Table 2.
Areas for rehabilitation improvement | Affected area | Methods that can be used with observed impacts |
---|---|---|
Movement disorders in Parkinson’s Disease | Basal ganglia [144] |
• Long-term deep brain stimulation of the subthalamic nuclei • Restorative effects of global structural and functional connectivity as a result of plasticity and neuroregeneration [145] • Stimulation of mesencephalic locomotor region [146] [analogous to the pedunculopontine nucleus in humans [147] |
Motor recovery after stroke | Unilateral cervical contusion [148] |
• Vagal nerve stimulation • Release of monoamines within cerebral cortex • Promotes plasticity of neural circuits and enhances motor learning [148, 149]. • Activity-dependent plasticity also occurs [150]. |
Allodynia | Mid-thoracic contusion SCI [151] | • Induces plasticity via stimulation to the nucleus raphe magnus to augment serotonin release [151]. |
Speech | Left fronto-temporo-parietal region (15708219) |
• Intensive speech therapy [152, 153] • Combined with pharmacological therapies [154–157] • Combined with noninvasive brain stimulation [158–161]. • Results are promising, but sample sizes have been small [162]. |
Eating and swallowing | Motor cortex |
• Sensory input essential as it drive changes in cortical circuitry [163]. • Neuromuscular stimulation induces plasticity changes [164]. |
Visual field and recognition | Visual cortex |
• Restitutive capacity is limited [165] • Compensatory mechanism are effective – shifting the visual field border towards the hemianopic side in hemianopia to improve spatial orientation and mobility [165]. • New visual functions – enhancement of the resolution to make it greater than that of the retina [165]. • Plasticity level in higher visual functions is unknown [166]. • Plasticity through cross-mode sharing of visual pathways with tactile or auditory pathways through extensive training and practice [167]. |
Optic Nerve | • Optic nerve with appropriate deletions of physiological “brakes” or additions of “facilitators” can regenerate centrally from the retinal ganglion cells [47]. | |
Cognitive (thinking, reasoning, judgment and memory) | Frontal cortex |
• NF training can lead to positive memory function and normalization of pathological brain activation patterns [168]. • Enriched environment promotes synaptic plasticity [169]. • Selective serotonin reuptake inhibitors administered acutely after brain injury may induce plasticity similar to that seen in the critical period [170]. • Normal plasticity becomes dysfunctional postinjury, failing to confer neuroprotection and to prevent further cell death. Therapies should target aspects of normal plasticity that are altered postinjury [171]. |
Bowel and bladder control | SCI above the sacrum |
• Early sacral neuromodulation following SCI reduces the extent of secondary injury and maladaptive neural restricting [172]. • Further evidence needed to support this theory. • EGFR inhibition promotes nerve regeneration in vitro and in vivo, with bladder function restored in rodents [173]. |
Emotional control | Fear memories | • Inhibition of NgR1 can help with the recovery of emotional control postinjury [174, 175]. |
NF Neurofeedback, SCI Spinal Cord Injury, EGFR epidermal growth factor receptor, NgR1 Neuronal Nogo-66 receptor 1