MAPEO DE LA PLASTICIDAD CORTICAL EN HUMANOS

Cortical map plasticity in humans

Pascual-Leone A, Cohen LG, Hallett M.

 

Brain 1993 Feb;116 ( Pt 1):39-52


Plasticity of the sensorimotor cortex representation of the reading finger in Braille readers.

Pascual-Leone A, Torres F.

Human Cortical Physiology Unit, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892.

We studied the organization of the somatosensory cortex in proficient Braille readers, recording somatosensory evoked potentials (SEPs) in 10 subjects and using transcranial magnetic stimulation (TMS) in five subjects, and compared the results with those of 15 control subjects. Somatosensory evoked potentials were elicited by a focal electrical stimulus to the tip of the index finger and recorded from a contralateral 4 x 4 grid of scalp electrodes centred around C3' and C4'. Transcranial magnetic stimulation, with an 8-shaped coil centred over the same scalp positions, was delivered simultaneously with, and at different intervals after, the finger stimulus. The results of the right index (reading) finger in Braille readers were compared with those of their left index (non-reading) finger and of the right and left index fingers of the control subjects. The scalp areas from which we recorded N20 and P22 components of the SEP with an amplitude of at least 70% of the maximal amplitude recorded in each trial were significantly larger in SEPs evoked from the reading fingers. Detection of the stimulus applied to the reading finger was blocked by TMS delivered over a larger contralateral scalp area and during a longer time window after the stimulus. These experiments suggest that reading Braille is associated with expansion of the sensorimotor cortical representation of the reading finger.

Transcranial Magnetic Stimulation Enhances Short-Term Brain Plasticity

For the first time, scientists studying how the brain reorganizes itself have shown that they can modify this process using a technique called transcranial magnetic stimulation (TMS). The finding suggests new ways to help people recover normal function after stroke, amputation, and other injuries.

TMS is a non-invasive technique that consists of a magnetic field emanating from a wire coil held outside the head. The magnetic field induces an electrical current in nearby regions of the brain. While TMS is often used to diagnose brain abnormalities, this report shows that it also can influence brain plasticity, or reorganization. This plasticity is thought to be responsible for much of the recovery seen in people who have suffered brain damage due to trauma, stroke, or other problems. The study, conducted by researchers at the National Institute of Neurological Disorders and Stroke (NINDS), is published in the February 1 issue of The Journal of Neuroscience.

Many studies in the last two decades have shown that the brain continually responds to changes in stimuli by reorganizing itself. These changes are often beneficial. For example, people who have been blind from an early age often use part of the brain region normally employed for vision to process sensations from their fingertips, which helps them read Braille. However, in other cases, brain reorganization may lead to problems such as phantom pain, which often develops after amputation. This study suggests that researchers might be able to use TMS or other strategies to enhance plasticity when it is beneficial (as in the blind) and to decrease it when it is harmful (as with phantom pain).

In the new study, researchers Leonardo G. Cohen, M.D., Ulf Ziemann, M.D., and Brian Corwell used a simple tourniquet around the elbow to shut off the blood supply to the forearm, blocking nerve signals to the brain and temporarily mimicking what occurs after amputation. The loss of normal signals caused the brain to reorganize. When the researchers applied TMS to the plastic cortex, or the part of the brain that was undergoing reorganization because of the tourniquet, the brain's responsiveness to stimuli increased, meaning that its plasticity was enhanced. However, when researchers applied TMS to the non-plastic cortex on the other side of the brain, the brain's responsiveness in the plastic cortex decreased. This shows that stimulation of the non-plastic cortex somehow inhibits plasticity on the opposite side of the brain.

"This paper addressed the possibility of modulating reorganization in a non-invasive way," says Dr. Cohen. "The technique used is not as important as the overall concept that we can increase and decrease plasticity." The ability to control brain reorganization after brain damage or injury could allow doctors to accelerate recovery and bring about more successful rehabilitation. Similar strategies could be developed to promote learning, a kind of brain reorganization that occurs every day.

Since the brain reorganization in this experiment occurred rapidly, it probably resulted from short-term strengthening of specific connections between neurons, rather than from sprouting of new connections, Dr. Cohen says. "New techniques or a reformulation of existing techniques might be able to induce more lasting effects," he adds. For example, long-term TMS or drug therapy, combined with practice or physical therapy, may be able to change brain circuitry as well as strengthen connections.

While these results are promising, much more research is needed before these strategies will be ready for clinical use. In most cases, researchers still need to learn whether the changes in brain function that they see after injury play a beneficial role by helping the brain to compensate, or if they are harmful or simply irrelevant, says Dr. Cohen. They also need to understand more about how plasticity occurs so they can design and test new strategies for controlling it.

The NINDS, one of the National Institutes of Health located in Bethesda, Maryland, is the nation's leading supporter of research on the brain and nervous system and a lead agency for the Congressionally designated Decade of the Brain

 

Transcranial Magnetic Stimulation May Help Regain Normal Brain Function

WASHINGTON, MD -- January 29, 1998 -- For the first time, scientists studying how the brain reorganises itself have shown that they can modify this process using a technique called transcranial magnetic stimulation (TMS). The finding suggests new ways to help people recover normal function after stroke, amputation and other injuries.

TMS is a non-invasive technique that consists of a magnetic field emanating from a wire coil held outside the head. The magnetic field induces an electrical current in nearby regions of the brain. While TMS is often used to diagnose brain abnormalities, this report shows that it also can influence brain plasticity, or reorganisation. This plasticity is thought to be responsible for much of the recovery seen in people who have suffered brain damage due to trauma, stroke, or other problems. The study, conducted by researchers at the National Institute of Neurological Disorders and Stroke (NINDS), is published in the Feb. 1 issue of The Journal of Neuroscience.

Many studies in the last two decades have shown that the brain continually responds to changes in stimuli by reorganising itself. These changes are often beneficial. For example, people who have been blind from an early age often use part of the brain region normally employed for vision to process sensations from their fingertips, which helps them read Braille. However, in other cases, brain reorganization may lead to problems such as phantom pain, which often develops after amputation. This study suggests that researchers might be able to use TMS or other strategies to enhance plasticity when it is beneficial (as in the blind) and to decrease it when it is harmful (as with phantom pain).

In the new study, researchers Leonardo Cohen, M.D., Ulf Ziemann, M.D., and Brian Corwell used a simple tourniquet around the elbow to shut off the blood supply to the forearm, blocking nerve signals to the brain and temporarily mimicking what occurs after amputation. The loss of normal signals caused the brain to reorganize.

When the researchers applied TMS to the plastic cortex, or the part of the brain that was undergoing reorganization because of the tourniquet, the brain's responsiveness to stimuli increased, meaning that its plasticity was enhanced. However, when researchers applied TMS to the non-plastic cortex on the other side of the brain, the brain's responsiveness in the plastic cortex decreased.

This shows that stimulation of the non-plastic cortex somehow inhibits plasticity on the opposite side of the brain.

"This paper addressed the possibility of modulating reorganization in a non-invasive way," Dr. Cohen said. "The technique used is not as important as the overall concept that we can increase and decrease plasticity."

The ability to control brain reorganization after brain damage or injury could allow doctors to accelerate recovery and bring about more successful rehabilitation. Similar strategies could be developed to promote learning, a kind of brain reorganization that occurs every day.

Since the brain reorganization in this experiment occurred rapidly, it probably resulted from short-term strengthening of specific connections between neurons, rather than from sprouting of new connections, Dr. Cohen said.

"New techniques or a reformulation of existing techniques might be able to induce more lasting effects," he added. For example, long-term TMS or drug therapy, combined with practice or physical therapy, may be able to change brain circuitry as well as strengthen connections.

While these results are promising, much more research is needed before these strategies will be ready for clinical use. In most cases, researchers still need to learn whether the changes in brain function that they see after injury play a beneficial role by helping the brain to compensate, or if they are harmful or simply irrelevant, Dr. Cohen said. They also need to understand more about how plasticity occurs so they can design and test new strategies for controlling it.

J Neurosci 1998 Sep 1;18(17):7000-7


Mechanisms of deafferentation-induced plasticity in human motor cortex.

Ziemann U, Hallett M, Cohen LG.

Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1428, USA.

Deafferentation induces rapid plastic changes in the cerebral cortex, probably via unmasking of pre-existent connections. Several mechanisms may contribute, such as changes in neuronal membrane excitability, removal of local inhibition, or various forms of short- or long-term synaptic plasticity. To understand further the mechanisms involved in cortical plasticity, we tested the effects of CNS-active drugs in a plasticity model, in which forearm ischemic nerve block (INB) was combined with low-frequency repetitive transcranial magnetic stimulation (rTMS) of the deafferented human motor cortex. rTMS was used to upregulate the plastic changes caused by INB. We studied six healthy subjects. In two control sessions without drug application, INB plus rTMS increased the motor-evoked potential (MEP) size and decreased intracortical inhibition (ICI) measured with single- and paired-pulse TMS in the biceps brachii muscle proximal to INB. A single oral dose of the benzodiazepine lorazepam (2 mg) or the voltage-gated Na+ and Ca2+ channel blocker lamotrigine (300 mg) abolished these changes. The NMDA receptor blocker dextromethorphan (150 mg) suppressed the reduction in ICI but not the increase in MEP size. With sleep deprivation, used to eliminate sedation as a major factor of these drug effects, INB plus rTMS induced changes similar to that seen in the control sessions. The findings suggest that (1) the INB plus rTMS-induced increase in MEP size involves rapid removal of GABA-related cortical inhibition and short-term changes in synaptic efficacy dependent on Na+ or Ca2+ channels and that (2) the long-lasting (>60 min) reduction in ICI is related to long-term potentiation-like mechanisms given its duration and the involvement of NMDA receptor activation.

J Neurosci 1998 Sep 1;18(17):7000-7


Mechanisms of deafferentation-induced plasticity in human motor cortex.

Ziemann U, Hallett M, Cohen LG.

Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1428, USA.

Deafferentation induces rapid plastic changes in the cerebral cortex, probably via unmasking of pre-existent connections. Several mechanisms may contribute, such as changes in neuronal membrane excitability, removal of local inhibition, or various forms of short- or long-term synaptic plasticity. To understand further the mechanisms involved in cortical plasticity, we tested the effects of CNS-active drugs in a plasticity model, in which forearm ischemic nerve block (INB) was combined with low-frequency repetitive transcranial magnetic stimulation (rTMS) of the deafferented human motor cortex. rTMS was used to upregulate the plastic changes caused by INB. We studied six healthy subjects. In two control sessions without drug application, INB plus rTMS increased the motor-evoked potential (MEP) size and decreased intracortical inhibition (ICI) measured with single- and paired-pulse TMS in the biceps brachii muscle proximal to INB. A single oral dose of the benzodiazepine lorazepam (2 mg) or the voltage-gated Na+ and Ca2+ channel blocker lamotrigine (300 mg) abolished these changes. The NMDA receptor blocker dextromethorphan (150 mg) suppressed the reduction in ICI but not the increase in MEP size. With sleep deprivation, used to eliminate sedation as a major factor of these drug effects, INB plus rTMS induced changes similar to that seen in the control sessions. The findings suggest that (1) the INB plus rTMS-induced increase in MEP size involves rapid removal of GABA-related cortical inhibition and short-term changes in synaptic efficacy dependent on Na+ or Ca2+ channels and that (2) the long-lasting (>60 min) reduction in ICI is related to long-term potentiation-like mechanisms given its duration and the involvement of NMDA receptor activation.

J Neurosci 1998 Feb 1;18(3):1115-23


Modulation of plasticity in human motor cortex after forearm ischemic nerve block.

Ziemann U, Corwell B, Cohen LG.

Human Cortical Physiology Unit, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.

Deafferentation leads to cortical reorganization that may be functionally beneficial or maladaptive. Therefore, we were interested in learning whether it is possible to purposely modulate deafferentation-induced reorganization. Transient forearm deafferentation was induced by ischemic nerve block (INB) in healthy volunteers. The following five interventions were tested: INB alone; INB plus low-frequency (0.1 Hz) repetitive transcranial magnetic stimulation of the motor cortex ipsilateral to INB (INB+rTMSi); rTMSi alone; INB plus rTMS of the motor cortex contralateral to INB (INB+rTMSc); and rTMSc alone. Plastic changes in the motor cortex contralateral to deafferentation were probed with TMS, measuring motor threshold (MT), motor evoked-potential (MEP) size, and intracortical inhibition (ICI) and facilitation (ICF) to the biceps brachii muscle proximal to the level of deafferentation. INB alone induced a moderate increase in MEP size, which was significantly enhanced by INB+rTMSc but blocked by INB+rTMSi. INB alone had no effect on ICI or ICF, whereas INB+rTMSc reduced ICI and increased ICF, and conversely, INB+rTMSi deepened ICI and suppressed ICF. rTMSi and rTMSc alone were ineffective in changing any of these parameters. These findings indicate that the deafferented motor cortex becomes modifiable by inputs that are normally subthreshold for inducing changes in excitability. The deafferentation-induced plastic changes can be up-regulated by direct stimulation of the "plastic" cortex and likely via inhibitory projections down-regulated by stimulation of the opposite cortex. This modulation of cortical plasticity by noninvasive means might be used to facilitate plasticity when it is primarily beneficial or to suppress it when it is predominately maladaptive.

 

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