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Review
, 14 (1), 34-38

Cortical Stimulation for Treatment of Neurological Disorders of Hyperexcitability: A Role of Homeostatic Plasticity

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Review

Cortical Stimulation for Treatment of Neurological Disorders of Hyperexcitability: A Role of Homeostatic Plasticity

Zhi Chai et al. Neural Regen Res.

Abstract

Hyperexcitability of neural network is a key neurophysiological mechanism in several neurological disorders including epilepsy, neuropathic pain, and tinnitus. Although standard paradigm of pharmacological management of them is to suppress this hyperexcitability, such as having been exemplified by the use of certain antiepileptic drugs, their frequent refractoriness to drug treatment suggests likely different pathophysiological mechanism. Because the pathogenesis in these disorders exhibits a transition from an initial activity loss after injury or sensory deprivation to subsequent hyperexcitability and paroxysmal discharges, this process can be regarded as a process of functional compensation similar to homeostatic plasticity regulation, in which a set level of activity in neural network is maintained after injury-induced activity loss through enhanced network excitability. Enhancing brain activity, such as cortical stimulation that is found to be effective in relieving symptoms of these disorders, may reduce such hyperexcitability through homeostatic plasticity mechanism. Here we review current evidence of homeostatic plasticity in the mechanism of acquired epilepsy, neuropathic pain, and tinnitus and the effects and mechanism of cortical stimulation. Establishing a role of homeostatic plasticity in these disorders may provide a theoretical basis on their pathogenesis as well as guide the development and application of therapeutic approaches through electrically or pharmacologically stimulating brain activity for treating these disorders.

Keywords: brain injury; cerebral cortex; cortical stimulation; epilepsy; homeostatic plasticity; hyperexcitability; neuropathic pain; tinnitus.

Conflict of interest statement

None

Figures

Figure 1
Figure 1
Two opposing strategies for controlling cortical hyperexcitability. (A) A homeostatic plasticity mechanism suggests that activity deprivation will cause neuronal homeostatic hyperexcitability (①) while activity enhancement reduces neuronal activity (②). (B) Development of neuropathic pain, acquired epilepsy, and tinnitus often involves primary lesion or pathology that causes initial deprivation of afferent input or directly injury of the cortex, which may contribute to the development of hyperexcitability through a homeostatic mechanism (①). This network hyperexcitability may be controlled either by enhancing excitatory activity so that the hyperexcitability can be reversed through the homeostatic mechanism (②) or by directly inhibiting activity by blocking glutamate transmission or enhancing GABAergic inhibition.

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