Positive Thought Disorder / Positive Formal Thought Disorder (PFTD)

1. Overview — What is Positive Thought Disorder? 

Positive Thought Disorder, or in its full academic term Positive Formal Thought Disorder (PFTD),
is a “cluster of abnormalities in thinking processes and language use” in which the abnormal features are “added on top of normal function” (excess / distortion), rather than something that is missing as in negative symptoms.

In psychiatric terminology, the term “formal thought” refers to the structure of thought:
for example, how sentences are organized, how topics are linked together, how a story is told in a way that others can understand.
It is not about the content of thought, which belongs in the category of delusions / overvalued ideas instead.

Therefore, Positive Thought Disorder focuses on:

“Patterns of thinking + ways of speaking/writing that deviate from normal structure so much that listeners cannot follow.”

The word “positive” here does not mean “good.”
It refers to symptoms that are “added” (positive symptoms),
similar to hallucinations and delusions, which are things the brain “creates on top of reality,”
rather than reductions or losses such as in negative thought disorder (e.g., very little speech, mental blankness, falling silent mid-sentence).

In real life, we often “see” Positive Thought Disorder through the patient’s speech, for example:

• They speak and go off-topic, jumping to something far away from the original point without realizing it.

• They tell stories in a highly rambling way, with excessive detail, to the point that no one remembers what the original topic was.

• They link sentences together in a way that makes little logical sense to the listener, even though the speaker is very confident in what they are saying.

• Sometimes it becomes completely incomprehensible (incoherent / word salad): the words are real, but they are arranged with no central thread.

Positive Thought Disorder is typically prominent in conditions such as:

• Schizophrenia

• Schizoaffective disorder

• Acute psychotic episode

and can also be seen to some extent in:

• Bipolar mania with psychosis, or

• Depression with psychotic features.

Clinically, in terms of the overall picture, it is grouped under “disorganization” symptoms,
together with other features such as disorganized behavior (bizarre, chaotic behavior), odd dressing, and behavior/speech that is not in tune with the situation.

What makes Positive Thought Disorder very important diagnostically is that:

• It is one of the “core dimensions” of psychosis in the schizophrenia spectrum.

• Sometimes, even if hallucinations or delusions are not very prominent, the pattern of disorganized speech/thought can serve as a major warning sign.

• It has a strong impact on daily functioning, because communication with other people essentially breaks down.

For example:

• Work meetings become incomprehensible.

• Written reports cannot be completed because the person cannot organize the structure.

• Family conversations turn into confusion or arguments, because nobody understands what the person is trying to say.

When clinicians encounter a patient with clearly evident Positive Thought Disorder,
doctors/therapists often have a very similar subjective experience:

“It’s hard to keep a focus. The sentences connect to each other in a strange way,
but the patient speaks with great confidence.
It’s as if there is some kind of logic in their head, but we just can’t access it.”

This is the core of Positive Thought Disorder:
the brain “is very active, keeps generating thoughts,”
but the structure and pathways of associations are so distorted that other people cannot access their inner world. 🌒🧠

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2. Core Symptoms — Key Clinical Features

Overall, Positive Thought Disorder means that “thoughts are still running, language production is still plentiful,” but
the direction and structure of those thoughts are distorted to the point that communication breaks down.

Below are the core symptoms, with clear illustrative examples:

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2.1 Loose associations / Derailment — Loose / Off-the-rails Associations

The brain is still “linking things together,” but those links are loose and illogical.

• The speaker feels that their ideas flow together very well.

• The listener, however, is confused and wonders: “How on earth are these things related?”

Example:

Doctor: “How have you been sleeping lately?”
Patient: “I sleep, yes. When I sleep I think about World War II. People these days don’t understand history, that’s why the subway is so expensive, and the dogs in my neighborhood bark really well.”

For the patient, there might be a chain of logic like:
sleep → dreams → war → government → inflation → transport costs → dogs barking because there are many people.
But for the listener, the topics are clearly jumping around without a coherent structure.

Key points to notice:

• This is not just “chatting and jumping between topics” like a normal talkative person.

• It is going off-topic even when the question is very clear.

• As they continue talking, we often feel: “Wait, we were talking about something else just a moment ago—how did we suddenly end up here?”

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2.2 Tangentiality — Persistently Off-topic, Circling Around the Core but Never Reaching It

The characteristic here is “consistently not answering the question directly.”

• When asked one clear question, the person will talk about many things, but

• they never actually touch on the core answer.

Example:

Doctor: “What brought you to see me today?”
Patient: “Well, this morning I went to the market. Markets these days are so crowded, and the traffic is terrible. The vendors are loud, and people have no manners. I think our country really has to fix this first, or our children will suffer.”

The stream of speech is long, but the patient never actually says what symptom brought them to see the doctor.

How is this different from Loose associations?

• Tangentiality = The person still seems to “circle around the general area of the original topic,” but never hits the core.

• Loose associations = The topics jump completely into another world.

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2.3 Circumstantiality — Overly Detailed, Rambling, But Eventually Comes Back to the Point

Patients will tell the story in excessive, unnecessary detail, wandering around.

• But, unlike tangentiality, they eventually come back to the point.

Example:

Doctor: “What time did you go to sleep last night?”
Patient: “Last night? Hmm… Before bed I had dinner with my mom. My mom cooks really well, she likes to add a lot of garlic. Then I washed the dishes, brushed my teeth—my toothbrush is blue, that’s my favorite color—then I went upstairs to my room. It was probably around midnight, I guess.”

The only answer the doctor needed was “around midnight,”
but the patient took them on a tour of the entire house first.

Key points:

• It is still comprehensible but very time- and energy-consuming to follow.

• In real-life functioning, if this happens frequently, it makes business conversations / meetings / presenting reports very cumbersome.

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2.4 Flight of ideas — Rapid Thoughts / Rapid Topic Changes (Common in Mania)

Very common in manic episodes.

• The person speaks very quickly / the content jumps very rapidly, because their mind is flooded with ideas.

• But each step in the topic change still has a faint logic or word-play/meaning connection.

Example:

“I know I have to start an online business; everything’s digital nowadays. The world is spinning fast like 5G, 6G, 7G, haha! I’ll go to America, to Silicon Valley. Do they have snow there? Snow is like ice, and ice reminds me of ice cream, now I’m hungry. My mom loves making desserts. My mom is talented, I’m talented too, I think I’m going to change the world.”

The topic changes very fast,
but we can still see a chain from digital → internet → America → snow → ice → ice cream → mom → self → greatness.
This is not word salad, but it is very fast and constantly switching tracks.

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2.5 Incoherence / Word salad — Fragmented Language, Incomprehensible Speech

This is more severe than loose associations or flight of ideas.

• It consists of real words, but they are arranged in a way that lacks coherent structure.

• The listener cannot extract any central meaning from it.

Example (capturing the feel):

“When the chair walks past the notebook, the house starts laughing, so the lightbulb ate yesterday’s lunch, and the sea has no door because dogs don’t like to run.”

This is not just “weird metaphors” like in poetry.
The entire sentence lacks any logical framework to hold onto.

Key points:

• Often seen in very severe psychosis.

• Frequently comes along with other severe symptoms such as motor disorganization, catatonia, or intense hallucinations.

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2.6 Clanging / Sound-based associations — Choosing Words by Sound, Not Meaning

Here, the brain chooses the next word because “it rhymes / sounds nice,”
not because it carries relevant meaning.

• The content drifts away from the topic because the focus is on sound rather than meaning.

Example:

“I walk on the street, feet, meet, heat, beat, neat, fleet, then repeat, complete, concrete, delete, elite…”

It sounds like wordplay / rap / random verse.
In some artistic contexts this might be normal,
but in Positive Thought Disorder it appears in situations where one would normally speak straightforwardly to communicate (e.g., answering the doctor’s question in a consultation).

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2.7 Neologisms — Making Up New Words

The patient uses words that do not exist in any language, yet uses them as if they were ordinary words.

• Sometimes they will explain what they mean; sometimes they will not.

Example:

“I’m being followed all the time by the Fironia people. They’re above the government. Everyone knows, but no one dares to talk about Fironia.”

If you ask, “What is Fironia?”
they may give a long explanation that it is a secret group / energy / entity controlling the world, etc., but the word itself has no origin in the language.

Key points:

• Different from slang or youth language because:
• No other language community uses it.
• There is no way to find an external origin for the term outside of the patient.

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2.8 Perseveration — Repeating the Same Phrase or Concept Over and Over

The person gets stuck on one word or topic repeatedly, even when the context has changed.

• It’s as if they “cannot get off the track” or “the needle is stuck in the groove.”

Example:

Doctor: “Do you feel like eating?”
Patient: “I have to go to school, I have to go to school, I have to go to school. If I don’t go, they’ll come take me. I have to go to school, I have to go to school…”

They answer every question with the same sentence, regardless of what the doctor asks.

Key points:

• This can be found in schizophrenia, brain injury, dementia, etc.

• In Positive Thought Disorder it appears together with other abnormal patterns of thinking/speech.

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2.9 Overall Picture of the Core Symptoms

The brain is still very active, but
the system that organizes thought → sentence → communication is out of balance.

• Listener’s perspective: They feel “I can’t grasp the main point / conversations are very difficult / I’m exhausted trying to decode what they say.”

• Speaker’s perspective: They feel “I’m speaking normally, why does no one understand me?”

This is why Positive Thought Disorder can seriously damage work performance, academic functioning, and relationships,
even when hallucinations/delusions are not necessarily the most prominent symptoms at the moment.

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3. Diagnostic Criteria — How Do We Decide It Is Positive Thought Disorder?

In theory, DSM-5-TR / ICD-11 use the term “Disorganized thinking (formal thought disorder)”,
reflected through “disorganized speech,” rather than the specific label “Positive Thought Disorder.”

Therefore, when a clinician makes a diagnosis, they treat it as a “symptom dimension” within a primary disorder such as schizophrenia, rather than a stand-alone disease.

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3.1 Presence of Clearly Abnormal Thought/Speech Patterns

We must observe patterns like those described under Core Symptoms, such as:

• loose associations

• tangentiality

• circumstantiality (to a degree that disrupts communication)

• flight of ideas (within a manic/psychotic context)

• incoherence / word salad

• clanging

• neologisms

• perseveration, etc.

It is not considered a formal thought disorder if:

• Someone just talks fast because they are excited.

• Someone simply chats and jumps between topics like a naturally talkative person.

• Someone has an eccentric speaking style, but listeners still “clearly understand the narrative structure.”

What matters is the degree to which it interferes with the listener’s understanding.
If the doctor/interviewer repeatedly has to ask for clarification, cut in, and interpret meaning,
→ it is starting to carry significant clinical weight.

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3.2 Genuine Impact on Communication (Functional Impairment in Communication)

Another key criterion is that the symptoms must:

• Cause conversations to be disjointed and difficult.

People around them (family, coworkers) feel like:

• “I can’t make sense of what they say.”

• “Every conversation with them slips into another world.”

• “Even when we ask them to explain something simple, they never manage to tell it clearly.”

Examples of real-life impact:

• Sending confusing work emails with unclear subject matters → mistakes / reprimands.

• Giving presentations where listeners “get lost” along the way → poor evaluations.

• Family discussions turning into arguments, because the other side feels the patient is evading questions or never answering directly.

In DSM/ICD, the phrase “clinically significant” means:
it affects functioning / relationships / self-care, not just “a bit of odd speech here and there.”

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3.3 Persistence and Clear Pattern (Not Just Temporary)

Clinicians consider it a Thought Disorder only when:

• The symptom appears repeatedly, not just:
• On days of extreme sleep deprivation,
• When intoxicated,
• Or when deliberately joking/reciting poetry.

• The same pattern is seen in multiple contexts:
• When talking to the doctor,
• When talking to relatives,
• When chatting in the ward or in the waiting room.

Examples of cases that “do not meet criteria”:

• A friend rambles because they’re hopped up on 5 cups of coffee and slept only 2 hours.

• Someone babbles because of a high fever, or is groggy and incoherent immediately after waking up.

Examples of more concerning scenarios:

• Relatives report: “In the last 3–4 months, every time we talk, they keep going off-topic.”

• The workplace complains: “Whenever we ask them to summarize something, it turns into a mess.”

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3.4 Association With a Primary Psychiatric Disorder (Underlying Disorder)

Positive Thought Disorder does not appear in isolation; it tends to:

• Be one of the core symptoms of disorders such as:
• Schizophrenia
• Schizoaffective disorder
• Schizophreniform disorder
• Brief psychotic disorder
• Bipolar disorder with psychotic features

• And often appears together with:
• Delusions (e.g., paranoid, grandiose)
• Hallucinations (e.g., auditory hallucinations)
• Negative symptoms (e.g., reduced speech, flat affect, anhedonia)
• Disorganized behavior

In diagnosing schizophrenia according to DSM-5:

• “Disorganized speech (e.g., frequent derailment or incoherence)”
  is counted as one of the Criterion A symptoms.

This means that the pattern of disorganized speech alone can serve as direct evidence of psychosis,
even when hallucinations or delusions are not very prominent during some phases.

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3.5 Not Due to Other Causes (Exclusion Criteria)

Before concluding that we are dealing with Positive (Formal) Thought Disorder within a psychotic disorder framework,
the clinician must systematically rule out other causes, such as:

• Substance / Medication-induced
• Intoxication with substances (e.g., methamphetamine, LSD, ketamine), alcohol, or certain medications.
• People who are “high” may talk in a disorganized way, but this is tied clearly to periods of substance use.

• Delirium
• Acute confusion due to medical conditions (e.g., severe infections, alcohol withdrawal, electrolyte imbalance).
• The person will have fluctuating level of consciousness, disorientation in time/place alongside weird speech.

• Dementia / Major Neurocognitive Disorder
• Progressive decline in cognition and memory.
• Speech may be disorganized because semantic memory is impaired, not necessarily due to a primary formal thought disorder as in schizophrenia.

• Aphasia / Focal brain injury (e.g., stroke, head trauma)
• Speech is abnormal because language centers in the brain are damaged.
• This must be distinguished from a psychosis-related thought disorder.

• Intellectual disability + baseline poor language skills
• Some people speak in a disorganized way because they never developed the skills to organize narratives,
  but they do not have psychosis.

Clinicians will use:

• Detailed history-taking (onset, course, triggers)

• Physical and neurological examination

• Sometimes blood tests / brain imaging (CT/MRI) / EEG

to confirm that the symptoms are not better explained by a neurological or medical condition.

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3.6 Assessment Tools

Besides the standard clinical interview, there are specific rating scales, such as:

• Scale for the Assessment of Thought, Language and Communication (TLC)
• Separates different types of symptoms: derailment, tangentiality, incoherence, clanging, etc.
• Rates the severity of each domain.

• PANSS (Positive and Negative Syndrome Scale)
• Contains subscales that assess disorganized thinking/disorganized speech.

• Clinical Mental Status Examination (MSE)
• Clinicians document a dedicated section “Thought form” separate from “Thought content.”
• This is where terms like loose associations, flight of ideas, word salad are recorded.

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3.7 Why “Lay People” Should Not Self-diagnose Based on a Few Odd Speech Episodes

Because in real life:

• Anyone can be rambling, messy, or off-topic in many situations, such as:
• Severe sleep deprivation,
• High stress,
• Heavy caffeine/sugar intake,
• Or excitement.

But that is not yet Positive Thought Disorder in the schizophrenia spectrum sense.

What turns it into a “psychiatric symptom” is:

• Severity — Conversations become almost impossible to follow.

• Persistence — It lasts for months/years, not just a couple of days.

• Impact on life (impairment) — Education, work, and relationships fall apart.

• Association with other psychotic symptoms — There are delusions, hallucinations, negative symptoms alongside it.

Therefore, the material in this section is well-suited as knowledge / educational content / academic reference.
But if it concerns “yourself or someone close to you” and you are starting to worry, it should be used as:

“A sign that suggests it might be time to see a psychiatrist / mental health professional for a proper assessment,”
not as a basis for 100% self-diagnosis.

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4. Subtypes or Specifiers — Subtypes of Positive Thought Disorder

We can categorize subtypes according to the dominant pattern, such as:

• Loose / Disorganized Type
• Dominated by “loose” associations and frequent topic changes.
• Topics jump around, but there is some faint internal logic in the patient’s own mind.

• Incoherent / Word Salad Type
• Thought/language becomes so fragmented that it is nearly incomprehensible.
• Often seen in very severe psychosis or in some cases of catatonia.

• Overinclusive / Circumstantial Type
• Overloading with details until the main point is lost.
• The person tries to capture every angle until their thinking becomes overloaded.

• Sound-Driven Type (Clanging / Rhyme-Driven)
• Chains of thought/speech follow “sound” instead of meaning.
• There is playful use of rhyme, sound associations, and alliteration.

• Manic Flight-of-Ideas Type
• Dominated by “speed” + topic switching based on loose associations.
• Listeners can sometimes see the logic, but cannot keep up because it is too fast.

• Neologism-Dominant Type
• The person creates many new words during storytelling.
• Others constantly have to ask what each new term means.

Clinically, these are usually not written as formal specifiers,
but used descriptively to characterize the individual patient’s pattern.

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5. Brain & Neurobiology — Brain and Biological Basis

First, the big picture:
Positive Formal Thought Disorder (PFTD) is thought to result from:

• Abnormal functioning of brain circuits related to language and executive function

• Neurotransmitter systems (dopamine / glutamate / GABA, etc.) disrupting the brain’s ability to “filter and organize” information

• Brain networks that are loosely or aberrantly connected

Large-scale review papers on FTD in schizophrenia confirm that it is a “multi-level phenomenon”—from genes, cells, and neurotransmitters to networks, all the way up to the level of disorganized language in everyday life. PubMed+1

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5.1 Dorsolateral Prefrontal Cortex (DLPFC) — The “Executive Chair” of Thought Organization

The DLPFC is the brain’s frontline area for:

• Working memory = holding key points in mind temporarily

• Executive control = choosing which thoughts to attend to and which to discard

• Organizing thought = arranging ideas into a coherent narrative

In people with FTD / disorganized thinking:

• Imaging studies show that DLPFC volume/function is reduced, or its connections are abnormal, particularly in psychosis and especially schizophrenia. PubMed Central+1

This leads to:

• Inability to maintain the “main storyline” → easy to go off-topic

• Failure to keep focus on the current question → constantly bringing up new topics

• Difficulty deciding what is “relevant” vs “irrelevant” → wanting to say everything

Connected symptoms:

• Loose associations

• Tangentiality

• Circumstantiality

• Flight of ideas (when combined with mania)

In simple terms, the DLPFC is like the “chairperson of a thought meeting.”
If the chairperson loses control, the brain is left with many people talking at once about different things.

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5.2 Temporal Lobe (Especially Superior Temporal Gyrus) — Language and “Meaning”

The Temporal lobe (TL), especially the Superior Temporal Gyrus (STG), is involved in:

• Auditory speech processing (hearing speech)

• Semantic processing (grasping the meaning of words/sentences)

• Linking words to form meaningful sentences

Structural brain studies in FTD have found that:

• The gray matter volume of the STG is reduced in schizophrenia patients with prominent FTD, compared to those without FTD and to healthy controls. VU Research+1

Consequences:

• The chain from “word → meaning → context” becomes distorted.

This leads to:

• Using words that do not fit the situation

• Word substitutions / sound play that are not related to content (clanging)

• New words (neologisms) that fall outside usual semantic fields

In summary: The temporal lobe is the “language + meaning” side.
If it is impaired, storytelling will fall out of alignment with the usual semantic map.

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5.3 Frontotemporal Connectivity — Communication Between “Structure” and “Content”

The crucial factor is not only individual brain regions, but also the “connections” between the frontal areas (DLPFC) and temporal regions (STG/MTG, etc.).

Recent structural & functional connectivity studies in psychosis have shown that:

• Patients with FTD have abnormal connectivity between prefrontal and temporal regions,

• especially within networks related to language and executive control. ResearchGate+1

Think of it like this:

• Frontal lobe = “the organizer”

• Temporal lobe = “the warehouse of meaning and language”

If the signal between these two parts is “loose / noisy / out of sync,” then:

• Thoughts are not adequately checked or filtered before they are spoken.

• The output is speech that listeners feel has a “broken structure.”

Some studies connect this idea with the concept that schizophrenia is a “functional disconnection disorder”—the brain is not “shut down,” but “misconnected” across multiple networks. arXiv+1

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5.4 Dopamine Dysregulation & Aberrant Salience — The Brain Assigns Importance to the Wrong Things

Dopamine remains a central player in psychosis:

• Many studies show dopamine presynaptic overactivity in mesolimbic/striatal pathways in schizophrenia and other psychoses. PubMed Central+1

Famous models such as the “aberrant salience hypothesis” propose that:

• Under normal conditions, the dopamine system highlights important stimuli to draw the brain’s attention.

• In psychosis, it “assigns importance to the wrong things”:
• Stimuli, thoughts, internal voices, minor coincidences → are given excessive significance.

This links to Positive Thought Disorder as follows:

• The brain is “firing dopamine in the wrong pattern.”

This causes:

• Thoughts that should be mere “background noise” to become “major topics.”

• The patient feels that these strange internal associations are crucial → so they talk about them continuously.

• Irrelevant things get chained together (A → B → C), even though for others A has nothing to do with C. DergiPark+1

In short:
If dopamine is a highlighter pen, then a psychotic brain is someone who highlights every line on the page.
Everything seems equally important, so thought pathways become scattered and bizarre.

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5.5 Glutamate, GABA, and NMDA Hypofunction — Networks Out of Sync

Newer work shows that dopamine alone is insufficient; we must also consider glutamate / GABA / NMDA receptors. Nature+1

The core ideas:

• NMDA receptor hypofunction (especially on GABAergic interneurons)
  → weakens the brain’s “brake” system → network firing becomes more chaotic.

• An imbalance between glutamate (excitatory) and GABA (inhibitory)
  → makes frontal–temporal circuits fire together in a “desynchronized” way.

As a result:

• Brain regions do not sync well within networks.

This leads to:

• Poor filtering of irrelevant information.

• Side thoughts that should be suppressed instead enter the current sentence.

• Loose associations, tangentiality, word salad, or clanging become more likely. Wiley Online Library+1

Some work suggests that cognitive dysfunction (attention, working memory, reasoning) driven by glutamate/NMDA abnormalities often appears before full-blown psychosis and predicts long-term outcomes in schizophrenia. Frontiers

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5.6 Neurocognitive Deficits — The Brain Can Think, But “Can’t Organize”

Behaviorally, formal thought disorder overlaps heavily with:

• Attention/vigilance deficits (easily distracted, poor sustained focus)

• Executive dysfunction (poor planning, sequencing, shifting focus)

• Semantic memory abnormalities (distorted access to word/concept meaning) PubMed+1

Mechanistically:

• When attention is impaired → too much noise is allowed into the sentence.

• When working memory is impaired → the person forgets what the original question or main topic was.

• When executive control is impaired → they cannot decide what to leave out of the story.

• When the semantic network is distorted → they pull up unusual words/meanings to replace normal ones.

This matches findings that patients with FTD often cannot suppress irrelevant information during language/cognitive tasks → irrelevant material intrudes and “occupies space” in the ongoing sentence. Wiley Online Library

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5.7 Inflammation & Neurodevelopment — The Distant Background

Recent studies are beginning to connect:

• Chronic low-grade inflammation,

with

• abnormal dopamine–glutamate interaction and damage to dendritic spines in the cortex,

which then impacts networks used for language + executive function. Springer+1

This fits with the broader view of schizophrenia/psychosis as a neurodevelopmental disorder:
the brain structures involved in language are “laid down abnormally” long before clear symptoms emerge in adolescence or early adulthood.

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5.8 Summary of Brain & Neurobiology for General Readers

To summarize in a way that lay people can understand:

Positive Thought Disorder = the brain still “thinks a lot and can talk,” but:

• The parts that control structure/ordering (DLPFC) are under-functioning. 

• The parts that handle language/meaning (Temporal lobe, STG) are out of balance. 

• Frontotemporal connections are loose, so “structure” and “content” don’t sync. 

• The dopamine + glutamate systems assign importance incorrectly and filter poorly. 

• Baseline cognitive skills (attention / working memory / semantic processing) are already impaired.

The result = the thoughts that come out appear “fragmented, rambling, off-structure,” even though inside the person feels everything makes perfect sense.

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6. Causes & Risk Factors

Again, Positive Thought Disorder is a symptom dimension, not a stand-alone illness.
We usually discuss it in the context of the Schizophrenia Spectrum or other psychotic disorders.

Therefore, the causes/risk factors for FTD largely overlap with those of these disorders,
but whether FTD is prominent or not depends on the combination of genes + brain development + environment in each individual.

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6.1 Genetics (Genetic Vulnerability)

People who have first-degree relatives (parents/siblings) with schizophrenia / schizoaffective disorder / psychotic disorders
have a higher chance of developing psychosis and the FTD dimension.

It follows a polygenic pattern = there is no single “magic gene”; instead, it is the combined effect of many small genes related to:

• Dopamine function

• Glutamate / NMDA systems

• Brain development before/after birth, etc. PubMed+1

Important:

• Genetics = increases “risk”

• It is not destiny.

• It must combine with other factors (stress, substances, trauma, etc.) for the illness to fully manifest.

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6.2 Neurodevelopmental Factors — Brain Development From the Womb Through Childhood

Our brains are “laid out” from the time we are in the womb → through childhood → adolescence.
If there are major disturbances in any of these phases, the structures/connections related to language and executive function may be altered.

Relevant examples:

• Intrauterine infections (e.g., influenza, rubella, maternal inflammation)

• Birth hypoxia (lack of oxygen during delivery)

• Childhood malnutrition, or lack of key nutrients needed for brain development

• Physical environmental factors, such as heavy metal exposure, or prenatal exposure to substances/ alcohol, etc. PubMed+1

Long-term consequences:

• The networks of frontal–temporal regions and the glutamate–dopamine system are laid down in atypical patterns.

• When the person later encounters stress/hormonal changes in adolescence → psychosis + FTD can emerge clearly.

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6.3 Substance Use — Drugs That Drive Dopamine & Glutamate

These substances do not necessarily “create illness from nothing,” but they can:

• Trigger latent vulnerability into an overt psychotic episode.

• Worsen disorganized thinking (FTD) dramatically.

Especially:

• Amphetamine / Methamphetamine
• Strongly increase dopamine → intensify aberrant salience → thoughts become more scattered. PubMed Central+1

• High-potency cannabis (high THC)
• Linked to risk of psychosis + disorganized thinking in individuals with genetic vulnerability.

• Hallucinogens (e.g., LSD, ketamine, PCP)
• Act on NMDA / glutamate → temporarily pull thought and perception networks away from reality.
• In very vulnerable individuals, this can lead to a prolonged psychotic state.

For Positive Thought Disorder specifically:

• These substances increase noise in the dopamine/glutamate systems,

• Making thought associations even more chaotic (loose associations, disorganized speech).

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6.4 Stress & Trauma — Psychological Stress and Trauma

There is substantial evidence that:

• Childhood trauma (e.g., physical abuse, sexual abuse, severe neglect)

• Chronic stress / social adversity (e.g., poverty, bullying, unsafe environments)

are linked to increased risk of psychosis and FTD through several mechanisms, such as:

• Stress system (HPA axis) dysregulation
• Chronically altered cortisol patterns → affect brain development.

• Dopamine system becoming hypersensitive
• Stressful events make the brain more likely to interpret the world in a threat-mode.

• Impact on cognitive & social cognitive development
• Children growing up in chaotic environments / lacking normal language modeling / lacking safe conversation
  → are more likely to develop disorganized thinking/language patterns as they grow.

In summary:
Trauma + chronic stress = lay the groundwork for brain networks involved in thinking and language to become fragile,
→ making it easier to develop PFTD when other triggers appear. PubMed+1

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6.5 Cognitive Style & Premorbid Traits — Pre-existing Thinking Style + Personality

Before full-blown illness, many individuals show premorbid traits, such as:

• Being “overinclusive” thinkers: they connect everything to everything, struggling to distinguish main themes from minor details.

• Preferring highly abstract thinking/speech, but having difficulty organizing it so others can follow.

• Exhibiting schizotypal traits: odd beliefs, magical thinking, slightly strange speech patterns visible long before clear psychosis. Wikipedia+1

When combined with:

• Genetic vulnerability

• Neurodevelopmental disturbances

• Stress / substance use

this previously “just quirky, eccentric thinking style” can be pushed to the next level and turn into Positive Thought Disorder as a true psychotic symptom.

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6.6 Course of Illness — Illness Phase and the Prominence of FTD

In Schizophrenia / Schizoaffective / Psychotic disorders:

• Prodromal phase / before full-blown illness
• Mild cognitive decline, social withdrawal, and slightly odd speech/thinking may appear.

• Acute psychotic phase
• Positive symptoms are most prominent: hallucinations, delusions, and disorganized thinking/speech (PFTD).
• FTD becomes very obvious → people around the patient begin to feel, “We can no longer have a normal conversation.”

• Chronic / residual phase
• If treatment is suboptimal or psychosis recurs multiple times,
• thinking and language networks wear down → both positive & negative thought disorders may persist.
• We see poverty of speech, thought blocking, plus intermittent off-topic thinking.

Put another way:

FTD = usually most prominent when the illness is active.
If untreated or repeatedly relapsing → brain networks degenerate → both “excess” and “deficit” types of thinking become long-term patterns.

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6.7 Other Social and Environmental Factors

Social psychiatry research also discusses factors like:

• Urbanicity — Growing up in large, crowded cities with high social stress → increases risk of psychosis.

• Minority stress / stigma / discrimination
• Increases chronic stress → indirectly affects dopamine–glutamate networks.

• Low family support / High expressed emotion (EE)
• Does not “create the illness from zero,” but worsens the illness course, leads to more relapses, and makes FTD more prominent over time.

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6.8 Summary of Causes & Risk Factors for General Readers

• Genes + Brain Foundations
• Multiple genes + brain development from the womb/childhood → networks responsible for language/thinking are laid down in atypical patterns.

• Brain Chemistry
• Dopamine, glutamate, GABA, and NMDA receptors are out of balance.
• The brain assigns importance to the wrong things and cannot filter information → thoughts go off-structure.

• Life Experiences
• Trauma, chronic stress, and social adversity further burden an already vulnerable brain system.

• Thinking Style and Personality
• People who already tend to overconnect ideas / think in highly abstract terms, when combined with biological vulnerability, can more easily develop FTD.

• Lack of Treatment / Recurrent Episodes
• The longer psychosis goes untreated, or the more often it relapses, the more brain networks deteriorate → FTD patterns become entrenched.

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7. Treatment & Management

Managing Positive Thought Disorder requires addressing both the underlying disorder and communication rehabilitation.

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7.1 Biological Treatment

Antipsychotic Medications

• The main goal is to reduce dopamine hyperactivity.

• They often reduce disorganized thinking, hallucinations, and delusions to some degree, in parallel.

Mood Stabilizers / Antimanic Agents

• Used when the symptoms occur within Bipolar / Mania with psychosis.

• Help decrease flight of ideas and improve emotional control.

Treating Comorbid/Contributing Factors

• Stopping/reducing substance use.

• Treating medical conditions that affect the brain (e.g., epilepsy, infections, metabolic problems).

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7.2 Psychosocial Treatment

Psychoeducation

• Explaining to both patients and families that strange or off-topic speech is a symptom of illness,
  not just “rambling / talking nonsense / lying.”

Cognitive Remediation / Cognitive Rehabilitation

• Training attention, working memory, and problem-solving.

• Reducing lapses in focus, improving the ability to sequence and structure thoughts.

Social Skills Training & Communication Training

• Practising how to answer questions directly; practising short & clear storytelling.

• Using role-play in group therapy or individual sessions.

CBT for Psychosis (CBTp)

• Helping patients recognize patterns in their own thinking.

• Training meta-cognition: “Am I going off-topic right now?” “Did I answer their question yet?”

Supportive Psychotherapy

• Supporting work and relationships.

• Emphasizing structured routines and reducing stressors that exacerbate symptoms.

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7.3 Environmental Adjustments

• Holding conversations in quiet spaces with minimal distractions.

• Using short, clear questions, one question at a time.

• Summarizing back to the patient what is being discussed to help “pull them back” to the main topic.

• Supporting adequate sleep and reducing sleep deprivation, which can markedly worsen symptoms.

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8. Notes — Additional Observations

Positive Thought Disorder is different from Negative Thought Disorder (e.g., poverty of speech, thought blocking):

• Positive = something is “added / exaggerated,” such as talking a lot, rambling, inventing words.

• Negative = something is “missing,” such as very little speech, very short answers, sudden silent blocks mid-sentence.

In some people, both positive and negative thought disorders can coexist:
for example, in one phase they talk excessively in an incoherent manner; in another phase, they become extremely quiet and cut off.

Disturbed thinking is a “core” feature of psychotic disorders, but many societies focus only on hallucinations and delusions,
which leads to the communication dimension being overlooked.

In real-life contexts:

• It makes study/work difficult, because the person cannot explain tasks or ask for help clearly.

• It affects relationships because others see them as “hard to talk to / nonsensical / always rambling.”

Good treatment does not only look at whether “the voices are gone,”
but also at how much the pattern of thinking and speech has improved.

Read Schizophrenia

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📚 References

Kircher, T. et al. (2018). “Formal thought disorders: from phenomenology to neurobiology.” The Lancet Psychiatry.
A classic large-scale review covering FTD from clinical phenomenology and subtyping to brain networks and cellular-level mechanisms in schizophrenia. ScienceDirect

Chen, J. et al. (2021). “Neurobiological substrates of the positive formal thought disorder in schizophrenia revealed by seed connectome-based predictive modeling.” NPJ Schizophrenia.
Uses resting-state fMRI + machine learning to identify brain networks directly associated with positive FTD in multi-center schizophrenia samples. PubMed Central

Cavelti, M. et al. (2018). “Is formal thought disorder in schizophrenia related to structural and functional aberrations in the language network?” Schizophrenia Bulletin.
Reviews evidence linking FTD with structural and functional abnormalities in the fronto–temporo–parietal language network, showing clear disruptions in frontal–temporal tracts. PubMed

Kerns, J. G. et al. (2002). “Cognitive impairments associated with formal thought disorder in schizophrenia.” Journal of Abnormal Psychology.
Shows that patients with prominent FTD commonly have marked executive dysfunction and semantic processing abnormalities, forming the neurocognitive basis under the thought disorder. PubMed

McCutcheon, R. A. et al. (2023). “Cognitive impairment in schizophrenia: aetiology, pathophysiology, and treatment.” Molecular Psychiatry.
A mega-scale review on cognitive deficits in schizophrenia (attention, working memory, executive function), framing them as central features of the illness and linking them to disorganization symptoms. Nature

Andreasen, N. C. (1986). “Scale for the Assessment of Thought, Language, and Communication (TLC).”
A classic FTD assessment scale that distinguishes subtypes such as derailment, tangentiality, incoherence, and clanging, widely used in FTD research. cssh.northeastern.edu+1

Kapur, S. (2003). “Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia.” American Journal of Psychiatry.
Proposes the dopamine–aberrant salience model, arguing that psychosis (including disorganized thinking) arises from dopamine “highlighting the wrong things” in the brain. PubMed+1

Balu, D. T. (2016). “The NMDA Receptor and Schizophrenia.” Current Pharmaceutical Design.
Reviews the role of NMDA hypofunction and glutamate–GABA imbalance in schizophrenia, connecting this with network dysregulation in language and executive functions. PubMed Central+1

Kruse, A. O. et al. (2022). “Glutamatergic dysfunction in schizophrenia.” Translational Psychiatry.
Summarizes evidence of glutamate abnormalities (especially frontal Glu) and their association with illness severity and cognition/language symptoms. Nature

Sharkey, R. J. et al. (2024). “Differences in the neural correlates of schizophrenia with and without formal thought disorder.” Molecular Psychiatry.
A recent imaging study (2024) comparing brain differences between schizophrenia with and without FTD, showing distinct patterns of volume loss in language-related regions. Nature

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