Evidence map›Paper›PMID 42897155›Full record

ArticleNPJ Parkinson's disease2026

Dopamine amplifies subthalamic long-latency responses to cortical stimulation in patients with Parkinson's disease.

Jean-Christin Beyer, Alessia Cavallo, Jojo Vanhoecke, Richard M Köhler, Bassam Al-Fatly, Gerd-Helge Schneider, Katharina Faust, Gregor A Brandt, Andrea A Kühn, Wolf-Julian Neumann

Abstract read
In one paragraph

Article in NPJ Parkinson's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Jean-Christin BeyerMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Alessia CavalloMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Jojo VanhoeckeMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Richard M KöhlerMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Bassam Al-FatlyMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Gerd-Helge SchneiderDepartment of Neurosurgery, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Katharina FaustDepartment of Neurosurgery, Universitätsklinikum Düsseldorf, Düsseldorf, Germany.
Gregor A BrandtMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Andrea A KühnMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Wolf-Julian NeumannMovement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. julian.neumann@charite.de.

Funding

European Research Council ReinforceBG 101077060German Research Foundation Project-ID 424778381 - TRR 295
6 · The paper itself

Abstract

The cortico-subthalamic hyperdirect pathway provides a rapid route for cortical influence over basal ganglia processing and is a key target of deep brain stimulation (DBS) in Parkinson's disease (PD). However, to what degree dopamine modulates signal transmission along this pathway in humans remains unclear. Using bidirectional cortical and subthalamic electrical stimulation while invasively recording evoked responses in 15 PD patients undergoing DBS surgery, we examined cortico-subthalamic communication across dopaminergic states. Cortical stimulation evoked a short-latency subthalamic response consistent with monosynaptic hyperdirect activation that was preserved across medication conditions. In contrast, longer-latency subthalamic responses showed significant dopaminergic modulation, while cortical responses to subthalamic stimulation remained unchanged. These results reveal a temporal dissociation within the cortex-basal ganglia network, whereby fast cortical transmission is unaffected by dopamine, which in turn amplifies slower network level communication to the subthalamic nucleus. This separation of fast and delayed components provides a mechanistic framework for understanding how dopamine shapes information flow in the cortex-basal ganglia system.

Identifiers

PMID42897155
PMCPMC13680478

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.