What Each Prefrontal Cortex Region Does, Which Network It Joins, and What Happens When It Fails

Neurofeedback providers inherit a prefrontal vocabulary built by anatomists, lesion neurologists, and imaging scientists who rarely spoke to one another. One colleague says dorsolateral, another says area 46, a third says central executive network, and all three may mean overlapping but not identical tissue. This post sorts the major prefrontal regions by Brodmann number, the network each joins, and the functions supported by human lesion and imaging studies. It then describes the symptoms that follow damage to each region and the disorders in which group-level differences appear, keeping the two kinds of evidence distinct.

Brodmann Numbers Describe Cell Layers, and the Layers Move From Brain to Brain

A Brodmann area is a patch of cortex that Korbinian Brodmann numbered in 1909 because its cytoarchitecture differed from that of its neighbors. Cytoarchitecture is the layering and density of cell bodies seen under a microscope. The numbers remain the common currency for describing prefrontal regions, so a provider needs to know what they can and cannot promise. They cannot promise a fixed location on any individual scalp.

Rajkowska and Goldman-Rakic (1995) remapped areas 9 and 46 in postmortem human brains and superimposed five reconstructions on the Talairach atlas, a standard coordinate space for the human brain. The maps showed overlap and considerable spread in each area's position across the five brains.

Amunts et al. (1999) found the same lesson in Broca's region. In 10 human brains, the borders of areas 44 and 45 did not consistently follow the sulci, the grooves visible on the brain's surface. Area 44 volume differed across subjects by up to a factor of 10.

Öngür et al. (2003) mapped the orbital and medial prefrontal cortex in human brains and subdivided it more finely than Brodmann had. This post uses their numbering for the orbital and medial surfaces. Newer maps keep subdividing the dorsolateral surface as well, so any list of Brodmann numbers is a snapshot of an atlas that is still being redrawn.

A Brodmann number names a cytoarchitectonic territory, not an address on any one person's scalp. The dorsolateral areas 9 and 46 and the ventrolateral areas 44 and 45 vary in position and size from one brain to the next. Their borders do not follow the sulci a clinician can see on a scan. Any statement of the form ‘electrode F3 sits over area 9’ is a population average with a wide margin, never a fact about the client in the chair.

This is also true of brain regions in general. It reinforces the need to view each client's brain as it is: similar to population averages in many respects, yet shaped by features unique to that client's history, genetics, and experience. Assessment and training therefore become specific to that individual, and change, or progress, must be interpreted as within-client results that are not necessarily generalizable to the broader population.

In practice, treat Brodmann labels as the language of the literature and scalp sites as the language of the clinic. When a report says a protocol targets area 46, read it as targeting the middle frontal gyrus in most people. A gyrus is a ridge of cortex on the brain's surface. When a client's qEEG shows a deviant score at F3, resist the urge to name a single Brodmann area as the culprit.

Three Large-Scale Networks Divide the Prefrontal Cortex Among Themselves

The second vocabulary is that of networks. It comes from resting-state functional connectivity, the correlation between spontaneous fMRI signals in distant regions while a person lies quietly in the scanner. Functional MRI tracks changes in blood oxygenation as a proxy for neural activity. Yeo et al. (2011) clustered these correlations from 1,000 adults and found seven cortical networks, in which association cortex formed distributed networks instead of local ones. Three of those networks anchor the discussion that follows.

Network labels attach to subregions and shift with the atlas used, so no prefrontal region belongs to a single network.

Seeley et al. (2007) separated two of them in healthy adults. A salience network, anchored by the dorsal anterior cingulate cortex and the frontoinsular cortex, connected strongly with subcortical and limbic structures. An executive-control network, the frontoparietal control network of later atlases, linked the dorsolateral prefrontal and parietal cortices. The two dissociated behaviorally: prescan anxiety ratings correlated with connectivity in the salience network, whereas executive task performance correlated with connectivity in the executive-control network.

The third is the default mode network, a set of regions with correlated activity at rest. It is associated with internally directed thought, and its activity typically falls during externally directed tasks. Raichle et al. (2001) identified it by showing that a consistent set of regions, including the medial prefrontal cortex, decreases its activity from a resting baseline when attention turns to a task.

Menon (2011) grouped these three into a triple-network model of psychopathology. In that model, the salience network switches control between the other two, and a failure of that switching appears across disorders. The model synthesizes other people's data and should be read as a framework, not as a finding.

The prefrontal cortex belongs to at least three distributed networks. The lateral surface, especially the dorsolateral prefrontal cortex, joins the frontoparietal control network that carries out effortful tasks. The dorsal anterior cingulate cortex anchors the salience network that decides what deserves control, attention, or both. The ventromedial prefrontal cortex belongs to the default mode network, which is associated with internal awareness and attention. A region's symptoms usually reflect the network it serves.

In practice, a frontal training site is a doorway into a network, not a switch on a region, and even that is a hypothesis. An electrode position does not identify which sources a protocol reinforces or show that a network was engaged. When a provider trains at Fz, the anatomy suggests alertness, effort, and conflict handling as candidate targets. When a provider trains at F3 or F4, it suggests the frontoparietal network's working memory and set-shifting functions. When training is designed to engage communication between sites, such as rewarding Fz and Pz to differentially modulate a specific EEG frequency, it may strengthen, reinforce, or exercise the same frontoparietal network. Treat these as hypotheses, not as expectations the anatomy has already secured.

A functional outcome measure can show whether the client improved; it cannot show that the intended region was engaged or that training caused the improvement. However, communication measures such as coherence, phase, and phase slope index can detect changes in network communication metrics that may suggest these networks were engaged.

The Dorsolateral Prefrontal Cortex Holds Information Online and Sets the Task

The dorsolateral prefrontal cortex (dlPFC) occupies the middle frontal gyrus and adjacent superior frontal gyrus and corresponds to Brodmann areas 9 and 46 (Rajkowska & Goldman-Rakic, 1995). It supplies the prefrontal nodes of the executive-control network (Seeley et al., 2007). It is the region most people mean when they say executive, and that shorthand is defensible.

Owen et al. (2005) pooled 24 imaging studies of the n-back task, in which a person reports whether the current item matches the one shown n items earlier. The task reliably engaged the dorsolateral and ventrolateral prefrontal cortex, the frontal pole, premotor and dorsal cingulate cortex, and the posterior parietal cortex. That list is the point. Working memory, the capacity to hold and manipulate information over seconds, is a network operation with the dlPFC as one node.

Lesion work adds precision. Barbey et al. (2013) tested 19 patients with dlPFC lesions against patients with lesions elsewhere and people without lesions. Damage to the dlPFC was associated with deficits in manipulating verbal and spatial information. The left dlPFC was necessary for manipulation within working memory and the right dlPFC for manipulation in broader reasoning. Holding information and rearranging it are separable, and dlPFC damage hits the rearranging.

Stuss and Alexander (2007) tested patients with focal frontal lesions across many tasks and argued against a single dysexecutive syndrome. Task setting, the ability to establish a stimulus-response rule, was associated with left lateral frontal damage. Performance monitoring was associated with right lateral frontal damage. Energization, the initiation and sustaining of a response, was associated with superior medial damage. These are lateral-frontal localizations, coarser than the dlPFC, and they do not reduce to a left-sets, right-checks rule for areas 9 and 46.

When the dlPFC underperforms, the clinical picture is a client who understands the plan and cannot execute it. Minzenberg et al. (2009) meta-analyzed 41 imaging studies of executive tasks in schizophrenia and found reduced activation in the left dlPFC and the anterior cingulate cortex, alongside increased activation elsewhere. The pattern argues against blanket hypofrontality, a global reduction in frontal activity, and for a specific control-network deficit.

Depression complicates the picture. Koenigs et al. (2008) studied combat veterans with penetrating head injuries and found that bilateral dorsal prefrontal lesions were associated with substantially higher depression scores than nonfrontal lesions. Hornak et al. (2003) found that patients with surgical dlPFC excisions performed normally on measures of emotion recognition, social behavior, and subjective emotional state. Together, these findings suggest that the dlPFC contributes more to mood control than to its generation, although each rests on one lesion sample.

The dorsolateral prefrontal cortex (areas 9 and 46 on the middle frontal gyrus) is the prefrontal end of the frontoparietal control network. It rearranges what is held in mind, and the wider lateral frontal cortex around it sets tasks on the left and monitors performance on the right. It shows reduced task activation in schizophrenia, and bilateral dorsal prefrontal damage was associated with higher depression scores in injured veterans. Its best-documented symptoms are execution failures.

For providers, F3 and F4 are the conventional sites for the dlPFC, and electrode placement alone does not demonstrate selective engagement. Choose outcome measures that require manipulation, not just span, such as backward digit span, an n-back task, or Trail Making Part B, and track them across sessions.

Improvement on those measures shows that the function changed. It does not show that the dlPFC was selectively trained or that the neurofeedback caused the change. A client who can repeat a phone number but cannot reorder it shows the dlPFC pattern the lesion data describe. Do not promise mood change from dlPFC training unless a mood measure is on the table and the plan says how it will be read.

The Ventrolateral Prefrontal Cortex Stops Actions and Produces Speech

The ventrolateral prefrontal cortex (vlPFC) lies on the inferior frontal gyrus and covers Brodmann areas 44, 45, and 47 (Amunts et al., 1999). Its two best-documented human functions are divided between the hemispheres. The right side helps initiate inhibitory control, and the left side supports speech production.

Aron et al. (2003) used the stop-signal task, which measures how quickly a person can cancel a response after a stop cue, in patients with right frontal lesions. Stop-signal reaction time correlated with the volume of damage to the right inferior frontal gyrus and not with damage elsewhere in the frontal lobe. That result supports a specific role for this tissue in response inhibition, the cancellation of a prepared or ongoing action. The lesion sample was small, so read the finding as strong single-study evidence and not as settled fact.

Choo et al. (2022) then asked what the right inferior frontal gyrus does when it stops an action. Patients with right inferior frontal lesions failed to trigger the stop far more often than controls, whereas stopping, once triggered, was preserved. The region appears to contribute to initiating inhibitory control, and a different system implements it. For a provider, an apparent failure of self-control may begin as a failure to trigger the stop, not to carry it out. The study does not say why the trigger fails.

On the left, the classical claim is Broca's. Broca's area is the left inferior frontal gyrus, conventionally areas 44 and 45, named for Paul Broca, who in 1861 linked damage there to loss of fluent speech. Dronkers et al. (2007) scanned the preserved brains of Broca's two original patients with high-resolution MRI. Leborgne's lesion extended far beyond the inferior frontal gyrus into deeper structures, whereas Lelong's lesion spared the anterior portion of what is now called Broca's area. The defensible position is to describe the left vlPFC as a speech-production area with wide connections whose damage rarely acts alone.

Providers most often meet response inhibition problems in ADHD, and imaging places part of that story in the pace of prefrontal maturation. Shaw et al. (2007) measured cortical thickness across 824 scans from 223 children with ADHD and 223 typically developing controls. Half of cortical points reached peak thickness at a median age of 10.5 years in the ADHD group and 7.5 years in controls. The delay was most prominent in prefrontal regions.

Norman et al. (2016) then compared meta-analyses of ADHD and obsessive-compulsive disorder. Patients with ADHD showed underactivation predominantly in the right ventrolateral prefrontal cortex during inhibitory control. These are group findings that describe delay and underactivation, and they do not establish a right vlPFC deficit in any individual child.

The ventrolateral prefrontal cortex, areas 44, 45, and 47 on the inferior frontal gyrus, does two lateralized jobs. On the right, it helps initiate inhibitory control, and the extent of damage there predicts how rapidly a person can stop. On the left, it supports speech production, although Broca's own cases had damage well beyond it. As a group, children with ADHD reach peak cortical thickness later than peers and underactivate the right ventrolateral cortex during inhibition.

The scalp sites nearest the vlPFC are F7 and F8, and electrode placement alone does not demonstrate selective engagement of the vlPFC. If a provider trains at F8 for impulsivity, the outcome measure should be a stopping measure, such as stop-signal reaction time or commission errors on a continuous performance test. That test measures sustained attention and counts responses to non-targets.

Before training, confirm that the client can trigger a stop at all, because lesion work suggests triggering can fail while stopping itself remains intact. When families ask about the maturation data, explain that the three-year figure is a group median for one cortical measure. It does not say whether a particular child's cortex is still thickening, and it does not predict a training timetable.

The Dorsal Anterior Cingulate Cortex Detects Conflict, Energizes Action, and Shapes the Body's Response to Effort

The anterior cingulate cortex (ACC) wraps around the front of the corpus callosum on the medial wall and includes Brodmann areas 24 and 32 (Öngür et al., 2003). The corpus callosum is the fiber bundle joining the hemispheres. Below the genu, the front bend of the corpus callosum, the subgenual territory also includes area 25 and area 33 (Palomero-Gallagher et al., 2015).

Its dorsal portion anchors the salience network described earlier (Seeley et al., 2007). Many imaging locations labeled dorsal ACC fall within the anterior midcingulate cortex (aMCC), a region behind the perigenual cingulate with distinct cell layering (Vogt et al., 2003). The adjacent dorsomedial prefrontal cortex (dmPFC), the medial parts of areas 8 and 9, forms with it the superior medial region that Stuss and Alexander (2007) tied to energization. The subgenual portion belongs instead to the ventromedial territory treated in a later section.

Kerns et al. (2004) gave the clearest single demonstration of what the dorsal ACC does. In a Stroop task, a person names the ink color of a word that spells a different color. Under fMRI, ACC activity on a high-conflict Stroop trial predicted greater prefrontal activity and a behavioral adjustment on the next trial. That is conflict monitoring: the ACC detects competition between responses and signals the lateral prefrontal cortex to increase control. The finding supports a monitoring contribution without making every cingulate signal an error signal.

The superior medial cortex also supplies energization. Stuss and Alexander (2007) found that patients with superior medial lesions were slow to initiate and sustain responses, a deficit they distinguished from task setting and monitoring. Clinically, this is the client who can do the task but cannot start it or keep it going without prompting. Camille et al. (2011) added a second function. Damage centered on the dorsal ACC impaired learning of which actions pay while sparing learning of which stimuli pay, and orbitofrontal damage produced the mirror-image deficit.

For a psychophysiologist, the dorsal cingulate has one more job. Critchley et al. (2003) ran fMRI with simultaneous electrocardiography while healthy adults performed cognitive and motor tasks. Dorsal ACC activity was related to cardiovascular arousal, indexed by heart rate and its variability. Three patients with focal cingulate damage then performed the same effortful tasks adequately but showed blunted cardiovascular responses. Because this is a case series of three patients, the finding supports a cingulate contribution to the bodily accompaniment of effort without naming the cingulate as the autonomic controller.

At the extreme, loss of this tissue silences behavior. As Devinsky et al. (1995) reviewed, reduced anterior cingulate activity after infarcts or surgery can contribute to akinetic mutism. In that state, a person is awake but neither moves nor speaks spontaneously.

Apathy, the loss of motivation and self-initiated activity, is a milder form of the same failure. Knutson et al. (2014) mapped caregiver-rated apathy onto lesion location in 176 veterans with penetrating brain injuries. Higher apathy scores were associated with left-hemisphere damage that included the anterior cingulate cortex, other frontal regions, the insula, and the supplementary motor area.

The obsessive-compulsive link has direct imaging support. Fitzgerald et al. (2005) recorded fMRI during an error-prone task in patients with obsessive-compulsive disorder and in controls. Patients showed greater error-related activity in the rostral ACC, and the response magnitude was associated with symptom severity. The sample was small.

Norman et al. (2016) complicate the picture, because patients with OCD in their meta-analysis showed reduced function and structure in the rostral and dorsal anterior cingulate. Hyperactive error signals and reduced task activation can coexist in the same territory, so a provider should not summarize the cingulate in OCD as simply too much or too little.

For EEG providers, this territory matters because it contributes to a scalp rhythm they can see. Ishii et al. (1999) recorded frontal midline theta, the theta rhythm that appears over the frontal midline during concentrated mental tasks, in four healthy adults. They used magnetoencephalography, which records the magnetic fields produced by cortical currents. They localized its source to the medial prefrontal cortex, including the anterior cingulate. Four subjects is a pilot-sized sample, so read the localization as an estimate.

Enriquez-Geppert et al. (2014) then reported that people can learn to raise it. Over eight sessions, a neurofeedback group increased frontal midline theta amplitude, whereas a pseudo-neurofeedback group did not. This is evidence that the measured EEG feature can be modified. It does not show selective engagement of the cingulate, and the clinical question belongs to other studies.

The dorsal anterior cingulate, within areas 24 and 32 and often the anterior midcingulate cortex, anchors the salience network. With the adjacent dorsomedial prefrontal cortex, it energizes the start and maintenance of behavior, detects response conflict, learns the value of actions, and contributes to the cardiovascular side of effort. Underactivity after lesions produces apathy and, at the extreme, akinetic mutism; in obsessive-compulsive disorder, error signals run hot while task activation runs low. Frontal midline theta recorded at Fz draws on medial frontal generators that include this tissue, and healthy adults can learn to increase it with neurofeedback.

In practice, Fz and FCz are the closest scalp sites to this system, and frontal midline theta is the scalp rhythm it contributes to, not a selective readout of it. When training here for apathy, low initiation, or poor error handling, measure those targets directly with a continuous performance test or a self-report scale of initiation. Record theta amplitude as a separate learning measure. A rise in trained theta is a training-phase quantity and says nothing about symptoms on its own. New or worsening loss of initiative warrants clinical assessment before increasing training demands.

The Dorsomedial Prefrontal Cortex Infers Other Minds, and One Patient Shows the Limit

The dorsomedial prefrontal cortex has a second life outside the control networks: it supports mentalizing, the inference of another person's beliefs, intentions, or feelings. Schurz et al. (2014) meta-analyzed imaging studies of theory of mind after sorting them by task type. The medial prefrontal cortex and the bilateral temporoparietal junction activated across every task type, supporting a core mentalizing network, while surrounding activation differed by task.

A single patient shows the limit of that association. Bird et al. (2004) reported patient G.T., whose bilateral anterior cerebral artery stroke damaged the medial frontal lobes extensively, including regions that imaging had marked as necessary for theory of mind. She had planning and memory difficulties, yet she performed adequately on several mentalizing tests. One case cannot settle the question, but it rules out a simple, universal medial frontal account of social inference.

The dorsomedial prefrontal cortex activated in every category of mentalizing task that the meta-analysis examined. Yet a patient with extensive bilateral medial frontal damage still passed several mentalizing tests. Imaging can show that a region is active during a task; only lesion evidence can show whether the region is necessary for it, and in this case, the one lesion study says it is not.

In practice, assess social interpretation directly instead of inferring it from a frontal midline finding, and keep it separate from planning and attention, which the same tissue also serves. Do not tell a client or family that a medial frontal abnormality explains social misunderstanding. The one relevant lesion case says it need not.

This may relate to broader network functions that, according to the meta-analysis, include the bilateral temporoparietal junction, an area known for receptive language interpretation. This includes both linear language (what is said or written) and the nonverbal components of communication such as tone of voice (prosody), facial expression, and body language. When these areas remain intact, some mentalizing abilities may remain, even in the face of a dorsomedial prefrontal cortex lesion.

The Ventromedial Prefrontal and Subgenual Cingulate Cortex Assign Value and Turn Off Fear

The ventromedial prefrontal cortex (vmPFC) is a functional label for the lower medial wall and the adjacent medial orbital surface. On the map of Öngür et al. (2003), it includes medial areas 10 and 11, area 14, area 25, and the ventral part of area 32. The subgenual cingulate cortex, the cingulate below the genu that includes area 25 and adjacent subgenual areas, is its most clinically famous piece. This territory belongs to the medial prefrontal component of the default mode network (Raichle et al., 2001).

Bartra et al. (2013) pooled 206 fMRI studies of subjective value, the worth an option holds for the individual. They identified a valuation system in the vmPFC and ventral striatum whose activity rose with value across many kinds of reward. The founding human observation is older and is a person. Damasio et al. (1994) reconstructed the path of the iron rod through Phineas Gage's skull. They estimated that the damage involved both the left and right prefrontal cortices, in a pattern matching modern patients with defects in decision making and emotional processing.

The reconstruction was an estimate from a skull without an autopsy of tissue, so the case illustrates a syndrome without proving precise localization of tissue damage.

Bechara et al. (1994) turned that syndrome into a laboratory measure with the Iowa Gambling Task. In this card game, decks that pay well in the short run cost more in the long run. Patients with ventromedial prefrontal damage kept choosing the disadvantageous decks while their intellect on standard tests remained normal. Insensitivity to future consequences alongside intact intelligence is exactly the profile that frustrates families and employers.

The same tissue supports the recall and expression of safety learning. Fear extinction is the learning of a new safety memory that suppresses a conditioned fear response. Milad et al. (2007) found that recall of extinction activated the vmPFC and hippocampus together in healthy adults, and vmPFC activation was associated with extinction memory strength.

Milad et al. (2009) then ran the same protocol in 16 people with posttraumatic stress disorder and 15 trauma-exposed controls. The PTSD group showed impaired extinction recall, with lower activation of the vmPFC and hippocampus during recall. The sample was small and the design cross-sectional, so the study links vmPFC underactivation with impaired extinction recall. It does not show which came first, or whether the memory was lost or merely not retrieved.

Mood disorders concentrate here. Drevets et al. (1997) found decreased activity and reduced gray matter volume in the prefrontal cortex ventral to the genu in familial bipolar and unipolar depression. Mayberg et al. (2005) reasoned that elevated area 25 metabolism in treatment-resistant depression could be treated with chronic deep brain stimulation, electrical stimulation through surgically implanted electrodes. They stimulated white matter beside the subgenual cingulate in six patients and reported sustained remission in four.

The stimulation targets white matter pathways beside area 25, not area 25 selectively. The two reports disagree on the direction of the activity difference, and the volume loss in the earlier sample is one plausible reason.

The open-label promise did not hold up in a controlled test. Holtzheimer et al. (2017) randomized patients with treatment-resistant depression to six months of active or sham subcallosal stimulation across multiple sites. The trial found no statistically significant difference in antidepressant efficacy between study arms.

Himes et al. (2025) later pooled open-label follow-up from 172 implanted patients across five studies. Their primary analyses covered 24 months, and smaller numbers followed to five years showed sustained improvement in depressive symptoms. That analysis has no sham arm, attrition rises with time, and four of its authors work for the device manufacturer, so it supports continued investigation, not a claim of efficacy.

Lesion data then point the opposite way from the dorsal cortex. Koenigs et al. (2008) found that veterans with bilateral vmPFC lesions had markedly lower depression scores than veterans with nonfrontal lesions, an association in that sample and not a general rule. The area 25 story therefore rests on strong anatomy, consistent imaging, a null sham-controlled trial, open-label long-term follow-up, and lesion evidence consistent with a contribution to depression. A provider should say all five.

The ventromedial prefrontal cortex, including subgenual area 25, assigns value to options, holds future consequences in view, and supports recall of the safety memory that extinguishes conditioned fear. Its damage leaves intelligence intact and decision-making poor, and in one veteran sample it was associated with lower depression scores. People with PTSD underactivate it when recalling safety, and familial depression shows reduced volume in the subgenual region. A sham-controlled trial of subcallosal deep brain stimulation found no significant advantage over sham, while open-label follow-up reports sustained improvement.

No scalp site sits over the vmPFC, and this is the region where a neurofeedback provider should be most modest. Fp1 and Fp2 project to the superior frontal gyrus at the frontal pole, and no surface montage isolates area 25 (Koessler et al., 2009, as summarized by Scrivener & Reader, 2022). That limit concerns what a provider can establish, not what training can affect, because feedback on a scalp signal may indirectly change connected regions. Conventional scalp EEG neurofeedback cannot selectively engage the vmPFC or area 25. Even swLORETA neurofeedback aimed at training area 25 should be approached cautiously in terms of its selective engagement of that Brodmann area.

To train this area as directly as possible, Sebern Fisher (2016) began using a location she labeled Fpo2, or right frontal pole orbital, which places the active sensor under the right eyebrow, above the eye. She reported resolution of anxiety and fear responses, and other clinicians have adopted this training location with similar results in some clients (personal experience). This area is also thought to influence the orbitomedial prefrontal cortex discussed below.

Some clients present with poor real-world decision-making despite intact test scores, or with a fear that will not extinguish despite good exposure work. Say that limit plainly, and make sure the plan includes therapies with direct evidence for those problems.

The Orbitofrontal Cortex Updates Reward Value and Restrains Social Behavior

The orbitofrontal cortex (OFC) is the cortex on the floor of the frontal lobe above the eye sockets. It covers areas 11, 13, and 14, with area 47 on its lateral edge (Öngür et al., 2003). The medial orbital cortex overlaps with the ventromedial territory described above, and most authors use OFC to refer to the central and lateral orbital surface.

Fellows and Farah (2003) compared patients with ventromedial frontal lesions, patients with dorsolateral frontal lesions, and healthy controls on a simple reversal learning task. In such a task, a previously rewarded choice becomes wrong, and the person must switch. Neither lesion group had trouble learning the initial pairing, and only the ventromedial group failed to reverse. The deficit is specific to updating value when the world changes.

Camille et al. (2011) sharpened the account. Orbitofrontal damage disrupted learning which stimuli pay while leaving learning which actions pay intact, the mirror image of the dorsal cingulate deficit described earlier.

Hornak et al. (2003) studied patients with circumscribed surgical excisions. Some patients with bilateral OFC lesions had deficits in identifying emotion in voices and faces. The bilateral group as a whole showed impaired social behavior and changes in subjective emotional state. Patients with dlPFC lesions performed normally on every measure.

This is the cleanest human dissociation between the orbital and dorsolateral surfaces. It is the reason a client with OFC damage can pass an executive battery and still lose friends.

The disease that targets this surface is behavioral variant frontotemporal dementia, a neurodegenerative disorder that erodes personality and social conduct.

Rosen et al. (2002) applied voxel-based morphometry, an automated comparison of gray matter density across whole brains, to eight patients with the frontal variant. They found gray matter loss concentrated in the ventromedial and posterior orbital frontal cortex, the insula, and the anterior cingulate cortex. Eight is a small sample, and the atrophy pattern matched the behavior.

Obsessive-compulsive disorder reaches this surface as well. Chamberlain et al. (2008) found that patients with OCD and their clinically unaffected relatives both underactivated the lateral orbitofrontal cortex during reversal learning. Reduced activation in relatives without symptoms points to a familial trait. It is neither a diagnostic test nor evidence that orbitofrontal dysfunction alone causes OCD.

The orbitofrontal cortex, areas 11, 13, 14, and 47 on the floor of the frontal lobe, updates the value of choices when outcomes change. It also supports the reading of emotion in faces and voices. Bilateral damage impairs reversal learning, social behavior, and subjective emotion while leaving dorsolateral executive tests intact. Frontotemporal degeneration that begins on this surface presents as a change in conduct.

In practice, no scalp electrode sits over the orbital surface, and the tissue lies beneath the frontal sinuses and the eye-movement artifact that providers spend their careers filtering out. Scalp neurofeedback cannot selectively engage the OFC, whatever indirect effects it may have.

A neurofeedback provider's contribution here is recognition. New-onset disinhibition, loss of empathy, or reckless spending in a client past midlife is a referral to neurology before it is a training plan. When behavior becomes repetitive, examine whether the client detects that outcomes have changed and can use that information to revise a choice.

The Frontopolar Cortex Juggles Goals and Remembers Intentions

The frontopolar cortex is Brodmann area 10 at the very front of the brain (Öngür et al., 2003). Most providers place it under Fp1 and Fp2, and it is the region least discussed in protocol manuals. One naming collision waits here. Bludau et al. (2014) mapped the human frontal pole and named its lateral area Fp1 and its medial area Fp2. Those are cytoarchitectonic areas, not electrode sites, and both electrode sites sit over cortex that contains both anatomical areas.

Burgess et al. (2007) proposed that the frontopolar cortex gates attention between current sensory input and self-generated thought, with medial area 10 supporting the former and lateral area 10 the latter. They also reported area 10 activation during prospective memory, remembering to carry out an intended action after a delay. Their account is a hypothesis with several lines of evidence, and a provider should present it as one. Owen et al. (2005) listed the frontal pole among the regions their n-back meta-analysis reliably engaged, which suggests a role alongside the dlPFC when tasks demand holding several subgoals at once.

Lesion work supports the multitasking account. Burgess et al. (2000) gave a multitasking procedure to 60 people with circumscribed lesions and 60 matched controls. People with lesions affecting the medial parts of areas 8, 9, and 10 showed rule-breaking and failures to switch tasks. The clinical picture is the client who passes standard executive tests and still cannot juggle several tasks or remember to act on an intention.

The frontopolar cortex, area 10, sits under Fp1 and Fp2 and has been proposed to gate attention between the outside world and self-generated thought. It activates during prospective memory and demanding working memory tasks. Its clinical signature is a failure to juggle goals and act on delayed intentions in a person whose standard executive scores look normal. The anatomical areas named Fp1 and Fp2 are not the electrode sites of the same name.

For a provider working at Fp1 or Fp2, the advantage is anatomical consistency. These sites projected onto the superior frontal gyrus in all 16 participants of one projection study (Koessler et al., 2009, as summarized by Scrivener & Reader, 2022). The disadvantage is artifact, since eye blinks and the frontalis muscle dominate these channels. Choose a prospective memory or dual-task outcome measure, and verify artifact rejection before trusting any change in band power.

What the Electrode Sees Is a Population Average and a Volume-Conducted Sum

Every section above ends at a scalp site, so the last question is how well the International 10-20 System finds the region a provider intends. That system is the standard scheme that spaces electrodes at 10% and 20% intervals of head measurements. Scrivener and Reader (2022) summarize the projection study by Koessler et al. (2009), who projected electrode positions onto the cortex of 16 healthy adults. Fp1 and Fp2 landed on the superior frontal gyrus in every participant, whereas most central and parietal electrodes spread across four different Brodmann areas.

In their own data from 20 adults, frontal electrodes were the least variable. C3 and C4, the sites providers use to find the motor cortex, lie closer to the postcentral than the precentral gyrus.

Two more limits deserve a sentence each. First, a scalp electrode records a sum of many cortical sources spread by volume conduction, the passive spread of electrical fields through brain tissue, fluid, skull, and scalp. The recorded activity therefore does not exclusively represent the nearest cortex (Scrivener & Reader, 2022). Second, the Brodmann areas themselves vary in position, as the first section showed (Rajkowska & Goldman-Rakic, 1995), so the electrode-to-area chain has two links, each carrying error.

A third limit belongs to the frontal sites in particular. Whitham et al. (2007) recorded scalp EEG in two subjects before and during complete neuromuscular paralysis. Power above 20 Hz was 10 to 200 times lower during paralysis. Ordinary scalp recordings of beta and gamma therefore carry substantial electromyography (EMG), the electrical activity of muscle. Two subjects are a tiny sample, but the paralysis design leaves little room for another explanation.

Frontal channels sit over the frontalis muscle of the forehead and near the temporalis muscle of the temple, so inspect for muscle before anyone calls fast frontal activity prefrontal dysfunction.

A scalp site is a population average with a margin of several millimeters in each axis, and the underlying Brodmann area moves from brain to brain on top of that. Frontal sites are the most consistent. Even a perfectly placed electrode, though, records a sum of sources spread by volume conduction, and above 20 Hz much of what it records is muscle. Claims of the form ‘F3 trains area 46’ should be spoken as approximations.

A workable response is to state the target as a gyrus and a network, keep the outcome measure functional, and add source-resolving methods when the anatomical question matters. If a client has an MRI, use it. Write the treatment note in the language this post has used: F3 over the middle frontal gyrus in the frontoparietal control network, expected function working memory, outcome measure n-back. And before interpreting any fast frontal rhythm, look at the raw trace for muscle. Think of training choices and their expected results as a scientific hypothesis to be tested with quantitative measures that allow disconfirmation and subsequent adjustment of the training protocol.

Integrative Summary

In human data, the prefrontal cortex resolves into six territories. The dorsolateral cortex, areas 9 and 46, holds and manipulates information within the frontoparietal control network (Barbey et al., 2013; Owen et al., 2005). Its best-documented failures are execution failures (Stuss & Alexander, 2007). The ventrolateral cortex (areas 44, 45, and 47) contributes to initiating inhibitory control on the right and supports speech on the left (Aron et al., 2003; Choo et al., 2022; Dronkers et al., 2007).

The dorsal anterior cingulate and dorsomedial cortex (areas 24, 32, and medial 8 and 9) detect conflict and energize action (Kerns et al., 2004; Stuss & Alexander, 2007). They learn the value of actions and contribute to the cardiovascular side of effort (Camille et al., 2011; Critchley et al., 2003). The same territory contributes to frontal midline theta and can contribute to apathy when damaged (Ishii et al., 1999; Knutson et al., 2014). In obsessive-compulsive disorder, its error signals run loud (Fitzgerald et al., 2005).

The ventromedial cortex and subgenual area 25 assign value and support extinction recall (Bechara et al., 1994; Milad et al., 2007). Extinction recall is the retrieval, after a delay, of the safety memory a person formed when a feared cue stopped predicting harm; when it fails, the old fear returns. Their damage was associated with lower depression scores in one lesion sample (Koenigs et al., 2008). The sham-controlled trial of subcallosal stimulation found no significant advantage over sham, and open-label follow-up reports sustained improvement (Himes et al., 2025; Holtzheimer et al., 2017).

The orbitofrontal cortex updates value when outcomes reverse and supports social conduct (Fellows & Farah, 2003; Hornak et al., 2003). Its degeneration presents as a change in character (Rosen et al., 2002). Frontopolar area 10 has been proposed to gate attention between the world and inner thought, and its damage was associated with multitasking failures (Burgess et al., 2000, 2007).

Two ideas integrate the six. First, each region is a node, and the network usually explains the symptom better than the node (Menon, 2011; Seeley et al., 2007; Yeo et al., 2011). Second, the electrode-to-region chain has two weak links. Brodmann areas move from brain to brain, and scalp sites carry millimeter-scale scatter and volume-conducted sources (Koessler et al., 2009; Rajkowska & Goldman-Rakic, 1995; Scrivener & Reader, 2022).

A provider who names the gyrus, names the network, chooses a functional outcome measure, and keeps trained EEG change separate from symptom change has stated the hypothesis clearly. That is a precondition for evidence-based treatment, not the same as having it. The rest is candor about what scalp recordings cannot selectively localize and what particular training protocols have not demonstrated.

Key Takeaways

1. Six territories organize the prefrontal map: dorsolateral areas 9 and 46, ventrolateral areas 44, 45, and 47, cingulate areas 24 and 32, ventromedial and orbitofrontal areas 10 to 14 and 25, and frontopolar area 10. Each shifts position from one brain to the next.

2. The dorsolateral cortex belongs to the frontoparietal control network and rearranges what is held in mind. The wider lateral frontal cortex sets tasks on the left and monitors performance on the right, and its best-documented failures are failures of execution.

3. The dorsal anterior cingulate anchors the salience network, detects conflict, energizes behavior, and contributes to frontal midline theta at Fz. Lesions there produce apathy, and in obsessive-compulsive disorder its error signals run hot.

4. The ventromedial and orbitofrontal cortex assign and update value, support recall of safety learning, and support social conduct. Scalp neurofeedback cannot selectively engage either, and a sham-controlled trial of subcallosal deep brain stimulation found no significant advantage over sham.

5. A scalp site is a population average with several millimeters of scatter, and fast frontal activity is often muscle. Name the gyrus and network, choose a functional outcome, and keep trained EEG change separate from symptom change.

Glossary

akinetic mutism: a state after bilateral medial frontal or cingulate damage in which a person is awake but neither moves nor speaks spontaneously.

anterior cingulate cortex (ACC): the cortex on the medial wall that wraps around the front of the corpus callosum, comprising Brodmann areas 24 and 32 with subgenual areas 25 and 33, and divided into dorsal, pregenual, and subgenual territories.

anterior midcingulate cortex (aMCC): the region behind the perigenual cingulate with distinct cell layering, within which many imaging locations labeled dorsal ACC fall.

apathy: diminished motivation and self-initiated activity.

behavioral variant frontotemporal dementia: the frontal variant of frontotemporal lobar degeneration, a neurodegenerative disorder that erodes personality and social conduct.

Broca's area: the region of the left inferior frontal gyrus, conventionally Brodmann areas 44 and 45, named for Paul Broca, who in 1861 linked damage there to loss of fluent speech; modern imaging of his cases shows their lesions extended well beyond it.

Brodmann area: one of the numbered cortical territories that Korbinian Brodmann defined in 1909 based on differences in cell layering.

conflict monitoring: the proposed anterior cingulate function of detecting competition between candidate responses and signaling the lateral prefrontal cortex to increase control.

cytoarchitecture: the layering, size, and density of cell bodies in a region of cortex as seen under a microscope.

deep brain stimulation: chronic electrical stimulation of a brain target through surgically implanted electrodes.

default mode network: the set of regions, including the medial prefrontal and posterior cingulate cortex, that show correlated activity at rest, are associated with self-referential and internally directed thought, and typically reduce their activity during externally directed tasks.

dorsolateral prefrontal cortex (dlPFC): the lateral prefrontal cortex on the middle and adjacent superior frontal gyri, Brodmann areas 9 and 46.

dorsomedial prefrontal cortex (dmPFC): the upper medial prefrontal cortex, the medial parts of Brodmann areas 8 and 9, adjacent to the dorsal anterior cingulate.

electromyography (EMG): the recording of electrical muscle activity, which can contaminate scalp EEG and does so most heavily above 20 Hz.

energization: the process of initiating and sustaining a response, which lesion studies localize to the superior medial frontal cortex.

extinction recall: the retrieval, after a delay, of the safety memory a person formed when a feared cue stopped predicting harm; when it fails, the old fear returns.

fear extinction: the learning of a new safety memory that suppresses a conditioned fear response; its recall in humans engages the ventromedial prefrontal cortex and hippocampus.

frontal midline theta: the theta rhythm that appears over the frontal midline during concentrated mental tasks, to which medial frontal generators, including the anterior cingulate, contribute.

frontoparietal control network: the executive-control network linking the dorsolateral prefrontal and lateral parietal cortices that carries out effortful tasks.

frontopolar cortex: Brodmann area 10 at the front of the frontal lobe, proposed to gate attention between the outside world and self-generated thought.

International 10-20 System: the standard scheme for placing scalp electrodes at 10% and 20% intervals of head measurements.

Iowa Gambling Task: a card game in which decks that pay well in the short run cost more in the long run, used to measure sensitivity to future consequences.

mentalizing: inferring another person's beliefs, intentions, or feelings.

n-back task: a working memory test in which items are presented one at a time and the person reports whether the current item matches the one shown n items earlier; raising n increases the load.

orbitofrontal cortex (OFC): the cortex on the floor of the frontal lobe above the eye sockets, Brodmann areas 11, 13, and 14 with area 47 on its lateral edge.

prospective memory: remembering to carry out an intended action after a delay.

response inhibition: the cancellation of a prepared or ongoing action; in humans the right inferior frontal gyrus contributes to initiating it.

resting-state functional connectivity: the correlation between spontaneous fMRI signals in distant brain regions while a person rests in the scanner.

reversal learning: a task in which a previously rewarded choice becomes the wrong one and the person must switch, used to measure value updating.

salience network: the network anchored by the dorsal anterior cingulate and frontoinsular cortex that connects with subcortical and limbic structures and decides what deserves control.

stop-signal task: a task that measures how quickly a person can cancel a response after a stop cue, yielding the stop-signal reaction time.

subgenual cingulate cortex: the cingulate cortex below the genu of the corpus callosum, including area 25 and adjacent subgenual areas, implicated in familial mood disorders.

subjective value: the worth an option holds for the individual making a choice.

Talairach atlas: a standardized three-dimensional coordinate system for the human brain, published in 1988, in which any location is specified by its distance in millimeters from the anterior commissure along three axes.

ventrolateral prefrontal cortex (vlPFC): the cortex of the inferior frontal gyrus, Brodmann areas 44, 45, and 47.

ventromedial prefrontal cortex (vmPFC): the lower medial wall and adjacent medial orbital surface, including medial areas 10 and 11, area 14, area 25, and ventral area 32.

volume conduction: the passive spread of electrical fields through brain tissue, fluid, skull, and scalp, which makes each scalp electrode record a sum of many sources.

voxel-based morphometry: an automated method that compares gray matter density across whole brains.

working memory: the capacity to hold and manipulate information over seconds.

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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 he 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 helps to maintain BCIA's certification programs. He is a recipient of AAPB's Distinguished Scientist Award and BFE's Lifetime Impact Award.

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