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 never know. Show all posts
Showing posts with label never know. Show all posts

Monday, January 27, 2020

Brain Cooling Tech Leads New Inventions in Thoracic Surgery

Would any of this be useful in responding to a stroke? We'll never know. 

All my previous research posts on this suggested no useful intervention. Obviously no protocols were ever written on hypothermia so everyone is still shooting in the dark. The result being that survivors are still screwed with no consequences to the doctors who haven't written up protocols on this. Don't you just love incompetence?

 

 

Brain Cooling Tech Leads New Inventions in Thoracic Surgery

NEW ORLEANS -- Innovations in brain cooling and augmented reality were featured, among other projects, at this year's Society of Thoracic Surgeons meeting.
Following the keynote lecture on technological innovation and entrepreneurship by Mark Cohen, MD, of University of Michigan in Ann Arbor, four contestants lined up their pleas for investment in front of judges and audience members at the conference's "Shark Tank" session.
The informal winner was a balloon catheter with a cooling pump that is designed to prevent ischemic injury to the brain during cardiac arrest or stroke. The project won 45% of audience votes (with only 20 people having voted, however).
Brain Cooling
Presenter Robert Schultz, MD, a resident in cardiac surgery at Alberta Health Services in Calgary, said that cooling in aortic surgery decreases strokes by 97% and the question was how to make this available to all surgeons, not just cardiac surgeons.
The device from his start-up, Voyage Biomedical, makes it possible to initiate cooling outside the operating room, cool the head by 10 °C in 10 minutes, and leave the rest of the body warm (never below 32 °C) and the heart beating, Schultz told the audience.
Eventually, the goal is to get the brain cooling device on ambulances and in ICUs. So far, it has been tested in pigs and human cadavers.
A judge during the session, Steven Bolling, MD, of University of Michigan Hospital in Ann Arbor, expressed concern about the intellectual property protection on Schultz's cooling balloon pump when he could easily recreate the technology at his own institution.
Nevertheless, Voyage already has enough money offered by investors to get to first-in-human trials by 2023, Schultz said.

Saturday, January 25, 2020

RhoA-ROCK Signaling as a Therapeutic Target in Traumatic Brain Injury

Would this help stroke survivors? We'll never know since we have NO STROKE LEADERSHIP and NO STROKE STRATEGY.

RhoA-ROCK Signaling as a Therapeutic Target in Traumatic Brain Injury

Shalaka Mulherkar 1 and Kimberley F. Tolias 1,2,* 1 Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA; mulherka@bcm.edu 2 Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA * Correspondence: tolias@bcm.edu
Received: 20 November 2019; Accepted: 16 January 2020; Published: 18 January 2020

Abstract: Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. TBIs, which range in severity from mild to severe, occur when a traumatic event, such as a fall, a traffic accident, or a blow, causes the brain to move rapidly within the skull, resulting in damage. Long-term consequences of TBI can include motor and cognitive deficits and emotional disturbances that result in a reduced quality of life and work productivity. Recovery from TBI can be challenging due to a lack of effective treatment options for repairing TBI-induced neural damage and alleviating functional impairments. Central nervous system (CNS) injury and disease are known to induce the activation of the small GTPase RhoA and its downstream effector Rho kinase (ROCK). Activation of this signaling pathway promotes cell death and the retraction and loss of neural processes and synapses, which mediate information flow and storage in the brain. Thus, inhibiting RhoA-ROCK signaling has emerged as a promising approach for treating CNS disorders. In this review, we discuss targeting the RhoA-ROCK pathway as a therapeutic strategy for treating TBI and summarize the recent advances in the development of RhoA-ROCK inhibitors.

Neuroplasticity and cognitive benefits associated with chronic intranasal oxytocin administration in aging

 Would this help stroke survivors? We'll never know since we have NO STROKE LEADERSHIP and NO STROKE STRATEGY.

Neuroplasticity and cognitive benefits associated with chronic intranasal oxytocin administration in aging


Stockholm University, Faculty of Social Sciences, Department of Psychology, Biological psychology.
Show others and affiliations
2019 (English)Conference paper, Oral presentation only (Other academic)
Abstract [en]
Oxytocin (OT) is a crucial chemical modulator of social behavior, and intranasal OT administration has potential as treatment for social deficits. Considerably less is known about OT’s effects on non-social cognition, a functional domain of particular relevance in aging. Brain mechanisms underlying OT’s benefits are not well understood but recent animal work suggests that repeated OT administration induces brain changes. To test this neuroplastic role of OT on the human brain and its potential for cognitive improvement in aging, we conducted a randomized double-blind study in older men (> 56 years), with 34 participants self-administering either 24 IUs OT or placebo (P) twice daily. Before and after 4-weeks intranasal administration, participants underwent MRI and processing speed assessment. Using voxel-based morphometry, gray matter (GM) volume was measured on T1-weighted anatomical images. Age, education, physical health, and image quality served as covariates and family-wise error rate determined statistical significance in regions of interest. Analyses were performed without awareness of the assigned treatment labels. Significant interactions between treatment (OT vs. P) and time (pre- vs. post-intervention) on GM volume for left amygdala, hippocampus, and putamen suggested increased regional GM volume following OT but not P. Further, OT-induced enlargement in putamen was associated with improved processing speed, while there was no brain−behavior correlation in the P group. These findings support the notion that amygdala, hippocampus, and putamen are key targets of OT’s neuroplastic potential on the human brain and chronic OT administration may constitute a potential treatment in counteracting cognitive decline in aging.  
Place, publisher, year, edition, pages
2019.
Keywords [en]
neuroplasticity, chronic intranasal oxytocin administration, aging
National Category
Psychology
Research subject
Psychology
Identifiers
URN: urn:nbn:se:su:diva-178081OAI: oai:DiVA.org:su-178081DiVA, id: diva2:1386531
Conference
Alpine Brain Imaging Meeting (ABIM), Champéry, Switzerland, January 6-10, 2019
Available from: 2020-01-17 Created: 2020-01-17 Last updated: 2020-01-20Bibliographically approved

Sunday, January 19, 2020

Blue light reduces organ injury from ischemia and reperfusion

Would wearing blue light googles immediately upon entering the ambulance or hospital prevent some of the reperfusion injury? We'll never know because we have NO leadership and NO strategy in stroke.

Blue light reduces organ injury from ischemia and reperfusion

Significance

It is well established that light regulates mammalian biology. And yet, we have been unable to define and thus harness the underlying mechanisms so as to apply them to alter the course of human disease. In this study we determine that the spectrum of light is a critical determinant of its effect on critical illness. We show that an acute and short (24 h) exposure to high-illuminance (1,400 lx) blue spectrum (peak 442 nm) light prior to ischemia/reperfusion (I/R) significantly attenuates the degree of organ injury. Our characterization of the biological mechanisms through which blue light beneficially alters the cellular response to I/R provides an opportunity to develop novel therapeutics for the prevention and treatment of many diseases.
Keywords: blue light, ischemia, reperfusion, organ injury, circadian rhythms

Abstract

Evidence suggests that light and circadian rhythms profoundly influence the physiologic capacity with which an organism responds to stress. However, the ramifications of light spectrum on the course of critical illness remain to be determined. Here, we show that acute exposure to bright blue spectrum light reduces organ injury by comparison with bright red spectrum or ambient white fluorescent light in two murine models of sterile insult: warm liver ischemia/reperfusion (I/R) and unilateral renal I/R. Exposure to bright blue light before I/R reduced hepatocellular injury and necrosis and reduced acute kidney injury and necrosis. In both models, blue light reduced neutrophil influx, as evidenced by reduced myeloperoxidase (MPO) within each organ, and reduced the release of high-mobility group box 1 (HMGB1), a neutrophil chemotactant and key mediator in the pathogenesis of I/R injury. The protective mechanism appeared to involve an optic pathway and was mediated, in part, by a sympathetic (β3 adrenergic) pathway that functioned independent of significant alterations in melatonin or corticosterone concentrations to regulate neutrophil recruitment. These data suggest that modifying the spectrum of light may offer therapeutic utility in sterile forms of cellular injury.

Thursday, May 2, 2019

Focused Transcranial Ultrasound for Treatment of Neurodegenerative Dementia

For our very likely descent into dementia, would this clearing be a preventative task our doctors should be doing? We'll never know since our doctors and hospital will never take responsibility for finding that answer. You're screwed because of incompetence.  

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

Focused Transcranial Ultrasound for Treatment of Neurodegenerative Dementia

Wednesday, August 15, 2018

Paralyzed mice regain movement in their legs with new treatment

Would this help in stroke? Since we have NO stroke leadership and NO stroke strategy we'll never know. This inhibiting movement by the KCC2 protein seems like a good investigative point to try for a spasticity solution. Does no one in stroke ever think at all?
https://www.researchgate.net/blog/post/paralyzed-mice-regain-movement-in-their-legs-with-new-treatment

The drug reactivates nerve pathways in partially severed spinal cords.
Most people with spinal cord injuries are paralyzed below the injury site, even if the cord is only partially severed. Researchers don’t know why the nerve pathways that are still intact also stop working. A new study provides a promising answer, and a path to restoring movement.

Researchers treated mice with partially severed spinal cords with a compound called CLP209. The drug was administered over eight to ten weeks. About 80 percent of the injured mice regained their ability to take steps. “Stepping is a first step towards motor functional recovery in animals, and perhaps humans,” says Boston Children’s Hospital researcher Zhigang He, who led the study.

A new approach is paying off


Many animal studies attempting to repair spinal cord damage have focused on getting nerve fibers to regenerate, or new ones to grow out of remaining healthy fibers. He and other researchers have achieved this, but they didn’t see the corresponding improvements in motor function they had hoped for.

He and his coauthors decided to try a different approach. They were inspired by treatments that stimulate the space around injured patients’ spinal cord with electric currents. When combined with rehabilitation training, this stimulation is the only treatment for spinal cord injury patients known to be effective. "However, in these studies, when you turn off the stimulation, the effect is gone,” says He.

The researchers set out to see if they could use drugs to mimic the stimulation caused by electric currents, so the effect would be longer-lasting. They tested several compounds known to alter the excitability of neurons. A small molecule called CLP209 worked best, and the treated mice remained more mobile than untreated mice up to two weeks after treatment stopped.

Results explain why remaining nerve pathways don’t function normally


The fact that CLP209 worked so well gives researchers a major clue as to why even intact nerve pathways fail after a spinal cord injury. The key seems to be a protein called KCC2, which CLP290 is known to activate.

To facilitate movement like walking, the spinal cord transmits the brain’s commands to muscles with two types of signals: those that inhibit muscles’ neurons and those that activate them. These opposing signals are what allow muscles to work in pairs, with one relaxing while the other contracts.

After a spinal cord injury, neurons that send signals inhibiting movement don’t produce enough of the KCC2 protein. As a result of this deficit, they don’t receive instructions from the brain to stop firing, and the overall spinal circuit is overwhelmed with inhibitory signals.

When the mice were treated with CLP290, the drug restored KCC2 levels, the brain’s commands to stop firing got through to inhibitory neurons, and signals resulting in movement were no longer overpowered.

"Too much excitation is not good, and too much inhibition is not good either,” says He. “You really need to get a balance. This hasn't been demonstrated in a rigorous way in spinal cord injury before."




A cross section of a mouse spinal cord, stained two different ways, showing increased expression of KCC2 in inhibitory neurons. Credit: Zhigang He Lab, Boston Children's Hospital

More research is needed to determine the treatment’s full potential


He and his colleagues are now exploring other drugs to activate KCC2 in spinal cord injuries. They hope their therapy could one day be combined with electrical stimulation techniques to maximize patients’ recovery.

They also hope they won’t be alone in exploring this type of drug’s potential. He says: “It would be great if other groups are willing to try this in their injury models. We hope that collectively we could find out the strengths and weaknesses of this approach and consider which patient populations could be targeted.”

Saturday, July 14, 2018

Autonomous multi-joint soft exosuit with augmentation-power-based control parameter tuning reduces energy cost of loaded walking

The energy cost of walking post-stroke has got to be extremely high. Would this help? We'll never know since there are no functioning neurons  in your stroke staff to realize this could help survivors walk. You're screwed. 
https://jneuroengrehab.biomedcentral.com/articles/10.1186/s12984-018-0410-y
  • Sangjun Lee,
  • Jinsoo Kim,
  • Lauren Baker,
  • Andrew Long,
  • Nikos Karavas,
  • Nicolas Menard,
  • Ignacio Galiana and
  • Conor J. WalshEmail author
Contributed equally
Journal of NeuroEngineering and Rehabilitation201815:66
Received: 15 December 2017
Accepted: 3 July 2018
Published: 13 July 2018





Abstract

Background
Soft exosuits are a recent approach for assisting human locomotion, which apply assistive torques to the wearer through functional apparel. Over the past few years, there has been growing recognition of the importance of control individualization for such gait assistive devices to maximize benefit to the wearer. In this paper, we present an updated version of autonomous multi-joint soft exosuit, including an online parameter tuning method that customizes control parameters for each individual based on positive ankle augmentation power.

Methods

The soft exosuit is designed to assist with plantarflexion, hip flexion, and hip extension while walking. A mobile actuation system is mounted on a military rucksack, and forces generated by the actuation system are transmitted via Bowden cables to the exosuit. The controller performs an iterative force-based position control of the Bowden cables on a step-by-step basis, delivering multi-articular (plantarflexion and hip flexion) assistance during push-off and hip extension assistance in early stance. To individualize the multi-articular assistance, an online parameter tuning method was developed that customizes two control parameters to maximize the positive augmentation power delivered to the ankle. To investigate the metabolic efficacy of the exosuit with wearer-specific parameters, human subject testing was conducted involving walking on a treadmill at 1.50 m s− 1 carrying a 6.8-kg loaded rucksack. Seven participants underwent the tuning process, and the metabolic cost of loaded walking was measured with and without wearing the exosuit using the individualized c
ontrol parameters.

Results

The online parameter tuning method was capable of customizing the control parameters, creating a positive ankle augmentation power map for each individual. The subject-specific control parameters and resultant assistance profile shapes varied across the study participants. The exosuit with the wearer-specific parameters significantly reduced the metabolic cost of load carriage by 14.88 ± 1.09% (P = 5 × 10− 5) compared to walking without wearing the device and by 22.03 ± 2.23% (P = 2 × 10− 5) compared to walking with the device unpowered.




Conclusion

The autonomous multi-joint soft exosuit with subject-specific control parameters tuned based on positive ankle augmentation power demonstrated the ability to improve human walking economy. Future studies will further investigate the effect of the augmentation-power-based control parameter tuning on wearer biomechanics and energetics.

Keywords

ExosuitAssistanceTuningAugmentation powerMetabolic cost



Introduction

Lower-limb assistive devices have been designed to assist with human locomotion [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12]. Recently, different groups have used rigid but lightweight mechanisms to create low-profile exoskeletons assisting with a specific target joint, and studies have shown that these devices may substantially reduce the energy cost of loaded [6] and unloaded [7, 8, 9, 10, 11, 12] wa
lking. For example, Lee et al. showed that their hip exoskeleton reduced the metabolic cost of walking by 21% compared to walking without wearing the device [12]. For ankle, Mooney et al. reported an 11% net benefit for walking [10] and an 8% net benefit for load carriage [6] using their autonomous ankle exoskeleton.
Our group has been developing soft exosuits that use functional textiles to anchor to the body and deliver assistance in parallel with the underlying muscles [13, 14, 15, 16, 17, 18, 19, 20]. In studies with tethered versions of the device, exosuits have been shown to significantly reduce the energy cost of regular walking [17, 20], walking with load [16, 19], and running [18]. For an autonomous version, Panizzolo et al. showed a 7% net metabolic reduction for loaded walking compared to equivalent-mass-removed condition (walking with the device unpowered but removing the equivalent mass of the device) [15].
Over the past few years, there has been a growing recognition on the importance of control individualization for such gait assistive devices to maximize one’s benefit; however, only a few studies so far have investigated methods to systematically customize the controller of assistive devices. Conventionally, researchers have used manual tuning to individualize the assistance of exoskeletons [12] or powered prostheses [3], where the wearer or an external operator subjectively tunes the control parameters based on the user’s perception or the observation of gait kinematics/kinetics. A challenge with a manual parameter tuning process is that it can involve a significant level of human subjective intervention, thus requiring expert knowledge and experience with the hardware. A more recent approach is human-in-the-loop optimization, where an optimization algorithm finds the optimal parameters that maximize one’s metabolic benefit, estimating the wearer’s instantaneous metabolic cost while walking [11, 20, 21, 22]. This approach holds advantages in that it automatically optimizes control parameters by directly monitoring the user’s metabolic cost; however, the current approach requires a user to wear respiratory measurement equipment throughout the process. The field of prosthetics has made efforts to bridge the gap between these two approaches [23, 24, 25, 26, 27]. Researchers have derived dynamic models of locomotion with specific types of powered prostheses and used computational algorithms, such as supervised learning [24], extremum seeking controller (ESC) [25], or adaptive dynamic programming (ADP) [26], to find optimal impedance control parameters in the model for each individual. Among them, Huang et al. suggested a method called cyber-expert tuning system for a powered knee prosthesis, where they implemented several decision rules of manual tuning into a computational algorithm based on data from the device’s own wearable sensors [27]. The approach of performing automatic parameter tuning with only device sensors is appealing as it opens the door to this being performed outside of a lab setting. However, it remains unclear how this approach can be applied to the devices augmenting the gait of healthy individuals, because it is currently unclear what may be proxy objective metrics for metabolic cost and how those metrics can be measured by body-worn sensors. Therefore, if a control tuning method can be developed based on an objective function that is easily measurable and strongly correlated with metabolic cost, it may greatly improve the energetic efficacy of a gait assistive device for healthy individuals.
In this paper, we present an updated version of the autonomous multi-joint soft exosuit aimed at overground walking in outdoor settings [28]. In addition, we propose an online parameter tuning method that automatically customizes assistance based on the positive power delivered to the ankle by the exosuit. This is based on the assumption that a positive correlation exists between the positive ankle augmentation power and the corresponding metabolic benefit [6, 10, 19, 29, 30, 31, 32, 33]. Given that this proxy objective metric can easily be measured by wearable sensors, we believe this augmentation-power-based parameter tuning approach holds a promise, given the desire to enable control individualization in unconstrained environments. Additionally, we present results from human subject testing demonstrating the metabolic efficacy of the soft exosuit with the subject-specific control parameters during loaded walking.
More at link. 


Saturday, June 9, 2018

Dietary approaches to treat MS-related fatigue: comparing the modified Paleolithic (Wahls Elimination) and low saturated fat (Swank) diets on perceived fatigue in persons with relapsing-remitting multiple sclerosis: study protocol for a randomized controlled trial

Would the exact same diet protocol help in stroke fatigue? We'll never know since we have NO stroke leadership that follows up interesting research that might help stroke recovery. You, your children and grandchildren are screwed until stroke survivors run the stroke associations.
https://trialsjournal.biomedcentral.com/articles/10.1186/s13063-018-2680-x
  • Terry WahlsEmail authorView ORCID ID profile,
  • Maria O. Scott,
  • Zaidoon Alshare,
  • Linda Rubenstein,
  • Warren Darling,
  • Lucas Carr,
  • Karen Smith,
  • Catherine A. Chenard,
  • Nicholas LaRocca and
  • Linda Snetselaar
Trials201819:309
Received: 21 December 2017
Accepted: 8 May 2018
Published: 4 June 2018

Abstract

Background

Fatigue is one of the most disabling symptoms of multiple sclerosis (MS) and contributes to diminishing quality of life. Although currently available interventions have had limited success in relieving MS-related fatigue, clinically significant reductions in perceived fatigue severity have been reported in a multimodal intervention pilot study that included a Paleolithic diet in addition to stress reduction, exercise, and electrical muscle stimulation. An optimal dietary approach to reducing MS-related fatigue has not been identified. To establish the specific effects of diet on MS symptoms, this study focuses on diet only instead of the previously tested multimodal intervention by comparing the effectiveness of two dietary patterns for the treatment of MS-related fatigue. The purpose of this study is to determine the impact of a modified Paleolithic and low saturated fat diet on perceived fatigue (primary outcome), cognitive and motor symptoms, and quality of life in persons with relapsing-remitting multiple sclerosis (RRMS).

Methods/design

This 36-week randomized clinical trial consists of three 12-week periods during which assessments of perceived fatigue, quality of life, motor and cognitive function, physical activity and sleep, diet quality, and social support for eating will be collected. The three 12-week periods will consist of the following:
  1. 1.
    Observation: Participants continue eating their usual diet.
  2. 2.
    Intervention: Participants will be randomized to a modified Paleolithic or low saturated fat diet for the intervention period. Participants will receive support from a registered dietitian (RD) through in-person coaching, telephone calls, and emails.
  3. 3.
    Follow-up: Participants will continue the study diet for an additional 12 weeks with minimal RD support to assess the ability of the participants to sustain the study diet on their own.

Discussion

Because fatigue is one of the most common and disabling symptoms of MS, effective management and reduction of MS-related fatigue has the potential to increase quality of life in this population. The results of this study will add to the evidence base for providing dietary recommendations to treat MS-related fatigue and other symptoms associated with this disease.

Trial registration

ClinicalTrials.gov, NCT02914964. Registered on 24 August 2016.

Keywords

Multiple sclerosisFatigueDietAccelerometerQuality of lifeInterventionSwank dietWahls elimination diet

Background

Fatigue is one of the most common and disabling symptoms of multiple sclerosis (MS), diminishing quality of life (QOL) and contributing to early exit from the workforce [1, 2]. MS-related fatigue is most commonly managed through multiple interventions, including disease-modifying drugs and stimulants, exercise, energy conservation, and stress management techniques [3]. Although exercise augmented by electrical muscle stimulation can be modestly effective in reducing perceived fatigue [4, 5], studies investigating the efficacy of pharmaceutical therapies have shown conflicting results [6, 7, 8]. Because drug treatment has not been effective, dietary interventions are being explored. Statistically and clinically significant reductions in perceived fatigue severity in persons with progressive multiple sclerosis (pwPMS) have been reported with use of a multimodal intervention consisting of a modified Paleolithic diet, stress reduction, exercise, and electrical muscle stimulation [4, 5].
Interventions considering the whole diet (vs. supplement-based, single-nutrient focus) have been used in treating or preventing diseases, including psoriasis [9], cancer [10, 11], and neurological diseases [12]. Emerging data support the notion that environmental rather than genetic factors are likely the predominant causes of MS [13]. Given that food consumed is a major component of the environment, it is conceivable that improving the quality of the diet may have a significant impact on the development of MS. The relationship between the quality of the diet and MS-related symptoms such as fatigue is unknown. In this study, we will compare two dietary patterns for the treatment of MS-related fatigue: the modified Paleolithic diet (Wahls elimination diet) and a low saturated fat diet (Swank diet).
One early dietary intervention for individuals with MS was based on the observation that high levels of saturated fat in the diet were associated with increased risk for MS in Norway [14, 15]. Dr. Roy Swank theorized that a diet high in saturated fats causes more rapid disease progression. Dr. Swank followed 144 patients with mild to more severe disability for 34 years. These individuals had agreed to consume a diet containing < 20 g of saturated fat per day and report their dietary adherence. The patients’ clinical outcomes were monitored, including physical and mental performance [16, 17, 18, 19, 20, 21]. The Swank study found that the number of relapses and progression of disability was associated strongly with dietary saturated fat consumption [17, 18, 19, 20, 21, 22]. The 50-year follow-up is a strength of the Swank study, but the absence of a control group and lack of brain imaging are limitations.
Consumption of vegetables has also been associated with favorable health outcomes related to MS. Notably, the mean daily serving of vegetables is associated with lower risk of developing obesity [23], which is a risk factor for and a common comorbid diagnosis of those with MS. Increased consumption of vegetables is associated with lower Expanded Disability Status Scale scores [24], insulin sensitivity, blood pressure, body weight, and body mass index (BMI). Considering these observations, researchers in a more recent randomized controlled trial used a vegetarian version of the Swank diet [25], also known as the McDougall diet. Measures included the Fatigue Severity Scale (FSS), 36-item Short Form Health Survey (SF-36) quality-of-life scores, lipids, weight, BMI, and brain magnetic resonance imaging (MRI) scans at baseline and at 1 year [26]. Favorable reductions in weight, BMI, and total cholesterol were observed, but no statistically significant differences in MRI findings or SF-36 quality-of-life scores were reported [26].
Another diet of interest to the MS community is a Paleolithic diet [27]. Dr. Loren Cordain’s recommendations for a modern version of the Paleolithic diet stresses the consumption of meats, vegetables, and fruits; excludes grains, legumes, and dairy [27, 28]; and excludes nightshade vegetables (potatoes, tomatoes, peppers, and eggplants) [29] for persons with rheumatoid arthritis. Recently tested for its impact on various biomarkers in healthy individuals, the Paleolithic diet was associated with improvements in blood pressure, BMI [30], total cholesterol, insulin sensitivity, fasting insulin, and arterial distensibility [31]. In a study of patients with type 2 diabetes, the Paleolithic diet was shown to be more satiating per calorie than the American Diabetes Association (ADA) diet, which encourages increased intake of vegetables, dietary fiber, whole-grain bread and cereal products, fruits, and berries and decreased intake of total fat with more unsaturated fat [32]. In a crossover study comparing the Paleolithic diet with the ADA diet, the Paleolithic diet was superior to the ADA diet with respect to improving blood pressure, lipid profile, and glycemic control [33]. Finally, in a randomized controlled study of obese persons with metabolic syndrome, comparison of the Paleolithic diet with the control diet, which was an isoenergetic diet based on Dutch dietary guidelines, the Paleolithic diet was associated with greater improvements in blood pressure, fasting levels of lipids, and weight loss than the control diet [34].
A modified version of the Paleolithic diet was shown to reduce perceived fatigue in pwPMS (either secondary or primary progressive multiple sclerosis [SPMS or PPMS, respectively]) [4, 5] as part of a multimodal intervention (modified Paleolithic diet, targeted vitamin supplementation, stress-reducing practices, exercise, and electrical muscle stimulation). The study diet stressed the consumption of more vegetables, with a target of 6 to 9 cups of vegetables and fruit per day, and recommended somewhat less meat than Paleolithic diets tested in the previously mentioned studies. At enrollment, study participants were consuming less than 1.5 servings of vegetables per day but raised this to an average of 8 servings per day by month 12 [5]. The dietary component of the multimodal intervention was significantly associated with favorable changes in mood and cognition between baseline and 12 months, whereas the nondietary components were not [25]. It is unknown whether the dietary component of the multimodal intervention also significantly contributed to the observed reduction in perceived fatigue [4, 5]; however, several participants anecdotally reported that deviations from the study diet resulted in a sharp worsening of their fatigue and noted that the fatigue resolved with stricter adherence to the study diet. Data from another pilot randomized controlled trial also showed significant reductions in perceived fatigue (as assessed by FSS) in individuals with relapsing-remitting multiple sclerosis (RRMS) following a modified Paleolithic diet intervention [35].
To establish the specific effects of diet on MS symptoms such as fatigue, this study focuses on diet only instead of the previously tested multimodal intervention. The modified Paleolithic diet continues to stress a high intake of vegetables but also eliminates foods to which some individuals may be sensitive: eggs and nightshade vegetables [29]. To enhance adherence and reduce the rate of dropout, which occurred early in the intervention among participants in a nondiet control group [35], control participants will be assigned a second diet, a low saturated fat (Swank) diet, which is also popular among the MS community and has research to support its efficacy.

Study design at the link.