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GI was also recorded in 24 age\u2010matched controls. GI scores related to pace, rhythm, and balance were derived from kinetics, and FOG was identified using kinematics. We compared GI performance related to FOG and DOPA, and GI\u2010LFP relationships between posterior\u2010sensorimotor versus central\u2010associative STN regions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      DOPA\n                      <jats:sup>OFF<\/jats:sup>\n                      , 12 patients with PD had FOG observed (FOG\u2010OBS, 263 episodes), occurring at a mean of 8 steps after GI, and 26 had no FOG observed (NOBS; FOG\u2010NOBS). GI pace scores were worse in FOG\u2010OBS than in FOG\u2010NOBS patients with PD, even when not followed by FOG, with weaker association with alpha\/low\u2010beta activity in the posterior STN. Although rhythm\/balance scores were similar between groups, their association with low\u2010beta activity was stronger in FOG\u2010OBS patients, with rhythm correlating more in the central STN and balance in the posterior STN. GI was worse preceding imminent FOG, with disrupted low\u2010beta GI\u2010LFP associations and emergent high\u2010beta correlations with reversed spatial distribution (pace\/rhythm\u2010posterior STN, balance\u2010central). Dopamine improved pace, rhythm, and FOG, and partially restored STN activity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>Our results reveal 3 distinct GI patterns in patients with PD associated with absence, predisposition to, or imminent occurrence of FOG, with STN neuronal modulations differing dynamically between the posterior and central subregions. These markers could support developing adaptive DBS strategies tailored for episodic gait impairments. 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