Abstract
Electromagnetic therapy is a non-invasive and safe approach for the management of several pathological conditions including neurodegenerative diseases. Parkinson’s disease is a neurodegenerative pathology caused by abnormal degeneration of dopaminergic neurons in the ventral tegmental area and substantia nigra pars compacta in the midbrain resulting in damage to the basal ganglia. Electromagnetic therapy has been extensively used in the clinical setting in the form of transcranial magnetic stimulation, repetitive transcranial magnetic stimulation, high-frequency transcranial magnetic stimulation and pulsed electromagnetic field therapy which can also be used in the domestic setting. In this review, we discuss the mechanisms and therapeutic applications of electromagnetic therapy to alleviate motor and non-motor deficits that characterize Parkinson’s disease.
Highlights
Parkinson’s disease Parkinson’s disease (PD) is one of the most common neurodegenerative diseases worldwide, second only to Alzheimer’s disease (AD) [1]
PD is caused by progressive loss of structure and function of dopaminergic neurons in the ventral tegmental area and substantia nigra pars compacta in the midbrain with subsequent damage to the basal ganglia (BG) [3]
Cerasa and coworkers observed that repetitive Transcranial magnetic stimulation (TMS) applied over the inferior frontal cortex reduced the amount of dyskinesia induced by a supramaximal single dose of levodopa in PD patients, suggesting that this area may play a key role in controlling the development of dyskinesia [139]
Summary
Parkinson’s disease Parkinson’s disease (PD) is one of the most common neurodegenerative diseases worldwide, second only to Alzheimer’s disease (AD) [1]. PD is caused by progressive loss of structure and function of dopaminergic neurons in the ventral tegmental area and substantia nigra pars compacta in the midbrain with subsequent damage to the basal ganglia (BG) [3]. Cumulative evidence supports the hypothesis that PD is the result of complex interactions among genetic abnormalities, environmental toxins and mitochondrial dysfunction [4,5,6]. The mechanisms of neuronal degeneration characterizing PD have been studied extensively and include a complex interplay. Pain syndrome and autonomic dysfunctions have been observed in PD patients [24,25,26]
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