Increased excitability in the primary motor cortex and supplementary motor area in patients with phantom limb pain after upper limb amputation

Dettmers, Christian; Adler, T.; Rzanny, R.; Schayck, Rudolf van; Gaser, Christian; Weiß, Thomas; Miltner, Wolfgang H. R.; Brückner, Lutz; Weiller, Cornelius

doi:10.1016/s0304-3940(01)01953-x

Cited by 87 publications

(75 citation statements)

References 10 publications

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“…If motor changes related to pain were to take place at the spinal level, sideto-side differences would be difficult to explain. In contrast, our data favor the cortical hypothesis [15,20,27,40], where pain-related modulation involves higher motor functions that are more lateralized.…”

Section: ■ Right-left Asymmetry In Motor Symptomssupporting

confidence: 48%

“…Other data suggest that pain-motor interactions take place at the cortical level. Functional MRI data showed increased activation in the primary motor cortex and the supplementary motor area in patients with phantom limb pain [15]. Data from patients with complex regional pain syndrome point to changes in intracortical motor excitability [40], motor cortical plasticity [27] and higher-order control of movement [20] related to the presence of chronic pain.…”

Section: ■ Interaction Between Pain and Motor Functionmentioning

confidence: 99%

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Pain and motor function in carpal tunnel syndrome

et al. 2008

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Motor symptoms may be found in approximately half of CTS hands. Clinical and neurographic signs of median nerve motor damage appear to be poorly correlated to motor symptoms. The factor that can help reconcile the discrepancy between motor symptoms and motor signs is pain. Pain modulation on motor function may take place at various anatomical levels in CTS. Nociceptive C-fibers may be involved in pain-motor interactions finally leading to motor symptoms.

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Section: ■ Right-left Asymmetry In Motor Symptomssupporting

confidence: 48%

Section: ■ Interaction Between Pain and Motor Functionmentioning

confidence: 99%

Pain and motor function in carpal tunnel syndrome

et al. 2008

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“…Additional evidence indicates that the increase of inhibitory neuronal activity in the deprived cortex may be the foundation of the poor recovery and pain observed in patients suffering from nerve injury (24,25,57). Moreover, previous studies suggested that these evoked increases in inhibitory activity are mediated through the transcallosal pathway (20,21).…”

Section: Discussionmentioning

confidence: 98%

Optogenetic-guided cortical plasticity after nerve injury

Downey

Bar‐Shir

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Peripheral nerve injury causes sensory dysfunctions that are thought to be attributable to changes in neuronal activity occurring in somatosensory cortices both contralateral and ipsilateral to the injury. Recent studies suggest that distorted functional response observed in deprived primary somatosensory cortex (S1) may be the result of an increase in inhibitory interneuron activity and is mediated by the transcallosal pathway. The goal of this study was to develop a strategy to manipulate and control the transcallosal activity to facilitate appropriate plasticity by guiding the cortical reorganization in a rat model of sensory deprivation. Since transcallosal fibers originate mainly from excitatory pyramidal neurons somata situated in laminae III and V, the excitatory neurons in rat S1 were engineered to express halorhodopsin, a light-sensitive chloride pump that triggers neuronal hyperpolarization. Results from electrophysiology, optical imaging, and functional MRI measurements are concordant with that within the deprived S1, activity in response to intact forepaw electrical stimulation was significantly increased by concurrent illumination of halorhodopsin over the healthy S1. Optogenetic manipulations effectively decreased the adverse inhibition of deprived cortex and revealed the major contribution of the transcallosal projections, showing interhemispheric neuroplasticity and thus, setting a foundation to develop improved rehabilitation strategies to restore cortical functions.recovery | amputation A lthough 20 million Americans suffer from peripheral nerve injury caused by trauma, metabolic, endocrine, and autoimmune disorders, there are few strategies to promote recovery. Surgical nerve repair and training of the injured limb are the classical rehabilitation approaches. Nevertheless, the clinical outcome in adults is generally poor, with persisting sensory dysfunction and pain (1).Recent evidence suggests that sensory dysfunctions caused by nerve injury should be attributable not only to the functional, cellular, and biochemical events occurring in peripheral nerve but also functional and anatomical changes occurring in cerebral cortical representations. It is well-documented in humans (2), non-human primates (3), cats (4), and rodents (5-7) that peripheral nerve injury can lead to expansion of neighboring cortical representation of peripheral regions within the affected (deprived) hemisphere (intrahemispheric neuroplasticity). Peripheral nerve injury and direct cortical lesions have been shown to also modify functional communication between cortical hemispheres (interhemispheric neuroplasticity) (8-19). Specifically, peripheral inputs normally evoking neuronal responses in the contralateral hemisphere cause inappropriate functional responses in the ipsilateral hemisphere. Previously, using singleunit electrophysiology recordings and juxtacellular labeling, it was shown that the inappropriate ipsilateral functional magnetic resonance imaging (fMRI) responses observed in deprived primary somatosensory cor...

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“…Most studies in upper limb amputees with phantom pain claim that it would be a correlate of functional remapping within the deafferented cortex (Ramachandran, 1993;Birbaumer et al, 1997;Borsook et al, 1998;Flor et al, 1998;Montoya et al, 1998;Lotze et al, 1999;Dettmers et al, 2001;Grüsser et al, 2001;Karl et al, 2001;Lotze et al, 2001;MacIver et al, 2008). The more intense the phantom pain, the more extensive the remapping observed in somatosensory and motor cortex (Flor et al, 2006).…”

Section: Functional Reorganization Related To Nonpainful Phantom Phenmentioning

confidence: 99%

Functional Expansion of Sensorimotor Representation and Structural Reorganization of Callosal Connections in Lower Limb Amputees

Simões¹,

Bramati²,

Rodrigues³

et al. 2012

J. Neurosci.

110

117

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Previous studies have indicated that amputation or deafferentation of a limb induces functional changes in sensory (S1) and motor (M1) cortices, related to phantom limb pain. However, the extent of cortical reorganization after lower limb amputation in patients with nonpainful phantom phenomena remains uncertain. In this study, we combined functional magnetic resonance (fMRI) and diffusion tensor imaging (DTI) to investigate the existence and extent of cortical and callosal plasticity in these subjects. Nine "painless" patients with lower limb amputation and nine control subjects (sex-and age-matched) underwent a 3-T MRI protocol, including fMRI with somatosensory stimulation. In amputees, we observed an expansion of activation maps of the stump in S1 and M1 of the deafferented hemisphere, spreading to neighboring regions that represent the trunk and upper limbs. We also observed that tactile stimulation of the intact foot in amputees induced a greater activation of ipsilateral S1, when compared with controls. These results demonstrate a functional remapping of S1 in lower limb amputees. However, in contrast to previous studies, these neuroplastic changes do not appear to be dependent on phantom pain but do also occur in those who reported only the presence of phantom sensation without pain. In addition, our findings indicate that amputation of a limb also induces changes in the cortical representation of the intact limb. Finally, DTI analysis showed structural changes in the corpus callosum of amputees, compatible with the hypothesis that phantom sensations may depend on inhibitory release in the sensorimotor cortex.

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Increased excitability in the primary motor cortex and supplementary motor area in patients with phantom limb pain after upper limb amputation

Cited by 87 publications

References 10 publications

Pain and motor function in carpal tunnel syndrome

Pain and motor function in carpal tunnel syndrome

Optogenetic-guided cortical plasticity after nerve injury

Functional Expansion of Sensorimotor Representation and Structural Reorganization of Callosal Connections in Lower Limb Amputees

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