Loop Dysfunction in Neurological and Psychiatric Disease

Loop Dysfunction in Neurological and Psychiatric Disease

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Citation anchors captured: 133

Citation contexts

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference} Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference} Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference} Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference} Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference} Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4 Modern circuit pathology of Parkinson’s disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...

• ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7; their phenomenology is contextualised by primate and patient single-unit work ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{2Citationpaper:paper-49ae95428ec6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9; their phenomenology is contextualised by primate and patient single-unit work ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2; their phenomenology is contextualised by primate and patient single-unit work ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5; their phenomenology is contextualised by primate and patient single-unit work ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8; their phenomenology is contextualised by primate and patient single-unit work ^{3Citationpaper:paper-542748ebb962Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0; their phenomenology is contextualised by primate and patient single-unit work ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3; their phenomenology is contextualised by primate and patient single-unit work ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6; their phenomenology is contextualised by primate and patient single-unit work ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{4Citationpaper:paper-a59069d2f96bModern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8; their phenomenology is contextualised by primate and patient single-unit work ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1; their phenomenology is contextualised by primate and patient single-unit work ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3 The clinical biomarker that has anchored loop pathology in PD is the beta-band burst. Prolonged pallidal beta bursts are a disease-specific feature of OFF-medication PD compared with dystonia or ON-medication PD ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4; their phenomenology is contextualised by primate and patient single-unit work ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5. Adaptive STN stimulation that triggers on burst onset yields ~30% greater motor improvement than con...

• ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6 Conflict 2 (60-Hz STN-DBS reproducibility). A second, related disagreement concerns axial symptoms. A single-centre PD trial reported that 60-Hz STN-DBS reduced laryngeal aspiration frequency by 57% and freezing of gait relative to 130 Hz ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7, while a subsequent narrative review concluded that the benefit, although replicated in some studies, was not confirmed in others and that methodological differences...

• ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8 Conflict 2 (60-Hz STN-DBS reproducibility). A second, related disagreement concerns axial symptoms. A single-centre PD trial reported that 60-Hz STN-DBS reduced laryngeal aspiration frequency by 57% and freezing of gait relative to 130 Hz ^{5Citationpaper:paper-8e35832dc5f6Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9, while a subsequent narrative review concluded that the benefit, although replicated in some studies, was not confirmed in others and that methodological differences...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}0 Conflict 2 (60-Hz STN-DBS reproducibility). A second, related disagreement concerns axial symptoms. A single-centre PD trial reported that 60-Hz STN-DBS reduced laryngeal aspiration frequency by 57% and freezing of gait relative to 130 Hz ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}1, while a subsequent narrative review concluded that the benefit, although replicated in some studies, was not confirmed in others and that methodological differences...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}2 Conflict 2 (60-Hz STN-DBS reproducibility). A second, related disagreement concerns axial symptoms. A single-centre PD trial reported that 60-Hz STN-DBS reduced laryngeal aspiration frequency by 57% and freezing of gait relative to 130 Hz ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}3, while a subsequent narrative review concluded that the benefit, although replicated in some studies, was not confirmed in others and that methodological differences...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}4 The promise of biomarker-driven, closed-loop DBS is to move from frequency dogma to circuit-state control. Conflict 3 (closed-loop triggers). That promise turns out to be biomarker- and target-specific. Movement-onset triggering for thalamic stimulation in essential tremor switches stimulation on for 80.4 ± 7.1% of the time tremor-evoking movements are present ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}5, and this strategy is feasibility-validate...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}6 The promise of biomarker-driven, closed-loop DBS is to move from frequency dogma to circuit-state control. Conflict 3 (closed-loop triggers). That promise turns out to be biomarker- and target-specific. Movement-onset triggering for thalamic stimulation in essential tremor switches stimulation on for 80.4 ± 7.1% of the time tremor-evoking movements are present ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}7, and this strategy is feasibility-validate...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}8 The promise of biomarker-driven, closed-loop DBS is to move from frequency dogma to circuit-state control. Conflict 3 (closed-loop triggers). That promise turns out to be biomarker- and target-specific. Movement-onset triggering for thalamic stimulation in essential tremor switches stimulation on for 80.4 ± 7.1% of the time tremor-evoking movements are present ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}9, and this strategy is feasibility-validate...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}00 The promise of biomarker-driven, closed-loop DBS is to move from frequency dogma to circuit-state control. Conflict 3 (closed-loop triggers). That promise turns out to be biomarker- and target-specific. Movement-onset triggering for thalamic stimulation in essential tremor switches stimulation on for 80.4 ± 7.1% of the time tremor-evoking movements are present ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}01, and this strategy is feasibility-validate...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}02 The promise of biomarker-driven, closed-loop DBS is to move from frequency dogma to circuit-state control. Conflict 3 (closed-loop triggers). That promise turns out to be biomarker- and target-specific. Movement-onset triggering for thalamic stimulation in essential tremor switches stimulation on for 80.4 ± 7.1% of the time tremor-evoking movements are present ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}03, and this strategy is feasibility-validate...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}04 The promise of biomarker-driven, closed-loop DBS is to move from frequency dogma to circuit-state control. Conflict 3 (closed-loop triggers). That promise turns out to be biomarker- and target-specific. Movement-onset triggering for thalamic stimulation in essential tremor switches stimulation on for 80.4 ± 7.1% of the time tremor-evoking movements are present ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}05, and this strategy is feasibility-validate...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}06 Dystonia is the cleanest case where a circuit-pathology view licenses divergent therapeutic targets. Bilateral GPi-DBS has the strongest controlled evidence base in primary generalised dystonia: BFMDRS movement scores improved from 46.3 ± 21.3 to 21.0 ± 14.1 at 12 months in the prospective trial ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}07, with 51% improvement at 1 year maintained at 58% at 3 years ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}08. Pallidal-DBS programming opt...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}09 Dystonia is the cleanest case where a circuit-pathology view licenses divergent therapeutic targets. Bilateral GPi-DBS has the strongest controlled evidence base in primary generalised dystonia: BFMDRS movement scores improved from 46.3 ± 21.3 to 21.0 ± 14.1 at 12 months in the prospective trial ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}10, with 51% improvement at 1 year maintained at 58% at 3 years ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}11. Pallidal-DBS programming opt...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}12 Dystonia is the cleanest case where a circuit-pathology view licenses divergent therapeutic targets. Bilateral GPi-DBS has the strongest controlled evidence base in primary generalised dystonia: BFMDRS movement scores improved from 46.3 ± 21.3 to 21.0 ± 14.1 at 12 months in the prospective trial ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}13, with 51% improvement at 1 year maintained at 58% at 3 years ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}14. Pallidal-DBS programming opt...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}15 Dystonia is the cleanest case where a circuit-pathology view licenses divergent therapeutic targets. Bilateral GPi-DBS has the strongest controlled evidence base in primary generalised dystonia: BFMDRS movement scores improved from 46.3 ± 21.3 to 21.0 ± 14.1 at 12 months in the prospective trial ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}16, with 51% improvement at 1 year maintained at 58% at 3 years ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}17. Pallidal-DBS programming opt...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}18 Dystonia is the cleanest case where a circuit-pathology view licenses divergent therapeutic targets. Bilateral GPi-DBS has the strongest controlled evidence base in primary generalised dystonia: BFMDRS movement scores improved from 46.3 ± 21.3 to 21.0 ± 14.1 at 12 months in the prospective trial ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}19, with 51% improvement at 1 year maintained at 58% at 3 years ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}20. Pallidal-DBS programming opt...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}21 Dystonia is the cleanest case where a circuit-pathology view licenses divergent therapeutic targets. Bilateral GPi-DBS has the strongest controlled evidence base in primary generalised dystonia: BFMDRS movement scores improved from 46.3 ± 21.3 to 21.0 ± 14.1 at 12 months in the prospective trial ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}22, with 51% improvement at 1 year maintained at 58% at 3 years ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}23. Pallidal-DBS programming opt...

• ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}24 Dystonia is the cleanest case where a circuit-pathology view licenses divergent therapeutic targets. Bilateral GPi-DBS has the strongest controlled evidence base in primary generalised dystonia: BFMDRS movement scores improved from 46.3 ± 21.3 to 21.0 ± 14.1 at 12 months in the prospective trial ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}25, with 51% improvement at 1 year maintained at 58% at 3 years ^{1Citationpaper:paper-d7b8b0eb6812Modern circuit pathology of Parkinson's disease (PD) inherits, but no longer obeys, the rate-model intuition. The original framework attributed hypo- and hyperkinetic disorders to opposing firing-rate disturbances within the basal-ganglia–thalamocortical motor circuit [DeLong1990]. That account survives as a useful summary statistic — single-unit recordings in awake PD patients still distinguish GPe (~42 Hz) from GP...content/sec_14_disease.md:line 9Open reference}26. Pallidal-DBS programming opt...

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