1. Probiotic use linked to improved symptoms of depression

    June 8, 2017 by Ashley

    From the McMaster University press release:

    Probiotics may relieve symptoms of depression, as well as help gastrointestinal upset, research from McMaster University has found.

    In a study published in the medical journal Gastroenterology, researchers of the Farncombe Family Digestive Health Research Institute found that twice as many adults with irritable bowel syndrome (IBS) reported improvements from co-existing depression when they took a specific probiotic than adults with IBS who took a placebo.

    The study provides further evidence of the microbiota environment in the intestines being in direct communication with the brain said senior author Dr. Premysl Bercik, an associate professor of medicine at McMaster and a gastroenterologist for Hamilton Health Sciences.

    “This study shows that consumption of a specific probiotic can improve both gut symptoms and psychological issues in IBS. This opens new avenues not only for the treatment of patients with functional bowel disorders but also for patients with primary psychiatric diseases,” he said.

    IBS is the most common gastrointestinal disorder in the world, and is highly prevalent in Canada. It affects the large intestine and patients suffer from abdominal pain and altered bowel habits like diarrhea and constipation. They are also frequently affected by chronic anxiety or depression.

    The pilot study involved 44 adults with IBS and mild to moderate anxiety or depression. They were followed for 10 weeks, as half took a daily dose of the probiotic Bifidobacterium longum NCC3001, while the others had a placebo.

    At six weeks, 14 of 22, or 64%, of the patients taking the probiotic had decreased depression scores, compared to seven of 22 (or 32%) of patients given placebo.

    Functional Magnetic Resonance Imaging (fMRI) showed that the improvement in depression scores was associated with changes in multiple brain areas involved in mood control.

    “This is the result of a decade long journey — from identifying the probiotic, testing it in preclinical models and investigating the pathways through which the signals from the gut reach the brain,” said Bercik.

    “The results of this pilot study are very promising but they have to be confirmed in a future, larger scale trial,” said Dr. Maria Pinto Sanchez, the first author and a McMaster clinical research fellow.


  2. Study finds ‘moral enhancement’ technologies neither feasible nor wise

    May 25, 2017 by Ashley

    From the North Carolina State University press release:

    A recent study by researchers at North Carolina State University and the Montreal Clinical Research Institute (IRCM) finds that “moral enhancement technologies” — which are discussed as ways of improving human behavior — are neither feasible nor wise, based on an assessment of existing research into these technologies.

    The idea behind moral enhancement technologies is to use biomedical techniques to make people more moral. For example, using drugs or surgical techniques to treat criminals who have exhibited moral defects.

    “There are existing ways that people have explored to manipulate morality, but the question we address in this paper is whether manipulating morality actually improves it,” says Veljko Dubljevic, lead author of the paper and an assistant professor of philosophy at NC State who studies the ethics of neuroscience and technology.

    Dubljevic and co-author Eric Racine of the IRCM reviewed the existing research on moral enhancement technologies that have been used in humans to assess the effects of these technologies and how they may apply in real-world circumstances.

    Specifically, the researchers looked at four types of pharmaceutical interventions and three neurostimulation techniques:

    • Oxytocin is a neuropeptide that plays a critical role in social cognition, bonding and affiliative behaviors, sometimes called “the moral molecule”;
    • Selective serotonin reuptake inhibitors (SSRIs) are often prescribed for depression, but have also been found to make people less aggressive;
    • Amphetamines, which some have argued can be used to enhance motivation to take action;
    • Beta blockers are often prescribed to treat high blood pressure, but have also been found to decrease implicit racist responses;
    • Transcranial magnetic stimulation (TMS) is a type of neurostimulation that has been used to treat depression, but has also been reported as changing the way people respond to moral dilemmas;
    • Transcranial direct current stimulation (TDCS) is an experimental form of neurostimulation that has also been reported as making people more utilitarian; and
    • Deep brain stimulation is a neurosurgical intervention that some have hypothesized as having the potential to enhance motivation.

    “What we found is that, yes, many of these techniques do have some effects,” Dubljevic says. “But these techniques are all blunt instruments, rather than finely tuned technologies that could be helpful. So, moral enhancement is really a bad idea.

    “In short, moral enhancement is not feasible — and even if it were, history shows us that using science to in an attempt to manipulate morality is not wise,” Dubljevic says.

    The researchers found different problems for each of the pharmaceutical approaches.

    Oxytocin does promote trust, but only in the in-group,” Dubljevic notes. “And it can decrease cooperation with out-group members of society, such as racial minorities, and selectively promote ethnocentrism, favoritism, and parochialism.”

    The researchers also found that amphetamines boost motivation for all types of behavior, not just moral behavior. Moreover, there are significant risks of addiction associated with amphetamines. Beta blockers were found not only to decrease racism, but to blunt all emotional response which puts their usefulness into doubt. SSRIs reduce aggression, but have serious side-effects, including an increased risk of suicide.

    In addition to physical side effects, the researchers also found a common problem with using either TMS or TCDS technologies.

    “Even if we could find a way to make these technologies work consistently, there are significant questions about whether being more utilitarian in one’s decision-making actually makes one more moral,” Dubljevic says.

    Lastly, the researchers found no evidence that deep brain stimulation had any effect whatsoever on moral behavior.

    “Our goal here is to share a cautionary note with those who are discussing different techniques for moral enhancement,” Dubljevic says. “I am in favor of research that is done responsibly, but against dangerous social experiments.”


  3. To improve chronic pain, get more sleep (coffee helps too)

    May 15, 2017 by Ashley

    From the Boston Children’s Hospital press release:

    New research from Boston Children’s Hospital and Beth Israel Deaconess Medical Center (BIDMC) shows that chronic sleep loss increases pain sensitivity. It suggests that chronic pain sufferers can get relief by getting more sleep, or, short of that, taking medications to promote wakefulness such as caffeine. Both approaches performed better than standard analgesics in a rigorous study in mice, described in the May 8, 2017 issue of Nature Medicine.

    Pain physiologist Alban Latremoliere, PhD, of Boston Children’s and sleep physiologist Chloe Alexandre, PhD, of BIDMC precisely measured the effects of acute or chronic sleep loss on sleepiness and sensitivity to both painful and non-painful stimuli. They then tested standard pain medications, like ibuprofen and morphine, as well as wakefulness-promoting agents like caffeine and modafinil. Their findings reveal an unexpected role for alertness in setting pain sensitivity.

    Keeping mice awake, through custom entertainment

    The team started by measuring normal sleep cycles, using tiny headsets that took electroencephalography (EEG) and electromyography (EMG) readings. “For each mouse, we have exact baseline data on how much they sleep and what their sensory sensitivity is,” says Latremoliere, who works in the lab of Clifford Woolf, PhD, in the F.M. Kirby Neurobiology Center at Boston Children’s.

    Next, unlike other sleep studies that force mice to stay awake walking treadmills or falling from platforms, Alexandre, Latremoliere and colleagues deprived mice of sleep in a way that mimics what happens with people: They entertained them.

    “We developed a protocol to chronically sleep-deprive mice in a non-stressful manner, by providing them with toys and activities at the time they were supposed to go to sleep, thereby extending the wake period,” says Alexandre, who works in the lab of Thomas Scammell, MD, at BIDMC. “This is similar to what most of us do when we stay awake a little bit too much watching late-night TV each weekday.”

    To keep the mice awake, researchers kept vigil, providing the mice with custom-made toys as interest flagged while being careful not to overstimulate them. “Mice love nesting, so when they started to get sleepy (as seen by their EEG/EMG pattern) we would give them nesting materials like a wipe or cotton ball,” says Latremoliere. “Rodents also like chewing, so we introduced a lot of activities based around chewing, for example, having to chew through something to get to a cotton ball.”

    In this way, they kept groups of six to 12 mice awake for as long as 12 hours in one session, or six hours for five consecutive days, monitoring sleepiness and stress hormones (to make sure they weren’t stressed) and testing for pain along the way.

    Pain sensitivity was measured in a blinded fashion by exposing mice to controlled amounts of heat, cold, pressure or capsaicin (the agent in hot chili peppers) and then measuring how long it took the animal to move away (or lick away the discomfort caused by capsaicin). The researchers also tested responses to non-painful stimuli, such as jumping when startled by a sudden loud sound.

    “We found that five consecutive days of moderate sleep deprivation can significantly exacerbate pain sensitivity over time in otherwise healthy mice,” says Alexandre. “The response was specific to pain, and was not due to a state of general hyperexcitability to any stimuli.”

    Analgesics vs. wake-promoting agents

    Surprisingly, common analgesics like ibuprofen did not block sleep-loss-induced pain hypersensitivity. Even morphine lost most of its efficacy in sleep-deprived mice. These observations suggest that patients using these drugs for pain relief might have to increase their dose to compensate for lost efficacy due to sleep loss, thereby increasing their risk for side effects.

    In contrast, both caffeine and modafinil, drugs used to promote wakefulness, successfully blocked the pain hypersensitivity caused by both acute and chronic sleep loss. Interestingly, in non-sleep-deprived mice, these compounds had no analgesic properties.

    “This represents a new kind of analgesic that hadn’t been considered before, one that depends on the biological state of the animal,” says Woolf, director of the Kirby Center at Boston Children’s. “Such drugs could help disrupt the chronic pain cycle, in which pain disrupts sleep, which then promotes pain, which further disrupts sleep.”

    A new approach to chronic pain?

    The researchers conclude that rather than just taking painkillers, patients with chronic pain might benefit from better sleep habits or sleep-promoting medications at night, coupled with daytime alertness-promoting agents to try to break the pain cycle. Some painkillers already include caffeine as an ingredient, although its mechanism of action isn’t yet known. Both caffeine and modafinil boost dopamine circuits in the brain, so that may provide a clue.

    “This work was supported by a novel NIH program that required a pain scientist to join a non-pain scientist to tackle a completely new area of research,” notes Scammel, professor of neurology at BIDMC. “This cross-disciplinary collaboration enabled our labs to discover unsuspected links between sleep and pain with actionable clinical implications for improving pain management.”

    “Many patients with chronic pain suffer from poor sleep and daytime fatigue, and some pain medications themselves can contribute to these co-morbidities,” notes Kiran Maski, MD, a specialist in sleep disorders at Boston Children’s. “This study suggests a novel approach to pain management that would be relatively easy to implement in clinical care. Clinical research is needed to understand what sleep duration is required and to test the efficacy of wake-promoting medications in chronic pain patients.”


  4. PTSD, certain prescriptions for PTSD may raise risk for dementia

    by Ashley

    From the American Geriatrics Society press release:

    Researchers are discovering that post-traumatic stress disorder (PTSD) is a significant risk factor in developing dementia. Dementia is a memory problem that affects a person’s ability to carry out usual tasks. Dementia is a leading cause of serious illness, disability, and death. It often requires care in a nursing home or other long-term care facility for people aged 65 and older.

    Until now, researchers didn’t know whether the kinds of medications used for people with PTSD could increase risks for dementia. (These medications include including antidepressants, antipsychotics, sedatives, or tranquilizers.) A new study, published in the Journal of the American Geriatrics Society, examined this connection.

    In their study, researchers examined information from 3,139,780 veterans aged 56 and older. At the beginning of the study, in 2003, the veterans were receiving health care from a Veterans Health Administration facility. Almost all the veterans were male and 82% were white.

    Of the veterans in the study, 5.4% had been diagnosed with PTSD. As the researchers looked at the data over the study’s nine-year follow-up period, they also included veterans who were diagnosed with dementia.

    Research has previously shown that veterans with PTSD are more likely to have health problems linked to a higher risk for dementia. These include traumatic brain injury, diabetes, chronic obstructive pulmonary disease (COPD), psychiatric disorders, substance abuse, and other health issues.

    In this study, researchers discovered that taking certain antidepressants, tranquilizers, sedatives, or antipsychotic medications significantly increased veterans’ risks for developing dementia compared to the risks for veterans who didn’t take such medications.

    Medicines that significantly increased dementia risk included:

    • Selective serotonin reuptake inhibitors (SSRIs)
    • Novel antidepressants
    • Atypical antipsychotics

    The increase in the risk of dementia for veterans taking the drugs was the same whether or not they were diagnosed with PTSD. (This is compared to veterans who weren’t taking these drugs.)

    What’s more, veterans who used three classes of medications were also more likely to be diagnosed with dementia whether or not they had PTSD. These medicines include:

    • Novel antidepressants
    • Serotonin-norepinephrine reuptake inhibitors (SNRIs)
    • Benzodiazepines

    The researchers noted that an interaction among these “psychoactive” drugs could potentially affect how PTSD impacts a person’s risk for developing dementia. The researchers concluded that further research should be conducted to learn more about PTSD and psychoactive drugs, including dosage, how long to take the medications, and which people could most benefit from them.


  5. Study looks at factors that may help in antidepressant selection

    May 2, 2017 by Ashley

    From the Elsevier Health Sciences press release:

    Selecting the antidepressant that will be most effective for a specific patient suffering from depression can be a “try and try again” process. Examining new personalized and precision psychiatry approaches, a new study in Personalized Medicine in Psychiatry shows that body mass index (BMI), sex of the patient, and symptom profile can be used to determine a personalized treatment that guides antidepressant choice and significantly improves patient outcome.

    “We are in the midst of a paradigm shift in the field of psychiatry, to find specific clinical and biological signals that help clinicians and patients decide what is the best treatment,” explained lead investigator Leanne Williams, PhD, VA Palo Alto Health Care System and the Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine. “This is the shift to incorporate precision medicine approaches to improve outcomes for patients. Our study adds new knowledge to this effort, and does so for two commonly associated chronic conditions, clinical depression and obesity, that need new treatment approaches. Our results have the potential for a significant impact on the majority of patients suffering from depression who are seen in primary care and community settlings.”

    Researchers analyzed data from 659 adults (ages 18-65) with clinical depression who completed the International Study to Predict Optimized Treatment in Depression (iSPOT-D). They were randomly assigned one of three antidepressants (venlafaxine-XR, sertraline, or escitalopram) and followed for eight weeks of treatment. Height and weight were recorded and each participant completed the 17-item Hamilton Rating Scale (a self-reported depression inventory) before and after treatment to measure change in depression severity. Patients who improved so substantially that they were no longer experiencing clinical symptoms were defined as “remitters.”

    The study found that for both men and women, having a larger BMI than patients of “normal” weight predicted remission for venlafaxine-XR specifically, due to a reduction in physical symptoms, including sleep disturbance, somatic anxiety, and appetite. Females with higher BMI were likely to remit regardless of medication type and this effect was related to a change in cognitive symptoms, including thoughts of suicide and guilt.

    These findings are very well suited for immediate translation into the primary care and community settings in which most patients are treated. Primary care doctors have access to information regarding patient sex, BMI (weight relevant to height), along with symptoms of depression.

    According to lead author Erin Green, PhD, VA Palo Alto Health Care System and the Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, “Although these findings require replication, they are ready for ‘prime time’ translation into clinical practice where there are currently no indicators and algorithms available for guiding treatment choice for patients with both depression and obesity.”

    “The future of psychiatry is in a precision, personalized medicine approach to refining diagnosis and tailoring treatments accordingly. This study demonstrates that currently available markers are poised to improve patient outcomes without introducing new costs. Markers such as BMI are likely to complement others being developed out of neuroimaging and genomics,” added Dr. Williams.


  6. Study suggests aspirin doesn’t help preserve cognitive function

    April 24, 2017 by Ashley

    From the Wiley press release:

    An analysis of published studies found no evidence that low-dose aspirin buffers against cognitive decline or dementia or improves cognitive test scores.

    The review and meta-analysis included eight studies with 36,196 participants who were an average of 65 years old and did not have cognitive impairment at baseline. Participants were followed for an average of six years.

    “Additional studies are needed to test the possibility that low-dose aspirin has beneficial effects when taken over a longer period and at an earlier age,” said Dr. Nicola Veronese, lead author of the Journal of the American Geriatrics Society study.


  7. APA study suggests patients more likely to refuse drug therapy than psychotherapy for mental health

    March 23, 2017 by Ashley

    From the American Psychological Association press release:

    People seeking help for mental disorders are more likely to refuse or not complete the recommended treatment if it involves only psychotropic drugs, according to a review of research published by the American Psychological Association.

    Researchers conducted a meta-analysis of 186 studies of patients seeking help for mental health issues that examined whether they accepted the treatment that was recommended and if they did, whether they completed it. Fifty-seven of the studies, comprising 6,693 patients, had a component that reported refusal of treatment recommendations, and 182 of the studies, comprising 17,891 patients, had a component reporting premature termination of treatment.

    After diagnosis, patients in the studies were recommended to drug-only therapy (pharmacotherapy), talk therapy (psychotherapy) or a combination of the two.

    “We found that rates of treatment refusal were about two times greater for pharmacotherapy alone compared with psychotherapy alone, particularly for the treatment of social anxiety disorder, depressive disorders and panic disorder,” said lead researcher Joshua Swift, PhD, of Idaho State University. “Rates of premature termination of therapy were also higher for pharmacotherapy alone, compared with psychotherapy alone, particularly for anorexia/bulimia and depressive disorders.”

    The research was published in the APA journal Psychotherapy.

    Across all the studies, the average treatment refusal rate was 8.2 percent. Patients who were offered pharmacotherapy alone were 1.76 times more likely to refuse treatment than patients who were offered psychotherapy alone. Once in treatment, the average premature termination rate was 21.9 percent, with patients on drug-only regimens 1.2 times more likely to drop out early. There was no significant difference for refusal or dropout rates between pharmacotherapy alone and combination treatments, or between psychotherapy alone and combination treatments.

    While Swift said the findings overall were expected, the researchers were most surprised by how large the differences were for some disorders. For example, patients diagnosed with depressive disorders were 2.16 times more likely to refuse pharmacotherapy alone and patients with panic disorders were almost three times more likely to refuse pharmacotherapy alone.

    The findings are especially interesting because, as a result of easier access, recent trends show that a greater percentage of mental health patients in the U.S. are engaging in pharmacotherapy than psychotherapy, according to co-author Roger Greenberg, PhD, SUNY Upstate Medical University.

    Some experts have argued that psychotherapy should be the first treatment option for many mental health disorders. Those arguments have been largely based on good treatment outcomes for talk therapy with fewer side effects and lower relapse rates, said Greenberg. “Our findings support that argument, showing that clients are more likely to be willing to start and continue psychotherapy than pharmacotherapy.”

    Swift and Greenberg theorized that patients may be more willing to engage in psychotherapy because many individuals who experience mental health problems recognize that the source of their problems may not be entirely biological.

    “Patients often desire an opportunity to talk with and work through their problems with a caring individual who might be able to help them better face their emotional experiences,” said Greenberg. “Psychotropic medications may help a lot of people, and I think some do see them as a relatively easy and potentially quick fix, but I think others view their problems as more complex and worry that medications will only provide a temporary or surface level solution for the difficulties they are facing in their lives.”

    While the meta-analysis provides information on refusal and dropout rates, the studies did not report the patients’ reasons for their actions, Swift noted. Going forward, research designed to identify these reasons could lead to additional strategies to improve initiation and completion rates for both therapies, he said. It is also important to note that participants in the research studies initially indicated they were willing to be assigned to any therapy, and therefore may not be representative of all consumers of treatment.


  8. Benzodiazepines, related drugs increase stroke risk among persons with Alzheimer’s disease

    January 25, 2017 by Ashley

    From the University of Eastern Finland media release:

    memory lossThe use of benzodiazepines and benzodiazepine-like drugs was associated with a 20 per cent increased risk of stroke among persons with Alzheimer’s disease, shows a recent study from the University of Eastern Finland. Benzodiazepines were associated with a similar risk of stroke as benzodiazepine-like drugs.

    The use of benzodiazepines and benzodiazepine-like drugs was associated with an increased risk of any stroke and ischemic stroke, whereas the association with hemorrhagic stroke was not significant. However, due to the small number of hemorrhagic stroke events in the study population, the possibility of such an association cannot be excluded. The findings are important, as benzodiazepines and benzodiazepine-like drugs were not previously known to predispose to strokes or other cerebrovascular events. Cardiovascular risk factors were taken into account in the analysis and they did not explain the association.

    The findings encourage a careful consideration of the use of benzodiazepines and benzodiazepine-like drugs among persons with Alzheimer’s disease, as stroke is one of the leading causes of death in this population group. Earlier, the researchers have also shown that these drugs are associated with an increased risk of hip fracture.

    The study was based on data from a nationwide register-based study (MEDALZ) conducted at the University of Eastern Finland in 2005-2011. The study population included 45,050 persons diagnosed with Alzheimer’s disease, and 22 per cent of them started using benzodiazepines or benzodiazepine-like drugs.

    The findings were published in International Clinical Psychopharmacology.


  9. The first-in-human clinical trial targeting Alzheimer’s tau protein

    December 13, 2016 by Ashley

    From the Karolinska Institutet media release:

    So far, many of the antibody drugs proposed to treat Alzheimer’s disease target only the amyloid plaques. Despite the latest clinical trial that is hailed as our best chance in the quest for treating AD, all later phase trials have failed with many causing severe side effects in the patients, such as abnormal accumulation of fluid and inflammation in the brain. One of the reasons for side effects, many speculate, is due to the antibody directing a reaction towards normal amyloid present in blood vessels or simply releasing beta-amyloid caught in the vessel wall.

    The authors of the study have developed a vaccine that stimulates the production of an antibody that specifically targets pathological tau, discovering its “Achilles’ heel.” It is able to do this because healthy tau undergoes a series of changes to its structure forming a new region that the antibody attacks. This new region (the “Achilles’ heel”), while not present in healthy tau, is present in diseased tau early on. Therefore, the antibody tackles all the different varieties of pathological tau. In addition to this important specificity, the antibody is coupled to a carrier molecule that generates a considerable immune response with the added benefit that it is not present in humans, thus avoiding the development of an immune reaction towards the body itself.

    Side effects have included a local reaction at the site of injection. This skin reaction is thought to occur due to the aluminum hydroxide, an adjuvant used in vaccines to enhance the body’s own antibody production. No other serious secondary effects were directly related to the vaccine. Overall, the safety of the drug and its ability to elicit an immune response were remarkable.

    While many trials against Alzheimer’s disease stubbornly continue to target amyloid, our study dares to attack the disease from another standpoint. This is the first active vaccination to harness the body’s ability to produce antibodies against pathological tau. Even though this study is only a phase 1 trial, its success so far gives the authors confidence that it may be the answer they are looking for to halt the progress of this devastating disease.


  10. Researchers use video gamelike test to study learning and recovery in stroke patients

    October 31, 2016 by Ashley

    From the Johns Hopkins Medicine media release:

    hospital stayA robotic arm and a virtual game were essential tools in a new study from researchers at Johns Hopkins Medicine. The study results suggest that while training doesn’t change neurological repair in chronic stroke patients, it can indeed help such patients learn new motor skills and achieve more independence in their daily lives.

    A report on the work is published in the journal Neurorehabilitation and Neural Repair on Oct. 27.

    “What we found is that physical rehab is not going to change the weakness caused by damaged brain cells in chronic patients, but it is going to change how well they can perform certain tasks, which can have a huge impact on a patient’s daily life,” says Pablo Celnik, M.D., director of the Department of Physical Medicine and Rehabilitation at Johns Hopkins.

    Brain damage from strokes occurs when the blood supply to the brain is blocked (ischemic stroke) or a blood vessel feeding brain tissue ruptures (hemorrhagic stroke). Depending on the extent of the stroke, the damage can cause partial or total paralysis, affecting motor function, balance, speech, sensation and other physical activities. Chronic stroke patients are those whose physical impairments persist more than six months after the stroke. Rehabilitation specialists measure the damage using the Fugl-Meyer Assessment (FMA), which measures the neurological damage wrought by a stroke on a scale from zero to 66.

    For the new study, the investigators recruited 10 chronic stroke patients with FMA scores of ?50 out of 66 and categorized them as having “mild to moderate” functional deficits for the purposes of the study, and 10 other patients with FMA scores of <50 out of 66 and categorized them as having “moderate to severe” impairment. A third group of 10 able-bodied participants served as a control group.

    All of the study participants were trained to control a simple video game using a using a robotic piece of equipment that held their dominant arm at 90 degrees from their bodies. This eliminated gravity as a burden for those whose arms were weakened by their strokes. The subjects were then taught to use the muscles around their elbow to move a cursor across a screen into small target windows.

    Participants’ performance in the game was measured during training sessions and skill assessment trials. A pre-training skill assessment was conducted to get a baseline from which to measure improvement. Participants were asked to move the cursor through the windows in time with a metronome and completed nine blocks of 10 trials at various speeds — 24, 30, 38, 45, 60, 80, 100, 110 and 120 beats per minute. The metronome prevented participants from slowing down to improve their accuracy, so the only way to show improvement was by becoming more skilled at the task.

    The next phase of the experiment had participants attend 30-minute training sessions for four consecutive days. They were asked to complete five blocks of 30 trials, all at their own pace, and were encouraged to improve their speed and accuracy in each consecutive block. Following the training sessions, participants’ skill levels were tested again in another skill assessment.

    Results showed that while each group’s skill level improved by the end of the training, those with greater motor impairment still demonstrated less skill in both the pre- and post-training assessments. All participants reached a plateau in their improvement around experimental days three and four.

    However, the study showed that there was considerable overlap between the post-training performance of the stroke patients and the pre-training performance of groups with less impairment. “When you look at the data, the post-training mild-to-moderate group is indistinguishable from the pre-training control group. And the same was true for post-training scores of those in the moderate-to-severe group and the mild-to-moderate group,” says Robert Hardwick, Ph.D., postdoctoral fellow in the Department of Neurology at the Johns Hopkins University School of Medicine.

    This is good news for patients because it means that even when there is little likelihood of further neurological recovery, it means I can still teach them new tasks through training,” says Celnik. “What is important is to not create false expectations of neurological recovery, while at the same time being hopeful that patients can learn within the boundaries of their neurological deficit to improve their lives.”

    According to the World Health Organization, 15 million people worldwide suffer a stroke each year. An estimated 5 million die, and another 5 million are left with lasting motor impairment. Celnik cautions that this study only included chronic stroke patients and that their future research plans include conducting similar studies in acute stroke patients — those within three months of the stroke — which could yield different results. “Maybe there is a different impact of training in the earlier stages of stroke damage,” says Celnik.