The effect of afferent electrical stimulation on synaptic plasticity within the sensorimotor cortex will be discussed. Afferent electrical stimulation induces a down regulation of inhibitory neural circuits and plays a critical role in strengthening excitatory synapses. Synaptic modifications such as long-term potentiation (LTP) mechanisms could be a crucial mechanism underlying this stimulation-induced cortical plasticity. LTP and long-term depression (LTD) of synaptic transmission are crucial factors for activity-dependent changes in the strength of synaptic connections. Many studies demonstrated that these pathways play an important role in cortical synaptic plasticity. Repeated activation of excitatory synapses induces both short-term potentiation (STP) and LTP. Both types of synaptic potentiation affect N-methyl-D-aspartate glutamate receptors leading to the formation of new synapses or the unmasking of excitatory amino acid receptors on motor neurons. This increased excitability localized within the sensorimotor cortex may reflect an increase in neuronal activity as a result of a dynamic interaction of various synaptic and cellular mechanisms due to the local processing of afferent electrical input to the sensorimotor cortex. The chapter reviews also the large number of studies using fMRI and TMS to examine the effects of afferent electrical input from the hand on the excitability of human sensorimotor cortex.
Part of the book: Synaptic Plasticity
With transcranial magnetic stimulation (TMS), the motor system in neuropsychiatric disorders has extensively been investigated, and effects of certain pharmacological agents have been monitored. The most consistent finding in neuropsychiatric disorders is a significant reduction of short-latency afferent inhibition (SAI). SAI provides a reliable biomarker of cortical cholinergic dysfunction in neuropsychiatric disorders. Cortical hyperexcitability and asymptomatic motor cortex functional reorganization in the early stages of neuropsychiatric disorders have been demonstrated by TMS. Together with high-density EEG TMS and paired-associative stimulation, TMS showed impaired cortical plasticity and functional connectivity across different neural networks in neuropsychiatric disorders. Neuromodulatory techniques, especially as repetitive TMS (rTMS), hold promise as a therapeutic tool for cognitive rehabilitation because rTMS can enhance cognitive functions in neuropsychiatric disorders.
Part of the book: Transcranial Magnetic Stimulation in Neuropsychiatry
Patients affected by muscular dystrophies often show CNS abnormalities. Patients with dystrophinopathies exhibit intellectual disabilities and mental retardation, while subjects with facioscapulohumeral muscular dystrophy (FSHD) often show epilepsy. Dystrophin and associated proteins have important roles in the CNS. Many patients with Duchenne and Becker muscular dystrophies (DMD/BMD) have cognitive impairment, learning disability, and variable degrees of mental retardation in addition to progressive muscular weakness. Unfortunately, the assessment of cortical function with TMS in DMD patients has not been able to delineate a clear picture and has yielded contradictory results. No TMS studies have been performed on BMD patients. Repetitive transcranial magnetic stimulation (rTMS) modulates cortical excitability, possibly by inducing a short-term increase in synaptic efficacy, and can be used to investigate motor cortex excitability in BMD patients. Changes in the size and threshold of motor evoked potentials (MEPs) and cortical silent period (CSP) duration evoked by rTMS delivered in 5 Hz trains of stimuli at suprathreshold intensity can be tested. Impaired muscular function might be partially compensated by an enhancement of motor excitability at the cortical level and/or at α-motoneuron level. TMS may thus offer a reliable means to characterize also important neurophysiologic and pathophysiologic aspects of cortical involvement in muscular dystrophy.
Part of the book: Muscular Dystrophies