Tremor, rigidity, slowness, and difficulty initiating movement are hallmarks of Parkinson’s disease (PD), and all seem to validate the condition’s designation as a movement disorder. But patients also have non-motor symptoms, including constipation, blood pressure swings, sleep disturbances, and apathy.

Why would a disorder presumed to be rooted in motor circuits produce symptoms that extend far beyond movement? And why are deep brain stimulation (DBS), levodopa (L-DOPA), and high-intensity focused ultrasound all effective in treating the condition, even though they act differently on different parts of the brain?

These are questions Nico U.F. Dosenbach, MD, PhD, and his colleagues have asked for years. And now, they think they’ve found the answer, hidden in a single brain circuit within the motor cortex called the somato-cognitive action network (SCAN).

First described in a 2023 study, the SCAN was discovered when precision brain imaging revealed that the classic map of the motor cortex is interrupted by zones that don’t control any particular body part but instead connect to regions involved in arousal, blood pressure, pain, and goal-directed behavior.

A study published earlier this year added to this growing body of evidence by showing that every effective PD therapy, regardless of mechanism, works by quieting dysfunction in this one network. Dosenbach thinks of the SCAN as the brain’s “actuator” — the system that sits between cognition and the body, translating intention into coordinated action.

This framework may help explain one of PD’s oldest puzzles. The typical PD prodrome that commonly involves constipation, sleep disturbances, and acting out dreams years before motor symptoms appear never fit the “movement disorder” label.

“People don’t go to the hospital because they’re constipated,” Dosenbach noted. “But once they can’t move, that’s when they present. The autonomic symptoms were always there because they’re part of the same circuit.”

If the framework holds, Dosenbach says the field may need to reconsider the current movement disorder classification.

“Parkinson’s is an action disorder, but because the motor symptoms are the most visible, they became dominant,” Dosenbach, professor of neurology at Washington University in St. Louis and senior author of both studies, told Medscape Medical News.

“I’ve given talks to movement disorders divisions, and I tell them: ‘You guys need to rename yourselves.’”

A Network Hidden in Plain Sight

For nearly a century, the motor cortex was understood through the work of Wilder Penfield, neurosurgeon who mapped the brain in awake epilepsy patients from the 1930s through the 1950s.

By electrically stimulating points along the cortex and observing which body parts twitched, Penfield created the famous “homunculus” — a distorted map of the body stretched across the brain, with discrete regions controlling the foot, hand, and mouth.

Dosenbach and his colleagues upended this textbook model in 2023. Using precision functional MRI, they discovered that between the foot, hand, and mouth regions are three “inter-effector” zones that don’t control any particular body part. These regions formed the structural basis of what the team named SCAN.

They found that symptoms of PD seemed to mirror SCAN connections, and the disease’s deficits aligned suspiciously well with the network’s purpose.

But to understand why SCAN might be so fundamental and why damage to it produces such a strange mix of symptoms, Dosenbach points to a 2024 evolutionary study of lampreys — jawless fish that diverged from other vertebrates roughly 500 million years ago. Lampreys possess sympathetic neurons, cells that drive fight-or-flight responses. But they don’t have limbs.

His hypothesis: If the circuitry for whole-body arousal and action existed before limbs evolved, then the limb-specific motor cortex came later. The SCAN may be the older system.

“Evolution designed a system that achieves goal-directed behavior,” he said.

One Circuit, Multiple Entry Points

In 2023, Dosenbach’s team had identified SCAN but lacked clinical data to prove that the network explained PD. In Beijing, China, Hesheng Liu, PhD, chief scientist of brain sciences at Changping Laboratory, had the clinical data — brain images amassed over many years — but lacked the framework needed to interpret it. The SCAN concept filled that gap.

Rather than compete, Liu and Dosenbach joined forces and conducted a study that combined datasets spanning DBS, transcranial magnetic stimulation (TMS), MR-guided focused ultrasound, and L-DOPA therapy.

The central finding of this research is that the SCAN is talking too much to the deeper parts of the brains of patients with PD in a pattern that researchers call “hyperconnectivity,” which jams the circuits that normally allow smooth, voluntary movement. They also found there was no hyperconnectivity in brain regions that control specific body parts; it was specific to the SCAN.

When the researchers looked at common PD treatments, a similar pattern emerged.

All three approved targets for DBS were more strongly wired to the SCAN than to the hand or foot areas of the motor cortex. In addition, across every treatment tested, the same pattern emerged: When therapy worked, the hyperconnectivity quieted. The quieter the connection, the more symptoms improved.

In 14 patients followed for a year after DBS surgery, the hyperconnectivity progressively declined. Focused ultrasound showed a similar pattern. When the lesion was placed closer to a SCAN-connected “hot spot” in the thalamus, patients did better.

L-DOPA also reduced the hyperconnectivity when patients were scanned before and after taking medication, suggesting that a pill and a brain stimulator may ultimately work through the same circuit.

But the strongest test came from within the study itself. Thirty-six patients were randomly assigned to receive TMS targeted either at the SCAN or at the regions Penfield mapped decades ago. Both groups improved, but patients in the SCAN group improved twice as much, with an average reduction of 13.5 vs 6.5 points on a standard symptom scale vs the comparison group.

“In the past, people tried TMS aimed at the motor cortex, and it kind of helped, but not more so than drugs, so it never caught on,” Dosenbach said. “They were shooting in the dark, as everyone’s brain is a little different, and sometimes, you’d hit the right spot by chance, but sometimes you’d miss.”

The TMS results also hinted at something DBS has failed to deliver: improvement in gait. Freezing mid-step is one of the most dangerous symptoms of PD because patients fall suddenly, often hitting their heads.

“Gait is the number one problem,” Dosenbach said. “DBS doesn’t help much with that. I’m excited the TMS trial suggested improvement.”

Remaining Questions

Rather than starting with a clinical label and working backward, the SCAN model starts with a circuit and asks how it’s broken, which is closer to precision medicine than treating all patients with PD the same way, said Alberto Espay, MD, MSc, who was not part of the study.

While the findings are a “step in the right direction,” more work is needed, Espay told Medscape Medical News.

“This is a small, single-center study that has not yet been put to the test with between-site reproducibility, scanner heterogeneity with regard to acquisition, and processing standardization,” said Espay, professor and endowed chair of the James J. and Joan A. Gardner Family Center for Parkinson’s Disease at the University of Cincinnati in Cincinnati.

SCAN hyperconnectivity cannot currently distinguish PD from other movement disorders, Espay noted, and, given the difficulty of separating the disorder from others using clinical features alone, an imaging biomarker faces a high bar. Even if the findings are replicated, they represent symptomatic treatment rather than disease modification, he added.

Joohi Jimenez-Shahed, MD, medical director of movement disorders neuromodulation at the Icahn School of Medicine at Mount Sinai in New York City, agreed the framework is promising but emphasized it’s not ready for the clinic. The findings will need to be reproduced across different contexts, likely first at academic centers with access to functional MRI and patients undergoing neuromodulation.

“SCAN mapping is not ready for prime time or as a standard of care, given the resources involved and this early phase of understanding,” said Jimenez-Shahed, who was not part of the research.

She also noted the TMS trial lacked a sham control arm, making it harder to rule out placebo effects. “It’s an intriguing finding,” she said, “but this should be investigated further in larger and well-designed studies.”

Still, she sees potential in how the framework validates patient experience.

“Many patients intuitively understand that when they ‘feel better’ they ‘perform better,’” she said. “The SCAN now provides evidence for the biological underpinnings of that connection.”

No Longer Just a Theory?

Dosenbach agrees that more research is needed and noted that the latest findings have implications for how future trials are designed.

“Most studies I’ve looked at don’t track anything but motor symptoms,” he said. “They’re not looking at whether they’re fixing the other problems. Now that we know it’s all in the same circuit, we need to add more measures.”

But if the SCAN framework holds, it offers both a deeper understanding of why PD produces its bewildering mix of symptoms and a roadmap for optimizing treatments that have worked for decades — without anyone knowing exactly why.

For the roughly 90% of patients with PD who will never receive DBS — because it’s invasive, expensive, or because their main symptoms don’t respond — the findings point toward alternatives.

TMS and low-intensity focused ultrasound can be added to existing regimens. And cortical SCAN targets offer a noninvasive entry point to the same circuit that DBS accesses surgically.

“There’s a clear, unmet, severe need. Patients are suffering. And with these results, I think it’s reasonable that patient expectations are high,” Dosenbach said.

It’s also reasonable to consider that it may be time to set aside the notion of PD as just a movement disorder, he said.

“It’s a big ask — to change how you think about the basic pathophysiology of Parkinson’s,” Dosenbach admitted.

But he emphasized that the research doesn’t just propose an idea; it tests one. Across DBS, TMS, focused ultrasound, and L-DOPA, the SCAN hypothesis held. “This isn’t just a theory anymore.”

The 2026 study was supported by Changping Laboratory, the National Institutes of Health (NIH), and the National Natural Science Foundation of China. Dosenbach has a financial interest in Turing Medical and may financially benefit if the company is successful in marketing FIRMM motion monitoring software products and may receive royalty income based on FIRMM technology developed at Washington University School of Medicine and licensed to Turing Medical. Dosenbach is also a co-founder of Turing Medical. Espay reported receiving consulting fees from NeuroDerm, Amneal, Acadia, Acorda, Kyowa Kirin, Supernus, and others, as well as grant support from the NIH and the Michael J. Fox Foundation. Jimenez-Shahed reported consulting relationships with Teva, Medtronic, and AbbVie.