Reacción a "Researchers study the role of a new brain network in Parkinson's disease"

Although the most striking symptoms of Parkinson's disease (PD) are motor-related (rigidity, tremor, slow movements, etc.), it is a systemic disease that affects organs in the body (the digestive system and cardiac function), the sleep-wake cycle, behavioural planning and motivation, and cognitive functions. In line with these observations, it is known that in addition to the death of dopamine-producing neurons in the substantia nigra and the dysfunction of subcortical neural circuits that control movement, PD is associated with alterations in the cerebral cortex and, above all, in the interaction between the cortex and subcortical structures (such as the subthalamic nucleus, thalamus, substantia nigra, or globus pallidus). This paper describes how the dysfunction of motor cortex structures collectively known as the Somato-Cognitive Action Network (SCAN) could be involved in the pathophysiology of PD. Studying the state of interaction between the SCAN and subcortical structures could be highly relevant for diagnosis and treatment.

The SCAN is a neural structure identified a few years ago in the motor cortex which, unlike traditional motor areas (which send specific motor commands to the muscles of the hand, mouth, arms, etc.), does not perform direct motor functions. The SCAN integrates movement with the cognitive processes of planning and behavioural motivation, as well as the state of the body's organs. The study describes:

• That the connectivity between the SCAN and the subcortical motor structures mentioned in the previous paragraph (monitored in several patient cohorts using complex imaging techniques) is altered in Parkinson's disease patients (what they call hyperconnectivity in PD) and not in patients with other neurological conditions such as essential tremor, dystonia or amyotrophic lateral sclerosis.
• There is a relationship between the degree of SCAN-subcortical structure hyperconnectivity and the severity of patients' symptoms: greater hyperconnectivity in more severe patients.
• SCAN-subcortical structure hyperconnectivity decreases when patients undergo therapies that improve PD (such as levodopa administration or deep brain stimulation).
• The application of repetitive transcranial magnetic stimulation to the cortex of patients with PD to modulate the SCAN decreases SCAN-subcortical structure hyperconnectivity and improves the symptoms of the disease.

The study concludes by highlighting the importance of SCAN-subcortical structure connectivity in the pathophysiology of PD. It suggests that the measurement of this connectivity could be used as a diagnostic biomarker for PD. The measurement of SCAN-subcortical structure connectivity could also be used to optimise treatments (e.g., to better define the sites where deep brain stimulation should be applied). Finally, the modulation of SCAN-subcortical structure connectivity using non-invasive techniques (transcranial magnetic stimulation) could be used as a treatment for PD.

This is a very interesting but complex piece of work, which in my opinion is well done. The techniques for measuring SCAN-subcortical structure connectivity are difficult to set up in a normal healthcare centre, and I therefore do not believe that this article will change daily clinical practice in the short term. However, it does represent a significant advance in our understanding of how all the alterations present in Parkinson's patients are generated. From a more scientific point of view, I would have liked to see a more precise description of the concept of SCAN-subcortical structure hyperconnectivity, which is essential to the study.