scholarly journals A review on treatment-induced neuronal reorganization in aphasia

2018 ◽  
Vol 12 ◽  
Author(s):  
Klara Schevenels ◽  
Bert De Smedt ◽  
Inge Zink ◽  
Maaike Vandermosten
2016 ◽  
Vol 2016 ◽  
pp. 1-20 ◽  
Author(s):  
Andrew C. Smith ◽  
Maria Knikou

Locomotor training is a classic rehabilitation approach utilized with the aim of improving sensorimotor function and walking ability in people with spinal cord injury (SCI). Recent studies have provided strong evidence that locomotor training of persons with clinically complete, motor complete, or motor incomplete SCI induces functional reorganization of spinal neuronal networks at multisegmental levels at rest and during assisted stepping. This neuronal reorganization coincides with improvements in motor function and decreased muscle cocontractions. In this review, we will discuss the manner in which spinal neuronal circuits are impaired and the evidence surrounding plasticity of neuronal activity after locomotor training in people with SCI. We conclude that we need to better understand the physiological changes underlying locomotor training, use physiological signals to probe recovery over the course of training, and utilize established and contemporary interventions simultaneously in larger scale research studies. Furthermore, the focus of our research questions needs to change from feasibility and efficacy to the following: what are the physiological mechanisms that make it work and for whom? The aforementioned will enable the scientific and clinical community to develop more effective rehabilitation protocols maximizing sensorimotor function recovery in people with SCI.


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
C. Salustri ◽  
F. Tecchio ◽  
F. Zappasodi ◽  
L. Tomasevic ◽  
M. Ercolani ◽  
...  

Objective. To verify whether systemic biometals dysfunctions affect neurotransmission in living Alzheimer’s disease (AD) patients.Methods. We performed a case-control study using magnetoencephalography to detect sensorimotor fields of AD patients, at rest and during median nerve stimulation. We analyzed position and amount of neurons synchronously activated by the stimulation in both hemispheres to investigate the capability of the primary somatosensory cortex to reorganize its circuitry disrupted by the disease. We also assessed systemic levels of copper, ceruloplasmin, non-Cp copper (i.e., copper not bound to ceruloplasmin), peroxides, transferrin, and total antioxidant capacity.Results. Patients’ sensorimotor generators appeared spatially shifted, despite no change of latency and strength, while spontaneous activity sources appeared unchanged. Neuronal reorganization was greater in moderately ill patients, while delta activity increased in severe patients. Non-Cp copper was the only biological variable appearing to be associated with patient sensorimotor transmission.Conclusions. Our data strengthen the notion that non-Cp copper, not copper in general, affects neuronal activity in AD.Significance. High plasticity in the disease early stages in regions controlling more commonly used body parts strengthens the notion that physical and cognitive activities are protective factors against progression of dementia.


2017 ◽  
Vol 24 (1) ◽  
pp. 22-35 ◽  
Author(s):  
Johanna L. Reichert ◽  
Veronika Schöpf

For the visual and auditory senses, an array of studies has reported on neuronal reorganization processes after sensory loss. In contrast to this, neuroplasticity has been investigated only scarcely after loss of the olfactory sense. The present review focuses on the current extent of literature on structural and functional neuroplasticity effects after loss, with a focus on magnetic resonance imaging–based studies. We also include findings on the regain of the olfactory sense, for example after successful olfactory training. Existing studies indicate that widespread structural changes beyond the level of the olfactory bulb occur in the brain after loss of the olfactory sense. Moreover, on a functional level, loss of olfactory input not only entails changes in olfaction-related brain regions but also in the trigeminal system. Existing evidence should be strengthened by future longitudinal studies, a more thorough investigation of the neuronal consequences of congenital anosmia, and the application of state-of-the-art neuroimaging methods, such as connectivity analyses and joint analyses of brain structure and function.


2018 ◽  
pp. 177-184
Author(s):  
Justin F. Averna ◽  
Alexander Bautista ◽  
George C. Chang Chien ◽  
Michael Saulino

Pain from spinal cord injury (SCI) is one of the pain syndromes that is recalcitrant to treatment. It is often a result of injury associated with mechanical trauma and vascular compromise of the spinal cord parenchyma. SCI pain is associated with substantial impact on the patient’s life, interfering with activities of daily living, effective rehabilitation, and quality of life. The underlying mechanism for the development of SCI pain includes neuronal hyperexcitability, reduced inhibition, neuronal reorganization, and plasticity. The diverse factors associated with SCI pain warrant the need for an interdisciplinary approach tailored to the individual patient. The goals of treatment should encompass four domains: pain management, spinal rehabilitation, psychological treatment, and social and environmental modification.


2001 ◽  
Vol 7 (S2) ◽  
pp. 660-661
Author(s):  
W. Gray (Jay) Jerome ◽  
Thomas J. Montine ◽  
Ariel Y. Deutch

Parkinson's disease (PD) is characterized by rigidity, tremor, bradykinesia, and postural instability. The proximate cause of these symptoms is striatal dopamine (DA) insufficiency. The motor symptoms of PD can be alleviated by DA replacement therapy. However, late in the course of the disease patients appear to become less responsive to DA replacement. This therapeutic change suggests the possibility of structural and/or functional defects in striatal medium spiny neurons, which receive convergent DA and cortical (glutamate) inputs.To understand the neuronal reorganization occurring in Parkinson's disease, we used ultrastructural methods to examine the striatum of rats with striatal dopaminergic deafferentation induced by unilateral intranigral injection of 6-hydroxydopamine. After a six month survival, rats were deeply anesthetized with pentobarbital and perfused with 4% paraformaldehyde-1 % glutaraldehdyde solution in 0.1M Sorenson's phosphate buffer (pH 7.4). The brains were removed, post-fixed for 12 hours, embedded in paraffin, and coronal sections cut through the striatum and midbrain.


2010 ◽  
Vol 4 (4) ◽  
pp. 290-303 ◽  
Author(s):  
E. I. Zakharova ◽  
A. M. Dudchenko ◽  
M. M. Svinov ◽  
M. M. Fedorova ◽  
E. L. Germanova

1997 ◽  
Vol 77 (2) ◽  
pp. 874-895 ◽  
Author(s):  
Andreas Straube ◽  
Albert F. Fuchs ◽  
Susan Usher ◽  
Farrel R. Robinson

Straube, Andreas, Albert F. Fuchs, Susan Usher, and Farrel R. Robinson. Characteristics of saccadic gain adaptation in rhesus macaques. J. Neurophysiol. 77: 874–895, 1997. We adapted the saccadic gain (saccadic amplitude/target step amplitude) by requiring monkeys to track a small spot that stepped to one side by 5, 10, or 15° and then, during the initial targeting saccade, jumped either forward or backward by a fixed percentage of the initial step. Saccadic gain increased or decreased, respectively, as a function of the number of adapting saccades made in that direction. The relation between gain and the number of adapting saccades was fit with an exponential function, yielding an asymptotic gain and a rate constant (the number of saccades to achieve 63% of the total change in gain). Backward intrasaccadic target jumps of 15, 30, and 50% of the initial target step reduced the asymptotic gain by an average of 12.2, 23.1, and 36.4%, respectively, with average rate constants of 163, 368, and 827 saccades, respectively. During 50% backward jumps, some saccades, especially those to larger target steps, became slower and lasted longer. Forward intrasaccadic jumps of 30% increased the asymptotic gain by 23.3% (average rate constant of 1,178 saccades). After we had caused adaptation, we induced recovery of gain toward normal by requiring the animal to track target steps without intrasaccadic jumps. Recovery following forward adaptation required about one third fewer saccades than the preceding gain increase. Recovery following backward adaptation required about the same average number of saccades as the preceding gain decrease. The first saccades of recovery were slightly less adapted than the last saccades of adaptation, suggesting that a small part of adaptation might have been strategic. After 50% backward jumps had reduced saccadic gain, the hypometric primary saccades during recovery were followed by hypometric corrective saccades, suggesting that they too had been adapted. When saccades of only one size underwent gain reduction, saccades to target steps of other amplitudes showed much less adaptation. Also, saccades in the direction opposite to that adapted were not adapted. Gain reductions endured if an adapted animal was placed in complete darkness for 20 h. These data indicate that saccadic gain adaptation is relatively specific to the adapted step and does not produce parametric changes of all saccades. Furthermore, adaptation is not a strategy, but involves enduring neuronal reorganization in the brain. We suggest that this paradigm engages mechanisms that determine saccadic gain in real life and therefore offers a reversible means to study their neuronal substrate.


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