Parkinsonism is a clinical syndrome characterized by akinesia/bradykinesia, muscle rigidity, resting tremor, and postural instability. Within the group of parkinsonisms is Parkinson’s disease, also known as neurodegenerative parkinsonian syndrome. The group of atypical parkinsonisms was established due to the existence of sporadic parkinsonisms that do not share the exact etiology of Parkinson’s disease. Additionally, parkinsonisms that arise from causes other than neurodegeneration have been classified as secondary parkinsonisms. With this in mind, given the diversity of etiologies that can trigger parkinsonism, it is crucial to understand the symptomatology and its relationship with the basal ganglia (including damage to the nigrostriatal pathway, neuroinflammation, and neuronal damage). Only then will it be possible to propose appropriate treatments for each variant of parkinsonism.

Background/Introduction: Parkinson’s disease (PD) is a progressive neurodegenerative disorder treated with deep brain stimulation (DBS) for advanced stages, targeting the subthalamic nucleus (STN) or the internal globus pallidus (GPi). Despite DBS’s symptomatic benefits, cerebrovascular events (CVEs) remain a concern. This study assessed CVE risk in PD patients undergoing DBS. Methods: We performed a systematic review and meta-analysis following PRISMA 2020 guidelines. Studies published between 2014 and 2024 that reported CVEs in PD patients treated with DBS-STN or DBS-GPi were included. Data on CVEs, DBS targets, perioperative period, and microelectrode recording (MER) use were extracted, and probability proportions were pooled using a random-effects model. Results: Twenty-three studies (4795 patients) were included. The overall CVE probability was 2.71% (95% CI: 2.27–3.18%). Descriptive probabilities were 2.56% (95% CI: 1.94–3.24%) for STN and 0.93% (95% CI: 0.00–3.08%) for GPi. Hemorrhagic events were most common (STN: 2.47%; GPi: 1.98%), while ischemic events were rare (STN: 0.07%; GPi: 1.98%). Note that GPi estimates are based on a considerably smaller population and should be interpreted with caution. Postoperative CVEs (1.74%) were more frequent than intraoperative events (0.17%), and MER use did not significantly alter risk (MER: 2.89% vs. NON-MER: 2.92%). Conclusions: Our results suggest that DBS in PD is associated with a relatively low CVE risk (~2.7%), with hemorrhage being the most frequent type; CVEs remain a potential risk factor. Comprehensive evaluation of patient-specific factors and further prospective studies focusing on CVE outcomes are essential to optimize DBS safety in managing PD.

Background: Parkinsonism, characterized by motor symptoms, is typically attributed to basal ganglia dysfunction. Recent evidence suggests that the cerebellum may also influence these symptoms. This study investigated Crus II, the dentate nucleus (DN), and the inferior olive (IO) in a rat model of parkinsonism induced by a bilateral ventrolateral striatal (VLS) lesion. Materials and Methods: Twenty-four male Wistar rats were divided into control (n = 12) and experimental (n = 12) groups. Monopolar electrodes were implanted in target structures. The experimental group received a bilateral VLS lesion. Animals underwent four weekly sessions of electrophysiological recordings and blind behavioral assessments (resting, grooming, locomotion, rearing, sniffing) via video tracking. Power spectral density (PSD) in the 300–500 Hz band was computed. Statistical analyses included Mann–Whitney U, Friedman with Wilcoxon post hoc, and Spearman correlation tests. Results: During weeks one and two, there were significant PSD increases in the experimental group compared to the control, particularly in Crus II—grooming (p = 0.005), locomotion (p = 0.007), and rearing (p = 0.026); in IO—sniffing (p = 0.0167); and in DN—grooming (p < 0.001) and locomotion (p = 0.0008). Additionally, intragroup analysis revealed significant PSD elevations relative to baseline in these structures. Significant correlations were observed only for grooming (negative correlations) and sniffing (positive correlations) across all cerebellar regions. Conclusions: These findings suggest compensatory cerebellar hyperactivity induced by VLS lesion, potentially modulating hypokinetic symptoms and highlighting dynamic network interactions. Interpretation warrants caution due to limitations inherent to the acute lesion model and experimental duration.

Parkinsonian symptoms such as tremors, rigidity, bradykinesia, and postural instability typically arise from basal ganglia dysfunction, but growing evidence suggests cerebellar circuits also play a key role. Here, we investigated multiunit activity (MUA) in the inferior olive (IO), dentate nucleus (DN), and Crus II of the cerebellum in a rat model of tract lesion-induced parkinsonism triggered by ventrolateral striatum (VLS) injury. Thirty-six male Wistar rats were divided into a Lesion group and an Intact group. Monopolar electrodes were implanted to record MUA in IO, DN, or Crus II for four consecutive weeks. Basal and tremor-associated signals were analyzed using generalized linear models and post hoc comparisons. In rats with VLS lesions, IO activity initially increased and then declined over time, whereas DN activity remained consistently elevated, suggesting compensatory upregulation. Crus II showed no significant shifts in baseline activity. During tremor episodes, all three structures exhibited distinct temporal fluctuations in MUA. These findings reveal cerebellar structure-specific responses to striatal injury and highlight the cerebellum’s role in both the acute and chronic phases of Parkinsonian motor dysfunction. Careful consideration of possible inflammatory responses to electrode implantation remains essential for future studies.

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Background: Parkinsonism entails pronounced basal ganglia dysfunction, but emerging research suggests that broader subcortical networks, specifically the cerebellum, play a vital role in functional motor compensation following circuit-level destabilization. This study sought to characterize the electrophysiological dynamics of Multi-Unit Activity (MUA) amplitude in Crus II, the dentate nucleus (DN), and the inferior olive (IO) following a focal mechanical lesion of the ventrolateral striatum (VLS) as a circuit-level perturbation model during spontaneous behaviors. Methods: Bilateral mechanical VLS lesions were induced in 24 male Wistar rats. MUA signals were chronically recorded over a four-week protocol during self-grooming, horizontal locomotion, and rearing behaviors. Results: Crus II and the IO exhibited a structure-specific “dynamic transition,” shifting from early-stage hyperexcitability to significant late-stage attenuation by W4 (p < 0.001), reflecting a divergence from control trajectories rather than internal temporal drift within the lesioned state. Conversely, the DN showed sustained hypoactivity compared to healthy controls throughout the recording period (p < 0.05). Despite these robust neurophysiological shifts, the syntactic organization of grooming and exploratory patterns remained phenotypically preserved, indicating functional sufficiency despite underlying circuit noise. Conclusions: VLS injury triggers a rapid distributed reorganization across the striato-cerebellar network. The cerebellum acts as an active adaptive node, recalibrating internal network gain to mask early Parkinsonian-like circuit dysfunction at the level of functional sufficiency and maintain motor performance through active homeostatic gain regulation.