The Von Economo Neurons in Frontoinsular and Anterior Cingulate Cortex in Great Apes and Humans

What This Research Found

Allman and colleagues' comprehensive study examines Von Economo neurons (VENs)—a distinctive type of brain cell found only in highly social species. These large, spindle-shaped neurons are concentrated in two regions critical for empathy and social cognition: the anterior insula and anterior cingulate cortex. The research reveals that VENs may be the cellular hardware underlying rapid social-emotional processing—the neural substrate of "gut feelings" about people and situations.

VENs have a unique structure suited for rapid signalling. Unlike the multipolar pyramidal neurons that dominate the cortex, VENs have a distinctive spindle shape with a single large apical dendrite and single basal dendrite. They are approximately three times larger than neighbouring neurons and have faster-conducting axons. This architecture suggests they evolved for rapid transmission of information—getting social-emotional signals to action centres quickly.

Their distribution is remarkably selective. VENs are found primarily in two interconnected regions: the anterior insula (involved in interoception, emotional awareness, and empathy) and the anterior cingulate cortex (involved in error monitoring, emotional regulation, and social decision-making). This strategic placement allows VENs to link emotional processing with autonomic responses and behavioural control.

The developmental timeline is critical. VENs appear late in fetal development (around 36 weeks gestation) but are sparse at birth. Their numbers increase dramatically during the first four years of life, reaching near-adult levels by age four. This postnatal development means VENs are shaped by early caregiving experiences in ways that prenatal neurons are not. The implications for understanding how early attachment affects empathy development are profound.

VENs express receptors for social bonding. These neurons show high levels of receptors for neurotransmitters involved in social bonding and emotional regulation—including serotonin, dopamine, and vasopressin. They are positioned to integrate emotional signals and relay them rapidly to autonomic centres. Damage to VEN-containing regions produces deficits in emotional awareness, empathy, and social decision-making.

Why This Matters for Survivors

Your abuser's empathy deficit may be neurobiologically real. One of the most confusing aspects of narcissistic abuse is the abuser's apparent inability to understand or care about the pain they cause. VEN research suggests this may not be a choice but a genuine neurological limitation. The cellular hardware that enables rapid empathic response may be compromised in individuals with narcissistic pathology. This doesn't excuse the abuse—adults are responsible for their behaviour regardless of neurobiology—but it helps explain why appeals to empathy so consistently fail.

Your "gut feelings" have a biological basis. Many survivors describe sensing something was wrong with their abuser before they could articulate what. This intuition, often dismissed as paranoia or oversensitivity, may reflect intact VEN function—your own social-emotional rapid processing system working as designed. When your gut told you something was off, it was likely detecting subtle social cues that your VENs integrated faster than conscious processing. Learning to trust this intuition again is part of recovery.

Early experience shapes empathy capacity. The postnatal development of VENs means that children who don't receive attuned caregiving during critical early years may develop with compromised empathy circuitry. This helps explain intergenerational patterns of narcissistic abuse: a parent whose own VENs didn't develop optimally may be unable to provide the attuned caregiving their child's VENs need to develop properly. Understanding this mechanism doesn't excuse the cycle, but it illuminates how it perpetuates.

Empathy is not just a moral choice. Narcissistic abusers are often told they need to "choose" to be more empathic, as if empathy were purely volitional. VEN research suggests that spontaneous, rapid empathic attunement depends on specific neural hardware. Some people may genuinely lack the cellular architecture for the kind of automatic empathy others experience. This reframes treatment expectations: cognitive empathy (learned rules about others' feelings) may be achievable where affective empathy (automatic emotional resonance) is not.

Clinical Implications

For psychiatrists, psychologists, and trauma-informed clinicians, VEN research provides neurobiological grounding for understanding empathy deficits and their treatment implications.

Assessment should distinguish empathy types. VEN-mediated empathy is rapid and automatic—the immediate "felt sense" of another's emotional state. This differs from cognitive empathy, which involves deliberate perspective-taking. Patients with compromised VEN function may show intact cognitive empathy (they can reason about others' feelings) while lacking affective empathy (they don't spontaneously feel what others feel). Assessment should distinguish these components, as treatment approaches and realistic goals differ.

Early intervention is neurobiologically justified. The postnatal development of VENs provides strong rationale for early intervention in at-risk families. Children whose early caregiving is disrupted are developing their empathy circuitry in suboptimal conditions. Intensive support during the first four years—when VENs are proliferating—may have lasting impact on empathy capacity. This argues for prioritising early childhood intervention over later remediation.

Treatment goals should be realistic about neurobiological limits. For adult patients with established empathy deficits, VEN research tempers expectations. If the cellular hardware for automatic empathy didn't develop properly, adult treatment may achieve compensatory strategies (learning social rules, reading cues cognitively) more readily than genuine affective empathy. This isn't therapeutic nihilism—meaningful change is possible—but realistic goal-setting prevents both clinician and patient frustration.

Survivor treatment benefits from neurobiological validation. For survivors, understanding that their abuser's empathy deficit likely has neurobiological substrates can be validating. It confirms that the emotional attunement they craved wasn't being withheld vindictively—it may never have been available. This can help survivors stop waiting for the empathy that won't come and redirect energy toward their own healing.

Broader Implications

VEN research extends beyond individual clinical encounters to illuminate how empathy—and its absence—shapes families, organisations, and societies.

The Developmental Window for Empathy

The postnatal development of VENs means that society-level factors affecting early childhood—parental leave policies, childcare quality, support for at-risk families—have neurobiological consequences. A society that doesn't support adequate early caregiving is a society that may be producing more individuals with compromised empathy circuitry. Investment in early childhood isn't just social welfare; it may literally be building the neural substrate for a more empathic population.

Intergenerational Transmission Mechanisms

The VEN developmental timeline provides a biological mechanism for intergenerational transmission of empathy deficits. A parent with compromised VEN function provides suboptimal emotional attunement during precisely the period when their child's VENs are developing. The child's VENs develop in an environment of emotional neglect, potentially producing another adult with compromised empathy capacity who then parents the next generation. Breaking this cycle requires intervention during the developmental window.

Evolutionary Perspective on Social Species

VENs appear only in highly social species with complex social structures. This convergent evolution—similar solutions arising independently in apes, elephants, and cetaceans—suggests that rapid social-emotional processing provides significant adaptive advantage for species that live in complex social groups. Human society depends on most members having intact empathy circuitry. When significant numbers lack this capacity, social cohesion suffers.

Implications for Leadership Selection

Research on VEN-containing regions shows reduced volume in individuals with narcissistic traits. Yet narcissistic individuals often seek and attain leadership positions. Understanding that empathy has specific neural substrates—not present equally in all brains—has implications for how we select leaders. Organisations and societies might benefit from assessing empathy capacity in leaders, though how to do so ethically remains challenging.

Criminal Justice and Responsibility

VEN research complicates questions of moral responsibility. If empathy deficits partly reflect developmental neurobiology, how should this affect how we understand and respond to harmful behaviour? The research doesn't eliminate responsibility—adults with empathy deficits can still learn rules and face consequences—but it does suggest that purely punitive approaches miss something important about the underlying condition.

Neurodiversity and Empathy Variation

VENs exist on a continuum; their number and function vary across individuals. This raises questions about neurodiversity: is low empathy capacity a disorder, a difference, or both depending on context? Some environments may actually reward low empathy (certain competitive contexts). Understanding empathy as partly neurobiological invites more nuanced thinking about what we consider pathological versus simply different.

Limitations and Considerations

Correlation versus causation. We know VENs are associated with empathy and located in empathy-related regions, but direct causal proof that VENs produce empathy remains incomplete. Other cell types and circuits contribute to empathic function.

Human studies are necessarily indirect. We cannot directly manipulate VENs in living humans. Much of what we know comes from post-mortem studies, comparative anatomy, and inference from lesion cases. Animal models help but have limits.

Individual variation is substantial. VEN counts vary significantly between individuals. We don't yet know how much variation is genetic versus environmental, or what threshold of VEN reduction produces clinically significant empathy deficits.

Development is complex. While VENs proliferate postnatally, many other factors also shape empathy development. Attributing empathy deficits solely to VEN development oversimplifies. Genetics, other neural circuits, and later experiences all contribute.

How This Research Is Used in the Book

Allman's VEN research appears in Chapter 7: Architecture of Structures to explain the cellular basis of empathy and social intuition:

"These cells enable the rapid integration of social and emotional information. VENs link the anterior insula directly to the anterior cingulate cortex, creating a fast pathway enabling social intuition. They are the cellular hardware of social intuition—the brain cells which allow a 'gut feeling' to guide behaviour before conscious deliberation."

The book uses VEN research to ground abstract concepts like "empathy deficit" in concrete neurobiology. Understanding that empathy depends on specific cells that develop postnatally helps explain both how narcissistic pathology develops and why it proves so resistant to change.

Historical Context

Von Economo neurons were first described by the Austrian neurologist Constantin von Economo in the 1920s during his studies of encephalitis lethargica. For decades, these distinctive spindle-shaped cells were considered a neuroanatomical curiosity without clear functional significance.

Beginning in the early 2000s, Allman's laboratory at Caltech transformed understanding of VENs. By demonstrating their presence specifically in highly social species—humans, great apes, elephants, whales—and their concentration in empathy-related brain regions, Allman established VENs as potentially crucial for social cognition. The 2010 paper synthesised a decade of this work, becoming the standard reference for VEN function.

Subsequent research has linked VEN abnormalities to conditions including autism, frontotemporal dementia, and—relevant to this book—reduced anterior insula volume in narcissistic personality disorder. VENs have moved from anatomical curiosity to central importance in understanding the neurobiology of social-emotional function.

Further Reading

• Craig, A.D. (2009). How do you feel—now? The anterior insula and human awareness. Nature Reviews Neuroscience, 10(1), 59-70.
• Seeley, W.W. et al. (2006). Early frontotemporal dementia targets neurons unique to apes and humans. Annals of Neurology, 60(6), 660-667.
• Fan, Y. et al. (2011). Is there a core neural network in empathy? NeuroImage, 54(3), 2446-2458.
• Schulze, L. et al. (2013). Gray matter abnormalities in patients with narcissistic personality disorder. Journal of Psychiatric Research, 47(10), 1363-1369.
• Von Economo, C. (1926). Eine neue Art Spezialzellen des Lobus cinguli und Lobus insulae. Zeitschrift für die gesamte Neurologie und Psychiatrie, 100, 706-712.