Capgras syndrome

1) Overview — What is Capgras syndrome?

Capgras syndrome (Capgras delusion) is a state of “impostor-themed delusion” belonging to the family of Delusional Misidentification Syndromes (DMS). It refers to a cluster of symptoms in which the brain can still “see” and “recognize the faces of familiar people” to some extent, but misinterprets them as if close others have been swapped out / replaced by strangers in disguise — whether that person is a spouse, partner, parent, child, or primary caregiver. The patient is not just saying “I feel distant from them” or “they’ve changed” as a metaphor; they genuinely believe, at a psychotic level, that “this is not the real person — this is an impostor.”

The name “Capgras” comes from French psychiatrist Joseph Capgras, who described a female patient who believed that the people around her had been replaced by dozens of “doubles” or “impostors.” He called this phenomenon “illusion des sosies”, or “the illusion of lookalike doubles,” which was later developed into the terms Capgras syndrome / Capgras delusion in later psychiatric literature.

The important point is that in Capgras, the patient is not deluded in the sense of “I don’t know who this is at all” like in prosopagnosia (face blindness). Instead, they are in the position of “I can tell they look exactly like the same person, but my heart tells me they’re not.” They see the same body shape, face, voice, gestures, and many matching features, but feel strange, distant, and unfamiliar — as if a stranger were wearing a mask of their loved one. The brain then constructs a “story” to explain this: the original person has been swapped out, and the one standing here now is an impostor.

Because of this, Capgras is classified as a “delusional misidentification” — not a visual or eye problem, but a problem at the level of interpreting familiarity and identity. The brain receives visual input normally, but the system that previously generated a sense of warmth, attachment, and safety when seeing the faces of close others no longer functions as before. This creates a gap between “the image that is seen” and “the feeling inside.” That gap is then filled in by a delusion.

Capgras is not a standalone “disorder” by itself in DSM-5-TR. Instead, it is regarded as one specific manifestation of delusion that can appear under several major diagnostic umbrellas, such as:

Schizophrenia spectrum and other psychotic disorders

Mood disorders with psychotic features, such as bipolar disorder or major depression with psychosis

Neurocognitive disorders, such as Alzheimer’s disease, Dementia with Lewy Bodies (DLB), or Parkinson’s disease dementia

Or Psychotic Disorder due to Another Medical Condition / following brain injury / stroke, etc.

In the group of dementias, especially Dementia with Lewy Bodies (DLB), Capgras is discussed very frequently, because these patients commonly have visual hallucinations, fluctuating levels of alertness, and pre-existing abnormalities in face processing. This makes “impostor stories” easy to generate and very convincing in daily life — to the point where some patients fear or hate their own spouse or partner, because they believe that person is an impersonator, not the original partner they once loved.

From a neuropsychological perspective, many theories propose that Capgras arises from abnormal connectivity between the face recognition system and the emotional–familiarity system (limbic/amygdala). That is, the brain can still say, “This face looks like my partner/mother,” but no emotional familiarity signal follows, so it feels as if one is looking at a stranger whose face happens to perfectly match their ex-partner. When this is combined with reduced function of frontal lobe circuits, which normally evaluate reasons and put the brakes on bizarre beliefs, the strange thought is no longer suppressed. It becomes a fully formed delusion that the person in front of them is an impostor.

Overall, Capgras syndrome is not about “overthinking” or “just having an active imagination.” It is a sign that the brain network which recognizes the identity of close others and gives faces their emotional meaning is seriously malfunctioning. This often occurs in the context of moderate–severe psychiatric illness or advanced dementia/neurological disease. If not properly assessed and managed, it can lead to severe family conflict, violence, or crisis-level stress for both the patient and caregivers.

2) Core Symptoms — Core features of Capgras syndrome

Big picture first:
Capgras does not mean “you see a face and can’t recognize it.”
It means: “You recognize that the face looks like the original person, but your heart/feelings say it isn’t.”
So the brain creates a “story” that this person has been swapped / replaced / is an impostor.

To explain this simply to readers, think of it in three layers:

Input: The visual–face recognition system = still functioning.

Feeling: The “familiarity/bonding” system = drops / is out of sync.

Story: The brain tries to find a reason → creates the delusion: “This is an impostor.”

From here we break it down into subpoints A–D in detail.

(A) The “impostor” delusion — Core belief structure

This is the heart of Capgras:

“They look exactly like my partner/mother, but inside they’re not the same person. They’ve been swapped / replaced.”

1. Content of the belief (content of delusion)

The focus is usually on “very close people”, such as:

Partner, spouse

Mother, father

Children

Primary caregiver

The person most frequently involved is the primary caregiver — the one who is physically closest and most involved in the patient’s life.

The patient will insist that:

This person is a “fake,” “stranger in disguise,” “robot/spy pretending to be them,” etc.

Some patients have “supporting theories”, such as:

There is a secret organization replacing people.
There is some hidden evil plan.
Or in dementia: there may be no clear conspiracy narrative, but they still firmly believe “this is not the real person.”

2. Key point: “Everything looks the same, but it’s not”

Patients will often say things like:

“The face looks the same, the voice is the same, but the feeling is wrong.”

This is different from conditions where the person truly cannot recognize faces, such as prosopagnosia:

Prosopagnosia: You see a face but can’t tell who it is.

Capgras: You know it looks like your partner, but you feel it’s not the same person.

3. The target of the delusion is not limited to “people”

Although the classic target is a close person, some cases (especially those with dementia/Parkinson’s/neurodegenerative disease) show that patients may:

Believe that pets have been swapped

e.g., “This dog is not my old dog. It looks the same, but it’s not.”

Or believe that the house/room/place has been replaced

e.g., “This house looks like ours, but it’s actually a fake house built to fool me.”

This is very useful in content writing, because it conveys the feeling of a “fake world” — like sci-fi meets psychology in real life.

4. Systematization of the delusion (expansion into a system)

In some people, the “impostor” idea does not stop at just one person but expands into a system, for example:

Starts with the partner → later thinks friends/relatives have been swapped too.

Eventually starts to believe that “the whole town is a fake stage.”

At this point it begins to overlap with persecutory delusions or other bizarre delusions.

For writing/blog purposes, you can map it as:

Level 1: Only one person (e.g., romantic partner).

Level 2: Multiple people + beginning of a conspiracy story.

Level 3: The entire world becomes a fake stage (very severe psychosis).

(B) Strong conviction + unshakable by evidence — the “full-blown delusion” tone

This is the signature that shows “this is not just overthinking/suspiciousness.”

1. 100% belief (delusional conviction)

Patients are often very confident that they can “see through” reality.

Even in the face of contradicting evidence, such as:

Old photos together

Shared events with deep and specific details

Audio/video recordings, etc.

They may say things like:

“Sure, there are photos, but the person in those photos is the one who got swapped out.”

Or “All of you are in on it together.”

This is the classic pattern of delusion:

Every new piece of information is interpreted in a way that fits the existing belief,
not used to test or disprove it.

2. Confabulation — Filling the gaps in the story

To make their story seem more logical, the brain will:

Add details, such as:

“I know because this person walks differently.”
“They hold the glass in their left hand, but my real partner always held it in their right.”

Even when these reasons are somewhat internally inconsistent, the patient does not feel that anything is strange.

For general readers, you can explain it as:

The brain is “reverse-engineering” the strange feeling → backfilling reasons that match it.

3. Double bookkeeping — Outwardly agreeing, but inwardly unchanged

Some people (especially those who are cognitively intact or have only mild dementia) may show this pattern:

In front of doctors/family: “Okay, okay, maybe I’m just overthinking.”

But deep inside, the belief remains 100% unchanged.

When they have a chance to be alone or time passes, the old belief returns in full force.

This explains why Capgras can “seem to fade temporarily in the clinic,” but becomes severe at home again.
→ This can lead to underestimating the danger if clinicians only go by what they see during the brief consultation.

(C) Emotional and behavioral consequences — where the “risk” and real-life drama come in

The delusion itself is intense, but the truly frightening part is the reaction that follows.

1. Common emotional responses

Suspicion / fear

Especially if they believe their close person has been replaced by a “dangerous impostor with bad intentions.”
The emotional state is often a mix of anger + fear + extreme loneliness.

Anger / resentment

Some believe the impostor is going to harm them or exploit them.

Sadness / sense of loss

In dementia/older adults, some will cry because they genuinely believe:

“My partner/child is gone. This is a fake. I miss the real one.”

This makes Capgras not just an odd symptom, but a deeply painful emotional wound for both the patient and the family.

2. Behavioral consequences

Avoidance / fleeing

Refusal to stay alone with the “impostor.”
Changing bedrooms / asking someone else to stay nearby instead.

Surveillance / checking / spying

Eavesdropping on phone calls, checking personal belongings.
Taking photos/recordings to “gather evidence” that this isn’t the real person.

Confrontation / aggression (this is a major safety flag)

Pushing, shouting, insulting, trying to drive the impostor out of the house.
In some international cases, this has escalated to physical assault or even homicide, due to the belief that the impostor is dangerous.

3. Impact on the surrounding system

The person who is seen as “the impostor” will:

Feel deeply hurt (“I really am their partner/child, but they no longer believe it.”)

Experience severe burnout, since they are both caregiving and constantly being accused.

The home environment turns into:

A psychological battlefield.

Every small gesture is interpreted by the patient as supporting their delusion.

For blogs/educational content, this section is what makes readers feel that Capgras is far more serious than they might have thought.

(D) Common patterns in Dementia with Lewy Bodies (DLB)

In DLB, Capgras often shows up as a “package” that looks like this:

Cognitive fluctuations

Some days they’re very clear; other days they’re very confused.
Capgras may be worse in the evening/night (classic “sundowning” style).

Visual hallucinations

Seeing people/objects/shadows/animals that aren’t there.
Combined with Capgras, the brain has a lot of “raw material” to spin impostor stories.
For example, seeing “a strange shadow behind my partner” → interpreted as “This is not the real partner.”

High anxiety + environmental sensitivity

Dim lighting, dark corners, reflections in mirrors → can easily trigger symptoms.
When someone changes clothes/hairstyle/glasses, it can be a key moment where Capgras flares up.

Neuroleptic sensitivity

People with DLB are often much more sensitive to antipsychotic medications than the general population.
This makes managing Capgras in DLB more difficult than in a typical schizophrenia case.

If you run a knowledge site like Nerdyssey, this part is pure gold, because it:

Shows how the presentation of Capgras in older adults differs from that in younger schizophrenia patients.

Explains why “stubborn refusal to accept reality” is not just stubbornness, but the product of genuinely altered brain circuits.

3) Diagnostic Criteria — Practical diagnostic approach to Capgras (in depth)

As mentioned earlier:

Capgras does not have its own standalone “disorder slot” in DSM-5-TR.

It is a “form of delusion” that must be placed under a larger diagnosis, such as:

Schizophrenia / Schizoaffective disorder

Delusional Disorder

Mood Disorder with Psychotic Features (e.g., Bipolar)

Dementia / DLB / Parkinson’s disease dementia

Psychotic Disorder due to Another Medical Condition, etc.

So when clinicians diagnose, they don’t just ask “Is this Capgras or not?”
They ask:

“This Capgras phenomenon is occurring within the framework of which disorder?”

We can lay this out as a stepwise workflow that works both in clinical practice and as an easy-to-read blog structure.

Step 1: First confirm — “Is this truly a delusion?”

We must distinguish between:

✅ Delusion

❌ Just “suspiciousness,” “overthinking,” “distrust,” or confusion due to impaired consciousness / drug effects

Criteria for a delusion:

A belief that is clearly false and out of line with reality (not just a different interpretation).

High conviction – does not change even when presented with clear contradictory evidence.

Impacts daily functioning, such as destroying relationships or causing aggression, etc.

If someone only says:

“Lately my partner’s behavior is so strange that I feel like they’re not the same person.”

but is still open to reasons, doubts themselves, and can consider alternatives → this is not yet a delusion.

Step 2: Assess the overall scope of psychosis

Questions in a clinical context might be:

Is there hallucination?

Hearing voices talking, commanding, seeing people or shadows, etc.

Is there disorganized speech/behavior?

Speech that jumps randomly from topic to topic with no logical connection.
Odd behaviors such as strange ritualistic rearranging of objects, inappropriate gestures, etc.

Are there negative symptoms?

Flattened affect (blunted emotional expression).
Speaking very little, lack of motivation (avolition).
Social withdrawal, etc.

If many of these show up → we start thinking Schizophrenia spectrum.
If there are very few or none, but the delusion is prominent → we lean more toward Delusional Disorder.

Step 3: Place it within DSM frameworks — Schizophrenia vs Delusional Disorder vs Mood

3.1 If it meets criteria for Schizophrenia / Schizoaffective

At least 2 of the Criterion A symptoms (delusions / hallucinations / disorganized speech / disorganized behavior / negative symptoms).

Duration ≥ 6 months (including prodromal and residual phases).

Marked decline in social, occupational, or self-care functioning.

In such cases, Capgras would be recorded as:

Schizophrenia, with Capgras delusion (a form of delusional misidentification).

Here, Capgras = a specification of the delusion, not the primary disorder name.

3.2 If they don’t meet schizophrenia criteria, but the delusion is prominent and lasts ≥ 1 month → think Delusional Disorder

Key criteria:

At least 1 delusional theme lasting ≥ 1 month.

Has never met Criterion A for schizophrenia.

Overall functioning is relatively preserved (except in areas directly affected by the delusion).

If hallucinations are present → they are not prominent and are consistent with the delusional theme.

In this case, Capgras would be framed as:

Delusional Disorder, with Capgras-type misidentification.

For article writing, you can create a comparison table:

Aspect	Schizophrenia + Capgras	Delusional Disorder + Capgras
Other sx	Often hallucinations, disorganized speech, negatives	Rare or minimal other psychotic features
Function	Decline in many areas	Decline mainly in areas affected by the delusion
Duration	≥ 6 months	≥ 1 month
Mood	May fluctuate but not central	Usually not the main axis

3.3 If symptoms are strongly tied to mood episodes → Mood Disorder with Psychotic Features

Examples:

During extreme manic episodes or very severe depressive episodes (major depression with psychotic features),

The delusion appears only when the mood state is severely pathological.

When mood improves → the delusion fades or disappears.

If Capgras appears only during mania and resolves once mood is stabilized → the primary framework is Bipolar I with psychotic features, not a “pure psychotic disorder.”

Step 4: If there is brain disease / older age / late-onset psychosis → think “secondary/neurologic” first

Red flag pointers:

Age > 50–60 with no previous psychosis history.

Other signs pointing to dementia, such as:

Impaired short-term memory.
Getting lost in familiar places.
Personality changes.

Or clear neurological disease, such as:

Parkinson’s disease.
History of stroke / head injury / epilepsy, etc.

In such cases, Capgras may be framed as:

Major neurocognitive disorder (e.g., DLB, Alzheimer’s) with psychotic features including Capgras-type misidentification,
or
Psychotic disorder due to another medical condition, if the pattern matches the underlying disease.

Clinical workflow (for article explanation):

Assess consciousness and cognition (cognitive assessment).

Take a full medical and medication history.

Look for acute confusion → if present → consider delirium.

Consider brain imaging / lab tests if there are red flags: rapid onset, focal neurological signs, etc.

Step 5: Differentiate from other conditions that “look similar but are not Capgras”

For a “Differential diagnosis” section, you can use this list:

Prosopagnosia (face blindness)

Cannot recognize faces → does not know who the person is.
Different from Capgras, where they know the face looks the same but feel it isn’t.

Simple suspiciousness / overvalued ideas

A partner may suspect infidelity and say, “You’re like a different person.”
But they still know they might be overthinking.
There is doubt, not 100% conviction.

Depersonalization / derealization

Feeling like “the world is fake” or “everything feels dreamlike.”
But still knows the people around them are the same people; it just feels strange/unreal.

Confusional state / delirium that is not a true delusion

The patient is confused about time, place, and people → may misname or say someone is “not the same person.”
But the belief is not fixed — it fluctuates with their level of consciousness.

People using metaphorical language

e.g., “My mom has changed so much; she’s like a different person.”
On probing, you find they mean “her personality/attitude has changed” → this is a metaphor, not a delusion.

Step 6: ICD-11 / Coding in systems (for documentation / pro-level blogs)

Key concept:

Code the primary disorder first → then mention “delusional misidentification (Capgras type)” in clinical notes or summaries.

ICD-11 includes categories for psychotic disorders and specifiers for misidentification delusions in various teaching materials and reviews.

When citing specific codes:

It’s best to open the WHO ICD-11 Browser directly.

Some codes/subcategories are arranged in ways that can confuse non-specialist writers.

For blog content, you don’t need to list every single code in detail; just help readers understand that:

Capgras = one manifestation of “misidentification delusion”
which can occur in multiple underlying disorders. When reading research, always check “Capgras within which diagnostic framework?”

Step 7: Red flags (safety issues)

It’s very useful to include a “Warning / Seek urgent medical help” box like this:

They start believing that people in the house are impostors and begin to show aggressive behaviors.

They start saying they want to run away from home because they’re afraid the “impostor” will harm them.

New-onset symptoms in an older adult, especially after an illness / surgery / medication change.

Severe hallucinations occur alongside the delusion (seeing strangers in the home, hearing command voices, etc.).

Emphasize clearly:

This content is for understanding,

It cannot be used to diagnose oneself or family members.

If there is suspicion, they should see a psychiatrist/neurologist for a full evaluation.

4) Subtypes or Specifiers — Clinical subtypes/identifiers

Capgras is usually categorized more as a phenomenology than an official subtype, but in clinical practice it is often divided in a pragmatic way as follows:

(1) Based on underlying etiology (etiology-based)

Psychiatric-associated: schizophrenia spectrum, delusional disorder, mood disorders with psychosis, etc.

Neurodegenerative-associated: DLB, Alzheimer’s disease, Parkinson’s disease dementia, etc. (as often seen in PMC review articles).

Brain injury/lesion-associated: post-stroke, TBI, tumors, epilepsy, etc. (frequently reported in case reports and reviews in NCBI).

(2) Based on temporal pattern

Acute/transient: short episodes that come and go (seen in delirium and certain phases of dementia/psychosis, as noted in PMC).

Chronic/persistent: long-standing, fixed delusional belief.

(3) Based on the “target” of the delusion

Only a single person (e.g., partner/caregiver).

Multiple people at once.

Includes pets/places (also reported).

(4) Co-existing DMS features

Some patients may simultaneously show features of other DMS (Fregoli, intermetamorphosis, subjective doubles) or shift between them. DMS review articles (e.g., ruj.uj.edu.pl) often describe this broader picture.

5) Brain & Neurobiology — Brain and neurobiological mechanisms of Capgras

5.1 The big model: “You know it’s them, but it doesn’t feel like them”

The classic work by Ellis & Young proposes that Capgras is the “mirror image” of prosopagnosia (face blindness) (Cambridge University Press & Assessment+1).

Prosopagnosia: The brain looks at a face but does not know who it is.

Capgras: The brain knows who it is, but the feeling of familiarity/bonding is gone.

This model divides face/person recognition into two levels:

Overt / Explicit recognition – conscious recognition

“Oh, that’s my mom’s face, that’s my partner’s face.”
Relies on the ventral visual stream, temporal lobe, fusiform face area, etc.

Covert / Implicit recognition – automatic emotional/autonomic response

Slight changes in heart rate, skin conductance, etc.
Linked to the amygdala, limbic system, and autonomic nervous system.

In normal individuals:

Seeing a face → recognition system says “Yes, that’s them” → emotional system provides a sense of familiarity/safety.

In Capgras:

The “see–recognize who it is” step is still relatively intact.

But the emotional/familiarity signal decreases or does not match.
→ The brain tries to explain this strange internal state by reasoning:

“This person isn’t really the same. They must be a fake.”

This is delusion as an explanation of a weird internal signal,
not just “randomly making things up,” but a radical misinterpretation of a sensorimotor–emotion mismatch (Cambridge University Press & Assessment+1).

5.2 Evidence from “automatic–familiarity” research

Several Capgras case studies have used skin conductance response (SCR) to measure autonomic responses when seeing faces:

Ellis et al. found that Capgras patients could consciously distinguish between faces of friends/family and strangers (explicit recognition),
but their SCR did not differ → their bodies did not register familiar faces as more “emotionally close” than strangers (Royal Society Publishing+1).

Some cases show “Capgras for voices”:

They recognize faces normally; SCR to faces may be normal.
But SCR to familiar voices is abnormal → suggesting that the familiarity system for voices is disrupted instead (ResearchGate).

In summary:

The person-recognition system does not consist of a single route; there are multiple modality-specific channels (face, voice, etc.), and each can be selectively impaired.

This can be used in creative content, for example, a character who believes their mother’s voice is fake, but her face seems normal.

5.3 Neural pathways involved — “From eyes → temporal → limbic → frontal”

From multiple neuropsychiatry and DMS lesion-mapping reviews (NCBI+2, Psychiatry Online+2), we can summarize the broad picture as:

Ventral visual stream / temporal lobe (occipito-temporal)

Handles object/face discrimination.
Includes regions such as the fusiform face area (FFA), which processes faces as “individuals.”

Connections to limbic system (especially the amygdala)

Familiar faces activate amygdala + autonomic responses more than unfamiliar faces.
In Capgras, this mechanism is disconnected or down-weighted, leading to the phenomenon of “seeing but not feeling that it’s the right person” (Cambridge University Press & Assessment+1).

Frontal lobe / belief evaluation network

The frontal regions, especially the prefrontal cortex, play a role in:

Evaluating the reasonableness of thoughts.
Suppressing beliefs that are too bizarre or incongruent with reality.

Lesion-based reviews show that DMS (including Capgras) are often associated with right frontal–temporal lesions (Psychiatry Online+1).

Two-stage model of delusions:

Perceptual/affective abnormality – wrong familiarity signal, weird internal cue.
Impaired belief evaluation – frontal networks stop properly filtering and rejecting odd interpretations.
→ Thus the “impostor theory” is allowed to solidify into a full-fledged delusional belief (UNCW+1).

5.4 Hypo- vs Hyper-familiarity — why DMS comes in multiple flavors (Capgras, Fregoli, etc.)

Newer DMS reviews introduce the framework of hypo-/hyper-familiarity (NCBI+1):

Capgras = hypofamiliarity

Things/people that should feel familiar → instead feel “wrong / strange / distant.”

Fregoli = hyperfamiliarity

Strangers → feel like “the same person disguised as different people.”

Overall, the same face–limbic–frontal network is involved, but the balance shifts in different directions:
→ producing different flavors of misidentification (impostor vs “same person in many disguises”).

In an article, you can illustrate this with a sliding scale graphic:

Left: hypofamiliarity → Capgras

Right: hyperfamiliarity → Fregoli

Middle: normal familiarity

5.5 Capgras and Dementia with Lewy Bodies (DLB) — why they pair so often

DLB is a disease where the “perception + attention + REM sleep + dopamine/acetylcholine” circuits all break down simultaneously, resulting in:

Prominent visual hallucinations

Fluctuating cognition – sometimes clear, sometimes very confused

REM sleep behavior disorder (RBD)

High sensitivity to antipsychotic drugs (neuroleptic sensitivity) (ScienceDirect+1)

This leads to:

Visual input that is already distorted/strange (shadows, figures, etc.).

Limbic–frontal circuits being destabilized → reality testing is impaired.

Older age + reduced cognitive reserve → easier to lose touch with reality.

Studies in DLB show a significantly higher rate of DMS (including Capgras) compared to other dementias (PMC+1).

Practical summary:

DLB is a brain state “optimized” for Capgras + hallucinations to appear, because both the visual content is distorted and the frontal reality-checking system is weakened.

5.6 Not just “missing familiarity signals,” but “loss of social meaning of faces”

Newer work suggests that Capgras patients do not only lose the simple familiarity signal; they also have trouble with:

Reading facial emotional expressions.

Matching multiple unfamiliar faces.

That is, face processing as a whole is affected in several subdomains (Cambridge University Press & Assessment+1).

So Capgras may be thought of as:

A disturbance of the “social meaning of faces,”
not just “not feeling familiar.”

In graphic form (perfect for Nerdyssey), you could show:

Bottom layer: visual features → face recognition.

Middle layer: familiarity / emotional tagging.

Top layer: social meaning + belief.

Capgras = primarily a breakdown of the top two layers.

6) Causes & Risk Factors — Causes and risk factors

Capgras does not arise from “one single disease.”

It is more like the tip of an iceberg produced by many disorders that disrupt the same network (face–limbic–frontal) in different ways.

We can divide things into three levels:

Disorders/conditions that change brain structure/chemistry.
Baseline risk factors (genetics, personality, etc.).
Acute triggers that precipitate the symptoms.

6.1 Main disorders/conditions commonly associated with Capgras

6.1.1 Psychiatric disorders

From StatPearls and various reviews (NCBI+2, nursingcenter.com+2), Capgras occurs frequently in:

Schizophrenia / Schizoaffective disorder

Both dopamine and frontal–temporal networks are disrupted.
Delusions are a core feature → it’s easy to attach anomalies of familiarity onto them as Capgras.

Bipolar disorder with psychotic features

During severe mania/depression, reality testing breaks down.
With co-factors (e.g., severe insomnia, stress), Capgras may appear transiently.

Major depressive disorder with psychosis

Especially late-life depression with early cognitive impairment.

Commonalities among these psychiatric disorders:

Dopamine/glutamate dysregulation, etc. → alters how stimuli are assigned salience.

Fronto-temporal dysconnectivity – networks that verify and inhibit false beliefs underfunction.

Context of high stress, poor sleep, social withdrawal → creates fertile ground for delusions to grow.

6.1.2 Neurodegenerative diseases / dementias

Capgras and other DMS are commonly found in (NCBI+2, PMC+2):

Dementia with Lewy Bodies (DLB)

Alzheimer’s disease (AD)

Parkinson’s disease dementia / advanced Parkinson’s disease

Mechanisms:

Neurodegeneration in temporal–parietal–frontal regions

Especially on the right side → affecting networks for face/familiarity/attention.

Hallucinations + fluctuating alertness

External world interpretation is noisy and unstable.
The brain uses “story-building” to manage confusing input → ideal ground for delusions.

Multiple neurotransmitter changes

Dopamine, acetylcholine, etc.
Affect both psychosis and attention/salience networks.

Systematic reviews of DMS in dementia show that DMS (including Capgras) are most common in DLB and AD (NCBI+2, PMC+2).

6.1.3 Brain injury / structural lesions

Many Capgras cases have been reported after:

Traumatic brain injury (TBI)

Stroke / cerebrovascular accident (CVA)

Brain tumors / pituitary tumors

Epilepsy, especially temporal lobe epilepsy (NCBI+2, Psychiatry Online+2).

Common lesion-mapping patterns:

Lesions/atrophy in the right frontal–temporal network.

Abnormalities in limbic connections.

Some cases show epileptic activity in the temporal lobe producing repeated “strange experiences,”
→ which the brain interprets as “people around me have changed / are impostors.”

You can phrase it like this:

Capgras in this group is the result of the brain being “shocked” such that the face–emotion–belief circuit is abruptly torn apart.

6.1.4 Other associated conditions

From reviews and case series (NCBI+2, Psychiatrist.com+2), Capgras has also been reported with:

Multiple sclerosis

Infectious or metabolic encephalopathy

Substance-related or medication-induced psychosis (less common but documented)

Postpartum psychosis, where some cases show DMS features including Capgras (Semantic Scholar).

The key idea:

Any “shock” that affects the same frontal–temporal–limbic network plus dramatically changes mood/thinking can produce Capgras as an “output.”

6.2 Individual-level risk factors

Although statistical data are still limited, case reports and reviews suggest trends such as:

Low cognitive reserve / lower educational attainment

When the brain is hit by physical/brain/psychiatric disease, it relies on less logical reasoning strategies,
→ making it easier for delusions to form.

Psychotic vulnerability / family history of psychotic disorders

e.g., genetic loading for schizophrenia spectrum.

Personality with high suspiciousness / preference for intuitive over analytic reasoning

When faced with small mismatches in familiarity, they more readily jump to complex conspiracy-type stories.

Strong attachment / unresolved conflict with the person who becomes the “Capgras target”

Old psychoanalytic theories suggest Capgras may involve underlying ambivalent love–hate conflicts; although today, neurocognitive models are more widely used (jneuropsychiatry.org).

6.3 Triggers that precipitate or exacerbate symptoms

These are tangible, real-world factors that you can present as a “tips” box:

Delirium / acute confusional state

Infections, dehydration, electrolyte imbalance, certain drugs, withdrawal, etc.
Cause fluctuations in attention and arousal → visual/auditory input is easily distorted.
Capgras may appear acutely during delirium and partially recede afterwards (nursingcenter.com+1).

Severe sleep deprivation + accumulated stress

Especially in people with pre-existing schizophrenia/bipolar disorder.
Sleep loss → dopamine/glutamate imbalance → psychotic flare.

Changes in environment

Moving house/room/changing caregiver.
In dementia: even rearranging furniture or night-time lighting can make the brain misinterpret faces in shadows as “impostors.”

Changes in the appearance of close others

Haircut, masks, new glasses, different usual clothing.
In a fragile network, even small changes can be taken as strong “evidence” of impostors.

Visual/hearing impairments

Cataracts, poor vision, hearing loss, etc.
Noisier input → the brain fills in with imagination → delusion-friendly environment.

6.4 A causal model you can use to explain Capgras simply

You can summarize Capgras as a three-layer model:

Foundation: Primary disease / brain damage

Schizophrenia, DLB, AD, Parkinson’s, TBI, stroke, etc.
Disrupts the face–emotion–belief circuit.

Pillars (modulators): Personality–genetics–coping

Suspicious worldview / belief in complex hidden plots.
Chronic stress, lack of social support, etc.

Tip (triggers): Acute events

Sleep loss, delirium, medications, moving house, changing caregivers, etc.
→ Ignite the delusion, leading to Capgras.

For an infographic: draw it as an iceberg:

The part above the water = “Belief that a close person has been swapped.”

Below the water = brain disease / psychiatric disorder / lesions / dementia, etc.

This is extremely “premium” for Nerdyssey, because it lets readers see that:

Capgras is not a floating hallucination, but a pathological signal from a brain struggling with a world it no longer perceives the way it used to.

7) Treatment & Management — Treatment and management

The core, “corporate but practical” mindset is:
Treat the cause + Reduce risk + Restore function.

7.1 First principle: Determine whether it is primary psychiatric or secondary neurologic/delirium

If there is delirium or clear physical illness → treat the underlying medical cause first (the delusion may greatly improve).

If dementia/DLB is suspected → medication strategy differs from schizophrenia because of neuroleptic sensitivity (ScienceDirect).

7.2 Medications (chosen according to the primary disorder)

(A) Antipsychotics

Often used when the delusion creates danger or severe disruption, especially in psychotic disorders (NCBI).

Caution in DLB/Parkinson’s: these patients may be extremely sensitive to neuroleptics and develop severe side effects. They require special, expert-guided approaches (ScienceDirect).

(B) In Lewy body dementia: consider cholinesterase inhibitors

LBD organizations and resources note that cholinesterase inhibitors can help with certain cognitive/behavioral symptoms in LBD, and there are mentions of improvement in Capgras-like symptoms in some cases (though results vary by individual) (Lewy Body Dementia Association+1).

Note: All medications must be prescribed and monitored by a physician, especially in older adults or those with dementia, due to side-effect and safety concerns.

7.3 Non-pharmacologic strategies (very important, often “faster-acting” at home)

The goal is to make the brain “feel safe and familiar” again, reducing the mismatch:

Avoid arguing directly that “this is the same person” (often escalates conflict) → use validation + redirection instead.

Reduce night-time triggers: shadows, mirrors, loud TV, darkness that promotes misinterpretation.

Maintain consistent routines: regular times for meals/sleep/activities.

Behavioral techniques:

The person labeled as an “impostor” should speak gently, keep an appropriate distance, and may start by speaking from another room before entering (to reduce shock on seeing their face).

Safety:

If there is a risk of aggression → keep physical distance, avoid confrontations, adapt the home environment to reduce accessible weapons/sharp objects (this is pure risk management).

7.4 When to urgently see a doctor / emergency

There is risk of harming the person perceived as an “impostor.”

New-onset symptoms in an older adult (must screen for delirium/medical causes immediately).

Neurological signs appear (severe confusion, unsteady gait, seizures, slurred speech, etc.).

8) Notes — Points content creators should know

Capgras is not about “just disliking someone’s face” or “overthinking.” It is a delusion arising from faulty processing of familiarity, which is why the stories feel realistically terrifying.

In dementia/DLB, symptoms often wax and wane and fluctuate with sleep quality, stress, and environment (PMC).

For character writing: the emotionally piercing core is

“They recognize the face, but their heart doesn’t feel it’s the same person,”
and the brain explains this with an impostor theory.
This is a perfect core for drama + horror even without adding any ghosts.

Read Schizophrenia

References

Shah KP, Vahia IV. Capgras Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2023. (ncbi.nlm.nih.gov)
Bashir S, Cummings J. Delusional Misidentification Syndromes. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2024. (ncbi.nlm.nih.gov)
Thaipisutikul P, Lobach I, Zweig Y, Golomb J. Capgras syndrome in dementia with Lewy bodies. J Geriatr Psychiatry Neurol. 2013;26(2):117–126. (PMC)
Ellis HD, Lewis MB. Capgras delusion: a window on face recognition. Trends Cogn Sci. 2001;5(4):149–156. (ScienceDirect+1)
Ellis HD. Reduced autonomic responses to faces in Capgras delusion. Proc R Soc Lond B. 1997;264:1085–1092. (JSTOR+1)
Darby RR, Joutsa J, Rueter J, Fox MD. Lesion-related delusional misidentification syndromes. J Neuropsychiatry Clin Neurosci. 2017;29(3):222–229. (Psychiatry Online+1)
Breen N, Caine D, Coltheart M. Models of face recognition and delusional misidentification: a critical review. (Review on two-route model). (ResearchGate)
Locke D, Diaz A. Young-onset dementia with Lewy bodies with Capgras syndrome. Prim Care Companion CNS Disord. 2022;24(3):21cr03098. (Psychiatrist.com)
Cleveland Clinic. Capgras Syndrome (Capgras Delusion): What It Is, Causes, Symptoms & Treatment. (Cleveland Clinic)
Verywell Health. Capgras Syndrome in Lewy Body Dementia. (Verywell Health)

Capgras syndrome / Capgras delusion / delusional misidentification syndrome / DMS / impostor delusion / delusion of doubles / face recognition deficit / familiarity processing / hypo-familiarity / right frontal lesion / right temporal lesion / limbic system / amygdala dysfunction / two-route model of face recognition / overt vs covert recognition / autonomic response to faces / schizophrenia spectrum / psychotic disorder / dementia with Lewy bodies / DLB / Parkinson’s disease dementia / Alzheimer’s disease psychosis / neurodegenerative disease / brain injury / traumatic brain injury (TBI) / stroke / neuropsychiatry / visual hallucinations / misidentification of loved ones / caregiver burden / risk of aggression / forensic implications / treatment with antipsychotics / cholinesterase inhibitors / non-pharmacologic management / environmental modification / validation and redirection / delusional belief / psychosis and violence

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