Restorative neurology and neuroscience
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Restor. Neurol. Neurosci. · Jan 2013
Differential involvement of the left frontal and temporal regions in verb naming: a tDCS treatment study.
In aphasic patients, some studies have already emphasized the efficacy of transcranial direct current stimulation (tDCS) during the treatment of noun retrieval deficits. To date, in the same population, there are have been no studies addressing tDCS effects in the recovery of verb retrieval deficits. In this study, we wanted to test the potential of tDCS to improve verb production in a group of aphasic patients. ⋯ These findings further confirm that tDCS represents a useful new therapeutic interventions for the rehabilitation of lexical deficits in aphasic patients.
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Restor. Neurol. Neurosci. · Jan 2013
Changes in thresholds for intracortical excitability in chronic stroke: more than just altered intracortical inhibition.
The purpose of the present study was to assess changes in thresholds for the onset of short intracortical inhibition (SICI) and intracortical facilitation (ICF) in individuals with chronic stroke compared to age-matched healthy adults and evaluate the relationship between these thresholds and motor function in the chronic stroke group. ⋯ Reduced thresholds for the onset of SICI and ICF observed in the present study indicate that both inhibitory and facilitatory systems mediate changes in cortical excitability in chronic stroke patients. The association between higher onset thresholds and motor function in the stroke group also suggests that these thresholds have potential utility for tracking functional motor improvements in patients with chronic stroke. This study provides new insights to further characterize changes in intracortical neurotransmission that play an important role in modulating neuroplasticity and the potential relationship between inhibitory and facilitatory networks and motor function post-stroke.
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Restor. Neurol. Neurosci. · Jan 2013
Plasticity of the contralateral motor cortex following focal traumatic brain injury in the rat.
Recovery is limited following traumatic brain injury (TBI) since injured axons regenerate poorly and replacement of lost cells is minimal. Behavioral improvements could instead be due to plasticity of uninjured brain regions. We hypothesized that plasticity of the uninjured hemisphere occurs contralateral to a focal TBI in the adult rat. Thus, we performed cortical mapping of the cortex contralateral to the TBI using intracortical microstimulation (ICMS). ⋯ Following focal TBI in the rat, our data suggest reorganization of cortical and/or subcortical regions in the uninjured hemisphere contralateral to a focal TBI leading to an altered responsiveness to ICMS. Although we cannot exclude that these changes are maladaptive, it is plausible that this plasticity process positively influences motor recovery after TBI.
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Restor. Neurol. Neurosci. · Jan 2013
Rescue of injured motoneurones by grafted neuroectodermal stem cells: effect of the location of graft.
Avulsion of one or more ventral roots from the spinal cord leads to the death of the majority of affected motoneurons. In this study we investigated whether immortalized clonal neuroectodermal stem cells applied to the injured cord in various ways impart neuroprotection on motoneurons otherwise destined to die. ⋯ This study provides evidence that neuroectodermal stem cell transplantation into the reimplanted ventral root induces as successful regeneration of injured motoneurons as stem cells grafted into the spinal cord.
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Restor. Neurol. Neurosci. · Jan 2013
Plastic changes in lumbar segments after thoracic spinal cord injuries in adult rats: an integrative view of spinal nociceptive dysfunctions.
Spinal cord injuries (SCI) cause motor, sensory and autonomic dysfunctions as well as neuropathic pain. We investigated plastic changes occurring in cord segments caudal to the lesion to assess their potential contribution to pain states after SCI. ⋯ The existence of hyperalgesia despite the boost of inhibitory elements in the spinal cord confirms the dysbalance between excitatory and inhibitory mechanisms, leading to a general disinhibition. Widespread dysfunctions in remote segments after central injuries contribute to the appearance of pain, and they may be new targets for therapies aimed to modulate spinal dysfunctions after injury.