|Areas for rehabilitation improvement||Affected area||Methods that can be used with observed impacts|
|Movement disorders in Parkinson’s Disease||Basal ganglia ||
• Long-term deep brain stimulation of the subthalamic nuclei|
• Restorative effects of global structural and functional connectivity as a result of plasticity and neuroregeneration 
• Stimulation of mesencephalic locomotor region  [analogous to the pedunculopontine nucleus in humans 
|Motor recovery after stroke||Unilateral cervical contusion ||
• 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 .
|Allodynia||Mid-thoracic contusion SCI ||• Induces plasticity via stimulation to the nucleus raphe magnus to augment serotonin release .|
|Speech||Left fronto-temporo-parietal region (15708219)||
• Intensive speech therapy [152, 153]|
• Combined with pharmacological therapies [154,155,156,157]
• Combined with noninvasive brain stimulation [158,159,160,161].
• Results are promising, but sample sizes have been small .
|Eating and swallowing||Motor cortex||
• Sensory input essential as it drive changes in cortical circuitry .|
• Neuromuscular stimulation induces plasticity changes .
|Visual field and recognition||Visual cortex||
• Restitutive capacity is limited |
• Compensatory mechanism are effective – shifting the visual field border towards the hemianopic side in hemianopia to improve spatial orientation and mobility .
• New visual functions – enhancement of the resolution to make it greater than that of the retina .
• Plasticity level in higher visual functions is unknown .
• Plasticity through cross-mode sharing of visual pathways with tactile or auditory pathways through extensive training and practice .
|Optic Nerve||• Optic nerve with appropriate deletions of physiological “brakes” or additions of “facilitators” can regenerate centrally from the retinal ganglion cells .|
|Cognitive (thinking, reasoning, judgment and memory)||Frontal cortex||
• NF training can lead to positive memory function and normalization of pathological brain activation patterns .|
• Enriched environment promotes synaptic plasticity .
• Selective serotonin reuptake inhibitors administered acutely after brain injury may induce plasticity similar to that seen in the critical period .
• 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 .
|Bowel and bladder control||SCI above the sacrum||
• Early sacral neuromodulation following SCI reduces the extent of secondary injury and maladaptive neural restricting .|
• Further evidence needed to support this theory.
• EGFR inhibition promotes nerve regeneration in vitro and in vivo, with bladder function restored in rodents .
|Emotional control||Fear memories||• Inhibition of NgR1 can help with the recovery of emotional control postinjury [174, 175].|