Ask your doctor why incompetence reigned and they did nothing with all this earlier research. Then call the president and ask when competent staff will be installed in the hospital. Because if they did nothing they are incompetent in my opinion! There is absolutely no excuse for not keeping up-to-date on research! Ask your doctor if googling this; 'focal muscle vibration therapy device' will get you the right device to buy.
focal muscle vibration (3 posts to May 2020)
Focal Muscle
Vibration (fMV) for Post-Stroke Motor Recovery: Multisite
Neuroplasticity Induction, Timing of Intervention, Clinical Approaches,
and Prospects from a Narrative Review
1
IRCCS Fondazione Don Carlo Gnocchi, 20148 Milan, Italy
2
Physical Medicine and Rehabilitation Division, Umberto I Hospital, 00185 Rome, Italy
3
Department of Human Neurosciences, “Sapienza” University of Rome, 00185 Rome, Italy
4
Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
5
Department of Chemistry and Drug Technologies, “Sapienza” University of Rome, 00185 Rome, Italy
6
Department of Neurology, Fatebenefratelli Hospital—Gemelli Isola, Isola Tiberina, 00186 Rome, Italy
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work and share the last authorship.
Vibration 2023, 6(3), 645-658; https://doi.org/10.3390/vibration6030040
Received: 5 July 2023
/
Revised: 1 August 2023
/
Accepted: 4 August 2023
/
Published: 8 August 2023
Abstract
Despite newly available therapies for acute stroke
and innovative prevention strategies, stroke remains the third leading
cause of disability-adjusted life-years (DALYs) lost worldwide, mostly
because more than half of stroke survivors aged 65 and over exhibit an
incomplete functional recovery of the paretic limb. Given that a
repeated sensory input is one of the most effective modulators of
cortical motor and somatosensory structures, focal muscle vibration
(fMV) is gaining growing interest as a safe, well-tolerated, and
non-invasive brain stimulation technique to promote motor recovery after
stroke with a long-lasting and clinically relevant improvement in
strength, step symmetry, gait, and kinematics parameters. In this
narrative review, we first summarize the structural (neural plasticity)
and functional changes (network relearning) triggered by the stroke
lesion and carried out at a brain and spinal cord level in an attempt to
recover from the loss of function. Then, we will focus on the fMV’s
plasticity-based mechanisms reporting evidence of a possible
concurrently acting multisite plasticity induced by fMV. Finally, to
understand what the most effective fMV rehabilitation protocol could be,
we will report the most recent evidence regarding the different
clinical approaches and timing of the fMV treatment, the related open
issues, and prospects.
1. Motor Recovery after Stroke and Neuroplasticity: From Stroke Lesion to Network Relearning
In
the last three decades, stroke has become a dramatic fast-growing
burden in the world. From 1990, the absolute number of cases increased
substantially as well as incident strokes (70.0%), deaths from stroke
(43.0%), prevalent strokes (102.0%), and disability as expressed by
disability-adjusted life-years lost—DALYs (143.0% DALYs) [1].
Despite newly available therapies for acute stroke and innovative
prevention strategies, stroke still remains the second-leading cause of
death, with an estimated global cost of over US$ 721 billion due to incomplete recovery [2] and frequent comorbidities [3,4,5].
Post-stroke
motor impairment represents a great part of this burden since, to date,
stroke remains the third leading cause of disability, and more than
half of stroke survivors aged 65 and over exhibit an incomplete
functional recovery after stroke with reduced mobility [2].
Motor recovery after stroke consists of improvement in two domains [6,7].
The first is the so-called “true recovery”, which refers to the
improvement of body function and structures, and the second is the
compensation, which indicates the patient’s ability to accomplish a goal
through adaptation of remaining elements or substitution with a new
approach. While the latter also depends on implicit and explicit
compensatory strategies, true recovery mainly depends on neuroplasticity
[8,9],
which consists of the brain’s natural property to reorganize, changing
properties, structures, and pathways to acquire or improve skills.
Neuroplasticity
can be defined as “adaptive plasticity” if the subtended plastic
changes facilitate full recovery of an involved function, whereas, in
the case of incomplete recovery or the occurrence of unwanted symptoms
(e.g., pain, compensatory movement patterns, and delayed-onset
involuntary movements) [10], it is called “maladaptive plasticity” [11,12,13,14,15].
Specifically, a growing body of evidence from neuroimaging and
neurophysiological studies shows that incomplete motor recovery after
stroke may be the result of maladaptive structural and functional
changes in perilesional and remote regions triggered by the focal brain
lesion. These maladaptive changes may lead to functional disconnection
in the apparently intact perilesional brain areas and to an altered
balance of excitatory and inhibitory influences within the motor
network, both in the affected and unaffected hemisphere [10,16,17,18].
It is worth noting that even though maladaptive changes hinder
functional recovery, they also represent the brain’s attempt to restore a
function loss through neuroplasticity and thus are susceptible to
recovery through plasticity-based rewiring [18].
In
this scenario, understanding both the structural and functional changes
that occur soon after a stroke and the mechanisms underlying motor
recovery, represents the fundamental basis for optimizing rehabilitative
interventions that can condition the dysfunctional cerebral structures
and network by enhancing the adaptive plasticity and even modulating the
maladaptive one [10,19,20].
After
a brain injury such as a stroke, the plasticity-based attempt to
recover the function loss involves three distinct but partially
overlapping phases [21]:
reversal of diaschisis with cell genesis and repair, functional
neuronal plasticity (e.g., changing properties of central monoaminergic
neuronal pathways) [22,23],
and neuroanatomical plasticity (i.e., the capability to establish and
consolidate new neural networks in response to a change in the
environment) [24].
Even though these changes occur both at a cortical and a peripheral
level, they mostly involve the cortex, the ideal site for the plasticity
to take place [25].
To
describe in detail all the mechanisms underlying brain plasticity goes
beyond our purpose. Therefore, we will mainly focus on synchronous
electrical hyperactivity that represents a measurable change observed in
several cortical areas as an immediate response to stroke and, most
importantly, it can be susceptible to modulation by non-invasive brain
stimulation techniques (NIBS) such as focal muscle vibration (fMV).
Being
responsible for the facilitation of activity-dependent plastic change,
cortical hyperactivity represents the electrical expression of neuronal
plasticity, which depends on the peculiar ability of neocortical neurons
to modify their response properties following prolonged alteration in
input activity [26].
Early
cortical hyperactivation can promote post-stroke plastic changes by
enhancing the synaptic activity that produces a long-lasting increase in
signal transmission between two neurons (i.e., long-term potentiation,
LTP). The GABA receptor’s downregulation and the NMDA receptor’s binding
site enhancement, both linked to LTP-related cellular plasticity
together with metabotropic and AMPA glutamatergic receptors, have indeed
been described as peculiar to the hyper-activated damaged cortex.
Besides
synaptic remodeling, synchronous electrical hyperactivity can also
promote axonal sprouting, which in turn plays a pivotal role in
promoting neuroanatomical plasticity, i.e., the capability to recruit
additional cortical regions to establish and consolidate new neural
networks and to even facilitate subsequent refocusing towards a shifted
sensorimotor cortical representation [24,27].
In the specific, the ischemic lesions induce both long-distance cortico–spinal axonal sprouting [28] and horizontal axonal sprouting between previously non-connected areas [29].
From
a functional and even “teleological” point of view, the role of changes
in perilesional and remote brain regions (i.e., in both the affected
and in the unaffected hemisphere) triggered in the very acute phase by
the focal brain lesion, as well as the role of the recruitment of remote
or secondary brain structures, is not completely understood [16,17,30].
In
general, this compensative recruitment is not “maladaptive” because
stroke patients with greater motor impairment show stronger recruitment
of secondary brain structures, and the disruption of these areas through
transcranial magnetic stimulation (TMS) has demonstrated that their
recruitment is functionally significant [31]. Nevertheless, it leads to an incomplete recovery [32]
because stroke patients with poorer recovery have a stronger (i.e.,
more widespread and often bilateral) cortical over-activation and a
greater amount of previously “silent” region recruitment [33].
A possible explanation is that the projections from ipsilateral neurons
located in non-primary motor areas are less numerous and less efficient
at exciting spinal cord motor neurons than those from M1 [27,34,35].
Moreover, the integrity of the lesioned hemisphere’s motor cortex
(ipsilesional M1) is related to better post-stroke motor recovery [34,36,37], so the modulation of ipsilesional M1 became one of the most effective targets for rehabilitation therapy [38,39].
In this sense, repetitive focal muscle vibration (fMV) represents a
very effective neuro-rehabilitative intervention that can induce
prolonged changes in the excitatory/inhibitory state of the primary
sensorimotor cortex directly acting on the paretic limb.
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