Genetic dystonia is a complex movement disorder with diverse clinical manifestations arising from pathogenic mutations in various genes. The growing body of research indicates shared pathomechanism among these genes, yet the neural dynamics facilitating this convergence are largely unexplored. We analyzed neural patterns within globus pallidus to identify shared neural dynamics underlying functional convergence across dystonia genes. We identified 1714 pallidal neurons, isolated from explorative microelectrode recordings collected during deep brain stimulation surgery, across 32 dystonic patients with mutations in AOPEP, GNAL, KMT2B, PANK2, PLA2G6, SGCE, THAP1, TOR1A, and VPS16 genes. Neural dynamics exhibited significant differences among dystonia genes. GNAL-THAP1 and SGCE-PANK2 pairs displayed variations across >70% of neural features (Mann–Whitney U-test, P ≤ 0.05). AOPEP, PANK2, and THAP1 neurons demonstrated higher firing regularity (Mann–Whitney U-test, P ≤ 0.05), while GNAL, PLA2G6, KMT2B, and SGCE shared a substantial fraction of bursting neurons (>26.6%), surpassing rates in other genes (one-sided Fisher Exact, P ≤ 0.05). TOR1A and VPS16 genes constituted an intermediate group bridging these two main gene groups. Hierarchical clustering algorithms, based on these neural dynamics, validated the findings from first-order comparisons. We observed that dystonia genes, even those without common molecular pathways, can still exhibit largely overlapping structures of neural patterns. We suggest that spiking regularity and neural bursts emerge as two primary candidates for convergent neural dynamics in the globus pallidus for genetic dystonia syndromes.