{'fraction_non_alphanumeric': 0.025029797377830752, 'fraction_numerical': 0.014302741358760428, 'mean_word_length': 5.268656716417911, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Altered fast and slow inactivation of the N440K Nav1.4 mutant in a periodic paralysis syndrome

among newly diagnosed patients with PD and diabetes compared to nondiabetic patients (20.2% in H&Y stage 3 vs 4.5%). These findings suggest that postural instability and gait difficulty (PIGD) may be the primary clinical factor driving increased motor burden among diabetic patients. PIGD is less dopamine-responsive than bradykinesia or rigidity and is closely tied to H&Y scoring. Axial motor impairment in PD is likely worsened by many nondopaminergic factors including white matter burden,2 polyneuropathy, and other diabetes-related medical comorbidities. Diabetes may represent a risk factor for disease burden in PD, albeit one that is more closely related to extranigral pathology unlikely to improve with escalating doses of levodopa.