Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,278 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.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
My conclusion is you don't understand ONE GODDAMN THING ABOUT SURVIVOR MOTIVATION/DEMORALIZATION, DO YOU?
You create EXACT 100% recovery protocols, and your survivor will be motivated
to do the millions of reps needed because they are looking forward to
100% recovery. GET THERE!
In stroke rehabilitation, VR-based technologies like the C-Mill treadmill combine physical and cognitive
training to enhance motivation and motor learning. While quantitative studies show functional benefits, little is known about
patients’ experiences.
Aim:
This study aims to explore stroke survivors’ subjective experiences of motivation during C-Mill
training. Method: A qualitative design was employed. Seven inpatients at Sunnaas Hospital who had engaged in gait
rehabilitation with C-Mill participated in semi-structured interviews. Data were transcribed verbatim and analyzed using
systematic text condensation.
Results:
One overarching theme - motivation - was identified, comprising two subthemes:
intrinsic and extrinsic motivation. The patients described how the C-Mill fostered intrinsic motivation by providing
challenging, meaningful, and engaging activities that reflected everyday-life situations. They experienced that the system
encouraged them to push their limits and attempt tasks they might otherwise hesitate to try, while still feeling supported and
safe. Additionally, the technology enhanced extrinsic motivation through engaging feedback mechanisms, including
gamification elements, and the visualization of performance statistics.
Conclusion:
C-Mill appears to constitute a promising
adjunct to conventional rehabilitation by strengthening motivation. Its technological features, including safety scaffolding,
gamification, and task variability, appeared to facilitate engagement and promote motivation.
1. Department of Diagnostic and Interventional Neuroradiology, Philipps University of Marburg, Marburg, Germany
2. Clinic of Diagnostic and Interventional Radiology, Philipps University of Marburg, Marburg, Germany
Abstract
Objectives:
This study aimed to determine whether automated net water uptake (NWU) measured on admission non-contrast computed tomography (CT) independently predicts futile recanalization (FR) in anterior-circulation large vessel occlusion (LVO) stroke treated with endovascular thrombectomy (EVT).
Methods:
This was a retrospective single-center cohort study that included consecutive patients presenting at a tertiary care stroke center between January 2023 and April 2025. Patients were included if they presented with an anterior circulation LVO and had successful recanalization (mTICI 2b–3). An automated platform (VEOcore/MRAY) provided the Alberta Stroke Program Early CT Score (ASPECTS), perfusion metrics, and NWU. Associations with FR were analyzed using logistic regression. Discrimination was evaluated using receiver operating characteristic (ROC) analysis and Youden’s J statistic to identify an optimal NWU threshold, reporting the area under the curve (AUC), sensitivity, specificity, and predictive values.
Results:
Among 91 patients, 62 (68.1%) achieved recanalization with a 90-day modified Rankin Scale (mRS) score of 0–4, and 29 (31.9%) met the criteria for FR (mRS score 5–6). Those with FR were older (81.6 ± 8.3 vs. 76.9 ± 10.7 years; p = 0.044) and had more severe strokes at presentation (median National Institutes of Health Stroke Scale [NIHSS] score of 16 [13–20] vs. 9.5 [6–15]; p < 0.001). NWU in the core was higher in FR (21.9% [7.0–29.4]) than in non-FR cases (3.0% [0.5–7.3]; p < 0.001) and correlated with 90-day mRS (Pearson r = 0.602; 95% CI 0.452–0.719; p < 0.001). In multivariable models, NWU remained independently associated with FR (odds ratio [OR] 1.15; 95% CI 1.06–1.24; p < 0.001).
Conclusion:
Automated NWU on admission CT is an independent, strongly discriminative predictor of FR and 90-day disability. A tiered strategy using >11.5% as a risk flag and >17.5% as a high-specificity rule-in threshold may enhance early triage, prognostication, and clinical trial stratification. Prospective multicenter validation is warranted.
Until 100%recovery research is out there, artificial intelligence
isn't going to do much good. Wrong goal: the only goal in stroke is 100%
recovery! GET THERE!Predictions and 'management' DO NOTHING FOR RECOVERY! If you are that fucking stupid; you need to be fired!
Weihua Song1,#, Shuai Si2,#, Yinghui Wang3, Hong Chang1,*, Xiaoying Tang2,*
1. Department of Neurology, Beijing Municipal Geriatric Medical Research Center, Xuanwu Hospital,
Capital Medical University, Beijing, China
2. School of Medical Technology, Zhengzhou Academy of Intelligent Technology, Beijing Institute of
Technology, Beijing, China
3. Luohe Orthopedic Hospital, Luohe, China
Corresponding author: Hong Chang (changhong@xwhosp.org); Xiaoying Tang (xiaoying@bit.edu.cn)
# Those authors contributed equally to this work
Abstract:
Artificial intelligence (AI) is being studied across the stroke care pathway, but evidence
from acute diagnosis, early prognosis, rehabilitation-outcome prediction, and long-term management is
often discussed without clearly separating these clinical tasks. This structured narrative review adds an
integrated framework that maps each application to its decision point, relevance to rehabilitation,
validation level, and readiness for clinical use. Unlike previous technology-centred reviews, it
explicitly separates acute prognostic evidence from rehabilitation-specific evidence and distinguishes
technical performance from transportability, clinical impact, and rehabilitation benefit. Acute imaging
and prognostic models may provide baseline information for later rehabilitation planning, but their
diagnostic or prognostic performance does not establish rehabilitation efficacy. Most rehabilitation
models and robotic, virtual-reality, brain-computer interface, wearable, and home-monitoring
applications remain supported mainly by internal validation or early exploratory studies. Small or
selected datasets, limited external and prospective validation, uncertain workflow effects, and sparse
patient-centred outcomes continue to constrain clinical interpretation
Department of Neurology, Wenzhou TCM Hospital of Zhejiang Chinese Medical University, Zhejiang, China
Abstract
Introduction:
Post-stroke depression (PSD) is common and disabling, yet mechanism-based, multi-target therapies that jointly curb neuroinflammation and support cell survival are scarce. We evaluated a Blood-Activating, Depression-Relieving (BADR) herbal formula for effects on PSD-relevant molecular hubs and microglial phenotypes.
Methods:
BADR constituents from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform were standardised and mapped to human protein targets. Target-disease interaction networks were assembled in Search Tool for the Retrieval of Interacting Genes/Proteins, clustered with Molecular Complex Detection, and functionally annotated via Kyoto Encyclopedia of Genes and Genomes Orthology-Based Annotation System (KEGG/GO). For experimental validation, BV2 microglia were activated with lipopolysaccharide (LPS; 24 h) and co-treated with BADR within a pre-established non-cytotoxic range; dexamethasone (1 μM) served as comparator. Outcomes included cytokines (IL-1β, TNF-α, IL-6; enzyme-linked immunosorbent assay), expression of selected nodes (EGFR, STAT3, JUN, PIK3CA, BCL2; quantitative real-time polymerase chain reaction/western blot), viability (Cell Counting Kit-8), and apoptosis (flow cytometry).
Results:
Network analysis highlighted two dense modules enriched for PI3K-AKT, JAK–STAT, and neuroactive-ligand signaling. Hubs included EGFR, AKT1, STAT3, JUN, PIK3CA, and BCL2, with EGFR, STAT3, PIK3CA, JUN, and BCL2 prioritised for cellular validation based on topology, pathway relevance, and compound-target connectivity. In BV2 cells, BADR attenuated LPS-induced IL-1β, TNF-α, and IL-6 surges, improved viability, and reduced total apoptosis, with directionally comparable effects to dexamethasone. Mechanistically, BADR down-regulated EGFR/JUN/STAT3/PIK3CA and restored BCL2 at transcript and protein levels.
Conclusion:
By converging network-level predictions with microglial phenotyping, the formula exerts coordinated anti-inflammatory and pro-survival effects centred on the EGFR-STAT3-PI3K nodes in a PSD-relevant context. These data provide a mechanistic rationale for further phosphorylation-level and in vivo validation toward multi-target PSD therapeutics.
Neurology content commonly referenced by physicians includes major clinical practice guidelines, diagnostic frameworks, therapeutic advances, landmark clinical trials, and validated clinical assessment tools. The following 10-item framework reflects widely used resources that inform neurologic care.
American Heart Association (AHA)/American Stroke Association (ASA) Acute Ischemic Stroke Guidelines — The AHA/ASA guideline for acute ischemic stroke provides evidence-based recommendations for prehospital care, emergency evaluation, intravenous and intra-arterial treatment, in-hospital management, and early secondary prevention.
AHA/ASA Primary Prevention of Stroke Guideline — The AHA/ASA guideline provides recommendations for first-stroke prevention through risk factor management, cardiovascular and brain health optimization, and lifespan-based prevention strategies. The 2024 update includes revised recommendations and additional guidance on sex-specific stroke risk factors.
National Institutes of Health Stroke Scale — The National Institutes of Health Stroke Scale is a validated clinical tool used to assess stroke severity by measuring neurological deficits across multiple functional domains.
Dopaminergic Therapy for Early Parkinson Disease Guideline – The American Academy of Neurology guideline provides recommendations for initiating dopaminergic treatment for motor symptoms in early Parkinson disease. The guidance compares levodopa, dopamine agonists, and related formulations, supporting clinician-patient discussions about expected motor benefit, dyskinesia risk, impulse control disorders, prescribing decisions, and safety monitoring.
International League Against Epilepsy Classification of the Epilepsies — The International League Against Epilepsy classification system organizes epilepsy diagnosis by seizure type, epilepsy type, and epilepsy syndrome. It also incorporates etiology at each stage of evaluation, helping guide diagnosis, treatment decisions, and patient management.
Anti-Amyloid Monoclonal Antibodies for Alzheimer Disease — Lecanemab and donanemab are anti-amyloid monoclonal antibodies approved for patients with early Alzheimer disease and confirmed amyloid pathology. These therapies target beta-amyloid in the brain and are administered to selected patients with mild cognitive impairment or mild dementia due to Alzheimer disease.
McDonald Criteria for Multiple Sclerosis — The McDonald criteria provide a diagnostic framework for multiple sclerosis in patients with a typical clinically isolated syndrome. The criteria use clinical findings, magnetic resonance imaging, cerebrospinal fluid markers, and evidence of lesion dissemination in time and space to support diagnosis while highlighting exclusion of alternative explanations for a patient’s presentation.
Calcitonin Gene-Related Peptide-Targeting Therapies for Migraine Prevention — The American Headache Society position statement recognizes calcitonin gene-related peptide-targeting therapies as first-line preventive treatment options for migraine. The guidance incorporates evidence on efficacy, safety, and tolerability for patients with episodic and chronic migraine.
DAWN and DEFUSE 3 Trials — The DAWN and DEFUSE 3 trials evaluated mechanical thrombectomy in patients with acute ischemic stroke who met specific clinical and imaging eligibility criteria. Both studies reported better 90-day functional outcomes among patients who underwent thrombectomy in addition to medical therapy compared with those who received medical therapy alone.
CLARITY AD Trial — The phase 3 CLARITY AD trial evaluated lecanemab in patients with early Alzheimer disease and evidence of amyloid pathology. Compared with placebo, lecanemab was associated with less decline on measures of cognition and function over 18 months.
Sources: Stroke, American Heart Association, National Institute of Neurological Disorders and Stroke, Neurology, American Headache Society, The New England Journal of Medicine, Alzheimer’s Association, The Lancet Neurology
In my 16 years writing this blog, I SEE NOTHING THAT SUGGESTS ANY GUARANTEED WAY TO GET RECOVERY! Hope is NOT GOOD ENOUGH! Do the work that delivers recovery!
The neurologist Orlando Swayne doesn’t suggest everyone can recover.(That's the problem in a nutshell, advocating the tyranny of low expectations to dumb down the survivor goals to what can currently be delivered! THAT IS GIVING UP BEFORE THE SURVIVOR EVEN STARTS! 100% recovery is the only goal in stroke! GET THERE!) But he does argue that early, targeted and intense therapy can sometimes bring about life-changing improvements – and we have a moral obligation to provide it
Prefer the Guardian on GoogleThe Guardian’s journalism is independent. We will earn a commission if you buy something through an affiliate link. Learn more.
Claire was in bad shape. She had been brought to the ward on a stretcher and hoisted on to a bed where she lay curled up in a ball. She was unable to speak, her eyes flat and face expressionless. While she could move her right arm a little, her left arm and both legs were immobile.
Life had changed dramatically for Claire, a mother of three in her late 30s, many months earlier, when she collapsed while on a night out with friends. A weakness in an artery at the base of her brain had ruptured, spilling blood around her frontal lobe. She was taken to hospital, where surgeons removed two side plate-sized pieces of bone from her skull to relieve the pressure on her brain. She spent months in intensive care.
Can a patient with such profound impairment improve in any meaningful way, especially so long after the event? That was the question for Orlando Swayne, a consultant neurologist and co-lead of the pioneering neurorehabilitation unit at the National hospital for Neurology and Neurosurgery, a Victorian redbrick building in Queen Square, central London.
(If your doctor doesn't reference
Pedro Bach-y-Rita who recovered fully back in 1958 with only a partial brain! Aren't you smart enough to duplicate that? Then you DON'T have a functioning stroke doctor! Get rid of them!)
It was a few years before the pandemic when Swayne first met Claire on the ward. She made eye contact but showed no other response. He knew from the referring hospital that she could write single-word answers to queries, but these revealed characteristic signs of the brain damage she had sustained. Before leaving her bedside to tend to other patients, Swayne asked if she had any questions. With a pencil clenched in her right hand, she wrote: “Questions, questions, questions,” and then tailed off into a wiggly line. The pathological repetition comes from a failure in the frontal lobe to keep actions moving along in sequence.
“There are some patients who start off, when we first work with them, severely impaired – and I mean very severely impaired,” says Swayne. Claire (not her real name) was one such patient.
If he had trusted only his lectures at medical school, Swayne might have considered Claire beyond help. Dogma held that broken brains didn’t mend. A brief flirtation with neurosurgery did nothing to dispel the view. “You see patients in a really terrible state and you think that’s them for life,” he says, “but you don’t see them for very long.”
You see patients in a really terrible state and you think that’s them for life
Swayne quickly decided against a career in neurosurgery, perhaps for the best. “I’m a bit clumsy,” he says, though this wasn’t the only reason. “Neurosurgery is all about the craft, and I’m not really a craft person. I like the people. I like the relationships and the human aspects, which you don’t get so much in neurosurgery.”
He moved into general medicine, then into neurology and stroke medicine, and over the next 20 years or so started to see patients long after their original admission. “I began to realise that some of these patients were improving. And the ones who were improving were the ones working with therapists,” he says. “I thought: ‘OK, I didn’t realise that was a thing. How does it work?’”
The answer, it seems, is to be found in the brain’s capacity for neuroplasticity, its ability to make new connections and reorganise in the face of changed circumstances. In his new book, How to Use a Fork: Stories of Mending the Broken Brain, Swayne argues that recent discoveries in this area have “profound implications” for patients and the therapy and care we owe them.
Swayne is at the piano murdering Chopin – his words, not mine – when I arrive at his north London home. Our chat clashes with his daughter leaving for gap year travels, a milestone I’d assumed would be infused with chaos, but a calmness prevails. A small black dog bounds over and then scoots away, before finding a spot on the kitchen sofa.
My copy of his book is a mess of folded corners, underlined passages and notes in the margin, but I confess, unfairly in retrospect, that I hadn’t relished reading it. For there is history here. Doctors have written books on neuroplasticity before and some made me deeply uncomfortable. To my mind, they peddled false hope through portrayals of miraculous recoveries. At worst, they seemed to imply that patients with severe brain injuries could rise up from their wheelchairs, speak fluently once again and overcome deep cognitive impairment if only they put their mind to it. I feared more of the same: show me a publisher that wants stories of patients whose lives are destroyed and remain so.
Swayne, it turns out, has read the same books and shares the concern. To be clear, he is not suggesting that everyone who suffers a huge stroke or brain injury can recover. His argument is that early, targeted and intense therapy can bring about life-changing improvements, and that we have a moral obligation, not to mention an economic one, to provide such care. “The perception of brain injury is that it is irreversible and irrecoverable from, and this is a corrective to that view,” he says. “There is hope, but clearly you have to balance that. Some people just don’t recover.”(Discounting
Pedro Bach-y-Rita who recovered fully back in 1958 with only a partial brain!)
Stroke is a leading cause of adult disability in the UK. It happens when a blood vessel, typically an artery, becomes blocked or bursts, and starves the brain of oxygen and nutrients. Within minutes, brain cells in the affected region begin to die. Depending on the location, a stroke can cause paralysis, loss of speech, blindness and other vision problems, impaired thinking, memory loss, personality changes, an inability to swallow, and more. Of the 12 million or so people globally who suffer a stroke each year, one in five dies within 30 days.
Many stroke patients show small improvements in the first few weeks, as swelling and inflammation subside. According to old-school thinking, that was as much as you could hope for. But it’s not the full story. The damage caused by stroke or brain injury drives chemical changes in the brain. These trigger neuronal growth processes that were last active in the developing brain. Surviving neurons are spurred into making new connections and to work around the dead tissue.
Of course, the brain constantly demonstrates some level of neuroplasticity. To learn a foreign language, or how to play a new instrument or fly a helicopter, your brain must forge new connections. The process redraws the functional maps in the brain, the neural territory called upon to perform particular tasks. So it is that black-cab drivers in London have more grey matter in the hippocampus after learning the Knowledge. Likewise, the amount of brain dedicated to using the index finger expands when people learn to read braille with it. But the process is sluggish in adults compared with children and those who have suffered recent stroke or brain injury.
After such events, neuroplasticity ramps up for several months. This is when intense, targeted therapy can have the most impact. “Even though the capacity for plasticity is greatest in the first few months, it doesn’t just switch off,” Swayne says. In one study, intensive therapy improved upper limb movement in patients 18 months after their strokes.
Claire’s early therapy sessions focused on positioning and stretching – to enable her to sit comfortably – and mouth, tongue and voice box exercises. But they were tough, and she quickly became too tired to continue. In time, though, her stamina improved and she engaged more with the therapists. Her gaze began to follow people walking past and she would sometimes move her mouth to speak in response to questions.
Her improvement gathered pace with music therapy. In those sessions, Claire used her stronger right hand to pluck guitar strings and shake maracas. Her therapists noticed more spontaneous facial expressions and she began to point to instruments, choosing, being proactive. Session after session, for four months, she was drilled to make choices, identify objects, to engage her mouth and tongue.
Swayne hadn’t caught up with the therapists in a while, but one day as he headed past Claire’s bay and said hello, she looked up and said: “What happened to your hair?” Swayne stopped dead. “That was an amazing moment,” he says. “If you work with a patient who’s not spoken for a year, and you do an intervention and they start speaking, it’s got to be a response to the therapy.”
Swayne confided in Claire about his disastrous encounter with a barber and later learned from the speech therapist that her language had been coming for a week or so. First it was single words, then phrases and short sentences. She had made progress with her right hand, too. Before long, she was playing Connect 4 with her boys and fellow patients on the ward, though her left side and right leg remained lifeless.
“She started communicating with her kids and with us, and that was enormous,” Swayne says. “Her left side will always remain weak because it’s very badly damaged, but she started using her right arm to do things, like use a phone and use a power chair. We had her cooking, and that was huge. She will always need help, but for quality of life it was transformational.”
There’s plenty still to learn about the brain’s ability to work around dead tissue, but details of some mechanisms are emerging. Delve into the motor cortex in the brain’s frontal lobe and you’ll find specialised neurons that drive limb movement. These are arranged vertically to send their messages to the spinal cord. But they are also linked by a mesh of horizontal connections. Normally, these horizontal connections are suppressed, but in the event of brain damage, the inhibition is relaxed and the connections activate. Surviving neurons can now recruit neighbours to their cause, though they need time and training to learn the new job.
There’s more to neuroplasticity than this, but the mechanism explains some of the stark limitations that doctors and their patients witness. When neural connections are completely lost, it seems no amount of therapy can bring them back. And while the brain can reorganise to some extent, there’s no evidence that a specialised region of the cortex can take on an entirely different role. If a stroke leaves your right arm limp, your visual cortex cannot take control of it any more than your kettle can make the morning toast. That said, movement, language, sensation and vision are not confined to small brain regions: they are distributed across networks that provide for some flexibility. For example, most people do the bulk of their language processing in the left side of the brain, but if it is damaged, there’s evidence that parts of the language network on the right side can take on some of the work.
Much of the immediate work with new stroke patients is to identify their impairments and the causes. If they are unable to use a fork, what is stopping them? Can they feel it? Are they too weak on that side? Can they coordinate their movements?
Therapists take impairments and break them down into steps that patients can be drilled on. There is, so far, no shortcut to the gruelling hours put in by the patients described in Swayne’s book. Thomas, a vicar who couldn’t speak after a stroke at the pulpit, had intensive speech therapy to retrain his swallowing and tongue movements. Christian, a mixologist at a swanky London hotel, relearned how to brush his teeth: turn the tap on, get the toothbrush, add the toothpaste. Vikas, a roofer who fell from three storeys up, had sessions in the kitchen to learn how to pay attention and multitask again.
It’s not just the direct damage that therapists have to contend with. The brain can create its own problems. Patricia, a catering assistant, had lost the use of her right arm. When asked to point to it, she would move it out of the way and keep searching among the bedclothes. She later believed the arm was a baby and became inconsolable when she thought it had died.
The therapy a patient receives after stroke is the most important determinant of how well they recover: will they be dependent on others or able to fend for themselves? Yet what most patients receive is grossly inadequate, Swayne says. Every working day, patients at stroke units in the UK should receive 45 minutes each of physio, occupational therapy and speech therapy. In 2020, an audit found that most patients received only 14, 13 and seven minutes per day, respectively.“It’s shocking,” says Swayne.
It is even worse when people leave hospital. Stroke units used to pass patients on to the community therapy team in their local area, but those networks were demolished by austerity economics. “It’s a real postcode lottery. There are some boroughs where you’re relieved you’re discharging the patient to that borough because they’ve actually got a speech therapist, whereas another borough is a desert,” Swayne says. “It’s frustrating, having worked with these patients for months, to then send them into the wilderness.” It’s common for patients to return a year or two later with complications, having had no therapy since leaving hospital.
The argument that proper rehabilitation is a luxury we cannot afford does not add up, Swayne adds. Early intensive therapy pays for itself by reducing the cost of long-term care. This will become ever more important as first-time strokes rise in the coming years. Today, strokes cost the UK economy an estimated £27bn a year, but only £3bn of that is driven by direct hospital care. The rest is lost economic productivity and the invisible costs of care. By 2035, the cost is predicted to more than triple to £75bn.
“People talk about the cost of these interventions, but if you do the maths, an admission might cost something like £40,000,” Swayne says. “That sounds like a lot of money, but if you look at the change in care costs, it isn’t, because it pays itself back pretty quickly.” Swayne did the sums for one patient: during his time in the rehabilitation unit, his care costs fell to £2,640 per week, meaning the cost was offset within four months of him going home, and would save tens or hundreds of thousands of pounds in the longer term.
uble. Care for traumatic brain injury is also badly neglected. Each year, more than 1 million people in England and Wales attend emergency departments for head injuries. Of the 200,000 or so who are admitted to hospital, about 40,000 have evidence of traumatic brain injury.
Many such patients are discharged within a couple of weeks. Superficially, they seem better: they can walk and talk. But often, important problems are simply not spotted. “What we now realise is that a majority of those patients have got cognitive changes that haven’t been picked up,” Swayne says. “You can see them walking down the street and they look fine, but they cannot function normally. There’s an invisible disability. It affects their relationships, their employment and they get into trouble with the police.”
And so, the hidden damage left by brain trauma can lead to lives falling apart. In one 2025 study, researchers found that nearly 90% of adult men in Scottish prisons had experienced severe head injury. That doesn’t mean that brain injury triggered their crimes: violent men experience more violence. But damage to specific brain regions might contribute to criminal behaviour, by making it harder for people to control their impulses, feel empathy and anticipate the consequences of their actions.
Researchers are looking at ways to make therapy more effective and – the holy grail – to reopen the window of enhanced neuroplasticity. New drugs, brain stimulation and virtual reality are all in the mix. If they succeed, patients could receive more beneficial therapy to boost their recovery. But for now, perhaps the best we can do is keep our brain healthy and protected.
“We all know what to do for brain health,” says Swayne. “We should exercise. We should be in a stimulating environment and have social interactions. We shouldn’t smoke or drink too much alcohol. There’s really strong evidence that all these things help with brain maintenance. By looking after your brain you’re giving yourself the best chance of recovery should you need it.”
How to Use a Fork: Stories of Mending the Broken Brain is published by Pan Macmillan on 4 June (£20). To support the Guardian, order a copy from guardianbookshop. Delivery charges may apply
