ADAPTIVE NEUROPLASTICITY ASSOCIATED WITH ISCHEMIC BRAIN DAMAGE AND ITS ROLE IN STROKE RECOVERY: THEORETICAL PREREQUISITES FOR EFFECTIVE NEUROREHABILITATION

We don't SPECIFICALLY know why a neuron gives up its' current job and takes on a neighbors. Thus, nothing on neuroplasticity is scientifically repeatable on demand. So, DEMAND your doctor give you EXACT PROTOCOLS to use. Don't allow your doctor to give you generalities or guidelines. This person understands that problem because of the word theoretical instead of detailing exactly how to deliver neuroplasticity exactly.

 ADAPTIVE NEUROPLASTICITY ASSOCIATED WITH ISCHEMIC
BRAIN DAMAGE AND ITS ROLE IN STROKE RECOVERY: THEORETICAL PREREQUISITES FOR EFFECTIVE NEUROREHABILITATION

Khairieva Mukhsina Farkhadovna

Bukhoro davlat Tibbet institutes

THESIS

https://orcid.org/0000-0002-0002-0015

xayriyeva.muxsina@bsmi.uz

https://doi.org/10.5281/zenodo.15227136

Ischemic brain damage, like other pathogenic factors, initiates the

reorganization of cortical centers and pathways outside the "nuclear zone" of

acute or chronic ischemia, which limits the spontaneous restoration of functions

in victims. Accordingly, knowledge of the basic patterns of post-ischemic

neuroplastic remodeling(This doesn't exist yet, so your incompetent doctor needs to get that research going! The problem has been known for decades which is why I consider your doctor incompetent for not even attempting to get it solved. It's as if survivor recovery is not in the job description! And that leads directly to board of directors incompetence for not setting correct goals!) is crucial for developing more effective rehabilitation

strategies for stroke patients. The article discusses modern concepts of

neuroplasticity: the main patterns of post-stroke reorganization of the central

nervous system, studied in rodents, as well as clinical markers of compensatory

and regenerative processes in conditions of chronic cerebral ischemia in

cerebrovascular diseases, which allows us to identify the mechanisms

underlying the remodeling of neural networks in the penumbra and

contralateral hemisphere against the background of ischemic damage. At the

same time, the analysis of electrophysiological experimental data demonstrated

the restructuring of functional connections in both hemispheres far beyond the

focus of cerebral infarction, and clinical and biochemical studies on the model of

chronic cerebral ischemia in patients helped to identify key trophic factors

determining compensatory and regenerative processes. The results obtained

make it possible to justify the use of noninvasive brain stimulation methods and

some pharmacological agents to accelerate the recovery of impaired functions in

patients with this profile, and therefore to form rehabilitation protocols using

robotic devices to promote the development of adaptive neuroplasticity and full-

fledged functional recovery.

In this regard, it seems relevant to analyze the results of recent

experimental and clinical studies that have studied the processes of

neuroplasticity in ischemic brain lesions in order to develop and implement new

rehabilitation strategies.

The term "brain plasticity" or "neuroplasticity" defines all (morphological

and functional) changes in neural networks and glial complexes that occur in the

central nervous system throughout a person's life [9]. These changes are not

only closely related to the mechanisms of learning, development, aging, and

adaptation to the environment, but also underlie adaptive neuroplasticity –

compensatory and regenerative reactions that occur during the formation of

pathomorphological and/or functional disorders caused by diseases or injuries

of the nervous system [10]. In particular, acute ischemia and chronic ischemia

cause multilevel (in the cerebral cortex, the penumbra zone of the affected

hemisphere and the contralateral hemisphere, subcortical and cerebrospinal

regions) neuroplastic reactions of neural networks with temporal and spatial

organization (Figure) [11, 12], and these changes are sensitive to subsequent

damage regardless of their nature [13, 14].

The degree and range of neuroplastic changes depend on the size and rate

of formation of ischemic brain damage (acute or chronic). In microinfarcts

developing in the cerebral cortex against the background of transient ischemic

attacks or chronic cerebral ischemia caused, for example, by small vessel

disease, periinfarction zones can compensate for lost functions in the shortest

possible time, which explains the existence of "mute" strokes [1, 2]. This is

especially true of the ventral premotor region, which, being in close relationship

with the primary motor cortex, produces and releases vascular endothelial

growth factor, which has angiogenic and neuroprotective properties in the early

period after a heart attack [12]. In rodents, after a stroke, there is a steady

reorganization of the motor map of the rostral zone of representation of the

forelimbs (premotor cortex) [2, 3, 4]. Accordingly, the development of secondary

post-ischemic metabolic disorders in it exacerbates the primary motor deficit

[5].

The mechanisms underlying cortical reorganization and restoration of

impaired functions remain not fully understood [1]. This is especially true of the

gamma-aminobutyric acid (GABA) system and neuroglia, which may play an

important role in the control of neuroplastic reactions. So far, it has been

established that the neuroglial matrix, which consists of condensed chondroitin

sulfate proteoglycans surrounding mainly the bodies of GABAergic neurons,

correlates according to the feedback principle with adaptive neuroplasticity and

repair of the brain due to interneurons containing parvalbumin [6]. The

significance of perineuronal networks has been thoroughly investigated during

the maturation of the visual system. They have been found to have a stabilizing

effect on mature neural networks and a negative effect on neuroplasticity [7, 8].

Thus, inhibition of perineuronal networks by injections of the bacterial enzyme

chondroitinase ABC after damage to the central nervous system accelerated the

restoration of sensorimotor functions [3-4], and a spontaneous decrease in the

number of perineuronal networks in the cortex in the penumbra area indicated

an increase in adaptive neuroplasticity [23]. In turn, increased GABAergic

activity after stroke did not improve recovery rates [2], but rather worsened

motor deficits [4]. Moreover, it has been clinically confirmed that an artificial

decrease in GABAergic activity had a positive effect on functional recovery [4].

A special role in the development of neurological deficits in acute and

chronic ischemia and further functional recovery is played by the hemisphere

contralateral to the actual lesion, since animal studies and clinical practice have

well shown that neuronal connections after acute ischemia change not only in

the damaged hemisphere of the brain, but also on the opposite side.

Due to the improvement of scientific methods, it has become possible to

study changes in remote brain regions with local ischemic damage based on the

concept of connectionism within the framework of microscopic (synapses),

mesoscopic (homotopic brain regions) and macroscopic (thalamo-cortical

connections) neuroplastic reactions.

References at link.