The brain has the innate ability to undergo neuronal plasticity, which refers to changes in its structure and functions in response to continued changes in the environment. Although these concepts are well established in animal slice preparation models, their application to a large number of human subjects could only be achieved using noninvasive brain stimulation (NIBS) techniques. In this review, we discuss the mechanisms of plasticity induction using NIBS techniques including transcranial magnetic stimulation (TMS), transcranial direct current stimulation (tDCS), transcranial alternating current stimulation (tACS), random noise stimulation (RNS), transcranial ultrasound stimulation (TUS), vagus nerve stimulation (VNS), and galvanic vestibular stimulation (GVS). We briefly introduce these techniques, explain the stimulation parameters and potential clinical implications. Although their mechanisms are different, all these NIBS techniques can be used to induce plasticity at the systems level, to examine the neurophysiology of brain circuits and have potential therapeutic use in psychiatric and neurological disorders. TMS is the most established technique for the treatment of brain disorders, and repetitive TMS is an approved treatment for medication-resistant depression. Although the data on the clinical utility of the other modes of stimulation are more limited, the electrical stimulation techniques (tDCS, tACS, RNS, VNS, GVS) have the advantage of lower cost, portability, applicability at home, and can readily be combined with training or rehabilitation. Further research is needed to expand the clinical utility of NIBS and test the combination of different modes of NIBS to optimize neuromodulation induced clinical benefits.

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Background: Idiopathic normal pressure hydrocephalus (iNPH) is characterized by the clinical triad of gait disturbance, urinary incontinence, and memory impairment with normal cerebrospinal fluid (CSF) pressure. Transcranial magnetic stimulation (TMS) has been used to assess the corticospinal motor pathways in patients with iNPH with conflicting results. Methods: Our study included 11 patients with iNPH and 13 healthy controls. All the subjects underwent TMS and resting motor threshold (RMT), central motor conduction time (CMCT), short-interval intracortical inhibition (SICI), intracortical facilitation, and silent period (SP) were recorded in the upper limb. Besides, RMT and CMCT in lower limb were also recorded. Cognitive assessments were done using mini-mental status examination, Montreal cognitive assessment (MoCA), and Addenbrooke’s cognitive evaluation III (ACE III). Same parameters were recorded 24 h of CSF (lumbar puncture, LP) drainage. Results: Mean age of the iNPH patients was 69.00 ± 6.71 years with age at onset being 66.64 ± 7.10 years. Duration of disease was 1.80 ± 1.25 years. A significant difference was noted in CMCT for the lower limb (CMCT-LL), SICI, and ipsilateral SP between pre-LP NPH and controls. Also, there was a significant difference in MoCA and ACE III between pre-LP NPH and controls. A significant reduction was observed in lower limb RMT between pre- and post-LP NPH patients. Post LP, there was a reduction in the lower limb CMCT and improvement in SICI. Conclusion: A significant prolongation of CMCT-LL was observed in NPH patients. Lumbar CSF drainage in them resulted in a significant reduction in lower limb RMT thereby suggesting an increase in cortical excitability.

Background: Rapid eye movement sleep behaviour disorder (RBD) is considered to be one of the most frequent and important prodromal symptoms of Parkinson’s disease (PD). We aimed to study the neurophysiological abnormalities in patients of PD-RBD and PD without RBD (PD-nRBD) using transcranial magnetic stimulation (TMS). Methods: Twenty patients each of PD-RBD and PD-nRBD were included in the study in addition to 20 age and gender-matched healthy controls. RBD was identified using the RBD screening questionnaire (RBDSQ). All the subjects were evaluated with single and paired-pulse TMS and parameters such as resting motor threshold (RMT), central motor conduction time (CMCT), silent period (SP), short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were recorded. Results: The mean age of the controls and PD patients with and without RBD was comparable. There were no significant differences in RMT, CMCT and silent period between the two patient groups. SICI was present in all the three groups with significant inhibition noted in PD-RBD group (p < 0.001). ICF was absent in patients of PD-RBD (0.19 ± 0.11) and PD-nRBD (0.7 ± 0.5) when compared to controls (1.88 ± 1.02) with profound impairment in patients with PD-RBD (p < 0.001). The mean MoCA score was found to be significantly different in all the three groups with a worse score in patients with RBD (23.10 ± 2.55; p < 0.001). Conclusions: PD-RBD patients have significantly greater inhibition and reduced intracortical facilitation suggesting enhanced GABAergic and reduced glutaminergic transmission. These abnormalities may underlie the different pathophysiological process observed in these patients.