Catatonia

the Differentiation between

Lethal Catatonia and

Neuroleptic Malignant

Syndrome

SAMIR EL ANSARY

Icu professor

Learning Objectives

• To review symptoms and signs of catatonia including lethal catatonia.

• To know the overlap between catatonia and neuroleptic malignant syndrome.

• To understand the role of ECT in both catatonia and neuroleptic malignant syndrome

CatatoniaDSM-IV criteria

• Motor immobility as evidenced by catalepsy (including waxy flexibility) or stupor;

• Excessive motor activity (purposeless, not influenced by external stimuli);

• Extreme negativism (motiveless resistance to all instructions or maintenance of a rigid posture against attempts to be moved) or Mutism.

Catatonia: DSM-IV criteria

• Peculiarities of voluntary movement as evidenced by posturing, stereotyped movements, prominent mannerisms, or prominent grimacing

• ECHOLALIA OR ECHOPRAXIA

A. At least 2 of the above features

B. Due to mental (eg: Schizophrenia or Mood Disorders) or medical disorder

C. Does not occur exclusively during the course of a Delirium

Catatonia: Phenomenology-1

• Posturing

– Spontaneous maintenance of posture (s), including mundane (e.g. sitting or standing for long periods without reacting).

• Limb posturing

• “Psychic pillow”

• Staring


Rigidity

Maintenance of a rigid position despite efforts to be moved, exclude if cog-wheeling or tremor present

Negativism

Apparently motiveless resistance to instructions or attempts to move/examine patients. Contrary behaviour, does exact opposite of instruction.


Waxy Flexability

During reposturing of patient, patient offers initial resistance before allowing himself to be repositioned, similar to that of a bending candle.


• Gegenhalten

–Continuous involuntary sustained muscle contraction When an affected muscle is passively stretched, the degree of resistance remains constant regardless of the rate at which the muscle is stretched.


• Mitgehen

– "Anglepoise lamp" arm raising in response to light pressure of finger, despite instructions to the contrary.


• Ambitendency

– Patient appears "motorically stuck" in indecisive, hesitant movement.

• Automatic Obedience

– Exaggerated cooperation with examiner's request or spontaneous continuation of movement requested.

Lethal Catatonia• Classic description (Pre-neuroleptic era):

– Intense motor excitement followed by hyperthermia and exhaustion or stupor

– Often prodromal phase of insomnia, anorexia, labile mood

– May demontrate catatonic signs, and be delirious-like (disorganized thinking, psychosis, destructive)

– May have rigidity, or flaccidity, in terminal stages

– Presence of acrocyanosis in some

– Fatal in 75-100%

Lethal Catatonia

• Post-neuroleptic era:

– Stupor may be predominant presentation

–Antipsychotics, benzo’s, etc. can decrease excitement

–Up to 10% inpatient psych. admission?

– Fatal in 60%?

Neuroleptic Malignant Syndrome: DSM-IV criteria

A. Development of severe rigidity and elevated temperature associated with the use of neuroleptic medication

B. 2 of the following: diaphoresis, dysphagia, tremor, incontinence, change LOC, mutism, tachycardia, elevated or labile BP, elevated WBC or CPK (may also observe myoclonus)

Neuroleptic Malignant Syndrome: DSM-IV criteria

A. Not due to another substance, or neurological disorder, or other general medical condition

B. Not better accounted for by a mental disorder

NMS and Medications

• Antipsychotic medications

• Withdrawal of L-Dopa or dopamine agonists

• Prochlorperazine (Stemetil)

• Metoclopramide (Maxeran)

• Tetrabenanzine (Nitoman)

NMS risk factors

• Exhaustion and Dehydration

• Agitation, Stress, Psychosis

• Higher potency, rapid titration, multiple I.M.’s

• Environmental heat a factor?

• Previous history (trait vulnerability?)

– 17% hx. of NMS

– 30% will develop NMS again upon re-challenge

NMS: Pathogenic Mechanisms

Simplified Pathophysiology of Neuroleptic Malignant Syndrome (NMS), and Elements of Sympathoadrenal Dysregulation

Item Sachdev NMS Scale (2005): total=36 Subtotal Score

Oral temperature 0 1 2 3 4 5 6 ____ ____

•Rigidity 0 1 2 3 ____

•Dysphagia 0 1 ____

•Resting tremor 0 1 2 ____ ____

•Systolic BP 0 1 ____

Diastolic BP 0 1 ____

•Tachycardia 0 1 ____

•Diaphoresis 0 1 ____

•Incontinence 0 1 ____

•Tachypnea 0 1 ____ ____

Altered LOC 0 1 2 3 4 5 6 ____ ____

•Posturing 0 1 ____

•Poverty of speech 0 1 ____

•Mutism 0 1 2 ____

•Choreiform 0 1 ____ ____

•Dystonia 0 1 ____

•CK level (U/L) 0 1 2 3 4 ____

•Leucocytosis 0 1 2 ____ ____

NMS Course• 0.2% of patients

• 16% develop within 24 hrs of exposure

• 66% develop within 1 week of exposure

• Virtually all by 1 month of exposure

• 63% recover within 1 week of elimination

• Virtually all recover by 1 month of elimination

• Should wait 2 weeks at least after recovery before re-challenge with antipsychotics

• 10-20% mortality rate

• Few have persistent catatonic and/or parkinsonianstate

NMS: Catatonic and Non-Catatonic

• Antecedent Catatonia may predispose to catatonic NMS

• Non-catatonic NMS more likely preceded by severe EPS and delirium

NMS and Catatonia: Similarities

• Appearance of catatonic symptoms in NMS

• Appearance of rigidity and hyperthermia in (lethal) catatonia

• Treatment with Lorazepam in NMS and Catatonia can improve

• ECT effective in both– Unable to distinguish from NMS in 22%

NMS and Catatonia: Differences

• Extreme (lead pipe) rigidity uncommon in catatonia

• Stereotypic signs of catatonia unusual in NMS

• Excitement then hyperthermia pre-neuroleptic in lethal catatonia; rigidity then hyperthermia post-neuroleptic in NMS

• Potentially effective treatments for NMS (dopamine agonists, dantrolene) less proven in catatonia

Similar Conditions: DDx

• Malignant Hyperthermia

• Anticholinergic Delirium

• Heatstroke

• Manic Delirium

• Serotonin Syndrome

• Abusable alcohol or drug withdrawal (eg: delirium tremens) and intoxication (eg: Ecstasy)

• Status epilepticus and other CNS conditions

• Systemic Conditions: infection, hyperthyroidism, pheochromocytoma, adrenal cortical abnormalities, other causes of rhabdomyolysis (eg: collapse)

Catatonia

• In the modern era, the most likely psychiatric cause for catatonia is

Bipolar Disorder, esp. Mania

–More likely when severe mania

Pathogenic Mechanisms: Catatonia

• Neurochemical substrates:

– D2 antagonists can worsen catatonia

– GABA-B, 5-HT1A agonists promote catatonia

– GABA-A, 5-HT2A, NMDA agonists reduce catatonia

–“Top Down Modulation”: subcortical and

cortical circuits reciprocally connect

– More GABA-mediated, rather than D2 mediated

Catatonia and PD: Differences

GABA

(lorazepam)

- Gaba-ergic mediated neuronal

inhibition in medial orbitofrontal

cortex

- Modulation of functional and

behavioral inhibition

NMDA

(Amantadine)

- Down-regulation of

glutamatergic-mediated

overexcitation in prefrontal and

orbitofrontal-parietal pathways

- Down-regulation of glutamatergic-

mediated overexcitation in

subcortical pathways

Dopamine - Top-down modulation of striatal

D-2 receptors predisposing for

neuroleptic-induced catatonia

-Compensation for striatal D-2 receptor deficit with "normalization" of "bottom-up modulation

Catatonia Parkinson

Catatonia Treatment

• Benzo’s effective in 70% (Lorazepam)

• ECT effective in 85%

• Antipsychotics effective in 7.5%, or may even worsen symptoms (neuroleptic-induced catatonia)

Catatonia: Treatment• Rule out medical condition

• Lorazepam 1-12mg/day, up to 72hrs. Trial– Specific GABA-A agonist

• Dantrolene to be considered if rigidity

• ECT is treatment of choice

• May consider mECT if recurrent

• Others:– Atypical Antipsychotic? (not for lethal catatonia)

– Amantadine?

– Memantine?

NMS Treatment

• Discontinue Antipsychotic Drug• Supportive Medical Treatments• Mild to Moderate NMS:

– Bromocryptine 2.5-5 mg q8h (up to 30mg/d)– Amantadine 100mg q8h (to 200-400mg/d)– May use Benzo (eg: Lorazepam 1-8 mg/d)

• Moderate to Severe NMS:– Dantrolene IV 1-2.5 mg/kg (1mg/kg q 6h)– ECT (bilateral, may even be daily)

NMS and ECT• 45 published cases from 1966, and 9 new cases

• Catatonia manifested in 76% of cases

• 63% complete and 28% partial recovery with ECT

• Onset of ECT response average 4 treatments, generally by 6 treatments

• 4 cases of cardiovascular complications

• Supports the use of succinylcholine unless familial malignant hyperthermia—only one case of hyperkalemia following ECT for NMS

NMS and ECT: Potential Use

–Severe NMS

–Differental between NMS and catatonia uncertain

–Psychotic depression is the underlying disorder

–Catatonia predominates in NMS

Catatonia Treatment Algorithm

Conclusions

• It can be difficult to differentiate NMS and catatonia in practice, and definitive treatments are similar

• Use of antipsychotics with less dopamine blockadeis probably less likely to produce NMS and less likely to be severe, according to the dopaminergichypothesis

• Both NMS and catatonia can be safely and effectively treated with ECT, providing precautions are considered

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

[email protected]

Catatonia

Health & Medicine

Transcript of Catatonia