Physiology and pathophysiology of the basal ganglia—thalamo—cortical networks

Low-frequency resting tremor is one of the cardinal signs of Parkinson's disease (PD) and occurs also in some of its animal models. Current physiological studies and models of the basal ganglia indicate that changes of discharge pattern and synchronization of basal ganglia neurons rather than modification in their discharge rate are crucial to the pathophysiology of PD. However, parkinsonian tremor is not strictly correlated with the synchronous oscillations in the basal ganglia networks. We therefore suggest that abnormal basal ganglia output enforces abnormal thalamo–cortical processing leading to akinesia, the main negative symptom of Parkinson's disease. The parkinsonian positive motor signs, such as tremor and rigidity, most likely evolve as a downstream compensatory mechanism.