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Where does excessive beta in Parkinson's disease originate? Insights from a case of unilateral cortico-pallidal pathway dysfunction
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DOI：10.1177/1877718x261471025.png)
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Abstract
En 中文
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<jats:bold>Detecting the source of abnormal beta oscillations in Parkinson's Disease: evidence from a case of impaired connection between cerebral cortex and basal ganglia.</jats:bold>
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<jats:p>In Parkinson's Disease, a key feature is an exaggerated, oscillatory activity in the brain called the “beta rhythm”, which occurs in the circuit, particularly relevant for motor functions, connecting the cortex (the outer brain layer) and the basal ganglia (the deeper structures). Scientists have long debated whether the exact source of this pathological activity was located in the cortex or in the basal ganglia. This report describes a critical clue from an unexpected event: a person with Parkinson's disease developed temporary swelling (edema) that affected both the sensorimotor cortex and the basal ganglia. Notably, this event was limited to one side of the brain and occurred in a subject who carried a medical device that enables recordings of the beta rhythm from inside the basal ganglia. In this peculiar case, the excessive beta rhythm on the affected side was completely suppressed and only returned once the swelling in the overlying sensorimotor cortex had resolved, even though the edema in the basal ganglia itself had recovered earlier. This unique observation suggests that the integrity of the cortex is essential for the pathological beta rhythm to occur in Parkinson's Disease, lending strong support to the theory that this disruptive electrical rhythm is generated in the cortex before spreading to deeper brain structures such as the basal ganglia.</jats:p>
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