Physio-NeuroModulation

Neuromodulation Concept in Physiotherapy ( By Emad A. Masseh )

Archive for July, 2007

Placebo Works in the Brain(Placebo-Neuromodulation)

Posted by neuromodulator on July 31, 2007

Researchers Demonstrate How Placebo Effect Works in the Brain Pain pathways in motion in the brain during the placebo effiect. Credit: Columbia University 

Columbia University scientists, with colleagues from the University of Michigan, have shown how the neurochemistry of the placebo effect can relieve pain in humans. The scientists found that the placebo effect caused the brains of test volunteers to release more of a natural painkiller.

The placebo effect is an improvement in a medical condition caused by a patient’s belief as opposed to actual treatment. Exactly how the positive expectations created by placebos translate into pain relief had been a mystery until now.Understanding how placebo effects work may give scientists insight into why many drugs have a range of effects on people, how drugs and other treatments work together with psychological states, and how psychology can be effectively used in treatment.The research team was led by Tor Wager, Columbia professor of psychology. “Placebo effects are often observed in clinical practice, but there have been relatively few scientific studies that document the kinds of diseases that can be influenced by placebo treatments and how the treatments work in the brain and body,” Wager said.“Yet, placebo groups are included in virtually every major clinical trial, which is a testament to their importance. Only in the past few years have scientists developed the tools to directly investigate how placebos work in the human brain.”

In the experiment, scientists applied a placebo cream to volunteers’ forearms; volunteers were told it was a pain reliever, though the cream was not. Next, a control cream was applied to a nearby area, and subjects were told it had no effect. Researchers then placed a painfully hot stimulus (similar to a very hot cup of coffee) to both forearm areas and used positron emission tomography (PET) scans to measure and compare brain activity during each application. They found that the placebo treatment caused the brain to release more opioids, a chemical produced by the body and released by the brain, to relieve pain.

The scientists discovered that in the first area treated with a placebo, which volunteers falsely believed to have been treated with a pain reliever, opioid release occurred in brain areas associated with pain relief—in particular, the periadqeductal gray, an area in the brainstem used in neurosurgical interventions to control chronic pain. They also found opioid release in the orbitofrontal cortex and anterior cingulate, parts of the cerebral cortex thought to be related to evaluating and orchestrating responses in the brain and body to deal with a perceived threat—producing, for example, the so-called flight-or-fight response.

“These results extend our knowledge of how beliefs and expectations affect the brain’s neurochemistry and show that one’s mental response to a challenge can affect the brain and body in ways that are relevant to health,” Wager explained. “Understanding these interactions can pave the way for new treatments that are informed by knowledge of mind-body interactions.”

Source: Columbia University

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Neural plasticity after peripheral nerve injury and regeneration

Posted by neuromodulator on July 24, 2007

 Prog Neurobiol. 2007 Jun 22; [Epub ahead of print

Navarro X, Vivó M, Valero-Cabré A.

Group of Neuroplasticity and Regeneration, Institute of Neurosciences and Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, E-08193 Bellaterra, Spain; Institut Guttmann, Badalona, Spain.

Injuries to the peripheral nerves result in partial or total loss of motor, sensory and autonomic functions conveyed by the lesioned nerves to the denervated segments of the body, due to the interruption of axons continuity, degeneration of nerve fibers distal to the lesion and eventual death of axotomized neurons. Injuries to the peripheral nervous system may thus result in considerable disability. After axotomy, neuronal phenotype switches from a transmitter to a regenerative state, inducing the down- and up-regulation of numerous cellular components as well as the synthesis de novo of some molecules normally not expressed in adult neurons. These changes in gene expression activate and regulate the pathways responsible for neuronal survival and axonal regeneration. Functional deficits caused by nerve injuries can be compensated by three neural mechanisms: the reinnervation of denervated targets by regeneration of injured axons, the reinnervation by collateral branching of undamaged axons, and the remodeling of nervous system circuitry related to the lost functions. Plasticity of central connections may compensate functionally for the lack of specificity in target reinnervation; plasticity in human has, however, limited effects on disturbed sensory localization or fine motor control after injuries, and may even result in maladaptive changes, such as neuropathic pain, hyperreflexia and dystonia. Recent research has uncovered that peripheral nerve injuries induce a concurrent cascade of events, at the systemic, cellular and molecular levels, initiated by the nerve injury and progressing throughout plastic changes at the spinal cord, brainstem relay nuclei, thalamus and brain cortex. Mechanisms for these changes are ubiquitous in central substrates and include neurochemical changes, functional alterations of excitatory and inhibitory connections, atrophy and degeneration of normal substrates, sprouting of new connections, and reorganization of somatosensory and motor maps. An important direction for ongoing research is the development of therapeutic strategies that enhance axonal regeneration, promote selective target reinnervation, but are also able to modulate central nervous system reorganization, amplifying those positive adaptive changes that help to improve functional recovery but also diminishing undesirable consequences.

PMID: 17643733 [PubMed - as supplied by publisher]

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Motor imagery and action observation

Posted by neuromodulator on July 7, 2007

Motor imagery and action observation: cognitive tools for rehabilitation.

Mulder T.    J Neural Transm. 2007 Jun 20; [Epub ahead of print

Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands.

Rehabilitation, for a large part may be seen as a learning process where old skills have to be re-acquired and new ones have to be learned on the basis of practice. Active exercising creates a flow of sensory (afferent) information. It is known that motor recovery and motor learning have many aspects in common. Both are largely based on response-produced sensory information. In the present article it is asked whether active physical exercise is always necessary for creating this sensory flow. Numerous studies have indicated that motor imagery may result in the same plastic changes in the motor system as actual physical practice. Motor imagery is the mental execution of a movement without any overt movement or without any peripheral (muscle) activation. It has been shown that motor imagery leads to the activation of the same brain areas as actual movement. The present article discusses the role that motor imagery may play in neurological rehabilitation. Furthermore, it will be discussed to what extent the observation of a movement performed by another subject may play a similar role in learning. It is concluded that, although the clinical evidence is still meager, the use of motor imagery in neurological rehabilitation may be defended on theoretical grounds and on the basis of the results of experimental studies with healthy subjects.

PMID: 17579805 [PubMed – as supplied by publisher

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Lateralization of motor imagery following stroke

Posted by neuromodulator on July 7, 2007

Clin Neurophysiol. 2007 Jun 18; [Epub ahead of print]

Stinear CM, Fleming MK, Barber PA, Byblow WD.

Department of Sport & Exercise Science, Movement Neuroscience Laboratory, University of Auckland, Private Bag 92019, Auckland, New Zealand.

OBJECTIVE: Motor imagery may activate the primary motor cortex (M1) and promote functional recovery following stroke. We investigated whether the hemisphere affected by stroke affects performance and M1 activity during motor imagery. METHODS: Twelve stroke patients (6 left, 6 right hemisphere) and eight healthy age-matched adults participated. Experiment 1 assessed the speed and ease of actual and imagined motor performance. Experiment 2 measured corticomotor excitability during imagined movement of each hand separately, and both hands together, using transcranial magnetic stimulation. RESULTS: For control participants, imagined movements were performed more slowly than actual movements, and right-hand MEPs were facilitated when they imagined moving their right hand or both hands together. Patients reported being able to imagine movements with either hand, despite no measurable facilitation of MEPs in the stroke-affected hand. In left hemisphere patients, MEPs were facilitated in the left hand during imagery of the right hand and both hands together. In right hemisphere patients, motor imagery did not facilitate MEPs in either hand. CONCLUSIONS: Motor imagery does not appear to facilitate the ipsilesional M1 following stroke. SIGNIFICANCE: Motor imagery may play a role in rehabilitating movement planning, but its role in directly facilitating corticomotor output appears limited.

PMID: 17581773 [PubMed - as supplied by publisher]

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Influence of mirror therapy on human motor cortex.

Posted by neuromodulator on July 7, 2007

Int J Neurosci. 2007 Jul;117(7):1039-48.

Fukumura K, Sugawara K, Tanabe S, Ushiba J, Tomita Y

Graduate School of Science and Technology, Keio University. Yokohama, Kanagawa. Japan.

This article investigates whether or not mirror therapy alters the neural mechanisms in human motor cortex. Six healthy volunteers participated. The study investigated the effects of three main factors of mirror therapy (observation of hand movements in a mirror, motor imagery of an assumed affected hand, and assistance in exercising the assumed affected hand) on excitability changes in the human motor cortex to clarify the contribution of each factor. The increase in motor-evoked potential (MEP) amplitudes during motor imagery tended to be larger with a mirror than without one. Moreover, MEP amplitudes increased greatly when movements were assisted. Watching the movement of one hand in a mirror makes it easier to move the other hand in the same way. Moreover, the increase in MEP amplitudes is related to the synergic effects of afferent information and motor imagery.

PMID: 17613113 [PubMed - in process]

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