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 amantadine. Show all posts
Showing posts with label amantadine. Show all posts

Monday, April 28, 2025

Amantadine continuation after hospital discharge for acute stroke requiring inpatient rehabilitation: a long-term follow-up study 1-5-25

 What did your hospital do with this from 13 years ago? NOTHING? Then they revel in their incompetence assuming that stroke survivors won't find out and don't care.  I bet absolutely fucking nothing has been done to get clinical research done and a stroke protocol written up.
  • amantadine (8 posts to February 2012)
  • Amantadine continuation after hospital discharge for acute stroke requiring inpatient rehabilitation: a long-term follow-up study 1-5-25

    Author links open overlay panel Haley R. Torr Pharm D 1Sara Penrod SLP-CCC 2, Jennifer Cote OTR/L 2, Sara E. Hanken PTMPT 2, Stephanie C. Chan MD 3, Riker MD 456Angela Leclerc MSPAPA-C 45, Teresa L. May DO 45, David B. Seder MD 4 >5 6 7, David J. Gagnon PharmD 1 67

    Abstract

    Objectives To describe the dosing strategy, safety, and effectiveness of amantadine in patients admitted to inpatient rehabilitation after stroke.
    Design Retrospective, single-center, cohort study
    90-bed, inpatient rehabilitation hospital
    Participants28 patients with amantadine started in a neuroICU after stroke and continued after transfer to rehabilitation; the median age was 67 years and 61% were male.

    Interventions

    Oral amantadine

    Main Outcome Measures

    Amantadine prescribing practices, adverse drug effects, and changes in recovery trajectory relative to dose changes.

    Results

    This cohort included 14 adult patients with intracerebral hemorrhage, 10 with subarachnoid hemorrhage, and 4 with acute ischemic stroke. The most common admitting amantadine dose was 100 mg twice daily. Inpatient rehabilitation lasted 27 (24-35) days, and amantadine was discontinued during rehabilitation in 6 patients (21%). Amantadine was prescribed to 22 patients (79%) at discharge from rehabilitation, most commonly 100 mg daily or twice daily, and was continued for 105 (39-510) days after admission to rehabilitation among the 17 patients with this data available. Twenty-one potential adverse events were identified among 16 (57%) patients, including confusion or delirium, sleeplessness, agitation, fatigue or lethargy, and spasticity; 8 of these (38%) occurred after reductions in amantadine dose.

    Conclusions

    Amantadine dosing was highly variable during inpatient rehabilitation, with trends for longer dosing after acute ischemic stroke and shorter for subarachnoid hemorrhage. Amantadine appeared well tolerated during and after inpatient rehabilitation, and most (22/28) patients were prescribed amantadine at discharge. Strategies to guide long-term use of amantadine following acute stroke require further prospective study.

    Keywords

    Amantadine
    Ischemic Stroke
    Subarachnoid Hemorrhage
    Cerebral Hemorrhage
    Rehabilitation
    Adverse Drug Effects
    Brain Injuries

    Saturday, April 19, 2025

    Neurostimulant Use for Rehabilitation and Recovery After Stroke: A Narrative Literature Review

     I see nothing here that even remotely states what should be done to get recovered! You got published but DID NOTHING for getting survivors recovered!

    Neurostimulant Use for Rehabilitation and Recovery After Stroke: A Narrative Literature Review

  • Abstract

    BACKGROUND:

    Stroke often results in significant impairments across various domains, including movement, language, cognition, and mood. Neurostimulants have been proposed as potential therapeutic interventions to enhance recovery in these areas.

    METHODS:

    This narrative literature review examines clinical trials investigating the efficacy of neurostimulants in poststroke recovery. It evaluates outcomes related to aphasia, motor deficits, cognition, fatigue, and depression.

    RESULTS:

    The qualitative analysis included 34 trials testing the following neurostimulants: methylphenidate (n=6), amphetamines (n=8), memantine (n=2), modafinil (n=2), levodopa (n=14), amantadine (n=1), bromocriptine (n=3), and ropinirole (n=1). Of the 34 studies, 31 were randomized, placebo-controlled (double-blind, n=27; single-blind, n=2; unblinded n=2), 2 were randomized and not placebo-controlled, and 1 was not randomized. Study design was either multiarm (n=23), crossover (n=10), or used subjects as their own control (n=1). Mean sample size was 49.4 (5–593).

    CONCLUSIONS:

    Current evidence suggests that memantine may be effective for aphasia, although few phase III trials exist, whereas bromocriptine and amphetamines lack sufficient evidence for long-term recovery of aphasia. Levodopa may improve motor aphasias but has not shown long-term benefits for motor recovery. Similarly, ropinirole has not been shown to improve poststroke motor outcomes. Methylphenidate has limited efficacy for cognitive improvement but may enhance poststroke functionality and mood. Modafinil may help with poststroke fatigue. In conclusion, there are promising results of positive effects of neurostimulants with few side effects, though studies are limited by heterogeneous designs and small sample sizes. Neurostimulant efficacy must be assessed in conjunction with specific rehabilitation modalities as part of larger, well-designed studies to best understand their effects on impairment.

    Graphical Abstract




    Get full access to this article

    Tuesday, February 23, 2021

    CURRENT OPINION Motor rehabilitation in stroke and traumatic brain injury: stimulating and intense

    What did your hospital do with this from 8 years ago? NOTHING? Then they revel in their incompetence assuming that stroke survivors won't find out and don't care. 

    amantadine 6 posts back to Feb. 2012 and I bet absolutely fucking nothing  has been done to get clinical research done and a stroke protocol written up.

    CURRENT OPINION Motor rehabilitation in stroke and traumatic brain injury: stimulating and intense

      Erika Y. Breceda a,b
    and Alexander W. Dromerick a,b
    a Washington DC Veterans Affairs Medical Center and
    b Medstar National Rehabilitation Hospital, Georgetown University Department of Rehabilitation Medicine, Washington, District of Columbia, USA Correspondence to Alexander W. Dromerick, MD, Medstar National Rehabilitation Hospital, Georgetown University Department of Rehabilitation Medicine, 102 Irving Street NW, Washington, DC 20010, USA.Tel: +1 202 877 1932; fax: +1 202 726 7521; e-mail: Alexander.W.Dromerick@medstar.net
    Curr Opin Neurol
     2013, 26:595–601DOI:10.1097/WCO.0000000000000024

    Purpose of review
    The purpose of this review is to provide an update on the latest neurorehabilitation literature for motor recovery in stroke and traumatic brain injury to assist clinical decision making and assessing future research directions.
    Recent findings
    The emerging approach to motor restoration is now multimodal. It engages the traditional multidisciplinary rehabilitation team, but incorporates highly structured activity-based therapies, pharmacology, brain stimulation and robotics. Clinical trial data support selective serotonin reuptake inhibitors and amantadine to assist motor recovery post stroke and traumatic brain injury, respectively. Similarly, there is continued support for intensity as a key factor in activity-based therapies, across skilled and nonskilled interventions.Aerobic training appears to have multiple benefits; increasing the capacity to meet the demands of hemiparetic gait improves endurance for activities of daily living while promoting cognition and mood.At this time, the primary benefit of robotic therapy lies in the delivery of highly intense and repetitive motor practice. Both transcranial direct current and magnetic stimulation therapies are in early stages, but have promise in motor and language restoration.
    Summary
    Advancements in neurorehabilitation have shifted treatment away from nonspecific activity regimens and amphetamines. As the body of knowledge grows, evidence-based practice using interventions targeted at specific subgroups becomes progressively more feasible.

    Thursday, March 26, 2020

    The role of amantadine in cognitive recovery early after traumatic brain injury: a systematic review

    WHOM is going to do the followup to see if this would help in stroke also? Nothing will occur since we have NO STROKE LEADERSHIP to contact with these suggestions.

    The role of amantadine in cognitive recovery early after traumatic brain injury: a systematic review




    Highlights

    •
    Cognitive dysfunction is a common sequela of traumatic brain injury.
    •
    Amantadine has been investigated in cognitive recovery after traumatic brain injury.
    •
    Amantadine is well tolerated; may hasten cognitive recovery in the intermediate-term.
    •
    Efficacy of amantadine in improving long-term cognitive recovery remains uncertain.

    Abstract

    We conducted an updated systematic review on the safety and efficacy of amantadine in cognitive recovery after traumatic brain injury (TBI), in order to determine if the current literature justifies its use in this clinical condition. A comprehensive search strategy was applied to three databases (PubMed, Scopus, and Cochrane). Only randomized clinical trials (RCTs) that compared the effect of amantadine and placebo in adults within 3 months of TBI were included in the review. Study characteristics, outcomes, and methodological quality were synthesized. This systematic review was conducted and presented in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). A quantitative synthesis (meta-analysis) was not feasible due to the large heterogeneity of studies identified.
    Three parallel RCTs and one cross-over RCT, with a total of 325 patients were included. All of the studies evaluated only severe TBI in adults. Amantadine was found to be well tolerated across the studies. Two RCTs reported improvement in the intermediate-term cognitive recovery (four to six weeks after end of treatment), using DRS (in both studies) and MMSE, GOS, and FIM-Cog (in one study). The effect of amantadine on the short-term (seven days to discharge) and long-term (six months from the injury) cognitive outcome was found not superior to placebo in two RCTs. The rate of severe adverse events was found to be consistently very low across the studies (the incidence of seizures, elevation in liver enzymes and cardiac death was 0.7%, 1.9%, and 0.3%, respectively). In conclusion, amantadine seems to be well tolerated and might hasten the rate of cognitive recovery in the intermediate-term outcome. However, the long-term effect of amantadine in cognitive recovery is not well defined and further large randomized clinical trials in refined subgroups of patients are needed to better define its application.

    Sunday, July 30, 2017

    Vegetative stroke patient, 36, was able to speak and move just 16 DAYS after being given a Parkinson's disease drug

    4 posts back to Feb. 2012 and I bet absolutely fucking nothing  has been done to get clinical research done and a stroke protocol written up.

    Vegetative stroke patient, 36, was able to speak and move just 16 DAYS after being given a Parkinson's disease drug

    • The unnamed patient was only being kept alive through medical intervention
    • Doctors thought the patient's only option was to be admitted to a nursing home
    • She was able to move and speak in short sentences due to the drug amantadine
    • The patient can now breathe independently, eat precut food and stand with help
    • Experts believe the drug may have pushed her 'above the threshold' for recovery
    A vegetative stroke patient who was completely unresponsive to what was going on around her, regained complete consciousness just 16 days after being given a Parkinson's disease drug, a case report reveals. 
    The unnamed woman, 36, who was only being kept alive by medical intervention, was able to speak in short sentences after being given the dopamine-boosting drug, known as amantadine.
    Unable to move, doctors thought her only option was to be admitted to a nursing home, yet the woman, believed to be from Berlin, can now eat and stand.
    Experts believe the drug may have pushed the woman, who was diagnosed with unresponsive wakefulness syndrome, 'above the threshold' for recovery.
    Amantadine is used to treat Parkinson's disease and 'flu. It is thought to increase levels of the 'feel-good' hormone dopamine in the brain. Dopamine is involved in regulating movement.

    Tuesday, March 24, 2015

    Clinical neurorestorative progress in traumatic brain injury

    Which of these therapies mentioned can also be used in stroke? Does your doctor know anything about this?
    http://www.dovepress.com/articles.php?article_id=20957
    Authors Huang H, Chen L, Huang H
    Published Date March 2015 Volume 2015:3 Pages 57—62
    DOI http://dx.doi.org/10.2147/JN.S74486
    Received 30 September 2014, Accepted 26 November 2014, Published 20 March 2015
    Approved for publication by Prof. Dr. Hari Shanker Sharma
    Huiling Huang,1 Lin Chen,2,3 Hongyun Huang4–6

    1Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Huanhu Hospital, Tianjin Neurosurgical Institute, Tianjin, People's Republic of China; 2Medical Center, Tsinghua University, Beijing, People's Republic of China; 3Tsinghua University Yuquan Hospital, Beijing, People's Republic of China; 4General Hospital of Chinese people's Armed Police Forces, 5Beijing Rehabilitation Hospital of Capital Medical University, Beijing, People's Republic of China; 6Beijing Hongtianji Neuroscience Academy, Beijing, People's Republic of China

    Abstract: Traumatic brain injury (TBI) is a leading cause of death and disability from trauma to the central nervous system. Besides the surgical interventions and symptomatic management, the conventional therapies for TBI and its sequelae are still limited. Recently emerging evidence suggests that some neurorestorative treatments appear to have a potential therapeutic role for TBI and improving the patient's quality of life. The current clinical neurorestorative strategies available in TBI include pharmacological treatments (recombinant human interleukin-1 receptor antagonist, amantadine, lithium, and valproate), the neuromodulation treatments (repetitive transcranial magnetic stimulation, transcranial direct current stimulation, and low-level laser therapy), cell transplantation (bone marrow stromal cells and umbilical cord stromal cells), and combined neurorehabilitation. In this review, we summarize the recent clinical neurorestorative progress in the management of neurodegeneration as well as cognitive and motor deficits after TBI; indeed further clinical trials are required to provide more robust evidence.

    Friday, September 13, 2013

    Amantadine - One of my first week suggestions

    I'm going to ask my doctor for this in the first week because of this reasoning; But before you do anything I suggest, ask your doctor.
    Study: Old flu drug speeds brain injury recovery

    Two different ways to get it;

    Amantadine Hydrochloride Oral tablet

    Amantadine Hydrochloride Oral solution

    No wonder neurologists have no respect, a neurologist should have been pushing hyperacute therapies that stop the neuronal cascade of death. But [crickets]. 

    My full 31 hyperacute ideas for the first week here; 

    http://oc1dean.blogspot.com/2013/03/what-i-am-going-to-insist-i-get-after.html 

     

    Saturday, November 3, 2012

    Question to StrokeSmart magazine

    They were asking for article ideas and this was mine. I'm sure they won't do anything about it.
    Where are we in the US about hyperacute therapies like Draculin, edaravone from Japan, enzognel from New Zealand? What should doctors be giving patients in the first days? fish oil?, statins?, anti-depressants? nitric oxide? ibuprofen? ceria nanoparticles? leg compressions? music? MMP-9? minocycline? levodopa? Honokiol? amantadine? melatonin? If you don't know about all of these you are pathetic.

    Dear dean,
    Last week, I sent you an important survey that National Stroke Association developed to help us in preparation for our relaunch of StrokeSmart™ magazine. If you haven’t already taken it, please take a few minutes to tell us more about your needs.
    Thank you for your feedback. Your information will shape the future of StrokeSmart magazine.
    Sincerely,
    signed by Taryn Fort
    Taryn Fort
    Director, Marketing and Communications


    And yes, I know I'm dammed arrogant, these are all documented in postings in my blog.  Ask your countries stroke association about these or your doctor and watch them sputter.

    Wednesday, February 29, 2012

    Study: Old flu drug speeds brain injury recovery

    Lets start studying this for stroke.
    http://www.lasvegassun.com/news/2012/feb/29/us-med-brain-injury-drug/

    Researchers are reporting the first treatment to speed recovery from severe brain injuries caused by falls and car crashes: a cheap flu medicine whose side benefits were discovered by accident decades ago.

    Severely injured patients who were given amantadine got better faster than those who received a dummy medicine. After four weeks, more people in the flu drug group could give reliable yes-and-no answers, follow commands or use a spoon or hairbrush _ things that few of them could do at the start. Far fewer patients who got amantadine remained in a vegetative state, 17 percent versus 32 percent.

    "This drug moved the needle in terms of speeding patient recovery, and that's not been shown before," said neuropsychologist Joseph Giacino of Boston's Spaulding Rehabilitation Hospital, co-leader of the study. He added: "It really does provide hope for a population that is viewed in many places as hopeless."

    Many doctors began using amantadine for brain injuries years ago, but until now there's never been a big study to show that it works. The results of the federally funded study appear in Thursday's New England Journal of Medicine.

    A neurologist who wasn't involved in the research called it an important step. But many questions remain, including whether people less severely injured would benefit, and whether amantadine actually improves patients' long-term outcome or just speeds up their recovery.

    Each year, an estimated 1.7 million Americans suffer a traumatic brain injury. Falls, car crashes, colliding with or getting hit by an object, and assaults are the leading causes. About three-quarters are concussions or other mild forms that heal over time. But about 52,000 people with brain injuries die each year and 275,000 are hospitalized, many with persistent, debilitating injuries, according to government figures.

    With no proven remedies to rely on, doctors have used a variety of medicines approved for other ailments in the hopes that they would help brain injury patients. Those decisions are based on "hunches and logic rather than data," said Dr. John Whyte, of the Moss Rehabilitation Research Institute in suburban Philadelphia. He led the study along with Giacino.

    Amantadine (uh-MAN'-tah-deen), an inexpensive generic, was approved for the flu in the mid-1960s. The first inkling that it might have other uses came a few years later when it appeared to improve Parkinson's symptoms in nursing home patients who got it. It was found to have an effect on the brain's dopamine system, whose many functions include movement and alertness, and it was later approved for Parkinson's.

    It's now commonly used for brain injuries, and the researchers felt it was important to find out "whether we're treating patients with a useful drug, a harmful drug or a useless drug," Whyte said.

    The study was done in the U.S., Denmark and Germany and involved 184 severely disabled patients, about 36 years old on average. About a third were in a vegetative state, meaning unconscious but with periods of wakefulness. The rest were minimally conscious, showing some signs of awareness. They were treated one to four months after getting injured, a period when a lot of patients get better on their own, Giacino noted.

    They were randomly assigned to receive amantadine or a dummy drug daily for four weeks. Both groups made small but significant improvement, but the rate of recovery was faster in the group getting amantadine. When treatment stopped, recovery in the drug group slowed. Two weeks later, the level of recovery in the two groups was about the same.

    There was no group difference in side effects, which included seizure, insomnia and rigid muscles.

    The study was short, and the effect on long-term outcome is unknown. But Giacino said the drug still has value even if it only hastens recovery.

    "What condition would we not jump for joy if we could have it over with faster?" he said.

    The study didn't include those with penetrating head injuries, like the gunshot wound former Rep. Gabrielle Giffords suffered, but Giacino said the drug should have similar effects in those patients. Whether it would work in patients with brain injuries not caused by trauma, such as a stroke, isn't known.

    Whyte said the researchers want to test the drug for longer periods.

    Dr. Ramon Diaz-Arrastia said the results were welcome news in a field that has seen many failed efforts. He is director of clinical research at the government's Center for Neuroscience and Regenerative Medicine, which works with the military and government scientists on brain injury research.

    "It's an important step toward developing better therapies," he said.

    Since amantadine is so commonly used, he said U.S. troops with severe brain injuries in Iraq or Afghanistan probably get it, or should get it now. Since 2000, some 233,000 troops have suffered traumatic brain injuries, including about 6,100 serious cases, many of them from bomb blasts or shrapnel.

    Laura Bacon said amantadine seems to be helping her brother recover from a car accident in Vermont last October. Nicholas Gnazzo, 47, of Rochester, N.H., was in a coma for weeks before he was taken for rehabilitation to Spaulding, where doctors put him on amantadine in January.

    Since then he has been more alert, able to communicate with nods or gestures _ like pointing to his eyes when he wants his glasses, his sister said. Giacino agreed her brother has gotten better, but whether it is because of the drug can't be determined. Gnazzo wasn't part of the study.

    "It's been four months now, and we know we still have a long way to go," Bacon said. "Anything that could be faster _ or feel faster to us _ is a positive."