Plasticity of Sensory and Motor Maps in Adult Mammals

Kaas, Jon H.

doi:10.1146/annurev.ne.14.030191.001033

Cited by 893 publications

(452 citation statements)

References 101 publications

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“…The incomplete reversal of the changes is compatible with experimental data (Jones, 1993) and might be explained by some kind of structural alterations in synaptic size or shape or the formation of new synapses (Darian-Smith and Gilbert, 1994;Kaas, 1991).…”

Section: Intracortical and Spinal Excitabilitysupporting

confidence: 81%

Modulation of motor cortex excitability after upper limb immobilization

Zanette

Manganotti

Fiaschi

et al. 2004

Clinical Neurophysiology

101

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Objective: To examine the mechanisms of disuse-induced plasticity following long-term limb immobilization. Methods: We studied 9 subjects, who underwent left upper limb immobilization for unilateral wrist fractures. All subjects were examined immediately after splint removal. Cortical motor maps, resting motor threshold (RMT), motor evoked potential (MEP) latency and MEP recruitment curves were studied from abductor pollicis brevis (APB) and flexor carpi radialis (FCR) muscles with single pulse transcranial magnetic stimulation (TMS). Paired pulse TMS was used to study intracortical inhibition and facilitation. Compound muscle action potentials (CMAPs) and F waves were obtained after median nerve stimulation. In 4/9 subjects the recording was repeated after 35 -41 days.Results: CMAP amplitude and RMT were reduced in APB muscle on the immobilized sides in comparison to the non-immobilized sides and controls after splint removal. CMAP amplitude and RMT were unchanged in FCR muscle. MEP latency and F waves were unchanged. MEP recruitment was significantly greater on the immobilized side at rest, but the asymmetry disappeared during voluntary muscle contraction. Paired pulse TMS showed an imbalance between inhibitory and excitatory networks, with a prevalence of excitation on the immobilized sides. A slight, non-significant change in the strength of corticospinal projections to the non-immobilized sides was found. TMS parameters were not correlated with hand dexterity. These abnormalities were largely normalized at the time of retesting in the four patients who were followed-up.Conclusions: Hyperexcitability occurs within the representation of single muscles, associated with changes in RMT and with an imbalance between intracortical inhibition and facilitation. These findings may be related to changes in the sensory input from the immobilized upper limb and/or in the discharge properties of the motor units.Significance: Different mechanisms may contribute to the reversible neuroplastic changes, which occur in response to long-term immobilization of the upper-limbs.

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Section: Intracortical and Spinal Excitabilitysupporting

confidence: 81%

Modulation of motor cortex excitability after upper limb immobilization

Zanette

Manganotti

Fiaschi

et al. 2004

Clinical Neurophysiology

101

View full text Add to dashboard Cite

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“…A maladaptive response to this loss of input causes expansion of the tonotopic map so that this affected portion now becomes responsive to the adjacent frequency at which hearing threshold is normal -the lesion-edge frequency ( Figure 7). Of relevance for human neuroimaging studies, animal research has shown that a restricted cochlear lesion in adult animals drives neuroplastic changes in the frequency gradient within primary auditory cortex (Robertson and Irvine, 1989;Kaas, 1991, Rajan et al, 1993Schwaber et al 1993;Irvine et al, 2001). One theory of TI proposes that it is a consequence of such cortical reorganisation (e.g., Salvi et al, 2000a).…”

Section: Iii) Reorganisation Of the Cortical Tonotopic Mapmentioning

confidence: 99%

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

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In this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power. AbstractIn this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power.

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“…In the sensory and motor cortex, for instance, repetitive electrical stimulation is known to induce receptive field plasticity of the sensorimotor representation. 106 Similarly, ablation of a particular sensorimotor representation in the cortex can trigger a functional reorganization of the surrounding nuclei to compensate for the lesion. 107 It is also possible that neuronal populations adjacent to a DBS electrode, but not directly affected by the stimulation, reorganize their intrinsic functionality.…”

Section: Effects On Coactivation Of Competing Motor Programsmentioning

confidence: 99%

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

et al. 2008

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Summary:Chronic electrical stimulation of the brain, known as deep brain stimulation (DBS), has become a preferred surgical treatment for medication-refractory movement disorders. Despite its remarkable clinical success, the therapeutic mechanisms of DBS are still not completely understood, limiting opportunities to improve treatment efficacy and simplify selection of stimulation parameters. This review addresses three questions essential to understanding the mechanisms of DBS. 1) How does DBS affect neuronal tissue in the vicinity of the active electrode or electrodes? 2) How do these changes translate into therapeutic benefit on motor symptoms? 3) How do these effects depend on the particular site of stimulation? Early hypotheses proposed that stimulation inhibited neuronal activity at the site of stimulation, mimicking the outcome of ablative surgeries. Recent studies have challenged that view, suggesting that although somatic activity near the DBS electrode may exhibit substantial inhibition or complex modulation patterns, the output from the stimulated nucleus follows the DBS pulse train by direct axonal excitation. The intrinsic activity is thus replaced by high-frequency activity that is time-locked to the stimulus and more regular in pattern. These changes in firing pattern are thought to prevent transmission of pathologic bursting and oscillatory activity, resulting in the reduction of disease symptoms through compensatory processing of sensorimotor information. Although promising, this theory does not entirely explain why DBS improves motor symptoms at different latencies. Understanding these processes on a physiological level will be critically important if we are to reach the full potential of this powerful tool.

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Plasticity of Sensory and Motor Maps in Adult Mammals

Cited by 893 publications

References 101 publications

Modulation of motor cortex excitability after upper limb immobilization

Modulation of motor cortex excitability after upper limb immobilization

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

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