Parkinson's Disease as a SCAN Disorder
- Fred Shaffer
- 9 hours ago
- 12 min read
The Homunculus Was Never the Whole Story
For nearly a century, textbooks have presented the primary motor cortex (M1) as a kind of neural switchboard, a strip of tissue along the brain's surface where each patch sends commands to a particular body part.
This is the famous "homunculus," the distorted little human draped across M1, with oversized hands and lips representing the brain's disproportionate investment in fine motor control. It is a powerful teaching image, and it is not wrong.
But a major new study in Nature argues that it is dangerously incomplete, in ways that matter for understanding Parkinson's disease and rethinking how we treat it (Ren et al., 2026).
The central discovery is that M1 is not simply a mosaic of body-part territories. Woven among those effector-specific zones (the patches that control the hand, the foot, the mouth) lies a second system called the somato-cognitive action network, or SCAN.
Unlike the effector zones, SCAN does not map neatly onto any single muscle group or limb. Instead, it coordinates action at a higher level, linking movement with arousal, internal physiological states, and behavioral motivation.
Think of it this way: the effector regions are like individual instrumentalists, each responsible for their own part, while SCAN is the conductor, shaping the timing, intensity, and context-sensitivity of the whole performance.
This reframes M1 as a hybrid structure, part motor output and part integration hub. It also helps resolve a long-standing puzzle: clinicians and researchers have repeatedly noticed that movements can activate multiple, seemingly unrelated patches of M1 at once, an observation that never made sense if M1 were purely a body-part map.
SCAN provides the explanation, because those "extra" activations are network nodes that help plan, guide, and contextualize action rather than merely execute it (Gordon et al., 2023; Ren et al., 2026).
Why Parkinson's Symptoms Have Never Fit a Simple Motor Pathway
What makes this finding urgent rather than merely interesting is its bearing on Parkinson's disease. Yes, Parkinson's is a movement disorder in which patients develop tremor, rigidity, and slowness of movement.
But Parkinson's also disrupts sleep architecture, destabilizes autonomic functions like blood pressure regulation, and impairs mood and cognition. Motor symptoms can worsen dramatically under stress yet paradoxically improve when patients listen to music or engage in rhythmic activity.
These features have always been difficult to reconcile with the idea that Parkinson's damages a simple limb-control pathway. If the disease only affected a circuit for moving the arm or the leg, why would anxiety make walking worse? Why would a familiar melody temporarily restore fluency of movement?
The SCAN framework offers a coherent answer: the circuit that degenerates in Parkinson's is not just a limb-specific motor pathway but a system that couples movement with arousal, internal regulation, and cognition, exactly the kind of system SCAN is built to serve (Armstrong & Okun, 2020; Bloem et al., 2021; Ren et al., 2026).
SCAN and Effector Zones Alternate at Millimeter Scale Inside M1
A critical anatomical detail makes this more than a theoretical reinterpretation. The Nature paper reports that SCAN regions do not cluster in one corner of M1; they are interleaved with effector-specific regions and alternate along the central sulcus, the deep groove separating frontal motor areas from parietal sensory areas. This spatial arrangement has profound practical consequences.
When a neurosurgeon places a stimulating electrode "in M1," or when a researcher delivers a magnetic pulse "to motor cortex," the functional tissue being engaged depends on millimeters of positioning. A spot on a SCAN node and a spot on an adjacent effector zone may be separated by a sliver of cortex, yet they belong to fundamentally different networks with different downstream effects.
Older neuroimaging studies, which often treated M1 as a uniform strip and averaged signals across it, may have been blurring a distinction that turns out to be clinically decisive (Ren et al., 2026).
Mapping Subcortical Connections to SCAN Through Resting-State Imaging
The empirical backbone of the paper is a large multimodal dataset of 863 participants spanning Parkinson's patients, healthy controls, and individuals with several comparison movement disorders.
The researchers used resting-state functional connectivity (RSFC), a technique that estimates how strongly two brain regions are coupled by measuring whether their spontaneous activity fluctuations rise and fall together when a person is lying quietly in an MRI scanner, not performing any task. The logic is that regions whose activity is tightly correlated at rest are likely part of the same functional circuit.
Using this approach, the team mapped how deep brain structures connect to different parts of the cortical surface. These structures include the substantia nigra (SN), the dopamine-producing region that degenerates in Parkinson's.
The first major finding challenges conventional assumptions: basal ganglia sites and related subcortical nodes implicated in Parkinson's disease preferentially connect to SCAN regions within M1, not to the effector-specific hand, foot, or mouth zones (Ren et al., 2026).
This is a striking reorientation. When the substantia nigra and its neighbors "talk" to motor cortex, they are not primarily addressing the patches that control individual body parts but rather the integrative nodes that coordinate whole actions in context.
The implication for motor control theory is significant: core motor subcortical structures may be tuned not only for controlling muscle output but for shaping the selection, sequencing, and context-appropriateness of action (DeLong & Wichmann, 2015; McGregor & Nelson, 2019; Ren et al., 2026).
In this view, "motor control" is not just about kinematics and force. It is about choosing the right action at the right time under the right conditions, precisely the kind of integrative function SCAN supports.
SCAN Hyperconnectivity Distinguishes Parkinson's From Other Movement Disorders
The second major finding is disease specificity. In Parkinson's patients, the connectivity between subcortical motor regions and SCAN nodes is not just present; it is abnormally elevated, a pattern the authors call "preferential hyperconnectivity."
Crucially, this pattern does not appear in healthy controls, and it is absent in patients with essential tremor, dystonia, and amyotrophic lateral sclerosis. That comparison set matters enormously because it demonstrates that this is not simply a generic consequence of having any motor disorder.
Something about Parkinson's pathophysiology specifically drives excessive coupling within the SCAN circuit. The degree of hyperconnectivity tracks clinical severity: patients with stronger SCAN-circuit coupling tend to have worse motor symptoms and more pronounced nonmotor features, including anxiety, depression, and cognitive difficulties.
This is exactly what the SCAN framework predicts (Ren et al., 2026).
If SCAN is the system that bridges action control with internal state regulation, then its disruption should produce a clinical picture that mixes motor impairment with autonomic, emotional, and cognitive disturbance. That is precisely the multidimensional syndrome clinicians observe in Parkinson's disease.
Deep Brain Stimulation "Sweet Spots" Align With SCAN, Not Effector Zones
The paper goes beyond describing a connectivity signature. It marshals evidence from multiple treatment modalities to argue that SCAN is not merely a passive biomarker but a causally relevant circuit.
The authors examine deep brain stimulation (DBS), in which surgeons implant electrodes in subcortical targets like the subthalamic nucleus (STN) and deliver continuous electrical pulses to modulate circuit activity.
They report that the most effective DBS electrode placements, the so-called "sweet spots" that produce the best clinical outcomes, show stronger connectivity to SCAN than to effector-specific motor regions.
Over time, successful DBS appears to reduce the abnormal hyperconnectivity between subcortex and SCAN, as though the stimulation is partially normalizing a circuit that had become pathologically over-coupled (Okun et al., 2012; Ren et al., 2026).
Cortical Recordings Reveal a Fast SCAN-to-STN Pathway
The researchers add an electrophysiological layer using electrocorticography (ECoG), a technique in which electrodes are placed directly on the brain's surface to record electrical activity with exquisite spatial and temporal precision.
In patients undergoing adaptive DBS with cortical recording electrodes, the strongest stimulation-evoked cortical potentials appeared at SCAN locations. This means that when the STN is electrically stimulated, the signal that reaches cortex "lands" preferentially on SCAN nodes (Ren et al., 2026).
The authors interpret this as evidence for a hyperdirect pathway, a fast, monosynaptic connection between cortex and STN that bypasses the longer, multi-step loop through the striatum.
The hyperdirect pathway has been theorized for years as a mechanism for rapid action cancellation and motor urgency, but the Nature paper grounds it in a specific cortical target: SCAN.
Medication effects reinforce the same story. Levodopa (L-DOPA), the dopamine precursor that remains the mainstay of Parkinson's pharmacotherapy, was associated with reduced hyperconnectivity between STN and SCAN, and patients whose SCAN-circuit coupling dropped more on medication showed greater motor improvement.
This convergence across electrical stimulation, direct cortical recording, and dopaminergic medication creates a mechanistic narrative with unusual coherence: SCAN is a cortical circuit that is functionally engaged by subcortical interventions, and the clinical expression of Parkinson's disease is tied to abnormal coupling within this circuit (Armstrong & Okun, 2020; Ren et al., 2026).
Personalized TMS Targeting of SCAN Nodes Outperforms Effector-Region Stimulation
Perhaps the most directly translatable finding involves noninvasive brain stimulation. The Nature paper reports a randomized clinical study using transcranial magnetic stimulation (TMS), a technique that delivers focused magnetic pulses through the scalp to alter cortical excitability without surgery.
The researchers used intermittent theta-burst stimulation (iTBS), a patterned protocol designed to produce longer-lasting changes in cortical activity than single-pulse approaches. The critical design choice was that stimulation targets were individualized using each patient's own functional brain map rather than selected from a generic atlas (Ren et al., 2026).
Half the participants received iTBS aimed at their personally identified SCAN nodes within M1; the other half received iTBS aimed at their effector-specific M1 regions.
Under the traditional "M1 as output map" model, stimulating an effector zone should be the most direct route to motor improvement, because you are targeting the tissue that directly controls muscles.
Instead, the SCAN-targeted group improved significantly more on motor symptoms, with differences emerging as early as the first week and persisting into the second.
SCAN-targeted stimulation also reduced the pathological STN-to-SCAN hyperconnectivity, while effector-targeted stimulation did not. This result suggests that in Parkinson's disease, the functional bottleneck is not at the level of individual muscle commands but at the level of action selection and coordination.
The most therapeutically productive "motor cortex" tissue is not the output zone; it is the integrative network that organizes action (Ren et al., 2026).
Proximity to SCAN-Connected Thalamic Targets Predicts Surgical Outcomes
The logic extends to neurosurgical lesioning. In a cohort of patients who underwent MRI-guided focused ultrasound (MRgFUS) thalamotomy, a technique that uses converging ultrasound beams guided by real-time MRI to create a precisely targeted lesion deep in the brain without opening the skull, the authors computed an optimal thalamic target based on which thalamic voxels showed the strongest connectivity to SCAN. They then measured how far each patient's actual lesion fell from that SCAN-defined optimum.
Patients whose lesions landed closer to the SCAN-connected target experienced greater motor improvement. When the same analysis was repeated using effector-specific connectivity as the targeting criterion, the relationship disappeared.
This finding has immediate relevance for surgical planning: it suggests that "where" within a traditional anatomical target like the ventral intermediate nucleus matters partly because of which functional circuit that particular spot engages (Ren et al., 2026).
Thalamic targeting, in other words, may be improved by thinking in terms of circuit alignment with SCAN rather than relying solely on canonical nuclear boundaries.
The broader implication is that functional network mapping could become a principled way to personalize lesion targets, consistent with the paper's repeated emphasis on patient-specific functional localization.
Reclassifying Parkinson's Disease as a Disorder of the Somato-Cognitive Action Network
Taken together, these findings support what the Nature authors call a reclassification: Parkinson's disease as a "SCAN disorder." This is not merely a relabeling; it changes the explanatory framework at every level.
At the level of anatomy, it says the most relevant M1 tissue is the interleaved SCAN nodes, not the effector map.
At the level of pathophysiology, it identifies selective SCAN-circuit hyperconnectivity as a core disease feature, one that bridges motor and nonmotor symptoms and distinguishes Parkinson's from other movement disorders (Ren et al., 2026).
At the level of treatment, it argues that interventions work, at least in part, by normalizing SCAN-circuit coupling and that patient-specific mapping of SCAN nodes can meaningfully improve outcomes for stimulation, medication targeting, and surgical lesioning.
For motor control theory more broadly, the paper pushes toward a view in which a "motor" circuit is fundamentally a control system for selecting and coordinating action in context, not just a relay for muscle commands.
That reconceptualization makes clinical sense of observations that have long seemed anomalous: why motor symptoms fluctuate with emotional state, why a dopamine circuit produces cognitive and autonomic symptoms, and why a deep brain structure like the STN can drive measurable cortical effects in planning-oriented rather than force-producing nodes (Helmich et al., 2020; McGregor & Nelson, 2019; Nutt et al., 2011).
Open Questions and the Path Forward
Important questions remain. It is not yet clear whether substantia nigra degeneration causes SCAN disruption, or whether early SCAN dysfunction could feed back and accelerate nigral degeneration. The causal arrow may point in both directions, creating a vicious cycle, but disentangling that sequence will require longitudinal studies that track patients from the earliest prodromal stages.
Additionally, while the comparison with essential tremor, dystonia, and ALS is informative, future work will need to determine whether SCAN-circuit disruption plays a role in other conditions that share features with Parkinson's, such as dementia with Lewy bodies or multiple system atrophy (Bonanni et al., 2010; Ren et al., 2026).
What is clear already is that this paper changes the conversation about M1 and about Parkinson's disease treatment strategy. "Motor cortex stimulation" can no longer be treated as a generic intervention. It becomes a circuit-informed procedure whose outcome depends critically on whether the chosen cortical target sits within SCAN or within an effector zone.
Functional network mapping, done at the individual patient level with millimeter-scale precision, moves from being a research luxury to a practical necessity for optimizing therapeutic outcomes.
The most therapeutically relevant "motor cortex" in Parkinson's disease, it turns out, is not the part that controls your hand. It is the part that decides what your hand should do, when it should do it, and how urgently it needs to happen: the integrative core of the somato-cognitive action network (Gordon et al., 2023; Ren et al., 2026).
Glossary
central sulcus: the major groove separating frontal motor regions from parietal somatosensory regions, along which SCAN and effector territories alternate.
deep brain stimulation (DBS): a neurosurgical therapy delivering continuous electrical stimulation to deep brain targets, commonly used in Parkinson's disease, with therapeutic effects linked here to SCAN-circuit connectivity.
electrocorticography (ECoG): recording of electrical activity from electrodes placed directly on the cortical surface, used in this study to measure DBS-evoked cortical responses and identify which cortical nodes receive the strongest subcortical signals.
effector-specific region: a cortical zone specialized for controlling a particular body part, such as the hand, foot, or mouth representations within M1.
hyperconnectivity: abnormally elevated functional connectivity between brain regions or networks, reported here for SCAN-to-subcortex coupling in Parkinson's disease.
hyperdirect pathway: a fast, monosynaptic route connecting cortex and the subthalamic nucleus, discussed here as the mechanism through which STN stimulation evokes cortical potentials preferentially at SCAN nodes.
intermittent theta-burst stimulation (iTBS): a patterned form of repetitive TMS designed to induce longer-lasting changes in cortical excitability, used in this study for SCAN-targeted M1 stimulation.
levodopa (L-DOPA): a dopamine precursor medication for Parkinson's disease, associated here with reduced STN-to-SCAN hyperconnectivity and corresponding motor improvement.
MRI-guided focused ultrasound (MRgFUS): a technique using converging ultrasound beams under real-time MRI guidance to create precisely targeted brain lesions without craniotomy, evaluated here using SCAN-based functional targeting in the thalamus.
primary motor cortex (M1): a frontal cortical strip historically depicted as a body-part map (the homunculus), now shown to contain interleaved SCAN nodes supporting action planning and coordination alongside effector output zones.
resting-state functional connectivity (RSFC): a measure of correlated spontaneous brain activity between regions when a person is at rest, used here to map circuit coupling between subcortical structures and cortical networks.
somato-cognitive action network (SCAN): a distributed network interwoven with effector regions in M1 that coordinates action with arousal, internal physiology, and motivation, and is identified here as a core circuit disrupted in Parkinson's disease.
substantia nigra (SN): a deep brain structure housing dopamine-producing neurons that progressively degenerate in Parkinson's disease, and which preferentially connects to SCAN nodes in M1.
transcranial magnetic stimulation (TMS): a noninvasive technique that uses magnetic pulses delivered through the scalp to influence cortical activity, shown here to be more effective for Parkinson's motor symptoms when targeted to SCAN nodes.
ventral intermediate nucleus (VIM): a thalamic region commonly targeted in tremor procedures, used here as a reference point while evaluating whether SCAN-based functional targeting improves surgical outcomes.
References
Armstrong, M. J., & Okun, M. S. (2020). Diagnosis and treatment of Parkinson disease: A review. JAMA, 323(6), 548–560.
Bloem, B. R., Okun, M. S., & Klein, C. (2021). Parkinson's disease. The Lancet, 397(10291), 2284–2303.
Bonanni, L., Thomas, A., Tiraboschi, P., Perfetti, B., Varanese, S., & Onofrj, M. (2010). EEG comparisons in early Alzheimer's disease, dementia with Lewy bodies and Parkinson's disease with dementia patients with a 2-year follow-up. Movement Disorders, 25(10), 1302–1304.
DeLong, M. R., & Wichmann, T. (2015). Basal ganglia circuits as targets for neuromodulation in Parkinson disease. JAMA Neurology, 72(11), 1354–1360.
Gordon, E. M., Jin, A., & Dosenbach, N. U. F. (2023). A somato-cognitive action network alternates with effector regions in motor cortex. Nature, 617(7960), 351–359.
Helmich, R. C., Janssen, M. J. R., Oyen, W. J. G., Bloem, B. R., & Toni, I. (2020). Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor. Brain, 143(5), 1498–1511.
Jensen, D., Berrington, A., & Voloh, B. (2023). A somatomotor network in human putamen. Nature Neuroscience, 26(7), 1165–1169.
McGregor, M. M., & Nelson, A. B. (2019). Circuit mechanisms of Parkinson's disease. Neuron, 101(6), 1042–1056.
Nutt, J. G., Bloem, B. R., Giladi, N., Hallett, M., Horak, F. B., & Nieuwboer, A. (2011). Freezing of gait: Moving forward on a mysterious clinical phenomenon. The Lancet Neurology, 10(8), 734–744.
Okun, M. S., et al. (2012). Subthalamic deep brain stimulation with a constant-current device in Parkinson's disease: An open-label randomised controlled trial. The Lancet Neurology, 11(2), 140–149.
Ren, J., Zhang, W., Dahmani, L., Gordon, E. M., Li, S., Zhou, Y., Long, Y., Huang, J., Zhu, Y., Guo, N., Jiang, C., Zhang, F., Bai, Y., Wei, W., Wu, Y., Bush, A., Vissani, M., Wei, L., Oehrn, C. R., … Liu, H. (2026). Parkinson's disease as a somato-cognitive action network disorder. Nature. Advance online publication. https://doi.org/10.1038/s41586-025-10059-1
About the Author
Fred Shaffer earned his PhD in Psychology from Oklahoma State University. He earned BCIA certifications in Biofeedback and HRV Biofeedback. Fred is an Allen Fellow and Professor of Psychology at Truman State University, where has has taught for 50 years. He is a Biological Psychologist who consults and lectures in heart rate variability biofeedback, Physiological Psychology, and Psychopharmacology. Fred helped to edit Evidence-Based Practice in Biofeedback and Neurofeedback (3rd and 4th eds.) and helped to maintain BCIA's certification programs.
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