Dystonia Europe is delighted to congratulate Dr. Roxanne Lofredi of Berlin, Germany, who has been announced as the recipient of the David Marsden Award 2026. She will receive €10,000 to support research on dystonia.
Dr. Lofredi is being recognised for her outstanding paper, “Striato-pallidal oscillatory connectivity correlates with symptom severity in dystonia patients”, which provides important new insights into the neurophysiological mechanisms underlying dystonia. Her work represents a significant contribution to advancing our understanding of the condition and may help guide future approaches to diagnosis and treatment.
David Marsden (1938–1998), was a British neurologist who made a significant contribution to the field of movement disorders. Dystonia Europe established the David Marsden Award in 2003, to acknowledge Prof Marsden’s work on the dystonias, and to honour the immense part he played in improving the lives of so many people who live with the condition. The aim of the award is to stimulate developing knowledge of and interest in dystonia through publications of aetiology, pathogenesis, diagnosis in dystonia or on the psycho social effects.
Dystonia Europe President Gill Ainsley said, “On behalf of Dystonia Europe, I warmly congratulate Dr Lofredi on this well-deserved recognition. Research like this is vital to improving life for those with dystonia. By deepening understanding of the condition, Dr Lofredi’s work brings us closer to effective treatments and better patient outcomes.”
Speaking on behalf of the judging panel, Prof Mark Edwards, said ”Roxanne Lofredi’s work is a deserved winner of the David Marsden Award. It leverages specialist recordings from the brain of people with dystonia, using deep brain stimulation electrodes, allowing Roxanne and her colleagues to look at the network of structures in the brain that are likely to generate dystonia. Importantly, her results showed a link between function of parts of this network and the severity of the dystonia in individual patients. This provides critical information about how one might change network function to directly improve the severity of dystonia. It’s very exciting work.”
About the winner
Dr. Roxanne Lofredi
Dr. Roxanne Lofredi is Junior Group Leader of the “Symptom Circuits Lab” within the Movement Disorders and Neuromodulation Unit at Charité – Universitätsmedizin Berlin. She is currently completing her neurology residency with specialization in movement disorders, with a particular focus on advanced neuromodulation therapies such as deep brain stimulation (DBS).
Dr. Lofredi studied medicine at Heidelberg University and Charité – Universitätsmedizin Berlin. She completed her doctoral thesis with highest honors at the Brain and Spine Institute in Paris, where she investigated neuronal circuit organization and inhibitory microcircuits.
During her postdoctorate under the supervision of Prof. Andrea Kühn at Charité Berlin, Dr. Lofredi developed extensive expertise in intracerebral neurophysiology, electrophysiological biomarkers, and network analysis. She further expanded her international research experience through fellowships at the University of Oxford with Prof. Peter Brown and at Aix-Marseille University with Prof. Alexandre Eusebio.
Dr. Lofredi has received multiple national and international awards and competitive grants, including the Young Investigator Award from the German Society of Clinical Neurophysiology, a Clinician Scientist Fellowship from the Berlin Institute of Health (BIH), and a Wellcome Trust Translational Partnership Fellowship. She currently leads projects within the Collaborative Research Center ReTune and was recently awarded an Else Kröner-Fresenius Foundation Reentry Grant.
Her research focuses on the neurophysiology of movement disorders, particularly dystonia and Parkinson’s disease. She investigates how abnormal brain oscillations and dysfunctional network connectivity may explain motor and sensory symptoms, and how these signals can be leveraged to develop more individualized treatment strategies.
About the research
Deep brain stimulation (DBS) is an established therapy for dystonia in which electrodes are implanted into specific brain regions to improve motor symptoms. However, the mechanisms underlying both dystonia and the therapeutic effects of DBS remain incompletely understood. Increasing evidence suggests that dystonia arises not from dysfunction of a single brain region, but from abnormal communication across distributed motor networks.
In the study “Striato-pallidal oscillatory connectivity correlates with symptom severity in dystonia patients,” Dr. Lofredi investigated the communication between different structures of the basal ganglia in patients undergoing DBS surgery. The basal ganglia are deep brain structures essential for the control and coordination of movement.
Using a specific type of DBS electrode, electrical activity was simultaneously recorded from interconnected basal ganglia regions in patients following DBS-surgery. This enabled direct investigation of neural communication within the human basal ganglia network. It was observed that patients with more severe dystonia symptoms exhibited stronger abnormal low-frequency synchronization between the striatum and the internal globus pallidus, two key nodes of the basal ganglia circuitry.
Importantly, the abnormal synchronization appeared to be specifically linked to the so-called “direct pathway,” a major communication route involved in facilitating movement. Stronger pathological coupling within this pathway was associated with greater symptom severity. These findings provide direct evidence that dystonia is characterized by abnormal network-level activity rather than isolated dysfunction of individual brain structures.
The study contributes to a better understanding of dystonia pathophysiology and supports the search for biomarkers that may guide future neuromodulation therapies. Current DBS systems deliver continuous stimulation with fixed settings, whereas future adaptive or “closed-loop” approaches may be capable of detecting pathological brain activity in real time and adjusting stimulation accordingly. Identification of neural signatures linked to symptom severity may therefore help improve individualized treatment strategies and clinical outcomes for patients with dystonia.
