Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 27,840 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
All due to my doctor and therapists completely failing at getting my left arm/hand recovered, they did nothing to cure my spasticity! Since I'm tending to my 95 year old Mom we get meals on wheels and there are usually small cups of fruit and pudding/Jello. I have to hope that I have something on the table hefty enough on the table to stop the cup from sliding. The pudding and Jello cups are impossible to get clean with your spoon. My left arm will never rest on the table and stay there and I can't get my fingers open and at the same time get them around the cup. This problem is all because of spasticity of which the ridiculous opinion of Dr. William M. Landau is preventing a solution. I shouldn't hope that schadenfreude
hits him but I do.
Experts don’t know how someone becomes a super-ager, though there were a
few differences in health and lifestyle behaviors between the two
groups in the Spanish study. Most notably, the super-agers had slightly
better physical health, both in terms of blood pressure and glucose
metabolism, and they performed better on a test of mobility.(I managed to do 14 and I'm 68 so I guess I passed. Getting an ejection seat recliner would mean you'll never pass the power test!)
The super-agers didn’t report doing more exercise at their current age
than the typical older adults, but they were more active in middle age.
They also reported better mental health.(I haven't been depressed a day in my life and I never will!)
What EXACT PROTOCOL does your competent? doctor have to boost your brain function post stroke? NONE? So you don't have a functioning stroke doctor? Why are you seeing them? Find someone better!
There is no way I could get my 95 year old Mom to work a smartphone without someone sitting next to her and guiding every key stroke.
Summary: Internet-based conversations can
significantly improve cognitive functions in socially isolated older
adults. The trial, known as I-CONECT, involved 186 participants aged 75
and older who engaged in structured video chats four times weekly, which
helped enhance memory and executive function, particularly among those
with mild cognitive impairment.
Over the course of a year, these
interactions not only increased cognitive scores but also improved
emotional well-being and increased connectivity in brain regions
associated with attention. The findings suggest that digital
conversations can be a viable strategy to combat social isolation and
its cognitive repercussions.
Key Facts:
Enhanced Cognitive Function:
Participants in the I-CONECT trial who engaged in frequent digital
conversations showed improvements in global cognitive test scores and
language-based executive functions.
Improved Emotional Well-Being:
Both the control and intervention groups experienced boosts in
emotional health, indicating that regular social contact, even brief,
can have positive effects.
Neurological Benefits:
Brain imaging revealed increased connectivity within the dorsal
attention network of the intervention group, highlighting the potential
of conversational interactions to enhance brain function.
Source: Harvard
Just talking to other
people can stimulate different brain functions among socially isolated
older adults, even when the interactions are internet-based, according
to a new clinical trial out of Massachusetts General Hospital.
The results are published in The Gerontologist.
“We
initiated the first proof of concept behavioral intervention study in
2010, nearly a decade prior to the COVID-19 pandemic drawing attention
to the detrimental effects of social isolation on our overall health,”
explained lead author Hiroko H. Dodge, the principal investigator of the
National Institutes of Health–funded trials.
Measures
of emotional well-being improved in both control and intervention
groups, suggesting that emotion can be boosted by brief weekly telephone
calls while improving cognitive function requires frequent
conversational engagement. Credit: Neuroscience News
The 186-participant phase 2 randomized trial, called I-CONECT, used
the internet and webcams to allow for conversational interactions
between trained interviewers and socially isolated individuals aged 75
years and older who had normal cognition or mild cognitive impairment.
Investigators
rotated conversation partners assigned to each participant to enhance
the novelty of the experience, provided user-friendly devices allowing
participants without any internet/webcam experience to easily engage in
video-based conversations, and encouraged conversations with
standardized daily themes and picture prompts.
Thirty-minute
conversations were conducted four times per week for six months and then
twice per week for an additional six months. A control group of similar
individuals did not participate in such conversations, but both the
intervention and control groups received weekly 10-minute telephone
check-ins.
After the initial six-month period, the intervention
group had a higher global cognitive test score compared with the control
group with a large effect size among those with mild cognitive
impairment. Also, intervention group participants with normal cognition
had scores indicating higher language-based executive function.
At
the end of final six-month period, intervention group participants with
mild cognitive impairment had test scores indicating better
memory-related brain function than those in the control group.
Measures
of emotional well-being improved in both control and intervention
groups, suggesting that emotion can be boosted by brief weekly telephone
calls while improving cognitive function requires frequent
conversational engagement.
Also, brain imaging tests showed that the intervention group had
increased connectivity within the dorsal attention network—a region
important for the maintenance of visuospatial attention—relative to the
control group, although this finding must be interpreted carefully
because of the limited number of participants assessed due to
COVID-19–related research restrictions.
Upon requests from former
trial participants asking to continuously have conversations, Dodge and
her colleagues have established a nonprofit organization, the I-CONNECT
Foundation. The foundation has been providing social interactions to
isolated older individuals in the community free of charge, using the
same materials used in the trial.
“Our next goal is to extend
these activities to reach more isolated individuals in need, as well as
to delve into the biological mechanisms underlying the impact of social
interactions on our brain functions,” said Dodge.
“Providing
frequent stimulating conversational interactions via the internet could
be an effective home-based dementia risk-reduction strategy against
social isolation and cognitive decline.
“We plan to extend this
therapy to geriatric outpatient populations, for which we are
currently fundraising, and also examine its effectiveness for mild to
moderate depressive symptoms.”
The team is also exploring the
possibility of providing conversational interactions via chatbot — an
artificial intelligence – trained robot that provides stimulating
conversations as a cost-effective intervention.
“We
are aware that human contacts are critically important for our
emotional well-being, but for cognitive stimulations, chatbots might
work as effectively as humans, which we are currently investigating,”
said Dodge, who serves as the director of Research Analytics at the
recently inaugurated Interdisciplinary Brain Center at MGH and is a
faculty member of the Harvard Medical School.
Funding: Funding was provided by the National Institute on Aging.
About this cognition and aging research news
Author: Tracy Hampton Source: Harvard Contact: Tracy Hampton – Harvard Image: The image is credited to Neuroscience News
Sleep comprises one third of our adult life. It is essential for
normal functioning; without it, we experience memory lapses, have
difficulty with concentration, experience mood alterations, become more
prone to accidents, perform poorly at work, experience breaches in
interpersonal relationships and develop more medical and psychiatric problems.
Animals deprived of sleep will experience metabolic abnormalities and
eventually die. Despite all of this information, however, we do not
fully understand the whys of sleep.
Scientists have yet to determine how physical and psychological
restorative processes are coordinated during sleep and why such a
behaviorally disconnected state is necessary to accomplish these tasks.
The clearance of beta-amyloid, a neurotoxic waste product that
accumulates in the brain during wakefulness, is enhanced during sleep.
This and similar information suggests that the restorative function of
sleep is a result of its importance in maintaining metabolic homeostasis
through the removal of toxins that accumulate during wakefulness.
From a behavioral standpoint, sleep is characterized by diminished
responsiveness to, and perceptual disengagement from, the environment.
In these ways, it is similar to coma, with the exception that it is
readily reversible. However, from a neurophysiologic standpoint, it
bears no resemblance to comatose state at all. During sleep, the brain
is highly active and undergoes characteristic changes that translate
into parallel changes, not just in the central nervous system (CNS), but
throughout the body. The apparent quiescence of the sleeper is a
product of active processes that diminish responsiveness to
environmental stimuli. Sleep seems to be an important aspect of the 4
Rs: rest, restore, rejuvenate and repair.
At the same time, there is a perceptual disengagement from the
environment. However, this disengagement is not complete when important
environmental sensory information is monitored, again emphasizing the
active nature of the brain during sleep. An example is the mother who
responds to the infant’s whimper yet sleeps through other loud noises of
lesser significance.
Decades of sleep research have confirmed Aserinsky and Kleitman’s
original discovery of rapid eye movement (REM) sleep in 1953 and have
conclusively demonstrated that sleep is comprised of two fundamentally
distinct states, REM and non-REM (NREM) sleep, which repeat in cyclical
(ultradian) fashion throughout the night, forming a pattern widely known
as sleep architecture (Figure 2-1).
Proper characterization of sleep stages necessitates the simultaneous
monitoring of the numerous physiologic parameters, a process known as
polysomnography. Minimally required are the electroencephalogram (EEG),
electro-oculogram (EOG) and electromyogram (EMG) of skeletal muscle,
usually the submentalis.
The Rechtschaffen and Kales (R & K) sleep scoring manual was
published in 1968, 15 years after REM sleep was discovered. For several
decades, the manual has provided the methodology for human sleep
research, dictating the scoring of sleep stages. Advances in the field
have warranted a re-appraisal of these evaluation systems for sleep. In
2007, the American Academy of Sleep Medicine (AASM)
standards manual provided revised criteria for scoring sleep stages,
including standardizing epoch length, redefining sleep terminology and
criteria, and simplifying certain scoring rules. Table 2-1 shows a comparison of the R&K and AASM sleep stage scoring systems.
In the American Academy of Sleep Medicine (AASM) Visual Scoring system,
sleep is classified into four stages: stages N1-N3 (NREM), and stage R
(REM). Patterns for each of these parameters during the sleep of a young
adult are depicted in Figures 2-2 through 2-4.
In addition to sleep scoring, the AASM criteria also include scoring of
arousals, respiratory events, sleep-related movement disorders and
cardiac abnormalities.
The relative distribution of sleep stages changes with age (Figure 2-5).
N3 sleep is maximal in children and diminishes markedly with age,
especially during adolescence. Seniors may have little or no N3 sleep.
The loss of N3 sleep with age may be a consequence of the diminution in
cortical synaptic activity. In contrast, N1 sleep increases with age.
With aging, there is a general tendency toward sleep fragmentation,
characterized by an increase in the frequency of awakenings and brief
arousals. Older adults with specific EEG sleep characteristics (sleep
latency >30 minutes, sleep efficiency <80%, REM sleep percentage
in the lowest or highest 15% of the total sample distribution) have an
excess risk of dying beyond that associated with age, gender, or medical
burden.
Cognitive mental processes seem to be at a low level during N1 sleep
since sleepers who are awakened from it usually report experiencing
thought fragments or vague images. Most individuals awakened from delta
(N3) sleep report no mental activity at all. In contrast, most sleepers
report dreams when awakened from REM sleep.
Sleep needs are quite variable from individual to individual.
Although the average nightly sleep duration is approximately 8 hours,
children obtain about 10 hours, and the elderly <7 hours. Sleep
lengths vary even within similar age groups, with some individuals
reportedly requiring as little as 3 hours of nightly sleep. The most
prudent answer to the question of “How much sleep do I need?” is that
amount of sleep that results in optimal daytime alertness, no need to
“catch up” on sleep on non-work days, and no tendency to fall asleep
unintentionally during the course of normal daytime hours. Achieving
sleep needs should lead to a sense of mental efficiency and well-being.
Enlarge Figure 2-1: Sleep Architecture of a Normal Adult. The horizontal axis portrays hours of sleep. Source: Kryger MH, et al, eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-2: Polysomnography of
Wake to Sleep Transition. Notes: The most marked change is visible on
the two electroencephalographic (EEG) channels (C3/A2 and O2/A1), where a
clear pattern of rhythmic α activity (8 cps) changes to a relatively
low-voltage, mixed-frequency pattern at about the middle of the figure.
The level of electromyographic (EMG) activity does not change markedly.
Slow eye movements (right outer canthus [ROC]/left outer canthus [LOC])
are present throughout this episode, preceding the EEG change by at
least 20 seconds. In general, the change in EEG patterns to stage N1 as
illustrated here is accepted as the onset of sleep. Source: Kryger MH,
et al, eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-3: FIGURE 2.3 —
Polysomnography of Non-REM Sleep. Notes: The four electroencephalogram
tracings depicted here are from a 19-year-old female volunteer. Each
tracing was recorded from a referential lead (C3/A2) on a Grass
Instruments (West Warwick, RI) Model 7D polygraph with a paper speed of
10 mm/sec, time constant of 0.3 sec, and 12-amplitude high-frequency
setting of 30 Hz. On the second tracing, the arrow indicates a K-complex
and the underlining shows two sleep spindles. Stages 1 and 2 correspond
to stages N1 and N2 in the current AASM scoring system, while stages 3
and 4 correspond to stage N3. Source: Kryger MH, et al, eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-4: Polysomnography of
Patient in REM Sleep. Notes: On the left side is a burst of several
rapid eye movements (out-of-phase deflections in right outer canthus
[ROC]/A1 and left outer canthus [LOC]/A2). On the right side, there are
additional rapid eye movements as well as twitches on the
electromyographic (EMG) lead. The interval between eye movement bursts
and twitches illustrates tonic REM sleep. Source: Kryger MH, et al,
eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-5: Sleep and Age.
Notes: Age-related percentile curves for sleep macrostructure and
arousals in 100 healthy Caucasian volunteers. (A) N1%. (B) N2%. (C) N3%.
(D) REM%. Circles represent women, squares represent men; figures show
10th, 25th, 50th, 75th and 90th percentile. Key: REM, rapid eye
movement. Source: Adapted from Mitterling T, et al. Sleep. 2015;38(6):867-875.
Polysomnography
Polysomnography is typically performed in specialized facilities called sleep disorders centers and laboratories. In preparation for polysomnography,
patients are introduced to their sleeping quarters during their initial
office-based evaluation and provisions are made for special needs. On
the night of the test, they arrive at the laboratory well in advance of
the study time to acclimate to the new environment. Studies are
conducted in noise-free and private rooms and comfort is maximized by
making rooms aesthetically pleasing.
As noted earlier, characterization of sleep stages requires, at the
minimum, an EEG, EOG and EMG of the submentalis. However, a typical
clinical polysomnogram also includes monitors for airflow at the nose
and mouth, respiratory-effort strain gauges placed around the chest and
abdomen, and noninvasive oxygen-saturation monitors that function by
introducing a beam of light through the skin. Other parameters include
the electrocardiogram and EMG of the anterior tibialis muscles, which
are intended to detect periodic leg movements (PLMs). Finally, a
patient’s gross body movements are continuously monitored by audiovisual
means (Figure 2-6).
Enlarge Figure 2-6: Patient Undergoing Polysomnography. Public domain image. Source: National Heart Lung and Blood Institute (NIH).
Mechanisms Underlying Sleep and Wakefulness
Sleep and wakefulness are believed to be the net effect of the
interaction of two opposing, mutually inhibitory, interdependent
processes (Figure 2-7).
Enlarge Figure 2-7: Brain Regions
Involved in Regulation of Sleep and Wakefulness. Source: Adapted from
Atkin T, et al. Pharmacol Rev. 2018;70(2):197-245.
Arousal Neurophysiology
The wake-promoting system is consists of noradrenergic, cholinergic
(ACh), serotoninergic (5-HT), dopaminergic and histaminergic (His)
neurons, which produce cortical arousal via two pathways: a dorsal route
through the thalamus and a ventral route through the hypothalamus and
basal forebrain (Table 2-2). The
dorsal branch of ascending neurons receives input from cholinergic cell
groups in the upper pons, the pedunculopontine and laterodorsal
tegmental nuclei, which facilitate transmission of signals from the
thalamus to the cerebral cortex.
The second branch of ascending neurons receives input from the
monoaminergic neurons in the upper brainstem and caudal hypothalamus.
This pathway also receives contributions from peptidergic neurons in the
lateral hypothalamus (LH) containing orexin and from basal forebrain
neurons containing acetylcholine and γ-aminobutyric acid (GABA). All of
these ascending arousal pathways traverse the region at the
midbrain-diencephalic junction, where it was observed that lesions
caused hypersomnolence.
The neuropeptide hypocretin/orexin plays an important role as a
stabilizer and maintainer of wakefulness, minimizing unplanned
transitions to the sleep state through the reinforcement of
wake-promoting signaling in the brain (Figure 2-8).
Orexin deficiency results in narcolepsy in many species, suggesting
that this system is particularly important for maintenance of
wakefulness, although not necessarily its initiation. Orexin neurons
receive abundant input from the limbic system and activate waking active
monoaminergic and cholinergic neurons in the hypothalamus and brainstem
regions to maintain a long, consolidated waking period. These neurons
also interact with systems that regulate emotion, reward and energy
homeostasis to maintain appropriate vigilance states.
After the identification of arousal centers more than 3 decades ago,
it remained unclear how the arousal system was turned “off” so that
sleep could be initiated and maintained. It was not until the mid-1990s
that the identity of this sleep-promoting circuitry was revealed. It was
demonstrated that wake-promoting neurons are inhibited during sleep by a
system of ventrolateral preoptic nucleus (VLPO) neurons, which contain
sleep-active cells that contain the inhibitory neurotransmitters GABA
and galanin.
Primarily active during sleep, VLPO neurons project to all of the
main cellular components in the hypothalamus and brainstem that
participate in arousal. Inhibition of the arousal system by the VLPO
during sleep is critical for the maintenance and consolidation of sleep.
Work by Batini and colleagues has provided support for the concept that
an active sleep-promoting area is located near the nucleus of the
solitary tract in the medulla, but this remains largely unconfirmed.
Because the VLPO neurons do not have orexin receptors, actions of the
orexin neurons are primarily to reinforce the wake-promoting systems
rather than to directly inhibit the VLPO (Figure 2-8).
Transitioning Between Wakefulness and Sleep
Transitions between the discrete states of wakefulness and sleep are
rapid and complete and can be described as a “flip-flop” switch. As
signaling from one side increases, so does its inhibitory influence on
the signaling of the opposing process (Figure 2-9).
As long as signaling from one side exceeds the other, that state is
maintained. While the flip-flop switch avoids prolonged intermediate
states between sleep and wakefulness, transitions can also occur with
little warning and may have negative consequences. To minimize unplanned
transitions from wake to sleep, wake signaling consists of redundant
pathways that are stabilized via orexin neuropeptides, collectively
making wake asymmetrically favored.
Enlarge Figure 2-9: The “Flip-Flop”
Switch Model of Arousal and Sleep. The mutual inhibition between VLPO
neurons and the monoaminergic cell groups forms a flip-flop switch,
which produces sharp transitions in state but is relatively unstable.
Source: Modified from Saper CB, et al. Nature.
2005;437(7063):1257-1263.
Factors Modulating Arousal and Sleep
There are many influences that affect the activity of the wake-sleep
circuit, which can be categorized within three major factors — circadian
rhythms, homeostatic drive and allostatic signaling.
The homeostatic influence is believed to be based on the accumulation
of the drive for sleep during prolonged wakefulness and relief of this
need during sleep. The mechanism for this homeostatic regulation may be
linked to the accumulation of a sleep-promoting substance (believed to
be adenosine) that enhances the activity of sleep-promoting cells and
reduces the activity of wake-promoting neurons.
Circadian rhythms are governed mainly by the suprachiasmatic nucleus
(SCN) area in the brain, which serves as a biological clock of roughly
24 hours. Signals from various areas in the body connect to the dorsal
and ventral subparaventricular zones, as well as the dorsomedial nucleus
of the hypothalamus (DMH). Neurons in these regions relay information
necessary for organizing daily cycles of wake–sleep and rhythms of body
temperature (Table 2-3). DMH neurons drive circadian
cycles of sleep, activity, feeding and corticosteroid secretion. These
integrative connections allow circadian rhythms to mold the daily cycles
of sleep-wakefulness in accordance with internal and external cues.
Rather than maintaining a rigid sleep/wake schedule, the physiologic
systems within the body are able to fluctuate to meet demands from
external forces via allostatic signaling. Allostatic signaling adapts
sleep and wakefulness to external behavioral events, such as
environmental, sensory, cognitive and emotional inputs. These are
thought to be mediated in part by cues from visceral sensory systems and
feeding regulatory systems to the arousal systems, involving inputs to
the SCN, VLPO and orexin neurons from corticolimbic sites.
The process of sleep is important for physical and mental restoration
and normal functioning, although the mechanism by which sleep produces
these effects is a matter of ongoing research. Nevertheless, the complex
array of changes that is seen both in the brain and the peripheral
organs during sleep is proof that sleep represents an active state that
is highly regulated. The states of sleep and wakefulness are governed by
different, but interconnected neural circuits in the brain, which are
mutually interdependent and inhibitory. The transition between the
distinct sleep/wake states is fast and complete, governed by many
factors, such as circadian rhythms, homeostatic drive and allostatic
signaling.
Doghramji K, Doghramji PP. Clinical Management of Insomnia, 3rd ed. Professional Communications Inc. 2023.
Dew MA, Hoch CC, Buysse DJ, et al. Healthy older adults’ sleep predicts all-cause mortality at 4 to 19 years of follow-up. Psychosom Med. 2003;65(1):63-73.=
Do we have ANYONE in the stroke medical world that looks at this and says; 'We need to do the same research for stroke survivors, and we'll assign these people to get it done!' That will never occur, there is NO STROKE LEADERSHIP ANYWHERE!
Introduction: Virtual reality (VR)-based
interventions to improve balance and mobility are gaining increasing
traction across patient populations. VR-based interventions are believed
to be more enjoyable and engaging for patients with traumatic brain
injury. This scoping review aims to summarize existing studies from the
literature that used VR to improve balance and mobility and determine
the gap in VR-based balance literature specific to individuals with
traumatic brain injury. Methods: Two authors independently searched the
literature using the search terms “Virtual Reality Traumatic Brain
Injury Lower Limb”, “Virtual Reality Traumatic Brain Injury Balance”,
and “Virtual Reality Traumatic Brain Injury Gait”. Results: A total of
seventeen studies, specifically, three randomized controlled trials, one
one-arm experimental study, two retrospective studies, two case
studies, one feasibility/usability study, one cohort study, and seven
diagnostic (validation) studies, met the inclusion criteria for this
review. The methodological quality of the studies evaluated using the
PEDro scale was fair. Discussion: Future studies should focus on
large-scale clinical trials using validated technology to determine its
effectiveness and dose–response characteristics. Additionally, standard
assessment tools need to be selected and utilized across interventional
studies aimed at improving balance and mobility to help compare results
between studies.
Each year in the United States, approximately 1.7 million individuals encounter traumatic brain injuries (TBIs) [1].
The immediate impacts of a traumatic brain injury may include
unconsciousness of varying length, depression, confusion, trouble
recalling the traumatic event or learning new information, speech
issues, and lack of coordination [2]. Some or all of the immediate impacts may be permanent [2].
Depending on intrinsic variables like length of unconsciousness and
post-traumatic amnesia, TBI is categorized as mild, moderate, or severe [3].
Most people with mild TBI (70–90% of TBI cases) experience rapid
recovery, allowing them to reach their pre-TBI health status [4].
Those who experience a TBI with symptoms surpassing three months are
considered to have transitioned from the acute to the chronic phase of
TBI [5].
Five years post-injury, 57% of moderate or severe chronic TBI patients
are moderately or severely disabled, with about 33% relying on others to
complete everyday activities [6].
Furthermore,
regardless of the extent of severity, health problems due to TBI can
cause long-term physical and neurological impairments, affecting the
person’s ability to perform daily activities and return to work [7]. About 30–65% of TBI patients report balance impairments sometime during their recovery [8]. Damage to the integration of sensory, motor, and musculoskeletal systems leads to balance issues [9,10].
Impaired balance leads to a higher risk of falls. Falls are the leading
cause of TBI-related hospitalizations. Multiple interventions are being
developed and evaluated to help improve balance deficits post-TBI. With
technological development, research utilizing novel technology to help
improve balance deficits post-TBI has been gaining traction over the
past decade.
Traditionally, the standard of
care for treating patients with chronic TBI-related balance issues has
consisted of various exercises prescribed by a physical therapist, such
as firm static standing, foam static standing, and weight-shifting
exercises. Physical therapists also use research-based sensory–motor
learning concepts available in the clinical setting [11,12]. Physical therapy focusing on sensory stimulation has become a growing trend as rehabilitation techniques modernize [13,14].
In the past decade, the integration of novel Virtual Reality (VR)
technology to treat balance issues associated with TBI has grown. VR is a
user–computer interface method that incorporates real-time simulation
of an environment or activity and permits user input through various
sensory channels [15].
Unlike traditional user interfaces, VR allows users to interact with a
three-dimensional simulated environment. In VR-integrated rehab, spatial
and temporal manipulations are employed to improve sensorimotor
training [15].
The physiological activation of brain areas is achieved using VR
rehabilitation programs, as it involves motor learning and repeated
practice with stimuli from multiple senses (audio, visual, motor, and
proprioceptive) [16].
VR-integrated
rehab has some benefits over the standard of care. VR rehabilitation
allows for precise, objective progress tracking and seems to motivate
patients more than traditional rehabilitation practices [17].
Additionally, using VR to treat TBI balance issues allows therapists to
control the stimuli and simulate environments tightly without risking
patient safety [18].
Finally, VR therapy has also shown greater ecological validity while
having the ability to create more affordable environments that can be
reused by other therapists [19].
Research
involving VR is broadly classified into three main
categories—immersive, non-immersive, and semi-immersive VR. The
immersive VR creates a 360-degree environment with a headset or goggles
that makes the user feel as though they are inside the virtual
environment. Second is the non-immersive VR, which displays content on a
device such as a television, computer screen, or any other surface and
allows the user to see the computer-generated environment on the screen [20].
Semi-immersive VR is a mixture of immersive and non-immersive VR,
allowing users to interact with the virtual environment while physically
connecting to their surroundings. The advancement in technology and
reduction in cost has allowed these VR devices to expand in scope and
thus become widespread in research [21].
While extensive research exists on utilizing VR for upper extremity
rehabilitation, research implementing VR to help improve gait and
balance deficiencies post-TBI is relatively new. Although systematic
reviews summarizing VR interventions on traumatic brain injuries exist,
most have focused only on upper extremity rehabilitation. Only one study
focused on reviewing five randomized controlled trials (RCT) related to
lower extremity VR rehabilitation [22].
A full scoping review of the literature to understand the existing role
of VR in balance research post-TBI is needed to determine research gaps
and future research directions [22].
This review aims to fill the gap in the literature by completing a full
scoping review of VR interventions aimed at improving balance and
mobility deficits in adults with TBI. This review will summarize
existing literature related to lower limb VR rehabilitation. This review
is essential as a starting point in guiding clinical practice. This
review will highlight existing gaps in the literature and evoke new
research ideas.
Hopefully your competent? doctor, hospital and therapists have already found these 400 action observation videos on YouTube so you can benefit from them. But I bet you'll have to tell them how to be competent!
Occupational therapists can improve stroke survivors’ hand and arm movement and participation in daily activities through action observation (AO). AO involves watching another person’s hand or arm complete a movement or task. While research supports the use of AO with stroke survivors, there is a delay in applying the information from AO research studies to stroke rehabilitation. Also, limited AO videos are available to occupational therapists which makesapplying AO challenging. The purpose of this capstone project was to increase awareness of AOand access to AO videos for stroke survivors, occupational therapists, and researchers.Collaboration with experts on AO and stroke rehabilitation was used to guide the development ofover 400 AO videos that were uploaded to YouTube for stroke survivors at an outpatient clinic.Educational materials about AO were created and given to the occupational therapists and stroke survivors at the outpatient clinic. The AO videos were also delivered to researchers from Georgia State University and the Georgia Institute of Technology to be used in future research endeavors.The AO resources developed in this project will help increase the use of AO in stroke rehabilitation and be used by researchers to better understand the mechanisms of AO and create better guidelines for applying AO.
Corticospinal
tract (CST) is the principal motor pathway; we aim to explore the
structural plasticity mechanism in CST during stroke rehabilitation.
Methods
A
total of 25 patients underwent diffusion tensor imaging before
rehabilitation (T1), 1-month post-rehabilitation (T2), 2 months
post-rehabilitation (T3), and 1-year post-discharge (T4). The CST was
segmented, and fractional anisotropy (FA), axial diffusion (AD), mean
diffusivity (MD), and radial diffusivity (RD) were determined using
automated fiber quantification tractography. Baseline level of
laterality index (LI) and motor function for correlation analysis.
Results
The FA values of all segments in the ipsilesional CST (IL-CST)
were lower compared with normal CST. Repeated measures analysis of
variance showed time-related effects on FA, AD, and MD of the IL-CST, and there were similar dynamic trends in these 3 parameters. At T1, FA, AD, and MD values of the mid-upper segments of IL-CST
(around the core lesions) were the lowest; at T2 and T3, values for the
mid-lower segments were lower than those at T1, while the values for
the mid-upper segments gradually increased; at T4, the values for almost
entire IL-CST were higher than before. The highest LI was
observed at T2, with a predominance in contralesional CST. The LIs for
the FA and AD at T1 were positively correlated with the change rate of
motor function.
Conclusions
IL-CST
showed aggravation followed by improvement from around the lesion to
the distal end. Balance of interhemispheric CST may be closely related
to motor function, and LIs for FA and AD may have predictive value for
mild-to-moderate stroke rehabilitation. Clinical Trial Registration. URL: http://www.chictr.org.cn; Unique Identifier: ChiCTR1800019474.
BOSTON — In this video, an expert reviews current topics in addiction
medicine, like ties between cannabis use and cardiovascular health,
buprenorphine access and pre-operative alcohol assessments.
According to Charlie Reznikoff, MD, FACP, FASAM, an associate professor of medicine at the University of Minnesota, there is “increasing evidence that cannabis use causes cardiovascular events,” such as “heart attacks, atrial fibrillation and worsened angina.”
“I don’t think we’ve ever recognized that fully,” he said. “But what
we’re seeing now is that Baby Boomers are aging up ... gaining more
medical illness and returning to cannabis use.”
While Baby Boomers may have used cannabis when they were younger, the
difference now is “they have more medical problems,” Reznikoff, who
presented at the ACP Internal Medicine Meeting, said.
Reznikoff also discussed the prevalence of “significant” racial disparities in addiction medicine, which “are resulting in disparities in death rates.”
“It’s really important for us to treat everyone, and to recognize that there are racial disparities,” he said.
Reference:
Reznikoff C. Addiction medicine: What's new in the clinic?
Presented at: ACP Internal Medicine Meeting; April 18-20, 2024; Boston.
But this goes against standard age-proofing your home:
One of the best ways
to age-proof a house is by having a master bedroom and bathroom on the
first floor, says Mark Hager, founder of AgeInPlace.com. “You want to
have everything you need on one level so that you don't have to climb
stairs as you get older,”
I'll be climbing stairs until the day I die. Or as we hear from our medical staff; 'Use it or lose it'.
Climbing stairs was associated with a 39% reduced risk for death from heart disease.
It was also associated with a 24% reduced risk for death from any cause.
In a meta-analysis of studies covering more than 400,000 people,
climbing stairs was associated with reduced risk for all-cause mortality
and death from heart disease.
“If you have the choice of taking the stairs or the lift, go for the stairs, as it will help your heart,” Sophie Paddock, MBBS,
interventional cardiologist at the University of East Anglia and
Norfolk and Norwich University Hospital Foundation Trust, Norwich, U.K.,
who presented the findings at ESC Preventive Cardiology 2024, said in a
press release. “Even brief bursts of physical activity have beneficial
health impacts, and short bouts of stair climbing should be an
achievable target to integrate into daily routines.”
Data were derived from Paddock S, et al. Optimal exercise
modalities for primary and secondary prevention. Presented at: ESC
Preventive Cardiology; April 25-27, 2024; Athens, Greece.
Paddock and colleagues reviewed nine studies with data from 480,520
participants and conducted a pooled analysis of five studies with
455,649 participants to determine the relationship between stair climbing
and all-cause and CV mortality. The pooled cohort included healthy
individuals as well as those with prior MI or peripheral artery disease.
The age range was 35 to 84 years and 53% were women.
Stair climbing was associated with a 39% reduced risk for CV mortality (RR = 0.61; 95% CI, 0.48-0.79; I2 = 84%; z-test = 3.76; P = .0002) and a 24% reduced risk for all-cause mortality (RR = 0.76; 95% CI, 0.62-0.94; I2 = 85%; z-test = 2.5; P = .01), according to the researchers.
In a qualitative synthesis, the researchers concluded that there was a
positive association between stair climbing and CVD including MI,
ischemic stroke and HF.
“Based on these results, we would encourage people to incorporate stair climbing
into their day-to-day lives,” Paddock said in the release. “Our study
suggested that the more stairs climbed, the greater the benefits — but
this needs to be confirmed. So, whether at work, home, or elsewhere,
take the stairs.”
The authors of the present study address an important and topical
question: What is the best imaging modality to define large core
infarcts?
Over the last 2 years, multiple RCTs (RESCUE-Japan Limit,
ANGEL-ASPECT, SELECT-2) have demonstrated the efficacy of endovascular
thrombectomy (EVT) for large core infarcts. These studies used a
combination of modalities to define large core, including non-contrast
head CT (NCCT) using the Alberta Stroke Program Early Computed
Tomography Score (ASPECTS), as well as advanced imaging, such as CT
perfusion (CTP) and MRI. More recently, in the TENSION trial, EVT
improved outcomes when NCCT/ASPECTS was used as the sole imaging
modality to measure core infarct size.
Here, the authors performed a retrospective cohort study to determine
whether functional outcomes differed when large core was defined by
NCCT versus CTP. Patients were selected from the International Stroke
Perfusion Imaging Registry (INSPIRE), a large cohort of patients with
acute ischemic stroke, all of whom underwent NCCT and CTP. Patients
included in this study represented a subset of the INSPIRE registry who
had large vessel occlusion treated with EVT. Large core was defined as
ASPECTS ≤5 by NCCT or core volume ≥70mL by CTP. The primary outcome was a
poor functional outcome as determined by a modified Rankin Scale (mRS)
score of 5-6 at 3 months.
In total, there were 1115 patients with LVO who underwent EVT, of
which 90 (8.1%) had ASPECTS ≤5 and 97 (8.7%) had CTP core ≥70 mL.
Patients were categorized into 1 of 4 groups: 1) ASPECTS >5 and
CTP<70mL (N=962); 2) ASPECTS ≤5 and CTP <70mL (N=56); 3) ASPECTS
>5 and CTP ≥70mL (N=63); and 4) ASPECTS ≤5 and CTP ≥70mL (N=34).
Compared to group 1 (no large core by NCCT or CTP), patients in group 2
(ASPECTS-defined large core) were equally likely to have a poor
functional outcome at 3 months (29% vs 23%, adjusted OR 1.84
[0.91–3.73]; P=0.089). Conversely, compared to group 1, patients in
group 3 (CTP-defined large core) were more likely to have a poor
functional outcome (60% vs 23%, adjusted OR 3.91 [2.01–7.60];
P<0.001). In a subgroup analysis, it was demonstrated that when EVT
was performed after 6 hours, patients with ASPECTS ≤5 were more likely
to have a poor outcome than those with ASPECTS >5 (50% versus 27%,
P=0.004), whereas when EVT was performed within 6 hours, there was no
difference in the proportion with a poor outcome between ASPECTS ≤5 vs
>5. CTP-defined large core showed increased likelihood of poor
outcome in both time strata.
The results of this study suggest that CTP-defined large core may
provide better prognostic information than ASPECTS-defined large core,
particularly during the early time window — when CTP is not recommended
in the current American Heart Association guidelines. These findings
provide some evidence that foregoing CTP for patients with large core
infarcts may lead to more patients undergoing EVT that are unlikely to
benefit.
In the general population, 8-hour time-restricted eating significantly increases risk of cardiovascular mortality.
A daily 8-hour time-restricted eating (TRE) plan is associated with a
significantly increased risk of cardiovascular mortality in the general
population and in patients with cardiovascular disease (CVD) or cancer,
compared with eating for a duration of 12 to 16 hours, according to
research presented at the American Heart Association’s Epidemiology and
Prevention/Lifestyle and Cardiometabolic Health Scientific Sessions
2024.
Researchers analyzed data on dietary patterns in participants from
the 2003 to 2018 National Health and Nutrition Examination Survey and
mortality data through December 31, 2019, from the National Death Index
database.
A total of 20,078 adults aged 20 years or older and not pregnant were
included. Their mean age was 48.5 years, 50% were men, 73.3% were
White, 17.9% were current smokers, and their mean body mass index was
28.7. In addition, 8.2% had CVD, and 11.0% had cancer.
Of the cohort, 414 individuals had a daily eating duration of less
than 8 hours, 1492 had a daily eating duration of 8 to less than 10
hours, 4832 had a daily eating duration of 10 to less than 12 hours,
11,831 had a daily eating duration of 12 to 16 hours, and 1509 had a
daily eating duration of more than 16 hours.
These
findings require replication but do not support long-term use of 8-hour
TRE for prevention of cardiovascular death nor for improving longevity.
For all-cause mortality, participants
with a daily eating duration of less than 8 hours had an overall hazard
ratio (HR) of 1.26 (95% CI, 0.91-1.74), compared with those who had a
duration of 12 to 16 hours. The HR was 1.14 (95% CI, 0.93-1.39) in
individuals with a daily eating duration of 8 to less than 10 hours,
1.05 (95% CI, 0.92-1.20) in those with a duration of 10 to less than 12
hours, and 0.99 (95% CI, 0.78-1.25) in those with a duration of longer
than 16 hours.
For cardiovascular mortality, the HR was 1.91 (95% CI, 1.20-3.03) in
individuals with a daily eating duration of less than 8 hours vs those
with a duration of 12 to 16 hours. The HR was 1.25 (95% CI, 0.92-1.71)
in those with a duration of 8 to less than 10 hours. Among patients with
CVD,
those with a daily eating duration of less than 8 hours had an HR for
cardiovascular mortality of 2.07 (95% CI, 1.14-3.78). In patients with
cancer, the HR for cardiovascular mortality was 3.04 (95% CI, 1.44-6.41)
for those with a daily eating duration of less than 8 hours.
Regarding cancer mortality, the overall HR for individuals with a
daily eating duration of less than 8 hours was 1.20 (95% CI, 0.62-2.32)
vs a reference group of those with an eating duration of 12 to 16 hours.
In patients with CVD, the HR for cancer mortality was 0.69 (95% CI,
0.25-1.90) for those with an eating duration of less than 8 hours and
1.33 (95% CI, 0.64-2.78) in those with a duration of greater than 16
hours. For patients with cancer, the HR for cancer mortality was 0.44
(95% CI, 0.13-1.49) in those with a daily eating duration of less than 8
hours.
“These findings require replication but do not support long-term use of 8-hour TRE for prevention of cardiovascular death nor for improving longevity,” the study authors concluded.
Chen M, Xu L, Van Horn L, et al. Association of 8-hour
time-restricted eating with all-cause and cause-specific mortality.
American Heart Association’s Epidemiology and Prevention/Lifestyle and
Cardiometabolic Health Scientific Sessions 2024. March 18-21, 2024,
Chicago, Illinois. Abstract P192.
![Figure 2-2: Polysomnography of Wake to Sleep Transition. Notes: The most marked change is visible on the two electroencephalographic (EEG) channels (C3/A2 and O2/A1), where a clear pattern of rhythmic α activity (8 cps) changes to a relatively low-voltage, mixed-frequency pattern at about the middle of the figure. The level of electromyographic (EMG) activity does not change markedly. Slow eye movements (right outer canthus [ROC]/left outer canthus [LOC]) are present throughout this episode, preceding the EEG change by at least 20 seconds. In general, the change in EEG patterns to stage N1 as illustrated here is accepted as the onset of sleep. Source: Kryger MH, et al, eds. <em>Principles and Practice of Sleep Medicine. 7th ed. </em>Philadelphia, PA: Elsevier Saunders; 2022.](https://www.healio.com/~/media/clinical-guidance/insomnia/overview/ch2normalsleep/figure22.webp)
![Figure 2-4: Polysomnography of Patient in REM Sleep. Notes: On the left side is a burst of several rapid eye movements (out-of-phase deflections in right outer canthus [ROC]/A1 and left outer canthus [LOC]/A2). On the right side, there are additional rapid eye movements as well as twitches on the electromyographic (EMG) lead. The interval between eye movement bursts and twitches illustrates tonic REM sleep. Source: Kryger MH, et al, eds. <em>Principles and Practice of Sleep Medicine. 7th ed</em>. Philadelphia, PA: Elsevier Saunders; 2022.](https://www.healio.com/~/media/clinical-guidance/insomnia/overview/ch2normalsleep/figure24.webp)
