Figure 1
Distributed oscillatory network underlying parkinsonian tremor. Schematic representation of the proposed network model in which parkinsonian tremor emerges from dynamic interactions among basal ganglia, thalamic, cerebellar, and cortical motor circuits. Oscillatory activity generated within basal ganglia loops (left) is transmitted to the thalamus (center), where it is integrated and relayed to the sensorimotor cortex (top), ultimately leading to peripheral tremor expression. The cerebellum (right) contributes to modulation and synchronization of network activity through cerebello–thalamo–cortical pathways. Bidirectional connections between these structures (arrows) reflect continuous feedback and state-dependent modulation within the motor network.
Figure 2
Flow diagram summarizing the steps involved in the literature search. Flowchart summarizing the identification, screening, eligibility, and inclusion of studies in the structured narrative review. A total of 499 records were identified through database searches (PubMed: n = 141; Scopus: n = 358), with 220 duplicates removed prior to screening. After screening 279 records, no studies were excluded at this stage. All 279 reports were assessed for eligibility, of which 202 were excluded (review articles: n = 39; other pathologies: n = 93; not related to tremor: n = 50; non-English: n = 20). An additional 10 studies were identified through reference screening. In total, 77 studies were included in the review.
Figure 3
Hierarchical organization of the distributed oscillatory network underlying parkinsonian tremor. Schematic representation of the proposed three-level network model. Nigral dopaminergic depletion (1) leads to hyperactivity of striatal D2 medium spiny neurons (2), which become increasingly responsive to cortical oscillations (3). This state promotes an alternating pattern of striatal inhibition onto the Gpe (4), resulting in fluctuations in GPe inhibitory output to the STN (5). In parallel, the STN receives direct excitatory input from the sensorimotor cortex via the hyperdirect pathway. During periods of STN disinhibition, STN activity exerts a strong glutamatergic drive onto the GPi (6) and, retrogradely, onto the GPe. The GPi, in turn, sends rhythmic GABAergic output to the VL TH (7). The VL thalamus maintains a close functional relationship with the cerebellum (10), which receives afferent input via the corticopontocerebellar pathway and projects predominantly through the dentate nucleus to the VL thalamus and putamen. Additional modulatory structures include the PPN (8), which receives afferent input from BG structures and sends reciprocal projections to these regions and to the TH, and the cZI (9), which interacts with the STN and may exert rhythmic inhibitory influences on motor thalamic nuclei. Through these interactions, thalamic neurons resonate and retransmit oscillatory activity to the sensorimotor cortex, ultimately enabling the peripheral expression of tremor (11).