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Friday, April 25, 2014

Adult brain and neuro-plasticity

As I have been sharing in other posts, plastic capacity of young brains has been tirelessly studied, but what does happen with the neuroplasticity of the adult brain?, are brain structures modifiable?. 

 It is known that there are critical periods which depend on the explosion of neural connections and they decay during lifetime, however, new research show a different vision, and now is said that is never too late to make a brain learn new tricks. 

  For example, according to preliminary studies in the laboratory of Michael Merzenich of the University of California at San Francisco, who is a pioneer in the understanding of plasticity, memory in pre senile individuals can, with the help of training, be dramatically rejuvenated, and his studies show that plasticity has no limits. Some times even if areas of the cortex, e.g. Broca's area are destroyed by a stroke, a brain attack or a brain tumor, patient is likely to recover function once moved the circuit affected by others who may have other capabilities (Shreeve2005).

Something remarkable both neurogenesis, synaptogenesis is the direct relationship between increased mental activity and physical exercise, which suggests that people could reduce the risk of neural diseases and thereby help to repair brain processes choosing mental challenges and a physically active life, that’s the reason a majority of researches are running environmental stimulation as an important part of the recovering process, demonstrating that the environment can affect on the brain structure, which opens up the possibility a complete new field on areas as architectural designs which could modify the way they build  homes, offices and schools in order to allow more enriched environments that seek better cognitive functioning.

But what about brains who suffers an injury?, current research indicates that plasticity exists, during the pre and post natal, recognizing the existence of critical periods to make this happens, however, once the synaptic connections are established and they break or deteriorate, the pattern of cortical reorganization  the functional recovery of different capabilities is not the same, while the basic mechanisms of plasticity are shared by all the cortex.

However, there are peculiarities in the patterns of recovery depending on the type of injury, mainly finding the following modalities: linguistic and sensory motor, neuropsychological injuries

Regarding the recovery of a motor injury, it is known that  structures of the cerebral cortex is constantly changing in response to training, or behavioral and motor acquisitions. It is thus that the construction of functional maps of motor areas that have been made possible thanks to the use of three neuroimaging techniques: Transcranial magnetic stimulation: which is one way not-invasive stimulation of the cerebral cortex, it’s one of the latest tools that have built-in neuroscience, both for purposes of study and research; functional magnetic resonance imaging: which are a type of magnetic resonance imaging in which the response is measured hemodynamics (blood flow) related to the neural activity in the brain or spinal cord; also we can find the Positron Emission Tomography: which is a technique used on nuclear medicine that produces a three-dimensional image of the body's functional processes,  these techniques that have made possible the understanding of the way in which the motor cortex adapts and changes in response to injury and therapeutic intervention.

Studies conducted in people with central hemiplegia, show that functional recovery through rehabilitation, produces mechanisms of plasticity that differ depending on the timing of the injury.

When the injury requires a longer recovery time and therefore more long-term treatment, permanent changes in the cerebral cortex are generated. In most of the cases new motor routes are created starting  at the motor cortex in the healthy hemisphere and are directed in a ipsilateral manner (contrary), in a way that takes place the functional recovery of the affected side. While in other less numerous group of patients, new axons from the motor cortex not damaged are wrongly projected bilaterally, producing a less functional recovery with intense movements in mirror, this is an example of wrong adaptive plasticity where the patient moves the left hand, at the same time that moves right hand (Diaz-Arribas, Pardo-Hervas, Tabares-washing, Rios-lago and Maestu, 2006) . 

Talking about linguistic recovery, neurobiological studies provide data corresponding to language and its configuration in a certain moment of neurodevelopmental, have allowed increasingly better understand the role of language and their behavior after injury.

In this sense it is known that children around 4 years old have very well located the representation of language in the left hemisphere, in the majority of cases, virtually unchanged in the adult. However, these studies have found evidence that brain cortex involved in linguistic functions is also sensitive to the experience, so the centers related to the language processes  are not stable over time, and expand or contract depending on the experience, since new words are learned or  we stop employ others throughout our life.

Apparently, this area is initially broader throughout the perisylvian areas, which are focusing as it reaches the competence in the language, on the basis of increased complexity and level of specialization, in such a way that the peripheral areas which originally related to the language retains this ability as a secondary capability latent, capable of supplementing or completing the linguistic function in case of injury of the primary area (Hernandez-Muela, Mules, and Mattos, 2004).

However, it is worth mentioning that lesions of the left hemisphere are associated with greater involvement of the normal activity of the right hemisphere and an atypical asymmetry in activations of the perisylvian during linguistic activities area, to a greater extent when the injury takes place in early stages, that when it happens at later stages in life (Gage, 2007).

In this way, as a result of brain plasticity that happens after injury occurred in early stages, diverse studies have been found an increase in the prefrontal, frontoparietal and lower bottom regions activation, for expressive language, and inferior temporal, temporary front and temporary regions for the receptive language. Probably, because these structures are related with the area responsible for functions associated to the language in early stages, that with the maturing and growing complexity of the neural connections, so these are free depending on the type of tasks, but retain this ability, latent form to resume its function in case of later injury (Gollin, 1981; Maciques, 2004; Tubino, 2004; Ginarte, 2007).

In this sense, an early lesion that took place before the first year of life, leads to an extensive reorganization both of the right and left hemisphere, this is known as adaptive plasticity, as occurs in the motor cortex, but there is evidence of plasticity in the regions responsible for the language after a neurological damage, may be different in the case of the motor domain (Diaz-Arribas, Pardo-Hervas, Tabares-Lavado, Rios-Lago and Maestú, 2006).

However, the plastic changes are not limited only to the motor cortex or the language, but it also occurs in sensory systems. In this regard, an example is the case of hearing, which requires connection with environmental sounds as stimuli and whose processing is important for verbal communication, so it is a decisive step for the acquisition of language. This sensory modality is known that there is an auditory critical period for language acquisition. So was demonstrated in studies conducted in deaf children after application of cochlear implants (Hernandez-muela, mules and Mattos, 2004).

  In this regard, in terms of language difficulties secondary to the existence of a sensory deficit by hearing loss, it is necessary to consider two situations: the first one, is when hearing loss takes place prior to the acquisition of language, in the very early stages, while a second situation occurs when the loss hearing occurs subsequent to the acquisition of the language.

     In the first case, the plasticity will be through a migration of the function, while in the second case, the potentiation will be to more long term and will require the support of cochlear implant (Coplan, 1985; Hernandez-Muela, Mules and Mattos, 2004).

The other sensory aspect to consider is the visual capacity, even tought plasticity of visual fields is not well known, it’s possible to talk about at least two situations, on the one hand, when the visual cortex is damaged by a traumatic injury, and when, despite the strength of the occipital cortex, or if by peripheral reasons, it is not possible to develop the vision.

With respect to the first situation, some descriptive studies show the transfer of function from the visual cortex to adjacent areas on the occipital cortex, such as posterior regions of the parietal and temporal lobes, similar to the hearing process, which is called plasticity by migration (Castroviejo, 1996; Deacon, 2000; Ginarte, 2007).

Talking about the second situation, which presents peripheral blindness, caused by tumors in the optic chiasm for example, may be determinants of blindness at very early stages, it has shown the existence of the so-called mode cross plasticity i.e. Permanent reorganization that allows in principle do not own capabilities to a certain area, which appears to increase or facilitate compensatory alternative perceptions of deficit sensory. These changes involve mechanisms neuroplasticos in which areas that processed certain information, accept, process, and respond to other types of information from different sensory modality (Hernandez-Muela, Mules, and Mattos, 2004; Ginarte, 2007).

This way is usually explained the process of plasticity of occipital cortex from blind children ocurred at early stages, which facilitates and at the same time is result of the learning to read Braille, which creating occipital cortex networks ranging from motor areas that allow the movement of the fingers on the paper, and the areas that usually is used for viewing the letters in compensation by the absence of vision. This widening of the cortical representation of the index finger may be due to two mechanisms: the first, by unmasking of silent connections (increase of synaptic efficacy), in the same area injured or deficient and adjacent, and the second, structural plasticity, while other studies have shown the expansion, in the cortex somatosensory representation of the finger index, fundamental Braille readingwith what it says is that people can "see" through their fingers, as they achieve recognition of shapes and even colors at the touch of a surface (Poch, 2001).


Díaz-Arribas, M., Pardo-Hervás, P., Tabares-Lavado, M., Ríos-Lago, M. y Maestú, F. (2006) Plasticidad del sistema nervioso central y estrategias de tratamiento para la reprogramación sensoriomotora: comparación de dos casos de accidente cerebrovascular isquémico en el territorio de la arteria cerebral media. Rev Neurol. 42 (3): 153-158

Hernández-Muela, S., Mulas, F. y  Mattos, L. (2004) Plasticidad neuronal funcional Rev Neurol. 38 (Supl 1): S58-S68.

Gage, F. (2007) Brain, repairs yourself. In Floyd E, Bloom (2007) The best of the brain from Scientific American: mind, matter, and tomorrow’s brain. Washington DC. Dana Press.
Ginarte, Y. (2007) La neuroplasticidad como base biológica de la rehabilitación cognitiva. Geroinfo. Vol. 2. No. 1. 31-38

Gollin. E. S. (1981) Developmental and plasticity: behavioral and biological aspects of variation in developmental. New York. Academic Press.

Maciques (2004)  Plasticidad Neuronal. Revista de neurología. 2 (3) 13-17.

Poch, M.L. (2001) Neurobiología del desarrollo temprano. Contextos educativos. 4. 79-94.

Shreeve, J. (2005) Cornina’s brain: all she is… is here. National Geographic. Vol. 207. num. 3.  6-12.

Tubino, M. (2004) Plasticidad y evolución: papel de la interacción cerebro – entorno. Revista de estudios neurolingüsticos. Vol. 2, número 1. 21-39.

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