Catatonic-Dominant

1. Overview — What is Catatonic-Dominant?

At its core, catatonia is a neuropsychiatric syndrome that centers on
“abnormalities in movement + responsiveness + interaction with the environment.”
It is not just someone being “quiet” or “still.” It means the body, facial expression, speech, and movements are all clearly and markedly abnormal.

Symptoms can lie on the “stopped / minimally responsive” side, such as:

Being motionless like a statue (stupor), sitting/lying still in one position without moving

Not speaking (mutism) even though the person is aware of sounds and questions

Remaining rigid in odd or fixed postures (posturing / catalepsy)

Showing bizarre resistance (negativism), e.g., being told to stand up but instead lying down; being told to turn left but turning right

Or they can lie on the “excessive / abnormal motor activity” side:

Pacing, moving around restlessly, appearing agitated or almost “manic,” but not calming down in response to verbal reassurance

And they can include other strange behaviors such as:

Repeating the same gestures or movements over and over (stereotypy, mannerism)

Repeating others’ speech (echolalia) or copying others’ movements (echopraxia) automatically

From the perspective of DSM-5 / DSM-5-TR

In older systems, there used to be a subtype called “catatonic type schizophrenia.”

In newer systems, this subtype has been removed,
because we now know that catatonia does not occur only in schizophrenia – it can appear in many different disorders.

So currently, DSM handles it by adding a specifier “with catatonia” after the primary diagnosis, for example:

Schizophrenia, with catatonia

Bipolar I disorder, with catatonia

Major depressive disorder, with catatonia

The logic is:

The primary disorder (e.g., schizophrenia / bipolar disorder) is the “main diagnosis,”

And then we add that “there is catatonia as a significant concurrent syndrome right now.”

On the ICD-11 side, catatonia is viewed a bit differently:

ICD-11 gives code 6A40 Catatonia as essentially a separate disorder entity.

Then it specifies whether that catatonia is:

associated with schizophrenia
associated with a mood disorder
or due to a medical condition / substance

In other words, ICD-11 views catatonia as a kind of “central syndrome”
that can emerge alongside many different disorders, instead of being tied specifically and exclusively to schizophrenia.

Therefore, when we use the term “Catatonic-Dominant” in writing / academic contexts:

We do not mean it as an official diagnostic label,

We mean it as a “presentation” or “pattern of clinical manifestation.”

It refers to cases where:

The person may have delusions / hallucinations / disorganized speech,

But the most prominent and overarching feature is catatonia.

For example:

A patient with schizophrenia who currently does not present with very obvious delusional content anymore, because they spend the entire day sitting still, not speaking, not eating, not getting up, and needing help with almost everything.

Or a bipolar patient who still has signs of mania / depression in the background, but on the ward right now, the clinically most worrying features are stupor + mutism + posturing.

So “Catatonic-Dominant” =

A case where catatonia becomes the central axis of the clinical picture.

When describing a patient to the team or in a case report, we might use wording like:

“This is a schizophrenia case with a catatonia-dominant presentation.”

This is used to convey that:

The underlying disorder may be schizophrenia / schizoaffective / mood disorder, etc.,

But “the first thing we urgently need to manage” is the catatonia itself, not just hallucinations or delusional thinking.

In terms of epidemiology:

Many studies have found that catatonia is not as rare as once believed.

In psychiatric inpatient samples or general hospital settings,
prevalence figures often range around 7–38%, depending on the specific population studied.

What is especially noteworthy is that:

Catatonia is found frequently in mood disorders
(especially bipolar disorder and severe major depression),

To the point that the field has largely stopped viewing it as “belonging to schizophrenia only.”

Short summary for opening a post:

Catatonic-Dominant describes a phase where the patient’s entire life is essentially “taken over” by catatonic symptoms –
their movement, responsiveness, and interaction with the world are all profoundly disturbed.
To the extent that, when clinicians describe the case, they don’t start with
“What hallucinations/delusions does this patient have?”
but rather with “Right now, they are sitting still, not speaking, not eating, and barely able to move at all.”

2. Core Symptoms — Main Symptoms in Catatonic-Dominant

First, the overall picture:

When we see a case of catatonia (especially a catatonic-dominant one),
the most striking thing is that “movement and responsiveness” break down across the whole system –
whether in the form of “stopping / slowing to near-zero”, “extreme agitation”, or “bizarre / repetitive movements.”

Broadly, we can group the symptoms into three clusters (which can co-occur in the same individual):

Markedly decreased or nearly absent movement (decreased psychomotor activity)

Excessive or abnormal increase in movement (increased psychomotor activity)

Abnormal, bizarre, or repetitive movements/behaviors (abnormal movements & behaviors)

It is very important to remember:
In a single person, they may switch from extreme slowing → extreme agitation → back to slowing over a few days (or in some cases, within hours).
Therefore, assessment must look at a “time window” of behavior, not just a 5-minute snapshot and then call it done.

2.1 “Slowed / Stopped” Cluster (Decreased psychomotor activity)

This group consists of patients who look as if someone has “switched off” their body and contact with the world –
but it is not deliberate or “pretending.”

1) Stupor

A state where the patient is extremely still and almost completely unresponsive to the environment.

They sit or lie in the same position for very long periods, do not turn toward sounds, and may not respond even when called or gently touched.

However, this is not a coma: on careful examination, some patients still have slight muscle tension / open their eyes / blink / turn their face away a little.

Critical points to watch for:

High risk of dehydration, malnutrition, pressure sores, muscle wasting, and blood clots (DVT/PE).
Some patients perceive everything but cannot move, leading to intense psychological suffering—as if they are “trapped inside their own body.”

2) Mutism

Speaking very little or not at all, despite no structural damage to the larynx or language centers.

When asked questions, the patient often remains silent, even though we may see signs that they hear and understand.

It needs to be differentiated from:

Selective mutism due to anxiety
Aphasia (language comprehension/production problems)

In catatonia, mutism typically co-occurs with stupor / staring / posturing and looks more like the motor system “shutting down” than a primary language problem.

3) Immobility / Motoric Immobility

Remaining in the same posture while sitting or standing for an abnormally long time, such as:

Sitting cross-legged and not getting up for hours
Standing in a corner in the same stance for a very long time

This is not simply “laziness.” When you try to move them, there is often no response or unusual resistance (negativism, waxy flexibility).

Direct consequences include muscle fatigue, joint stiffness, and fall risk if the person maintains a poorly balanced posture for too long.

4) Staring

Staring fixedly, barely blinking, with a rigid, vacant gaze.

Some patients stare in one direction the whole time; others stare at the examiner with almost no facial expression.

People around them often misinterpret this as being “spaced out” or “disinterested,”
but in fact it is a recognized catatonic sign and is included in several rating scales such as the Bush–Francis Catatonia Rating Scale (BFCRS).

5) Withdrawal

No eye contact, no response, no participation in basic activities.

The person may not eat by themselves, not get up to use the bathroom, and require assistance with nearly everything.

On the surface, this can look like “extreme depression” or “being stubborn and uncooperative.”

But in catatonia it usually comes with other motor components, such as posturing, stupor, or mutism.

Overall, this “slowed / immobile” cluster is what many newer studies have found to be more predictive of a catatonia diagnosis than odd behaviors alone.

2.2 “Excessive / Uncontrolled” Cluster (Increased psychomotor activity)

This cluster presents as “excited, almost manic” – but with the distinctive features of catatonia.

Agitation not influenced by external stimuli

The patient is highly restless, pacing, pulling at objects, scrunching their clothes, tearing at bedsheets, etc., continuously.

It may look like panic or anger, but the key is:

Verbal reassurance, calm talking, or environmental changes hardly reduce the agitation at all.

Some patients can swing in and out of other catatonic features, for example:

Suddenly shifting from a whole day of sitting immobile to walking restlessly, grabbing at things, and pulling out tubes or lines.

Risks include:

Unintentional self-harm or harm to others
Pulling out feeding tubes, IV lines, or other medical devices

Some conceptual frameworks call this cluster “excited catatonia,” which is often severe and can progress to malignant catatonia if untreated.

2.3 Abnormal Movements & Behaviors Cluster

These are the classic signs of catatonia, forming part of the 12 criteria in DSM-5.

1) Posturing

The patient assumes and maintains an odd or inappropriate posture (or even a seemingly normal posture that is clearly unsuitable for the situation) and holds it for a long time.

For example, raising an arm and keeping it held up; tilting the head at an odd angle and not moving.

The key difference from catalepsy is that posturing = the patient adopts and maintains the position by themselves,
not as a result of the examiner placing them in that posture.

2) Catalepsy

The clinician physically places the patient’s arm/leg/body into a posture—such as flexing the arm, lifting it up, etc.

After the clinician lets go, the patient remains in that posture, as if they were a wax figure.

Often found together with waxy flexibility (mild resistance) and some rigidity.

3) Waxy Flexibility

When we try to change the patient’s limb position, we feel a kind of “soft resistance” –
like bending wax: neither rigidly stiff nor completely relaxed.

Once the limb is moved to a new position, the patient holds that position instead of returning to the original one.

In teaching, the distinction is often stressed as:

Posturing / catalepsy = the position being maintained
Waxy flexibility = the quality of muscle tone/resistance we feel while moving the limb.

4) Negativism

“Unmotivated opposition” to instructions or external stimuli, such as:

Being told to stand up → instead, lying motionless
Being told to turn left → turning right
Or simply failing to respond to any command at all

This isn’t ordinary stubbornness; it occurs even without emotional conflict or obvious reason, and often recurs alongside other catatonic signs.

5) Stereotypy

Repeated movements without an obvious goal, such as:

Walking in circles
Waving hands repeatedly in the same pattern
Repeating the same phrase over and over

This differs from obsessive rituals in OCD:

Stereotypy in catatonia tends to look empty and meaningless,
And it does not clearly reduce anxiety in the way OCD rituals do.

6) Mannerism

Movements that resemble normal behavior but are exaggerated or stylized in an odd way, e.g.:

An overly dramatic bow or greeting
Walking as if constantly performing on stage

This is not just personality style; it is inappropriate to the context/time, and often appears with other catatonic signs.

7) Grimacing

Holding odd facial expressions for periods of time, such as a strange smile, wide eyes, or twisted mouth.

These expressions are incongruent with the emotional context (e.g., talking about a sad topic while pulling a comical face).

Grimacing is one of the items scored in scales like the BFCRS.

8) Echolalia

The patient repeats words or phrases spoken by others, like an echo.

Ask “How do you feel today?” → the patient responds, “How do you feel today?”

There is typically no new content added by the patient, suggesting a disruption in the planning and generation of spontaneous speech.

9) Echopraxia

The patient mirrors the examiner’s movements, such as:

The examiner scratches their cheek → the patient scratches their cheek.
The examiner shifts their chair → the patient makes a similar movement.

Sometimes this is subtle and requires careful observation of timing and pattern to detect.

This full set of symptoms does not need to be “all present” in a single individual,
but in clear catatonia, we typically see some combination of several of these signs.
These are exactly what DSM-5 and ICD-11 use to define the 12 core symptoms in their diagnostic criteria.

2.4 How to Understand “Catatonic-Dominant” Clinically?

In the context of schizophrenia / mood disorders / other major psychiatric illnesses,
the term “catatonic-dominant” is used to describe cases where:

The patient already has a primary disorder (e.g., schizophrenia),

But the current episode is dominated by catatonic motor symptoms.

On an inpatient ward, this looks like:

The nursing team is not primarily discussing
“What voices is the patient hearing today?”

Instead, they are saying things like:

“Today they still refuse to eat, won’t get up, won’t speak,”
or “Today they were running around, pulling out tubes, grabbing everything.”

That is why a catatonic-dominant presentation:

Pushes physical risks to the forefront:

dehydration, malnutrition, aspiration, DVT/PE, rhabdomyolysis, autonomic instability, etc.

Many studies have also found that:

A substantial number of patients remember what happened during their catatonic state quite vividly,
even when they appeared to have no reaction at the time.

If care is not delivered respectfully and safely, the whole episode can become an additional traumatic experience for the patient.

3. Diagnostic Criteria

3.1 DSM-5 / DSM-5-TR Catatonia

Definition in DSM-5

DSM-5 does not treat catatonia as a standalone disorder in most cases, but as a specifier or associated diagnosis, such as:

Catatonia associated with another mental disorder

Catatonic disorder due to another medical condition

Unspecified catatonia

The core diagnostic rule is: there must be ≥ 3 of the following 12 symptoms:

Stupor – marked reduction of psychomotor activity and reactivity to the environment
Catalepsy – passive induction of a posture, which is then maintained
Waxy flexibility – slight, even resistance to positioning by the examiner, with limbs staying where placed
Mutism – little or no verbal response (not due to aphasia)
Negativism – opposition or no response to instructions or external stimuli without a clear motive
Posturing – spontaneous maintenance of a posture held against gravity
Mannerism – odd, circumstantial caricature of normal actions
Stereotypy – repetitive, non-goal-directed movements
Agitation, not influenced by external stimuli – severe restlessness that does not respond to environmental or interpersonal attempts to calm
Grimacing – odd facial expressions held for periods of time
Echolalia – mimicking another’s speech
Echopraxia – mimicking another’s movements

Additional contextual requirements

The symptoms must:

Cause clinically significant distress to the patient or family,
Or produce severe functional impairment (e.g., inability to eat, drink, or perform basic self-care).

And they must not be better explained by other conditions, such as:

Neuroleptic Malignant Syndrome (NMS)
Delirium due to an acute medical condition
Locked-in syndrome, or other coma states, etc.

Duration

DSM-5 does not specify a strict minimum duration for catatonia.

Review articles suggest that symptoms can appear over hours to days, then evolve in pattern or persist for weeks if untreated.

In real-world practice, clinicians focus more on:

The pattern of symptoms,
Their continuity,
And the degree of impairment,
rather than on a rigid number of days.

Using DSM-5 criteria in a Schizophrenia Catatonic-Dominant case

1. First, diagnose Schizophrenia using the core criteria (delusions, hallucinations, disorganized speech, negative symptoms, etc.).

2. Then assess whether the current episode has ≥ 3 of the 12 catatonia symptoms.

3. If yes → add the specifier:

Schizophrenia, with catatonia

4. In explanatory language, we might informally say:

“Schizophrenia – catatonic-dominant presentation”
to convey that, here and now, catatonia is the main clinical problem.

3.2 ICD-11 Catatonia

Definition in ICD-11

ICD-11 defines catatonia as a “marked disturbance in the voluntary control of movements,”
with symptoms such as:

Extreme slowing or absence of motor activity

Mutism

Purposeless motor activity unrelated to external stimuli

Rigid / unusual / bizarre postures maintained over time

Resistance to instructions or attempts to move the person

Or automatic obedience (following commands in an automatic, excessive way)

ICD-11 divides catatonia into subcodes, for example:

6A40 Catatonia associated with another mental disorder

Catatonia induced by substances or medications

Secondary catatonia syndrome (due to a medical condition)

Unspecified catatonia

Number of symptoms

ICD-11 essentially uses the same principle as DSM-5:
there must be ≥ 3 symptoms from the clusters of decreased / increased / abnormal psychomotor activity.

Some explanatory documents suggest that:

When multiple hyperactivity features are present, they should be counted as one cluster
so we don’t overdiagnose catatonia purely based on agitation.

Key emphasis in ICD-11

It repeatedly highlights catatonia as a “psychomotor syndrome” that can occur in:

Mood disorders
Schizophrenia / primary psychotic disorders
Autism spectrum disorder
And various medical / neurological illnesses.

It clearly recommends that clinicians code both the underlying condition and catatonia, e.g.:

Schizophrenia + 6A40 Catatonia associated with schizophrenia

3.3 Clinical Assessment Tools (Bush–Francis CRS and others)

Even though DSM-5 and ICD-11 list the symptoms clearly, in practice clinicians often rely on standardized rating scales:

Bush–Francis Catatonia Rating Scale (BFCRS)

Contains 23 items (full CRS) and a 14-item screening version.

Covers signs such as excitement, immobility/stupor, mutism, staring, posturing/catalepsy, grimacing, echopraxia/echolalia, etc.

Typical use:

If at least 2 of the first 14 items score 2 or more → this is considered indicative of “catatonia” at a screening level.

Advantages:

Helps ensure consistent assessment across team members.
Useful for tracking severity before and after treatment (e.g., after lorazepam or ECT).

There are other tools as well (Modified Rogers Scale, DSM-based checklists),
but BFCRS is one of the most widely used instruments.

3.4 Differential Diagnosis and Pitfalls

Diagnosing catatonia is not simply “checking off 3 boxes and you’re done” –
the clinician must also rule out other conditions that can look similar:

1) Neuroleptic Malignant Syndrome (NMS)

Features:

High fever
Marked rigidity
Autonomic instability (abnormal blood pressure, pulse, sweating)
Often associated with use of, or rapid dose escalation of, antipsychotics

NMS and malignant catatonia share many overlapping features:
rigidity, stupor, autonomic dysregulation, fever.

Some authors see them as part of the same spectrum.

Differentiation relies heavily on medication history and lab tests (e.g., markedly elevated CPK).

2) Serotonin Syndrome / Acute Dystonic Reactions / Other EPS

These also involve abnormal motor signs and autonomic changes.

However, they commonly present with:

Clonus, hyperreflexia, mydriasis (in serotonin syndrome)
Focal dystonic postures (in acute dystonia)

A detailed medication history (SSRIs, MAOIs, antipsychotics, etc.) is crucial to distinguish these conditions.

3) Delirium, Encephalopathy, Coma States

Delirium can be hypoactive (appearing sluggish) or hyperactive (agitated), similar to catatonia.

ICD-11 and many review papers emphasize that we must carefully assess:

Level of consciousness,
Fluctuations in attention,
Changes in awareness.

Some cases may have both delirium and catatonia at the same time,
so we must avoid viewing the situation through only one lens.

4) Severe Depression / Negative Symptoms of Schizophrenia / Personality Traits

Someone with very severe depression may lie still, not get up, and show no interest in anything → resembling stupor.

Someone with severe negative symptoms (avolition, alogia, anhedonia) may appear emotionally flat and socially withdrawn.

The difference is:

Catatonia tends to show specific motor patterns (posturing, waxy flexibility, echolalia, etc.).
And the lorazepam challenge often produces a striking improvement in catatonia that is not typical of ordinary depression.

Short recap for these sections:

The Core Symptoms of catatonic-dominant cases are profound psychomotor changes –
severe slowing/immobility, excessive agitation, and abnormal/bizarre movements (posturing, echolalia, etc.) often combined in the same person.

The Diagnostic Criteria (DSM-5 / ICD-11) both rely on “≥ 3 symptoms out of a list of 12”
in the context of a psychiatric or medical disorder, while also ruling out mimicking conditions.

When these symptoms dominate the overall clinical picture, we call it a catatonic-dominant presentation,
a group with high physical risk that requires rapid diagnosis and treatment.

4. Subtypes or Specifiers — Key Forms

In real-world practice, clinicians tend to talk about “forms of catatonia” rather than strictly formal subcodes:

4.1 Retarded Catatonia (the most common form)

Main features: slowed, still, mute, unresponsive.

Core symptoms: stupor, mutism, posturing, withdrawal, staring.

Several studies have found that “retarded catatonia” is the most frequently observed pattern
(in some samples, more than 90%).

4.2 Excited Catatonia

Essentially the opposite of the first type: hyperactive + severe agitation.

The person moves excessively, may talk a lot, or show repetitive behaviors,
and may look “manic” or “out of control,” but does not respond well to typical calming strategies.

Risks:

Self-harm or aggression,
Accidents,
Physical exhaustion.

4.3 Malignant Catatonia

A severe form with fever, autonomic instability, labile blood pressure, tachycardia, profuse sweating, etc.

Clinically very similar to NMS and considered a medical emergency → requires urgent treatment (often ECT + ICU-level care).

4.4 Based on Underlying Condition (Associated Conditions)

Catatonia associated with:

Schizophrenia / schizoaffective disorder

Mood disorders (bipolar disorder, major depression) – more common than previously assumed

Neurodevelopmental disorders – such as autism spectrum disorder, intellectual disability

Autoimmune / neurological conditions – e.g., NMDAR encephalitis and other forms of autoimmune encephalitis

In the context of “Catatonic-Dominant Schizophrenia”, this means:

The core diagnosis is schizophrenia,

But the current episode is dominated by catatonic symptoms.

ICD-11 recommends coding both the schizophrenia and the associated catatonia.

5. Brain & Neurobiology — Brain and Neural Mechanisms

The big-picture view of catatonia (including catatonic-dominant presentations) from a brain perspective is:

It is not a “weird personality” or someone “refusing to move.”
It is a disorder of brain networks that control movement, initiation of actions, and the link between thought and behavior.

It is a psychomotor syndrome arising from dysfunction across multiple brain circuits at once:
structural networks, neurotransmitter systems, and often immune/inflammatory mechanisms that affect the brain.

5.1 Brain Circuits Involved

Recent neuroimaging research suggests that several key networks are affected in catatonia:

5.1.1 Cortico–Striato–Thalamo–Cortical Loops

These are crucial because they form the backbone of planning, initiating, and regulating posture and movement.

Key structures:

Supplementary Motor Area (SMA)

Prepares voluntary movements before they are executed.
When impaired → the brain struggles to “issue the start command,”
so patients may remain still even while internally aware.

Anterior Cingulate Cortex (ACC)

Involved in deciding to start/stop actions, motivation, and conflict monitoring.
Dysfunction → patients may feel as if they can’t “press the start button” or are stuck in a perpetual state of indecision.

Basal Ganglia (Striatum, Globus Pallidus, etc.)

Work as the central “on–off switch” for motor commands from the cortex.
In catatonia, it is hypothesized that the balance between direct and indirect pathways is disrupted,
leading to abnormal initiation or inhibition of movements.

Thalamus

Acts as a relay and filter, sending processed signals back to the cortex.
If its function is disrupted, the “think–move” loop cannot complete properly.

fMRI and diffusion imaging studies in patients with catatonia (in schizophrenia and mood disorders) often show abnormal connectivity in these circuits –
for example, reduced or altered connections between motor cortex, basal ganglia, and thalamus compared to controls.

In short:

Circuits that should smoothly translate “intention → action” become stuck loops,
leaving the body “frozen” in a posture or moving in ways that do not respond to the environment.

5.1.2 Self-Awareness and Emotional Networks

Beyond pure motor circuitry, other networks support self-awareness and contextual processing:

Medial prefrontal cortex, posterior cingulate, insula, etc.

Involved in self-awareness, interoception, and the sense of agency.

Dysfunction in these regions may help explain why:

Some people in catatonia report feeling “cut off from their own body,”

Or feel they cannot control their body even though they perceive the environment clearly.

Systematic reviews suggest that catatonia is best understood as a network disorder,
rather than being caused by a single discrete lesion.

5.2 Structural and Connectivity Changes

MRI and DTI (Diffusion Tensor Imaging) studies show recurring patterns:

Gray matter changes

Slight reductions in gray matter volume in parts of the frontal–parietal–motor networks
in catatonic patients compared to psychiatric patients without catatonia.

White matter microstructure

Abnormalities in the fiber tracts connecting motor cortices with the basal ganglia and thalamus.
In some studies, fractional anisotropy (FA) is altered along these tracts,
suggesting abnormal signal conduction.

A simple way to phrase this in an article:

Brain imaging shows that catatonia is not purely a “psychological” phenomenon.
There are measurable changes in the structure and connectivity of motor–executive circuits,
resembling what we see in other movement disorders such as Parkinson’s disease or dystonia –
except that here, it is wrapped inside a primarily psychiatric clinical context.

5.3 Neurotransmitters — GABA, Glutamate, Dopamine

A key point is that catatonia seems to involve multiple neurotransmitter imbalances at once,
not just dopamine as in the older, schizophrenia-centered model.

5.3.1 GABA Hypothesis

The most striking clinical evidence is the often rapid and robust response to benzodiazepines (e.g., lorazepam).

Benzodiazepines enhance GABA-A receptor activity, increasing inhibitory tone in key circuits.

The hypothesis:

In catatonia, GABA-mediated inhibition in motor/prefrontal circuits may be too low or mis-timed,
causing abnormal synchronization of motor outputs → freezing, odd postures, lack of responsiveness.

Giving benzodiazepines restores inhibitory balance, leading to dramatic relief of symptoms in many cases.

You can frame it simply as:

A healthy brain has a GABA “brake system” to pace and coordinate movement.
In catatonia, the brake system malfunctions—some parts don’t brake at all, others brake at the wrong time.
Benzodiazepines “recalibrate the brakes,” which is why some patients seem to “switch back on” and start moving and talking again.

5.3.2 Glutamate / NMDA

Evidence from autoimmune encephalitis, especially anti–NMDA receptor encephalitis:

Many patients present with psychosis + catatonia + movement disorders + seizures in a single syndrome.

The underlying mechanism is antibodies disrupting NMDA receptor function.

Several reviews propose that a subset of catatonia is essentially a glutamatergic disorder.

There are reports of compounds such as amantadine, memantine (special NMDA antagonists), and ketamine being used in refractory catatonia (resistant to benzodiazepines/ECT), with some improvement in individual cases.
However:

This remains a specialist-level approach based on case reports/small series,

It is not yet standard of care.

Overall:

Abnormal glutamate/NMDA signaling may be one of the “core engines” of catatonia,
particularly in forms linked to autoimmune brain disease.

5.3.3 Dopamine and Overlap with NMS

In schizophrenia, dopamine (especially mesolimbic) is central.

Using antipsychotics that strongly block D2 receptors, or adjusting doses too quickly,
can, in some individuals, trigger syndromes that resemble catatonia / malignant catatonia

or progress to Neuroleptic Malignant Syndrome (NMS).

NMS and malignant catatonia overlap strongly:

Rigidity, stupor, autonomic instability, fever.

Some researchers view them as part of a continuum,
differing mainly in trigger and the specific neurotransmitter profile that “collapses” most severely.

You can explain it on the site as:

When we suppress dopamine in the basal ganglia too aggressively,
the motor control system of the whole body may “lock up,”
producing a clinical picture similar to catatonia or NMS.
This is why clinicians must be very cautious when using antipsychotics in patients who are prone to catatonia.

5.4 Immune System and Inflammation

In the last 10–15 years, research has shown that the immune system plays an important role in some forms of catatonia, especially:

Autoimmune encephalitis, such as anti–NMDA receptor encephalitis

Typical course:

Patients often start with emotional and behavioral changes, insomnia, irritability, auditory hallucinations, delusions,

Then gradually develop:

Catatonia (sitting still, fixed postures, slowed response)
Movement disorders (jerks, abnormal postures)
Seizures, autonomic instability (blood pressure/heart rate fluctuations) and other neurological signs.

Paraneoplastic syndromes – immune reactions associated with certain cancers that inflame the brain and can produce catatonia.

Review articles suggest that catatonia may be a final common pathway of different forms of brain inflammation or immune activation:

Regardless of whether the primary trigger is psychosis, mood disorder, autoantibodies, or metabolic factors—
if the process sufficiently disturbs motor + limbic networks, it can manifest as catatonia.

Key takeaway for readers:

Some cases of catatonia are not purely psychiatric,
but are warning signs of serious neurological illnesses (e.g., autoimmune encephalitis).

Hence most guidelines emphasize:

If catatonia appears in someone with no prior psychotic history,
Or in someone who also has clear neurological signs,
→ thorough medical and immune workup is urgently needed.

6. Causes & Risk Factors

Catatonia is an end-stage syndrome that can arise from many different pathways.
It is not a single disease with a single cause.
We therefore need to think in terms of “etiological groups” instead of cramming everything under “schizophrenia.”

6.1 Primary Psychiatric Conditions

Schizophrenia / Schizoaffective Disorder / Other Psychotic Disorders

Historically, catatonia was viewed as a subtype of schizophrenia.

Now we know:

Catatonia in schizophrenia is less common than in mood disorders,
But when it does occur, it is often severe, associated with a chronic course and need for intensive treatment (e.g., ECT + clozapine in some).

In a catatonic-dominant schizophrenia picture:

Positive symptoms (hallucinations/delusions) may be less prominent than the psychomotor symptoms,

Patients may spend a long time in hospital just to stabilize nutrition, mobility, and physical rehabilitation.

Mood Disorders — Bipolar Disorder & Major Depressive Disorder

Modern research has found that catatonia is common in bipolar disorder.

It can occur in:

Manic episodes (excited catatonia with agitation),
Severe depressive episodes (with stupor, mutism, withdrawal).

MDD patients with catatonia tend to have very severe depression and are at high risk of self-neglect and medical complications if not treated promptly.

Others in the Schizophrenia Spectrum / Psychotic Disorders

Conditions like brief psychotic disorder, schizophreniform disorder can occasionally present with catatonia.

This is why DSM-5 introduced the broader category “catatonia associated with another mental disorder.”

6.2 Neurodevelopmental & Intellectual Disorders

Autism Spectrum Disorder (ASD)

There are reports of pediatric / adolescent catatonia in young people with ASD.

Typical scenario:

A young person with autism who previously functioned fairly well
Suddenly becomes slowed, speaks less, sits immobile, shows intensified repetitive movements, and stops responding to commands.

This is often misinterpreted as “worsening autism” or “teenage defiance,”
when in fact it is catatonia superimposed on ASD.

Intellectual Developmental Disorders (IDDs)

In individuals with low IQ or longstanding developmental problems,
the onset of catatonia is very hard to detect.

It is frequently misattributed to:

“Slowing down due to aging,”
“Non-compliance or stubbornness.”

Studies in older adults with IDD show that catatonia is often overlooked,
even though it responds well to benzodiazepines/ECT and treatment can significantly improve function.

6.3 Medical / Neurologic / Autoimmune Conditions

This group is crucial because it represents secondary catatonia,
where finding and treating the underlying cause can dramatically improve the syndrome.

Encephalitis (brain inflammation)

Both infectious (e.g., viral encephalitis) and autoimmune encephalitis (e.g., anti-NMDAR).

Patients often begin with psychiatric symptoms (hallucinations, delusions, sleep disturbance),
and then develop:

Catatonia
Movement disorders (jerking, restlessness)
Seizures, altered consciousness

If clinicians don’t consider this possibility, treatment may focus solely on psychiatry and miss a dangerous brain disease.

Structural / Degenerative Brain Disorders

Brain tumors, strokes in certain regions (especially frontal–basal ganglia circuits),
and neurodegenerative diseases (e.g., Parkinson’s disease, dementia with Lewy bodies, frontotemporal dementia)
can all present with catatonic features, particularly during acute exacerbations or under stress.

Metabolic / Systemic Conditions

Severe hyponatremia (low sodium), advanced hepatic/renal failure, and profound vitamin B12 deficiency
have all been associated with catatonic states.

Heavy alcohol use, or withdrawal from certain substances, can also be linked to catatonia in some cases.

Infections / Sepsis

Critically ill ICU patients with sepsis or severe infections can develop states resembling catatonia mixed with delirium.

Distinguishing pure delirium from delirium with catatonia requires rating scales and clinical experience.

6.4 Substances and Medications (Substance / Medication-Induced)

Antipsychotics

High-potency typical antipsychotics, or rapid changes in antipsychotic regimens,
can trigger:

Catatonia in some individuals,
Or progression to NMS (overlapping with malignant catatonia).

Guidelines generally recommend:

If catatonia emerges after antipsychotic changes → consider antipsychotic-induced catatonia / NMS,
and review stopping or reducing the antipsychotic under close medical supervision.

Abrupt Benzodiazepine Discontinuation (BZD Withdrawal)

Individuals who have used benzodiazepines long-term and suddenly stop them may develop withdrawal catatonia.

The picture can include:

High anxiety, severe insomnia, followed by abnormal motor symptoms, stupor, or agitation.

Treatment = reinstating benzodiazepines and then gradually tapering under supervision.

GABA-B Agonists and Drugs Affecting Serotonin / Glutamate

Substances such as baclofen, and some drugs that strongly increase/decrease serotonin or glutamate,
have been linked in case reports to catatonia.

Although not yet recognized as major causative factors, they show that heavy interference with GABA / glutamate systems can destabilize psychomotor control.

6.5 Other General Risk Factors

Beyond primary causes, there are “amplifiers” that raise an individual’s risk of developing catatonia:

Past History of Catatonia

If someone has had one episode of catatonia, their risk of recurrence in later stress episodes is increased,
especially if the underlying disorder remains unstable or effective medications are stopped/reduced rapidly.

Severe Psychiatric Illness + Frequent Hospitalizations

Patients with severe schizophrenia or bipolar disorder, long inpatient stays, and multiple medications
are at higher risk of catatonia due to:

The illness itself, and
Frequent medication changes or abrupt discontinuations.

Severe Stress / Untreated Acute Psychiatric Episodes

Intense psychosocial stress, chronic sleep deprivation, or prolonged uncontrolled psychosis/mood episodes
can act as triggers that push brain circuits into a “collapse” state, resulting in catatonia.

Older Age and Intellectual Disability

In these populations, catatonia is frequently misattributed to:

“Normal slowing due to old age,”
“Their usual personality,” or “just non-cooperative.”

In reality, it may be treatable catatonia, and recognizing it can greatly improve quality of life,
as patients may regain mobility and communication once appropriately treated.

6.6 Linking Back to “Catatonic-Dominant”

When we put everything together, catatonic-dominant presentations are:

Endpoints where multiple brain networks fail simultaneously –
motor circuits, limbic circuits, immune–brain interactions, and neurotransmitter systems.

The root causes may include:

Primary psychiatric illnesses (schizophrenia, bipolar disorder, MDD)

Brain inflammation / autoimmune disease

Metabolic problems, medications, or withdrawal states

If we don’t adopt this integrated view, we risk:

Focusing only on surface narratives like “They’re not cooperating,” “They’re stubborn,” or “They’re just depressed,”

While missing the fact that the brain is actually in systemic dysfunction.

For your website, you can wrap this message like:

Catatonia (especially catatonic-dominant forms) is not a single disease,
but a “language” the brain uses to tell us that
the circuits for movement, intention, and self-awareness are in serious trouble.
The trigger might be a psychiatric illness, a neurological disorder, immune dysregulation, medications, or overwhelming stress.
Recognizing it as a brain syndrome, rather than mere stubbornness or laziness,
is the key to proper treatment and preventing long-term harm.

7. Treatment & Management

Important: Catatonia is often a medical-psychiatric emergency, especially when there is risk of dehydration, malnutrition, or organ failure.
The information below is for educational purposes only and is not personal medical advice. Actual treatment must be planned and supervised by psychiatrists/medical teams.

7.1 Initial Assessment

Perform a full physical exam, check vital signs, and order labs (electrolytes, renal/hepatic function, etc.).

Rule out look-alike conditions such as NMS, serotonin syndrome, acute dystonia, status epilepticus, delirium, coma, etc.

Assess for risks such as:

Not eating or drinking
Fall risk, aspiration risk
Abnormal blood pressure or heart rate

7.2 Benzodiazepines (Lorazepam Challenge)

Benzodiazepines (especially lorazepam) are the most widely used first-line treatment.

Typically, a “lorazepam challenge” is performed → the medication is given, and clinicians observe the response over 5–10 minutes.

In many patients, there is striking improvement, which also supports the diagnosis of catatonia.

Dosage is then adjusted according to response (by the physician) and gradually tapered once the syndrome improves.

7.3 Electroconvulsive Therapy (ECT)

ECT is considered when:

There is no adequate response to benzodiazepines, or

The presentation is malignant catatonia / life-threatening.

Current guidelines treat ECT as the treatment of choice in severe or refractory cases.
Studies note that some chronic catatonia patients benefit from ECT combined with clozapine over the long term.

7.4 Management of Other Medications

Antipsychotics

In schizophrenia, antipsychotics are crucial for long-term management of the underlying disorder.

But during an acute catatonic episode, aggressive antipsychotic use can worsen catatonia or precipitate NMS.

Many guidelines recommend:

First stabilize catatonia with benzodiazepines/ECT,
Then cautiously optimize antipsychotics.

Glutamate Modulators

Agents like amantadine, memantine, ketamine have shown benefit in some treatment-resistant catatonia cases,
but remain specialist options with limited evidence (case reports/small series).

7.5 Long-Term Management

Stabilize and treat the underlying disorder (schizophrenia, bipolar, MDD, ASD, etc.).

Provide psychoeducation to patients and families about catatonia and early warning signs.

Plan relapse prevention: medication adherence, stress reduction, regular psychiatric follow-up.

Incorporate rehabilitation: physical therapy, movement rehabilitation, re-engagement with daily activities and social interaction.

8. Notes — Key Points for Catatonic-Dominant

Catatonia does not always mean “standing like a statue.”

Some patients are hyperactive / excited, resembling mania or severe agitation.

It is more common than many people think, and often missed clinically:

Teams and relatives may interpret it as “non-cooperative,” “lazy,” or “just deeply depressed.”

In Schizophrenia with a Catatonic-Dominant presentation:

If we focus only on delusions/hallucinations and neglect catatonia,
the patient faces high physical risks: DVT, pulmonary embolism, malnutrition, aspiration pneumonia, etc.

Early diagnosis and treatment:

Markedly improves outcomes, especially with timely benzodiazepines and/or ECT.

For lay readers / content creators:

Emphasize that this knowledge is for understanding, not for self-diagnosis.

If you see someone who is:

Non-responsive, “frozen” in posture, or repeating strange movements
In the context of serious psychiatric illness or severe medical illness
→ it is a warning sign that they need urgent medical evaluation.

Read Schizophrenia

References

Rogers JP, Pollak TA, Blackman G, et al. Catatonia: clinical overview of the diagnosis, treatment, and clinical challenges. Medicines (Basel). 2021.
Edinoff AN, Kaufman SE, Hollier J, et al. Catatonia: clinical perspectives and neurobiological underpinnings. StatPearls Publishing.
Jain A, Mitra P, Tripathi A. Catatonic schizophrenia. StatPearls Publishing.
Walther S, Stegmayer K, Wilson JE, Heckers S. Structure and neural mechanisms of catatonia. CNS Spectrums.
Rogers JP, et al. Catatonia and the immune system: a review. The Lancet Psychiatry.
Ariza-Salamanca DF, et al. Molecular and cellular mechanisms leading to catatonia. Frontiers in Molecular Neuroscience.
Cattarinussi G, et al. Brain mechanisms underlying catatonia: a systematic review. European Psychiatry.
World Health Organization. ICD-11 – 6A40 Catatonia; Schizophrenia or other primary psychotic disorders.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. (DSM-5 / DSM-5-TR).
Dubovsky SL. Catatonia: how to identify and treat it. Current Psychiatry.

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