With Catatonia

🧠 Overview 

Bipolar I Disorder with Catatonia
A subtype of Bipolar I Disorder in which an episode (either mania or major depressive episode) presents with catatonia. This means the brain is unable to regulate behavior and movement normally during that mood episode.

In clinical notation, specify:

Bipolar I Disorder, current episode manic (or depressed), with catatonia

🔹 Why the “with Catatonia” specifier matters

Catatonia is often overlooked because patients may appear quiet and still, leading clinicians or family to misinterpret it as ordinary depression or delirium. In reality, the brain is in an acute psychomotor shutdown or overload.
Without timely, appropriate treatment—e.g., benzodiazepines or ECT—patients may progress to malignant catatonia, a life-threatening emergency (akin to Neuroleptic Malignant Syndrome).

🔹 What “Catatonia” means in brain terms

Catatonia is not just “freezing” or “rigidity.” It reflects a desynchrony between motor control circuits and emotion–motor integration.
Key regions and systems—basal ganglia, thalamus, prefrontal cortex, and the GABA–glutamate system—become imbalanced, leading to faulty motor commands (e.g., holding a posture, mutism, oppositional resistance, or purposeless repetitive acts).
Some patients swing to the opposite extreme: prolonged immobility or severe purposeless hyperactivity.

🔹 Relationship to Bipolar I Disorder

During manic or depressive episodes, dopamine and GABA systems that govern behavior are already fluctuating.
If a severe or abrupt disequilibrium occurs (e.g., prolonged sleep loss, discontinuation of mood stabilizers, stimulant overuse, or neuroinflammation), the psychomotor circuit can “crash”, producing catatonia on top of the mood episode.

🔹 How it differs from “typical” Bipolar I

Feature	Bipolar I (typical)	Bipolar I with Catatonia
Mood	Extreme mania/depression	Mania/depression plus loss of motor control
Movement	Faster or slower per mood	Marked abnormalities (freezing, rigidity, repetition, non-response)
Communication	Talkative or reduced speech	May be mute
Responsiveness	Some awareness	May fail to respond to external stimuli
Risks	Risky behavior in mania	Life-threatening risk if untreated (catatonia)

🔹 Prevalence and clinical presentation

• Roughly ~10% among acutely ill psychiatric inpatients.
• In mood disorders, rates can reach 17–47%, especially during mania.
• Onset may be abrupt and resolve within days if treated promptly; untreated >1–2 weeks risks malignant catatonia or medical complications (dehydration, thrombosis, arrhythmia).

🔹 Common misconceptions

• “Just depression” → may actually be depressive episode with catatonia.
• “Only a medication side effect” → catatonia often responds to benzodiazepines.
• “Psychosis or NMS” → must be differentiated carefully; management differs.

🔹 Summary

Bipolar I Disorder with Catatonia = a mood episode in which motor–behavioral control shuts down.
It’s a psychiatric emergency: delays can lead to metabolic collapse, infection, or death.
With correct, timely treatment, patients often improve rapidly and may return to baseline within days.

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⚙️ Core Symptoms 

Per DSM-5-TR, diagnosis requires ≥3 of 12 symptoms below—each reflects psychomotor control dysregulation:

Symptom	Explanation	Real-world example
1. Stupor	No response; no speech or movement	Sits motionless, eyes open as if “asleep awake”
2. Catalepsy	Maintains imposed posture abnormally long	Arm remains raised for many minutes after being positioned
3. Waxy Flexibility	Limbs feel “waxy”; can be placed and left in odd positions	Nurse positions arm; it stays there
4. Mutism	Little or no verbal response despite intact neuromuscular function	Repeated questions go unanswered
5. Negativism	Non-response or resistance without reason	Asked to raise hand, the patient refuses or does the opposite
6. Posturing	Spontaneously holds bizarre/uncomfortable postures	Holds head down or one arm up for long periods
7. Mannerisms	Odd, purposeful-seeming movements	Saluting or waving repeatedly without context
8. Stereotypy	Repetitive, non-goal-directed behaviors	Pacing, repeating phrases, tapping continuously
9. Agitation (not stimulus-driven)	Severe restlessness without external trigger	Sudden running or arm-flailing
10. Grimacing	Abnormal facial expressions	Fixed smile; intermittent facial contortions
11. Echolalia	Repeats others’ words	Doctor: “How are you?” Patient: “How are you?”
12. Echopraxia	Imitates others’ actions	Doctor raises hand; patient mirrors immediately

🌀 Two principal phenotypes

Hypokinetic (Retarded) Type

• Most common: stillness, silence, no eating/drinking.
• Often linked to excess inhibitory drive / GABA pathway imbalance → motor execution “stalls.”
• Untreated risks: dehydration, thrombosis, collapse.

Hyperkinetic (Excited) Type

• Opposite profile: excessive, purposeless movement, verbal/motor repetition, severe agitation.
• Linked to excess glutamate–dopamine activation.
• Uncontrolled cases can escalate to malignant catatonia.

⚠️ Malignant Catatonia (Life-threatening)

A combined psychiatric–medical emergency with autonomic failure and metabolic collapse.

Key features:

• High fever
• Rigidity
• Autonomic instability (HR/BP)
• Markedly elevated CPK (NMS-like)
• Confusion or coma

Urgent treatment:

• IV lorazepam challenge
• ECT within 24–48 hours if inadequate response

🧩 Brain Systems—at a glance

System	Role	When dysregulated
Basal Ganglia	Start/stop movement	Slowness, “freezing,” motor blocks
Prefrontal Cortex	Top-down behavioral control	Poor adaptation to stimuli
GABAergic	Inhibitory control	Hypoactive → over-movement; hyper-inhibitory → immobility
Glutamatergic (NMDA)	Excitatory signaling	Over-excitation → purposeless/repetitive acts
Dopamine pathways	Motivation & initiation	Fluctuations in mania can trigger catatonia

Bottom line:

Catatonia = loss of synchronization between thought–emotion–movement.
It can occur in manic or depressive episodes of Bipolar I and is highly treatable if recognized promptly.

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Diagnostic Criteria

• Confirm Bipolar I: at least one manic episode per DSM-5-TR (after ruling out substances/medical causes).
• Add the specifier “with catatonia” when, during the mood episode, ≥3 of the 12 DSM catatonia features are present. BFCRS may aid screening/severity (14-item screen; 23-item severity).

Differential diagnosis: NMS, delirium, encephalitis, heat stroke, etc. MC and NMS overlap; antipsychotic exposure and associated signs help differentiate. MC typically responds rapidly to benzodiazepines/ECT.

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Subtypes or Specifiers (Related)

• Catatonia specifier (main focus here) for manic/depressive episodes in Bipolar I (DSM-5-TR).
• Clinical catatonia forms: hypokinetic vs excited; malignant catatonia (emergency).
• Other Bipolar specifiers that may co-occur: with psychotic features, mixed features, anxious distress, rapid cycling, peripartum onset, seasonal pattern. “With catatonia” is an added specifier, not a separate Bipolar type.

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🧠 Brain & Neurobiology

Catatonia in patients with Bipolar I Disorder is not merely “freezing” or “rigidity.” It reflects simultaneous dysregulation across multiple brain systems—especially three core neurotransmitter systems: GABA, glutamate, and dopamine.

🔹 1) GABAergic System (the brain’s inhibitory system)

• Normally, GABA-A receptors inhibit neuronal firing within motor and limbic circuits.
• In catatonia, GABA-A hypoactivity (reduced function) → inadequate inhibition → motor circuits “stall” or become desynchronized.
• Key evidence: patients often respond dramatically to benzodiazepines (e.g., lorazepam), which are positive allosteric modulators of GABA-A. Once given, inhibitory tone is restored and motor control can “reset” within hours.

Summary:

• Low GABA → brain “locks up.”
• Benzodiazepines → raise GABA → improvement within ~20–60 minutes.

🔹 2) Glutamatergic System (the brain’s excitatory system)

• Another mechanism is NMDA hyperactivity—excess glutamatergic drive in regions such as the cortex and basal ganglia → excitotoxic stress that disrupts motor-circuit coordination.
• Studies show that NMDA antagonists (e.g., amantadine, memantine) can alleviate catatonia in benzodiazepine-refractory cases.
• This mechanism overlaps with autoimmune encephalitis (e.g., anti-NMDA receptor encephalitis), which can also produce catatonia.

Summary:

• Excess glutamate → overexcited brain → confused/repetitive movements.
• NMDA antagonists → help re-balance excitatory tone.

🔹 3) Dopaminergic System (dopamine)

• Dopamine is crucial for drive and movement initiation.
• Strong D2 receptor blockade (e.g., high-potency antipsychotics or overly high doses) can trigger catatonia or NMS-like reactions.
• Conversely, dopaminergic overactivity (as in mania) can produce hyperactive catatonia (repetition, purposeless movement).

Summary:

• Too little dopamine → rigidity/stupor.
• Too much dopamine → hyperactivity/agitation.
• The goal is to balance GABA–glutamate–dopamine.

🔹 4) Relevant Neural Circuits

• Basal Ganglia–Thalamo-Cortical Loop: governs start/stop of movement → when signaling between basal ganglia and motor cortex goes awry, patients freeze or repeat actions.
• Prefrontal–Limbic Pathways: integrate emotion with behavior → if limbic overactivation occurs while prefrontal control is inhibited, the brain “wants to move” but cannot execute.
• Cerebellum & Parietal Cortex: planning/coordination of movement (fMRI often shows hypoperfusion here during catatonia).

🔹 5) Catatonia as a Network Disorder

Multiple neuroimaging modalities (fMRI, PET, SPECT) indicate catatonia is not damage to a single spot, but rather network dysconnectivity. In short, the motor–limbic–cognitive circuits fall out of sync → the brain issues commands that the body fails to carry out.

🔹 6) Immune & Inflammatory Dimension (Neuroinflammation)

Some patients show elevated cytokines or antibodies to NMDA or GABA-B receptors. This may explain why certain cases respond to NMDA antagonists or, in autoimmune catatonia, to anti-inflammatory/immunologic treatments (e.g., corticosteroids, IVIG).

🧩 Brain Mechanism—Bottom Line

Catatonia = circuit breakdown caused by neurotransmitter imbalance (GABA↓ / glutamate↑ / fluctuating dopamine) and disconnection across motor–limbic–prefrontal networks, leaving the brain unable to command normal responses.

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⚠️ Causes & Risk Factors

In Bipolar I, catatonia is usually triggered by abrupt biological and environmental shifts that destabilize neural circuits. Think in three broad buckets:

🔹 1) Biological Factors

• Neurotransmitter volatility during mood episodes — mania ↑dopamine; depression ↓GABA.
• Basal ganglia circuit abnormalities (seen on imaging).
• Bipolar-spectrum genetics → greater limbic vulnerability.
• Neuroinflammation / autoimmune encephalitis (especially anti-NMDA, GAD65 antibodies).
• Metabolic problems: hyponatremia, hepatic encephalopathy, hypocalcemia, etc.

🔹 2) Pharmacological Triggers

• Starting/escalating antipsychotics—especially high-potency (e.g., haloperidol) → excessive D2 blockade → catatonic stupor or NMS-like states.
• Abrupt benzodiazepine withdrawal → sudden GABA drop → catatonic relapse.
• Stimulants (amphetamines, cocaine) → glutamate/dopamine surges → excited catatonia.
• Lithium toxicity or sodium depletion while on lithium.

🔹 3) Medical / Environmental Factors

• Dehydration, malnutrition, chronic infection → metabolic stress to the brain.
• Extreme psychosocial stress or prolonged insomnia.
• History of catatonia → higher recurrence risk.
• Physical immobilization or prolonged hospitalization.

🔹 4) Bipolar-Specific Contributors

• Severely manic episodes → dopamine surges → psychomotor short-circuit.
• Depressive episodes with psychotic features → excessive inhibitory tone (GABA) → motor shutdown.
• Mixed features (simultaneous high–low mood) → acute limbic–motor chaos.

🧩 Etiology—Bottom Line

Catatonia rarely has a single cause. It is the convergence of factors: neurotransmitter imbalance + brain stress + medication/medical contributors.

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Treatment & Management

Principle: Treat catatonia first, alongside mood-episode care.

Benzodiazepines (first-line)

• Lorazepam challenge: 1–2 mg IV (IM/PO if needed); reassess in ~20–60 min (IV). ≥50% improvement supports catatonia; continue/titrate until remission (many cases resolve in 3–7 days).
• Use BFCRS to monitor severity/response.

Electroconvulsive Therapy (ECT)

• Indications: non-response to lorazepam, severe/unsafe presentations, malignant catatonia, or biological instability (autonomic dysregulation, fever, high CPK, poor intake).
• Common schedule: 3×/week; more frequent for malignant cases as needed.

NMDA antagonists (refractory/adjunct)

• Amantadine (e.g., 100–500 mg, 2–3×/day) or Memantine (5–20 mg/day) show benefits in case series when benzodiazepines/ECT are limited.

Mood-episode management (after catatonia improves)

• Mania: lithium/valproate/lamotrigine; cautious use of SGAs.
• Depression: follow BD-I depression guidance; avoid switching to mania.

Antipsychotic precautions

• In acute catatonia—especially malignant—avoid or hold dopamine-blocking agents if possible (worsening/NMS risk). Once catatonia clearly remits, reintroduce slowly with close monitoring only if essential.

Supportive care

• Prevent complications of immobility/poor intake: fluids/nutrition, DVT prophylaxis, pressure-injury care, aspiration precautions, close monitoring of temp/HR/BP/CK, and workup for infection/metabolic/encephalitic causes as indicated.

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Notes (Practice Points)

• Do not delay: a lorazepam challenge both aids diagnosis and initiates treatment, reducing complications.
• Track with BFCRS: baseline and serial scores after medication/ECT to quantify response and coordinate care.
• MC vs NMS: significant overlap—review antipsychotic exposure, fever/autonomic signs/CK, and consider early ECT in high-risk cases.
• Search for medical drivers (autoimmune, infectious, metabolic), especially if non-responsive or if systemic signs are present.

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References (Key Sources)

• American Psychiatric Association. Highlights of Changes from DSM-IV-TR to DSM-5 (catatonia as specifier and standalone condition).
• StatPearls. Catatonia (core features; ≥3-symptom criterion).
• Edinoff AN et al., 2021. Catatonia: Clinical Overview… (DSM criteria and treatment overview).
• Rogers JP et al., 2023. BAP Evidence-based consensus guidelines for catatonia (lorazepam challenge, ECT, NMDA antagonists).
• ICD-11 concept of catatonia (≥3 symptoms; as independent entity and as associated with other mental disorders).
• Prevalence and mood-disorder data (meta-analyses/reviews).
• Malignant catatonia—features and management (reviews/handbooks).
• NMDA antagonists (amantadine/memantine) in refractory cases—BAP guidelines & 2024 systematic reviews.
• BFCRS (Bush–Francis Catatonia Rating Scale) manuals and teaching materials.

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