Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,483 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. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?
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.
A study investigated the origin of ataxia in the
brain of patients with stroke. A significant number of the stroke
lesions in the patients were located outside the cerebellum.
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FULL STORY
A new study by the University of Turku
and Turku University Hospital in Finland investigated the origin of
ataxia in the brain of patients with stroke. A significant number of the
stroke lesions in the patients were located outside the cerebellum.
A recent study by a Finnish
research group found that, contrary to the information usually taught in
medical schools, more than half of the cerebrovascular diseases that
caused ataxia were located entirely outside the cerebellum and
cerebellar peduncles. However, these lesions localized to a brain
network, connected to the cerebellum.
Areas of the brain in those with stroke were analyzed for lesion activity and functional connectivity.
In 54% of those with acute limb ataxia resulting from stroke, lesions were found outside the cerebellum.
For individuals with stroke, lesions that cause ataxia of the limbs
occur in different regions of the brain but are connected by a common
network, according to new research published in Neurology.
“Generally, ataxia is strongly associated with lesions in the
cerebellum or its direct connections, transversing through the
cerebellar peduncles or through the spinocerebellar tracts,” Oliver Liesmaki, MD, MSc, of the department of clinical neurosciences at the University of Turku in Finland, and colleagues wrote.
The latest research out of Finland found that brain lesions in
stroke which cause limb ataxia may not be centrally located but are part
of a common network.Image: Adobe Stock
As prior research has established that ataxia may also occur without
damage to the cerebellum, Liesmaki and colleagues sought to investigate
whether lesions in the brain due to stroke that result in limb ataxia can be identified as part of a common neural network.
Their prospective cohort study included 197 individuals (mean age,
67.2 years; 39% women) with new-onset stroke and visible lesions on CT
or MRI who were admitted to Turku University Hospital (TUH) during the
years 2020 and 2021. All participants were examined following stroke
while still admitted to the hospital, then again at a 4-month follow up
to determine the presence of limb ataxia.
The researchers analyzed the location of brain lesions from 133
individuals (23 with, 110 without limb ataxia). Any nonbrain tissue were
removed from imaging sources via computerized software.
The researchers then compared, on a voxel-by-voxel basis, whole-brain
lesion locations and their functional connectivity from all patients,
utilizing data from 1,000 healthy volunteers from the Brain Genome
Superstruct Project via voxel-based lesion-symptom mapping as well as
lesion network mapping.
A separate independent confirmation dataset was compiled from an
additional 96 individuals diagnosed with new-onset stroke from TUH and
included in data analyses.
The findings were confirmed in an independent cohort of patients with stroke who had identical clinical assessments.
According to the results, at baseline, 35 individuals were diagnosed
with new-onset acute limb ataxia and 162 were not. At the 4-month follow
up, four additional patients had developed late-onset limb ataxia. A
total of 118 individuals were not diagnosed with ataxia at any point (n =
40 with missing follow-up data).
Liesmaki and colleagues wrote that, in 54% of the patients with acute
limb ataxia, lesions were found outside the cerebellum and cerebellar
peduncles, with no discernible associations between specific lesion
locations and ataxia occurrence.
However, the researchers reported that lesions causing acute limb ataxia were
connected to a common network centered on the intermediate zone
cerebellum and cerebellar peduncles (lesion connectivity in patients
with acute limb ataxia vs. those without, pFWE < 0.05), with similar
results found when comparing both patient groups when excluding lesions
in the cerebellum and cerebellar peduncles (pFWE < 0.05).
These findings were replicated within the independent stroke dataset (OR = 2.27; 95% CI, 1.32–3.91) for limb ataxia.
“Our findings lend insight into the mechanisms of extracerebellar
lesions causing limb ataxia, which may help(NOT GOOD ENOUGH!) in clinical localization of
lesions causing limb ataxia and possibly also avoiding ataxia in
neurosurgical treatments of brain disorders,” Liesmaki and colleagues
wrote.
Disclosures:
Liesmaki reports no relevant financial disclosures. Please see
the study for all other authors’ relevant financial disclosures. The
study was funded by the Finnish Medical Foundation, the Instrumentarium
Research Foundation, the Sigrid Juselius Foundation, the Finnish
Foundation for Alcohol Studies and Turku University Hospital.
In case you want your doctor to use this to treat your ataxic gait.
What is Ataxic Gait?
Ataxic gait is often characterized by difficulty walking in a
straight line, lateral veering, poor balance, a widened base of support,
inconsistent arm motion, and lack of repeatability. These symptoms
often resemble gait seen under the influence of alcohol.
If you want to evaluate your ataxia yourself in violation of doctor's purview, here you go.
by
Judy George, Senior Staff Writer, MedPage Today
March 26, 2021
A novel stimulator device to treat gait deficits in multiple sclerosis (MS) patients with mild to moderate symptoms earned a nod from the FDA Friday.
The device, known as the Portable Neuromodulation Stimulator (PoNS),
generates electrical pulses on the tongue to stimulate trigeminal and
facial nerves to treat motor deficits. To be available by prescription,
it is to be used only as part of a supervised therapeutic exercise
program in MS patients 22 and older, the agency said. The FDA authorized
the device through its "de novo" premarket review pathway for new
devices posing low to moderate risks for adverse effects.
"MS
is one of the most common neurological diseases in young adults.
Today's authorization offers a valuable new aid in physical therapy and
increases the value of additional therapies for those who live with MS
on a daily basis," Christopher Loftus, MD, acting director of the Office
of Neurological and Physical Medicine Devices in the FDA's Center for
Devices and Radiological Health, said in a statement.
Most people with MS experience their first symptoms between the ages
of 20 and 40 and the disease occurs more frequently in women than in
men. MS can cause a variety of symptoms, including problems with walking
and balance.
The PoNS device delivers mild neuromuscular electrical stimulation to
the dorsal surface of the patient's tongue. A control unit, worn around
the neck, sends signals to a mouthpiece the patient holds lightly in
place with their lips and teeth. A therapist can view usage data later
to identify "potential areas of missed or shortened sessions," the FDA
noted.
Two
clinical studies underpinned the agency's favorable review. One
involved 20 MS patients with gait deficits (10 who used PoNS; 10 who
used a sham device), the PoNS group showed "statistically significant
and clinically significant" improvement in Dynamic Gait Index (DGI)
scores at 14 weeks not seen in controls, the FDA said.
The other study, in 14 patients, demonstrated improvements from
baseline in sensory organization task scores (but not in DGI scores) at
14 weeks. No serious safety adverse events were reported in the clinical
studies or retrospective analysis of real-world data.
The PoNS device should not be used by patients with penetrating brain
injuries, neurodegenerative diseases, oral health problems, chronic
infectious diseases, unmanaged hypertension or diabetes, pacemakers, or a
history of seizures, the FDA cautioned. "Because the PoNS device
delivers electrical stimulation directly to the surface of the tongue,
precautions for use are similar to those for transcutaneous electrical
nerve stimulation," the agency said. Electrical stimulation should not
be used if there is an active or suspected malignant tumor, near recent
bleeding or open wounds, or in areas that lack normal sensation. The
PoNS device has not been tested on and should not be used by people
under age 22, who are pregnant, or who are sensitive to nickel, gold, or
copper.
This was device maker Helius Medical's second attempt to win FDA authorization; the agency rejected the PoNS device
in 2019 when the company sought clearance through the less rigorous
510(k) pathway, though it had been approved in Canada. It had been
featured extensively in the media after former television host Montel Williams promoted the device in 2016, which he used to treat his MS symptoms.
Judy George
covers neurology and neuroscience news for MedPage Today, writing about
brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy,
autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep,
pain, and more. Follow
I could have done none of these tests, dead brain kinda prevents that. So what protocols are out there to recover hand/finger function due to dead brain?
So you accurately described a problem, but provided NOTHING to solve that problem. Good to know how useless this research was.
Cerebellar
ataxia refers to the disturbance in movement resulting from cerebellar
dysfunction. It manifests as inaccurate movements with delayed onset and
overshoot, especially when movements are repetitive or rhythmic.
Identification of ataxia is integral to the diagnosis and assessment of
severity, and is important in monitoring progression and improvement.
Ataxia is identified and assessed by clinicians observing subjects
perform standardised movement tasks that emphasise ataxic movements. Our
aim in this paper was to use data recorded from motion sensors worn
while subjects performed these tasks, in order to make an objective
assessment of ataxia that accurately modelled the clinical assessment.
The selected model accurately (96.4%) predicted the clinical scores for ataxia and correlated well with clinical scores of the severity of ataxia (rho=0.8, rho=0.8, p<0.001).
The severity estimation was also considered in a 4-level scale to
provide a rating that is familiar to the current clinically-used rating
of upper limb impairments. The combination of FCT and FTT performed as
well as all four test combined in predicting the presence and severity
of ataxia.
Conclusion
Individual
bedside tests can be emulated using features derived from sensors worn
while bedside tests of cerebellar ataxia were being performed. Each test
emphasises different aspects of stability, timing, accuracy and
rhythmicity of movements. Using the current models it is possible to
model the clinician in identifying ataxia and assessing severity but
also to identify those test which provide the optimum set of data.
Trial registration
Human Research and Ethics Committee, Royal Victorian Eye and Ear
Hospital, East Melbourne, Australia (HREC Reference Number: 11/994H/16).
Repeated gait training with a flexible knee brace and an oil damper
hinged ankle-foot orthosis (GSD, Gaitsolution Design, Kawamura Gishi,
Osaka, Japan) improved the gait abnormalities and speed in a stroke
patient with ataxic hemiparesis. Here, we report on a female in her 50s
with a cerebral infarction in the posterolateral thalamus. She had
ataxic hemiparesis in her lower left leg. While walking, her knee was
bending at initial contact and loading response due to the ataxic
hemiparesis, and her gait speed remained at 52.2 m/min. To reconstruct
the inverted pendulum model, we provided gait training with a flexible
knee brace and GSD. As a result, her gait abnormalities were resolved
and her gait speed improved up to 72.6 m/min. We speculated that the one
of the reasons for the improvement in gait speed was the adjustment of
the task difficulty to address the gait abnormality due to the ataxic
hemiplegia, and repeating gait training with an inverted pendulum model.
We concluded that providing repeated gait training with a flexible knee
brace and GSD to construct the inverted pendulum model may improve the
gait abnormalities and speed in patients with ataxic hemiparesis.
What has your doctor found out about how many and what kind of perturbations are needed for your fall prevention and balance stability? OR HAS YOUR DOCTOR DONE NOTHING, LIKE USUAL? Are you expected to figure this out on your own?
Damage to the cerebellum can
affect neural structures involved in locomotion, causing gait and
balance disorders. However, the integrity of cerebellum does not seem to
be critical in managing sudden and unexpected environmental changes
such as disturbances during walking. The cerebellum also plays a
functional role in motor learning. Only a few effective therapies exist
for individuals with cerebellar ataxia. With these in mind, we aimed at
investigating: (1) corrective response of participants with cerebellar
ataxia (CA) to unexpected gait perturbations; and (2) the effectiveness
of a perturbation-based training to improve their dynamic stability
during balance recovery responses and steady walking. Specifically, we
hypothesized that: (1) CA group can show a corrective behavior similar
to that of a healthy control group; (2) the exposure to a
perturbation-based treatment can exploit residual learning capability,
thus improving their dynamic stability during balance recovery responses
and steady locomotion.
Methods
Ten participants with
cerebellar ataxia and eight age-matched healthy adults were exposed to a
single perturbation-based training session. The Active Tethered Pelvic
Assist Device applied unexpected waist-pull perturbations while
participants walked on a treadmill. Spatio-temporal parameters and
dynamic stability were determined during corrective responses and steady
locomotion, before and after the training. The ANalysis Of VAriance was
the main statistical test used to assess the effects of group (healthy
vs CA) and training (baseline vs post) on spatio-temporal parameters of
the gait and margin of stability.
Results
Data analysis revealed that
individuals with cerebellar ataxia behaved differently from healthy
volunteers: (1) they retained a wider base of support during corrective
responses and steady gait both before and after the training; (2) due to
the training, patients improved their anterior-posterior margin of
stability during steady walking only.
Conclusions
Our results revealed that
participants with cerebellar ataxia could still rely on their learning
capability to modify the gait towards a safer behavior. However, they
could not take advantage from their residual learning capability while
managing sudden and unexpected perturbations. Accordingly, the proposed
training paradigm can be considered as a promising approach to improve
balance control during steady walking in these individuals.
1Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
2Institute of Medical Biometry and Epidemiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
3Department of Neurology, Charité, University of Medicine Berlin, Berlin, Germany
Background: The aim of this prospective
study was to investigate clinical deficits of patients with isolated
cerebellar stroke applying a dedicated clinical score, the modified
International Cooperative Ataxia Rating Scale (MICARS) and identifying
factors that influence recovery.
Methods: Fifteen patients with acute
isolated cerebellar stroke received a standard stroke MRI on the day of
admission and were clinically assessed using the mRS, NIHSS and the
modified International Cooperative Ataxia Rating Scale (MICARS) on day
1, 3, 7, 30, and 90. A generalized linear model for repeated measures
was employed to analyze the effect of stroke lesion location, volume,
days after stroke, patient age, and MICARS score at admission on the
total MICARS score.
Results: Median patient age was 54
years, lesion location in most cases was right (87%) and in the PICA
territory (11/15). Median lesion volume was 3.2 ml. Median NIHSS was 1.
The median MICARS decreased from on day 1 with 23–4 at day 90. The
generalized linear model identified MICARS score at day 1, lesion
location, days after admission and the interaction of the last two on
the total MICARS score, whereas there was no significant effect of
stroke volume or patient age.
Conclusions: Isolated cerebellar stroke
can present with low NIHSS while more specific scales like the MICARS
indicate a severe deficit. Patient age at onset of stroke and lesion
volume had no significant effect on recovery from cerebellar symptoms as
opposed to severity of symptoms at admission and lesion location.
Introduction
Acute cerebellar stroke is a relatively rare subtype of
acute stroke representing approximately 3% of all ischemic and
hemorrhagic strokes (1, 2).
Clinical symptoms of cerebellar stroke are manifold and can be subtle
so that they are often not recognized at hospital admission (2).
Symptoms are frequently underestimated or missed by standard clinical
stroke scores such as the National Institutes of Health Stroke Scale
(NIHSS). Dedicated clinical scales such as the MICARS are available (3) but not widely used in routine stroke diagnostic and treatment.
Imaging of cerebellar stroke also may be challenging.
Whereas small ischemic lesions in the cerebellum are detectable by
magnetic resonance diffusion weighed imaging (DWI), identification may
be difficult or impossible on computed tomography (CT) (4).
Missed diagnosis of cerebellar stroke is not only detrimental to the
diagnostic work up of stroke etiology of individual patients but can
also lead to serious complications (4).
Studies addressing the clinical course and functional
outcome of patients with isolated cerebellar stroke are scarce, and
little is known about factors that influence recovery from isolated
cerebellar stroke. Therefore, we aimed to investigate the clinical
course and prognostic factors of clinical deficits caused by isolated
ischemic cerebellar stroke confirmed by Magnetic resonance imaging (MRI)
in a prospective study applying a dedicated cerebellar symptom rating
scale.
Just in case you have ataxia from your stroke. You can see how long it takes for your doctor to set this up as a protocol. They don't tell you what type of tDCS(anodal tDCS? cathodal tDCS? HD-tDCS?) Electrical Stimulation Helps Ataxia Symptoms
by Judy George, Contributing Writer, MedPage Today
Action Points
Brain and spinal cord direct current electrical stimulation appeared effective in treating symptoms of neurodegenerative ataxia.
Note that the least affected ataxia patients tended to have the greatest benefit.
Direct
current electrical stimulation to the brain and spinal cord appeared
effective in treating symptoms of neurodegenerative ataxia, researchers
in Italy said.
In a double-blind, randomized, crossover trial,
ataxia patients who had transcranial direct current stimulation (tDCS)
showed improvement in all performance areas, motor cortex excitability,
and cerebellar brain inhibition compared with sham stimulation, reported
Barbara Borroni, MD, of the University of Brescia, and co-authors in Neurology.
"We
found that treatment with concurrent cerebellar and spinal electrical
stimulation in patients with ataxia may reduce clinical symptoms,
improve quality of life and restore the physiological inhibition,
mediated by the cerebellum, on the motor cortex," co-author Alberto
Benussi, MD, also of the University of Brescia, told MedPage Today.
"This is of particular relevance in light of limited pharmacologic and
nonpharmacologic treatment options for patients with ataxia."
tDCS delivers a low-voltage electrical current to the scalp or spine. It is non-invasive and has been studied in chronic pain, post-stroke dysphagia, and as adjunctive treatment in bipolar depression.
For most hereditary and sporadic ataxias, no effective treatment
exists. While tDCS has shown promise in posture, gait, and kinetic
functions in ataxia patients, much research focused on the brain alone,
not the brain and spinal cord together.
In this study, researchers studied 20 patients with different kinds
of cerebellar ataxia. Patients were an average of age 55 and had ataxia
an average of 13 years.
They randomized patients 1:1. Each group received cerebello-spinal
stimulation (2 mA for 20 minutes) or sham stimulation for 5 days a week
for 2 weeks; after a 3-month washout period, patients received the
opposite treatment.
At
baseline and follow-up, researchers evaluated cerebello-motor
connectivity with transcranial magnetic stimulation. They used the Scale for the Assessment and Rating of Ataxia (SARA) and the International Cooperative Ataxia Rating Scale (ICARS) to evaluate cerebellar deficits, the 9-Hole Peg Test (9HPT) to gauge finger dexterity and upper limb coordination, and the 8-meter walking time (8MW) to assess gait speed.
Compared with sham, cerebello-spinal tDCS showed a significant
improvement in all performance scores, in motor cortex excitability, and
in cerebellar brain inhibition. In the 8MW test, for example,
participants took an average of 9.4 seconds at baseline and 7.8 seconds 1
month after tDCS treatment. In the 9HPT test, they took an average of
53 seconds at baseline to place and remove pegs from a peg board, and 47
seconds to complete the task 1 month later.
The least affected ataxia patients tended to have the greatest
benefit. "If we consider that repeated sessions of electrical
stimulation have been shown to induce and enhance neuronal plasticity
with long-term after-effects, it is reasonable to believe that patients
who were least affected, and thus with an increased plasticity
potential, might be the ones to benefit the most after this treatment,"
Benussi said.
The effects of tDCS lasted 3 months, but may be lost after that. "On
the basis of this observation, patients should receive stimulation
treatment 5 d/wk for 2 weeks or possibly more, potentially repeated once
a month to maintain effectiveness," wrote Shinsuke Fujioka, MD, of
Fukuoka University in Japan, and colleagues in an accompanying editorial.
While frequent follow-up visits may be challenging for ataxia
patients, portable stimulators might help, they added. But other
problems remain to be solved: "How many times do we treat patients per
time period? What is the best interval between treatments? What is the
optimal stimulus intensity?"
This
trial had a small sample size with a heterogeneous population, so
associations need to be made with caution, the authors pointed out. And
further research is needed to increase the duration and intensity of
improvements, Benussi noted.
"Another important aspect we are trying to figure out is if the
stimulation may improve cognitive symptoms in patients with ataxia,
characterized by deficits in executive functions, spatial cognition and
language, which are frequently overlooked in this patient population,"
he added.
The study was supported by the Italian Association for Alzheimer Research Onlus COOP.
Borroni
and Benussi disclosed no relevant relationships with industry.
Co-authors disclosed relevant relationships with GE Healthcare,
Eli-Lilly, Actelion Ltd Pharmaceuticals, Nutricia, PIAM, Lansgstone
Technology, UCB Pharma, and Chiesi Pharmaceuticals.
Fujioka disclosed relevant relationships with Parkinsonism and Related Disorders, the Polish Journal of Neurology and Neurosurgery,
and support from JSPS KAKENHI. Co-authors disclosed relevant
relationships with Acadia Pharmaceuticals, Gerson Lerhman, Coleman
Research Group, and the Michael J. Fox Foundation.
Reviewed by Robert Jasmer, MD
Associate Clinical Professor of Medicine, University of California,
San Francisco and Dorothy Caputo,
MA, BSN, RN, Nurse Planner
The ataxia gait is also possible post-stroke but this research does nothing to help. All it does is analysis, NO suggestion on how to solve the ataxia problems. You are on your own once again.
It is quite difficult to
evaluate ataxic gait quantitatively in clinical practice. The aim of
this study was to analyze the characteristics of ataxic gait using a
triaxial accelerometer and to develop a novel biomarker of integrated
gate parameters for ataxic gait.
Methods
Sixty-one patients with
spinocerebellar ataxia (SCA) or multiple system atrophy with predominant
cerebellar ataxia (MSA-C) and 57 healthy control subjects were
enrolled. The subjects were instructed to walk 10 m for a total of 12
times on a flat floor at their usual walking speed with a triaxial
accelerometer attached to their back. Gait velocity, cadence, step
length, step regularity, step symmetry, and degree of body sway were
evaluated. Principal component analysis (PCA) was used to analyze the
multivariate gait parameters. The Scale for the Assessment and Rating of
Ataxia (SARA) was evaluated on the same day of the 10-m walk trial.
Results
PCA divided the gait
parameters into four principal components in the controls and into two
principal components in the patients. The four principal components in
the controls were similar to those found in earlier studies. The second
principal component in the patients had relevant factor loading values
for gait velocity, step length, regularity, and symmetry in addition to
the degree of body sway in the medio-lateral direction. The second
principal component score (PCS) in the patients was significantly
correlated with disease duration and the SARA score of gait (ρ = −0.363, p = 0.004; ρ = −0.574, p < 0.001, respectively).
Conclusions
PCA revealed the main
component of ataxic gait. The PCS of the main component was
significantly different between the patients and controls, and it was
well correlated with disease duration and the SARA score of gait in the
patients. We propose that this score provides a novel method to assess
the severity of ataxic gait quantitatively using a triaxial
accelerometer.
I bet your doctor will never suggest this solution for your ataxia from your stroke. It is too damned difficult to translate an intervention for MS to one for stroke. http://www.medpagetoday.com/mastery-of-medicine/neurology-mastery-in-ms/61506?
A rehabilitative dance program based on classical ballet improved
ataxia among multiple sclerosis (MS) patients in a pilot study,
researchers reported here.
Among the six patients enrolled in the program, all had significant
improvements on most measures of the International Cooperative Ataxia
Rating Scale (ICARS), Citlali Lopez-Ortiz, PhD, of the University of Illinois at Urbana-Champaign, and colleagues reported at the Society for Neuroscience meeting here.
"Animal models have shown that exercise increases myelination," Lopez-Ortiz told MedPage Today.
"We think this sort of more heavily loaded, whole body exercise might
be pushing some of the mechanisms that are improving conduction in MS so
that we see improved coordination and reduction in ataxia."
The benefit of exercise and rehabilitation has been established, but
there has been little focus on improving agility and smoothness of
movement in exercise interventions for those with MS, the researchers
said.
So they developed a targeted exercise intervention based on classical
ballet training with the goal of improving agility, balance, ataxia,
and smoothness of movement in MS. The program relies on knowledge about
the nature of motor impairment and sensory processing as well as on the
whole body movement associated with conservatory training in classical
ballet, Lopez-Ortiz said.
"We think dance is important because it uses music, and research has
identified that there is an effect of entrainment facilitation of
movement when a rhythm is given to you. Dance couples music and movement
intrinsically. Also, classical ballet has a high cognitive demand,
involving the entire body all the time. Of all possible forms of dance,
it is the most demanding, but it creates the most dexterous people on
the planet. It's a technique that has been developed over 500 years, and
over that time people have been able to identify what really works in
training the motor system."
The researchers enrolled six patients with MS, ages 49 to 65, with
Expanded Disability Status Scale (EDSS) scores ranging from 4.5 to 6.5
-- indicating walking impairment -- into the 16 week pilot study that
involved two hour long classes per week.
The
primary investigator, who has a Bolshoi Ballet Academy Teacher
Certification and neuromuscular rehabilitation expertise, led the
classes.
Balance was assessed using the Mini-BESTest, and ataxia was measured on the International Cooperative Ataxia Rating Scale.
Smoothness of gait was measured by calculating s-indexes of 29
reflective markers placed on anatomical landmarks of the body in a 5
meter walk test.
Overall, the researchers found that gait smoothness significantly
improved on all measures at all locations, including the upper arm,
elbow, upper leg, and knee.
Patients also had a significant, 42%, improvement on the
Mini-BESTest, which Lopez-Ortiz noted far surpassed results in the
literature for other exercise interventions.
"Previous
literature on exercise interventions in MS shows improvements of about
10% to 15% in balance and walking ability in early-stage disease," she
told MedPage Today. "In this study, although it's a pilot and
we're still collecting data, we see improvement of 42% in balance and
walking ability combined."
The team also found a benefit for ataxia, with significant
improvement on all measures of ICARS (including posture and gait and
kinetic), with the exception of the oculomotor test.
Lopez-Ortiz noted that dance provides motivation, social
interactions, emotional expression, music, and targeted physical tasks
in a single program centered on movement rehabilitation. Also, the cost
of dance is a fraction of that of traditional pharmacological
interventions for MS, she pointed out.
Next steps include doing a larger clinical trial, as well as digging further into the potential mechanisms behind the benefits.
Lopez-Ortiz said that the team has also tested this dance program in
children with cerebral palsy and adults with Parkinson's disease, and
has seen improvements in movement quality as well as clinical
improvements "that make a difference in peoples' lives. Most commonly,
it improves balance, but it also improves measures of coordination and
movement in general."
The study was supported by the National Multiple Sclerosis Society.
Lopez-Ortiz disclosed no financial relationships with industry.
Reviewed by F. Perry Wilson, MD, MSCE
Assistant Professor, Section of Nephrology, Yale School of Medicine
and Dorothy Caputo, MA, BSN, RN,
Nurse Planner
A nicotinic drug approved for smoking cessation significantly improved the walking ability of patients suffering from an inherited form of ataxia, reports a new clinical study led by University of South Florida researchers.
The randomized controlled clinical trial investigated the effectiveness of varenicline (Chantix) in treating spinocerebellar ataxia type 3, or SCA3. The findings were published online earlier this month in Neurology, the journal of the American Academy of Neuroscience.
Lead author Dr. Theresa Zesiewicz and colleagues at the USF Ataxia Research Center collaborated with researchers from Beth Israel Deaconess Medical Center in Boston, MA, and from the David Geffen School of Medicine at UCLA in Los Angeles, CA.
Spinocerebellar ataxia impairs the brain and spinal cord causing progressive difficulty with coordination of movements, including walking. The uncoordinated movements, or ataxia, is a neurological symptom with no treatment or cure and can lead to serious fall-related injuries.
"This is the first clinical trial in patients with ataxia showing that nicotinic acetycholine agonists improve symptoms associated with the ability to stand straight and walk," said Dr. Zesiewicz, professor of neurology and director of the USF Ataxia Research Center. "Patients receiving varenicline could walk with more ease, with less help and faster than those in the placebo group."
The double-blind multicenter study evaluated 20 adult patients with genetically confirmed SCA3. Half the patients received 1 mg. of varenicline twice a day, and the other half received placebo. At the end of the eight-week study, patients taking varenecline performed significantly better on measures of gait, stance, rapid alternating movements and a timed 25-foot walk than those who did not. The drug was fairly well tolerated, with mild nausea being the most common side effect.
The study authors suggest that varenicline's ability to improve ataxia may be associated with the drug's ability to act at several different sites in the brain affected by nicotine.
Study co-author Lynn Wecker, PhD, a distinguished research professor at USF Health, is investigating the cellular and molecular mechanisms mediating the effects of varenicline and other nicotinic agonists. Dr. Wecker and colleagues, supported by a five-year grant funded by the National Institute of Neurological Disorders and Stroke, have shown that several drugs affecting neuronal nicotinic receptors improve gait and balance in an animal model of SCA3.
Further preclinical research is needed to understand how nicotinic acetylcholine agonists improve ataxia, and larger clinical studies with more patients are needed to identify other neurodegenerative diseases that may benefit from nicotinic medications, the authors conclude.
Alina Nickel
Bastian Cheng
Hans Pinnschmidt
Emine Arpa1, 
Christos Ganos
Christian Gerloff
Götz Thomalla