Neurorrehabilitation from the point of view of neuro plasticity
The action carried out by the human being is based. For many years, CNS was considered a functionally immutable and anatomically static structure.
The scientific advances achieved in Neuro Plasticity, with the application of modern technologies, has strengthened interest in the study of the plasticity of the nervous system, after brain lesions of diverse etiologies, neuro plasticity is the property of the nervous system of modifying its operation andTo reorganize in compensation to environmental changes or injuries, the most frequent cause of motor disability in adults are vascular accidents (stroke) and cranioecephalic traumas, the recovery of the injury that takes place after weeks, months or years is related to certainPhenomena such as: dendritic growth, the formation of new synapses, functional reorganization in the injured area, or the participation of other neighboring areas or homologous of the contralateral hemisphere.
One of the most frequent pathologies of alteration of motor sensitive pathways are vascular stroke, this type of injury causes very varied morphofunctional alterations according to various factors such as the injured area, the type of stroke, etc. After the occurrence of a stroke, a complex reorganization pattern in the different stages of this picture, this due to the activation of histological, neurochemical and neuroplastic mechanisms,
Pathophysiology and anatomopathologist of the ischemic vascular accident
Vascular occlusion brings with it a waterfall of chemical events produced by a dynamic interaction between neurons, astrocytes, fibroblasts, smooth and endothelial muscle cells, which in turn interact with the elements of the blood and lead to cell death by hypoxia or ischemia.
Hypoxia and cerebral ischemia can be divided according to clinical criteria in focal or multifocal ischemia by vascular occlusion;Global ischemia due to total cardiovascular pumping and decrease in irrigation and diffuse hypoxia dueOf collateral blood vessels, in the transition zones between the tissue with normal irrigation and the central nucleus with severe ischemia, the blood flow is reduced moderately, this moderately ischemic tissue ring is called ischemic gloom and although the brain cells in thisregion remain viable for longer than the ischemic nucleus cells, both will die if the suppression of the proper blood flow continues.
Focal cerebral ischemia sufficient to cause clinical signs or symptoms is 15 to 30 minutes, causing an irreversible lesion in specific, very vulnerable neurons, if the ischemia lasts an hour or more, the infarction of part or the entireAffected vascular territory, brain damage dueGlobal cerebral ischemia for more than 5 to 10 minutes is usually incompatible with the recovery of consciousness in north thermal people.
In the tissue with severe ischemia, they remain sufficient high energy compounds to preserve normal function only a few seconds, and glycogen, glucose, phosphocreatine and ATP are exhausted in a few minutes, shortly after the tissue begins to lose its structural integrity.
With the failure of energy -dependent pumps, the membranes of neuronal and glial cells are depolarized and allow the entry of sodium and calcium and the output of potassium ions, the high intracellular calcium originates an abrupt depolarization of the membrane, the intenseNeuronal membrane depolarization conditions the release of excessive quantities of glutamate and other exciting neurotransmitters9 and inhibitors, which can further exacerbate the lesion.
Glutamate stimulates membrane receptors such as NMDA (N-Methyl-Kida), which is responsible for the remarkable increase in CA and the implementation of the ischemic waterfall, which originates cell death, the increase of CA is a factorKey in the processes that lead to irreversible neuronal damage, since it activates a series of enzymes that condition the expression of several immediate response genes, glutamate is the most powerful biochemical predictor of progressive cerebral infarction;Plasma levels greater than 200: m/l in the first 24h since the beginning of the symptomatology, predict the deterioneurological with a 92% probability
Ischemic gloom and therapeutic window zone
The obstruction of a cerebral blood vessel causes 2 types of neuronal tissue injuries, immediate and late, this situation offers a useful period of several hours for the rescue of the neurons called, ischemic penumbra zone, thus enabling theReversion of the initial neurological deficit and the preservation of brain tissue. It is considered as the only treatable area, its duration determines the time when effective therapeutic measures could be applied.
Logically, the period of time during which the gloom persists, represents a potential therapeutic opportunity window, the viability of cells in the penumbra area has limited time since the decrease in oxygen and glycogen reserves trigger various pathological processes, that lead to brain death, the gloom has been delimited as an encephalic area with an increase in the oxygen extraction fraction and it is shown that the volume of gloom that escapes the final volume of infarction is highly correlated with neurological recovery.
Glia cells in cerebral ischemia
Astrocytes play a fundamental role in stroke, both in the establishment of the definitive lesion, and in the tissue repair23. During ischemia, astrocyte edema is the first observed morphological change, being one of the factors responsible for the decrease in glutamate reuptake, glial cells that survive the ischemic episode suffer a process of hypertrophy and proliferation, known as gliosisreactive, which has been related to neuro mechanisms protection and repair of ischemic lesions.
Neuro plasticity and neurorrehabilitation
Scientific research and clinical practice in patients with CNS injury, has allowed to recognize the possibility of partial or total recovery of lost functions, observing some restitution of the function of the affected areas, for which various mechanisms such as such mechanisms have been postulatedAs axonal and dendritic growth, establishment of new synapses, changes in the operation of the existing ones and the increase in activity of parallel to the injured, these being spontaneous mechanism or generated by the therapeutic intervention, it has been shown that the nervous system isremode it continuously throughout life and after ACV damage, through experience and learning in response to activity.
Functional plasticity
According to Grafman and Litvan (1999), in the human being, evidence of at least four forms of functional plasticity has been observed:
- The adaptation of homologous areas (contralateral, by disinhibition mechanism).
- Plasticity of cross modalities (reallocation of functions to an area not primarily intended for
- process a particular modality).
- The expansion of somatotopic maps (functional reorganization).
- Compensatory unmasking (disinhibition – functional reorganization).
These forms of plasticity are nothing more than expressions of the reinforcement factors of synaptic activity, readjustment of inhibition and disinhibition in the cortical circuit and, probably, the establishment of new synapses as a result of the emergence of new dendritic and axonal collaterals.
Functional plasticity
According to Grafman and Litvan, there have been evidence of at least four forms of functional plasticity:
- The adaptation of homologous areas (contralateral, by
- disinhibition mechanism).
- Plasticity of crossed modalities (reallocation of
- functions to an area not primarily intended for
- process a particular modality).
- The expansion of topical somato maps (functional reorganization).
- Compensatory unmasking (disinhibition – functional eorganization).
- In the particular case of motor lesions, accessory roads can be.
- Fibers preserved in the previous and posterior arms of the internal capsule and in the brain trunk.
- The ipsilateral motor cortex next to the direct pyramidal beam (not decused). This has been corroborated by transcranial magnetic stimulation and PET, with measurement of the regional cerebral flow.
- Multiple parallel systems with overlap of cortical areas and connections with medulla.
Another functional recovery mechanism is what is known as level transfer, which can be from a lower than one lower level, or vice versa, in the case of motor lesions, the transfer can be from a higher volitional level of movement to a lower oneAutomated, thus, in case of paresis of a superior member due to cortical lesion, which prevents the patient from making volitional movements with said member, more consolidated forms of activity are used, such as automatic movements of both members, inserted in combined actions (work therapy, ludotherapy). Transfer of a lower level of a higher movement is what can be seen in the rehabilitation of subcortical lesions with hemiparesis.
Synaptic plasticity
Initially, synapsis were considered immutable in their functional properties as welding points between the components of an electrical circuit, studies carried out later, have been demonstrating the plastic properties of synapse32, these plastic capabilities of synaptic connections can be expressed in a different way according to their Duration and the mechanisms involved, for example, there are mechanisms that lead to transitory changes in synaptic efficacy in the order of milliseconds to minutes example of these mechanisms are facilitation or inhibition by paired pulses and post -static potentiation other more lasting forms such as the so -called Long -term potentiation (LTP) is considered the best model of functional change in synaptic connectivity dependent on the activity The LTP implies stable structural changes and depends on various mechanisms such as: the creation of new synapses by growth and expression of dendrites aimed at helping to recover the function; the functional reorganization in the damaged area itself, changing the nature of its preprogrammed function to facilitate adequate functioning; and the participation of neighboring or collateral areas to replace the function by functional reorganization of the cortex, perhaps through the disinhibition of redundant roads and circuits.
LTP mechanisms
Morphological changes: there is evidence that in late phases (greater than 8 hours), detectable changes in the morphology of synapses that could be involved in the LTP may appear. For example, an increase in the number of perforated synapse has been observed, with divided transmission areas that later become double dendritic spines37 which, apparently, represent a local synaptic proliferation process the succession of mechanisms involved in the LTPbegins with changes in the functional area and culminates with growth processes.
- Presynaptic Changes: You can achieve more synaptic efficacy through:
- Increase in the amount of neurotransmitter released by the presynaptic terminal.
- Increase in the affinity of postsynaptic receptors by neurotransmitter.
- Increased postsynaptic receptors density.
The mechanisms described so far take place, and mainly affect the post-synptic components, which does not exclude the participation of presynaptic elements. The LTP presynaptic component requires the activation of postsynaptic neurons to occur. It has been proposed that the postsynaptic neuron releases a messenger that disseminates retrogradely to the presynaptic terminal and there causes the changes.
Cortical plasticity
Several forms of the neuroplastic process in the human brain have been described, plasticity can follow three processes.
- PLASTICITY OF THE MOTOR MAP OF THE INFARATED PERITIES AREAS.
- The increase in activity in areas of the injured hemisphere, such as the supplementary area42, or the premoTor cortex.
- The neuroplastic changes of the ipsilateral hemisphere to the most affected body part.
Studies in the visual cortex have documented the importance of plastic processes in the development of the functional capacities of this system44. Similar mechanisms operate in other areas such as somatosensory, motor, auditory and association areas.
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