is an excerpt of the Health Rounds newsletter, where we present latest medical studies on Tuesdays and Thursdays)

    By Nancy Lapid

    Dec 3 (Reuters) - Stroke patients who can't get to the hospital quickly enough to be eligible for the usual clot-busting treatments may ​soon have another option, results from a mid-stage trial suggest.

    Currently available thrombolytic drugs must be given within a few hours after ‌symptoms begin. That narrow window can rule out patients who did not, or could not, seek help promptly because they didn’t immediately recognize their symptoms, as well as those who wake ‌up with symptoms of a stroke that may have started hours earlier.

    The experimental drug being developed by Silver Creek Pharmaceuticals and dubbed scp776 inhibits apoptosis, a process in which injured cells self-destruct.

    The drug keeps injured cells alive by delivering a hormone called insulin-like growth factor 1, or IGF-1, which activates the cells’ natural repair pathways.

    In 119 patients who came to emergency departments on average about 12 hours after stroke onset - for whom there was no approved drug treatment - ⁠scp776 resulted in clinically meaningful improvements in outcomes compared ‌to a placebo, researchers reported at the 2025 World Stroke Congress in Barcelona.

    “It’s very promising to see a therapy that leverages the brain’s own recovery mechanisms to improve stroke outcomes in the clinic,” Silver Creek Chief Scientific Officer Kris ‍Kuchenbecker said in a statement.

    At the time of hospital discharge, or by day 7 after symptom onset, patients receiving scp776 had on average a clinically significant 2.26-point higher score on the 42-point NIH Stroke Scale compared to those who received a placebo, although the difference was just short of statistical significance.

    At 90 days, the treatment ​had resulted in a 15% increase in the relative proportion of patients achieving functional independence, researchers reported.

    The drug has received FDA Fast Track designation ‌for acute ischemic strokes caused by blockages in the arteries that carry blood to the brain. The Food and Drug Administration awards the designation to speed development and review of treatments for serious conditions where there is an unmet need.

    “Scp776 harnesses the well-understood repair power of growth factors in a targeted way, finally delivering on the vast preclinical evidence of therapeutic benefit of IGF-1,” Kuchenbecker said.

    AI IMPROVES SCREENING FOR FETAL HEART PROBLEMS

    Artificial intelligence software can improve fetal screening for congenital heart defects, according to results of a new study.

    Using a tool from medical company BrightHeart, researchers analyzed 200 fetal ultrasound ⁠scans obtained during the second trimester of pregnancy from women at 11 medical centers ​in two countries, including 100 with at least one suspicious finding.

    Seven obstetrician-gynecologists and seven doctors ​who specialize in high-risk pregnancies reviewed each examination in randomized order, both with and without AI assistance, looking for findings that might indicate the presence of a severe heart defect.

    The physicians detected more suspicious lesions, and in less time, with ‍AI than without, according to a report ⁠in Obstetrics & Gynecology.

    Overall, their detection rate rose from 82% to more than 97%, with an 18% reduction in reading time and 19% improvement in confidence scores.

    “Our study should prompt and encourage future research into AI-assisted software's ability to improve detection rates... (and) reduce the variability and ⁠inequity of detection of congenital heart defects globally,” study co-leader Dr. Andrei Rebarber of the Icahn School of Medicine at Mount Sinai said in a statement.

    “The future for prenatal diagnostic ‌imaging is bright when AI software is employed as an adjunct to physician interpretation.”

    (To receive the full newsletter in your inbox ‌for free sign up here)

    (Reporting by Nancy Lapid; Editing by Bill Berkrot)

    Saturday, February 8, 2025

    Revalesio announces new analyses from Phase 2 RESCUE study assessing RNS60 in acute ischaemic stroke

     You'll have to ask your competent? doctor which of the 5 causes of the neuronal cascade of death in the first week is being addressed! 

    I wish they had used the proper term; penumbra, and specified exactly how many millions of neurons were saved.

    I consider the Rankin scale useless, not objective except for #6, dead?

    NIHSS and the Berthel Index ARE NOT DAMAGE DIAGNOSES, they do not give you the 3d location of your dead and damaged neurons. In my opinion, they are FUCKING WORTHLESS to getting you recovered! 

    The latest here:

    Revalesio announces new analyses from Phase 2 RESCUE study assessing RNS60 in acute ischaemic stroke

    Revalesio has announced new analyses of the completed Phase 2 RESCUE clinical trial evaluating its drug candidate RNS60 in acute ischaemic stroke that demonstrate a nominally significant lowering of infarct growth in patients treated less than 12 hours from last known well. The lowering of infarct growth correlated with clinically meaningful improvements in several functional stroke measures for assessing a patient’s recovery(None of which are worth a damn, about helping you get recovered!), including the modified Rankin scale (mRS), Barthel index (BI), and National Institutes of Health stroke scale (NIHSS), the company claims in a recent press release.

    These results were delivered during an oral presentation at the ongoing International Stroke Conference (ISC; 5–7 February, Los Angeles, USA).

    “This analysis of the RESCUE trial adds further information regarding the beneficial effects of RNS60, confirming that it has favourable effects on MRI [magnetic resonance imaging]-confirmed ischaemic lesion growth that translated into improved clinical outcomes,” said former World Stroke Organization (WSO) president Marc Fisher (Beth Israel Deaconess Medical Center, Boston, USA). “These are exciting results that suggest that RNS60 should be evaluated in a large Phase 3 clinical trial that will hopefully confirm its benefits and lead to approval as the first therapeutic agent in decades to demonstrate significant efficacy in improving outcomes for acute ischaemic stroke patients.”

    In RESCUE—a multicentre, double-blinded, placebo-controlled, randomised Phase 2 clinical trial—Revalesio evaluated the safety and initial efficacy of RNS60. Eighty-two participants with acute ischaemic stroke eligible for endovascular therapy (EVT) were enrolled and received either intravenous RNS60 0.5mL/kg/h (low dose), RNS60 1mL/kg/h (high dose), or placebo, starting before completion of EVT and continuing for 48 hours.

    The trial had two primary endpoints: safety and mortality. Secondary endpoints for the study assessed disability based on mRS scores, changes in the size of the stroke measured via MRI at 48 hours, and additional standard stroke scales like BI and NIHSS.

    Highlights from the oral presentation—given by Revalesio’s acting chief medical officer Jordan Dubow on 5 February at ISC 2025—are as follows:

    • The high dose of RNS60 significantly lowered infarct growth by 50% (nominal p<0.05) when compared to placebo, based on imaging performed at approximately 48 hours compared to immediately post-EVT, both in patients treated within 12 hours and 24 hours of last known well
    • The high dose of RNS60 was also numerically better than placebo for each prespecified functional endpoint at day 90 (mRS, with 72% of subjects on high-dose RNS60 being independent [mRS 0–2] at day 90 compared to 37% on placebo; BI, with 72% of subjects on high-dose RNS60 returning to normal activities of daily living [BI³ 95] compared to 37% on placebo; and patient health status as measured by the EQ-5D-5L index, with 1 being ideal, which was 0.79 for RNS60 subjects and 0.57 for placebo)
    • RNS60 was safe and well tolerated

    “As the number-one cause of disability worldwide, the impact of stroke is staggering, accounting for US$721 billion annually to the global healthcare system,” said Bert van den Bergh, Revalesio’s executive chairman of the board of directors. “Additionally, more than 80% of patients in the USA have no treatment options following a stroke, underscoring the significant need for new and effective treatment options. These highly encouraging results further demonstrate the potential of RNS60 to greatly reduce the likelihood of disability in patients following a stroke, and we plan to advance RNS60 into a Phase 3 clinical trial in order to bring this promising therapy to patients.”

    Initial topline results from the RESCUE Phase 2 study—which evaluated patients who were 24 hours from last known well, and saw RNS60 meet its safety- and mortality-related endpoints—were presented as a late-breaking oral presentation at last year’s ISC (7–9 February 2024, Phoenix, USA).

    Tuesday, December 10, 2024

    Brain’s Quit-or-Wait Dilemma: How We Decide to Persist or Move On

     Ask your competent? doctor for the EXACT DAMAGE to these areas and how that will affect your ability to recover from your stroke with NOTHING FROM YOUR DOCTOR!

    I know that's asking a lot of your doctor, but competent doctors will have an EXACT DAMAGE DIAGNOSIS from your stroke.  NIHSS and the Berthel Index ARE NOT DAMAGE DIAGNOSES, they do not give you the 3d location of your dead and damaged neurons. In my opinion, they are FUCKING WORTHLESS to getting you recovered!

    Brain’s Quit-or-Wait Dilemma: How We Decide to Persist or Move On

    Summary: New research sheds light on how the brain’s prefrontal cortex evaluates whether to persist or quit in uncertain situations. Using tasks mimicking real-life dilemmas, researchers found that different brain regions influence patience and adaptability.

    Damage to the ventromedial prefrontal cortex reduced persistence, while damage to other areas impaired learning from feedback. These findings highlight the complex calculations our brains perform to weigh rewards, shedding light on behaviors tied to anxiety, addiction, and depression.

    Key Facts:

    • Brain Regions and Patience: The ventromedial prefrontal cortex is crucial for evaluating the value of waiting, while other regions affect adaptability in decision-making.
    • Lesions and Impairment: Individuals with brain damage in specific areas showed reduced persistence or struggled to learn when quitting was the better choice.
    • Broader Implications: Insights could help address conditions like addiction and depression, where persistence and reward processing are often altered.

    Source: University of Pennsylvania

    You’re standing at a bus stop, waiting for a ride that seems like it will never come. At first, you’re hopeful that it will be here any second. But as the minutes laggardly drag on, doubt creeps in. Should you keep waiting, or is it smarter to start walking or call for a ride? 

    “It’s a classic dilemma. “Do you persist with the belief that the bus is on its way, or do you cut your losses and move on to something else?” asks Joe Kable, a psychologist in the School of Arts & Sciences at the University of Pennsylvania. 

    The question isn’t just whether you have the patience to wait, he says.

    “It’s about understanding when it pays off to stick with something and when cutting your losses is the better choice.”

    Kable draws parallels to two competing ideas on perseverance: Penn professor Angela Duckworth’s bestseller “Grit,” which champions the value of persistence, and “Quit” by Penn alum Annie Duke, which explores the wisdom of knowing when to let go. 

    In a paper published in the Journal of Neuroscience, Kable, collaborator Joe McGuire of Boston University, and a team of researchers examine the neural underpinnings that belie one’s decision to persist or quit, “and how the brain’s executive function helps us decide when to wait or walk away.”

    The research looks at individuals with damage to different parts of the prefrontal cortex, the seat of executive decision-making, revealing how the brain evaluates uncertainty and guides those split-second decisions. 

    These findings could bear implications for understanding and potentially treating conditions like anxiety, depression, substance abuse, and addiction, which often involve altered reward processing and persistence behaviors. 

    Lessons gleaned from the waiting game

    Kable and his team investigated how different regions of the frontal cortex influence decisions to persist or quit using a task designed to mimic real-world dilemmas.

    In the experiment, participants decided when to “cash out” coins that increased in value over time. Some coins matured quickly while others required a longer wait, depending on the task condition.

    “We wanted to create a situation where persistence sometimes paid off and sometimes didn’t,” Kable says.

    In the high-persistence (HP) condition, maturation times were uniformly distributed, so always waiting until the coin reached its maximum value was optimal.

    In the limited-persistence condition, the maturation times followed a heavy-tailed distribution, meaning that if the coin did not mature within the first couple of seconds, it was better to stop waiting.

    Participants weren’t told about these distributions, forcing them to learn from experience.

    Their study had 18 controls and 31 participants with brain lesions, grouped by the affected regions of their frontal cortex.

    The lesion groups included people with damage to the ventromedial prefrontal cortex (vmPFC), the dorsomedial prefrontal cortex (dmPFC), or anterior insula (AI), and a “frontal control” group with lesions in other areas of the frontal cortex.

    By comparing these groups, the researchers aimed to pinpoint the specific contributions of different brain regions to persistence and quitting.

    “By studying individuals with these specific lesions, we could directly test how different parts of the brain contribute to persistence versus quitting,” says Camilla van Geen, first author of the study and a Ph.D. candidate in the Kable Lab.

    The team found that participants with vmPFC damage waited less overall, particularly in the HP condition where persistence was the optimal strategy.

    “The vmPFC seems to play a crucial role in evaluating the subjective value of waiting,” van Geen says.

    “Damage to this area doesn’t just reduce patience; it fundamentally alters how people assess whether persistence is worthwhile in the first place.”

    However, participants with lesions in the dmPFC or AI showed a different pattern of impairment, Kable says. They waited about the same amount of time in both conditions, failing to distinguish between situations where persistence was advantageous and those where it wasn’t.

    “It wasn’t just a matter of self-control,” Kable says.

    “These participants couldn’t adjust their strategies based on feedback from the environment, particularly from experiences where quitting was the better decision.”

    Van Geen also used a computational model to further analyze these decision-making processes, which revealed that the vmPFC group had a lower baseline willingness to wait, while the dmPFC/AI group struggled to learn from quit trials. 

    A dynamic relationship with rewards

    “This isn’t just about self-control or impulsivity; it’s about how our brains estimate value and adapt in real time to decide when waiting pays off,” van Geen says.

    One surprising finding was that individuals with lesions in the lateral prefrontal cortex, a region often associated with self-control, performed just as well as healthy controls.

    This result suggests that while the vmPFC helps determine the baseline value of waiting and the dmPFC and AI contribute to learning from feedback, the lateral prefrontal cortex may not be as central to persistence as previously thought. 

    “We often think of persistence as a good thing and quitting as a failure,” van Geen says.

    “But really, they’re two sides of the same coin. Both require complex mental calculations and both can be the right choice depending on the situation.”

    As a follow-up, the researchers are turning their attention to neurotransmitters like dopamine and serotonin to better understand how these systems influence persistence.

    “We’ve completed a study where participants take drugs that enhance these systems to see how it affects their willingness to wait,” Kable says.

    “The preliminary results suggest serotonin plays a particularly interesting role, but we’re still working through the data.”

    Future work will also focus on how brain regions and neurotransmitter systems interact. “Do these systems influence each other, or do they operate independently? That’s one of the big questions we’re tackling next,” Kable says. 

    Joseph W. Kable is the Jean-Marie Kneeley President’s Distinguished Professor of Psychology at the University of Pennsylvania’s School of Arts & Sciences.

    Camilla van Geen is a Ph.D. candidate in Penn Arts & Sciences.

    Other authors are Yixin Chen of Boston University, Rebecca Kazinka of the University of Minnesota, and Avinash R Vaidya of the NIDA Intramural Research Program.

    Funding: The research was supported by the National Institutes of Health (grants R01-DA029149, F32-DA030870, and R21-MH124095  and award ZIA DA000642), and the National Science Foundation (Grant BCS-1755757).

    About this self-control and neuroscience research news

    Author: Nathi Magubane
    Source: University of Pennsylvania
    Contact: Nathi Magubane – University of Pennsylvania
    Image: The image is credited to Neuroscience News

    Original Research: Closed access.
    Lesions to different regions of frontal cortex have dissociable effects on voluntary persistence” by Joe Kable et al. Journal of Neuroscience