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Catatonia - Pathophysiology, Diagnosis and Management
Catatonia - Pathophysiology, Diagnosis and Management
Catatonic Schizophrenia
For instance, neuroleptic malignant syndrome is a serious complication that can develop
if catatonia is left untreated and has a mortality rate of approximately 10%. [Strawn et al
2007]
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Reduced GABA-A receptor activity in the right lateral orbitofrontal and right
posterior parietal cortex, which would explain the motor and affective symptoms but
not behavioural catatonic symptoms. Furthermore, this explains the efficacy of
benzodiazepines, which increase GABA activity and are therapeutically effective in up
to 70% of patients.
Glutamate is an excitatory neurotransmitter and glutamatergic abnormalities in the
basal ganglia have been suggested to be a driver of catatonia-related glutamate
hyperactivity. Therapeutic recovery with the NMDA-antagonist, amantadine, is
gradual and therefore NMDA receptors are likely to be a secondary mechanism
(unlike GABA-A receptors)
Dysfunctional dopamine metabolism was originally hypothesised to be linked to
catatonia during the 1970’s however the data is inconsistent. Evidence of sudden and
massive dopamine blockade in the striatal dopaminergic system does, however,
explain why antipsychotics such as haloperidol can exacerbate the syndrome (i.e.
neuroleptic-induced catatonia).
Catatonia may also be an evolutionary fear response to imminent danger that is
similar to the animal defence strategy of tonic immobility. [Moskowitz et al 2004] The
‘death feint’ is an instinctive response to predators that detect movement but in
humans of today is now inappropriately triggered by modern-day threats.
DIAGNOSIS
The classical clinical feature of catatonia is stupor, which is characterised by immobility
and mutism. Another classic symptom is posturing, whereby the patient positions
themselves in an uncomfortable position against gravity with complete akinesia.
Catatonia is an identifiable syndrome that is well characterised and defined in the DSM-V
as a separate clinical diagnosis to schizophrenia. [APA 2013]
Although the catatonic subtype of schizophrenia has been deleted from the DSM,
catatonia is still included as a specifier for schizophrenia and major mood disorders
(bipolar disorder, major depressive disorder, and other mental, and neurodevelopmental
disorders).
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A new residual diagnostic category of catatonia not otherwise specified (NOS) is added in
patients with psychiatric conditions other than schizophrenia or mood disorders or when
the general medical condition is not immediately recognised. [Luchini et al. 2015]
Classification of Catatonia
There are several proposed classifications of catatonia, which is outside the scope of this
article. For further reading, please refer to Luchini F et al., 2015
Taylor and Fink proposed that catatonia should be classified as an independent entity with
three subtypes:[Taylor and Fink, 2003]
One key difference highlighted between NMS and catatonia is that malignant catatonia
starts with psychotic excitement while NMS starts with severe extrapyramidal muscular
rigidity.
Rating Scales
The video below shows the signs of waxy flexibility, forced grasping, opposition,
negativism and aversion.
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Catatonia
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Waxy Flexibility
Parkinson’s disease –Akinesia and rigidity are commonly associated with Parkinson’s
disease; however, catatonia also has strong affective and behavioural abnormalities
that do not generally occur in cases of Parkinson’s disease. Tremor is also notably
absent in catatonia.
Extra-pyramidal side-effects (EPSE) – Adverse events commonly observed with
antipsychotics that can present with immobility, rigidity, and staring. Postural
instability can be exacerbated by benzodiazepines, and so the distinction between
EPS and catatonia is important.
Neuroleptic malignant syndrome – A serious adverse event associated with
antipsychotics that is characterised by rigidity and mutism however, autonomic
instability differentiates this syndrome from catatonia.
Nonconvulsive status epilepticus – Often indistinguishable from catatonia however,
an electroencephalogram (EEG) can assist in making the correct diagnosis.
Abulia or akinetic mutism – Moderate or severely diminished motivation that can
result in the absence of speech or movement; however, visual tracking is preserved. It
does not present with negativism or echophenomena.
Locked-in syndrome – Complete paralysis caused by ventral pontine lesions, which
may be detectable by MRI or by brainstem potential examination.
Vegetative state – Often a secondary feature of severe cerebral injury that can be
distinguished from catatonia by an abnormal EEG.
Stiff-person syndrome – An autoimmune disorder characterised by lower extremity
stiffness and spasms that are very painful, and as such patients are generally not
mute like catatonic patients. A GAD65 antibody seropositive result is indicative of
stiff-person syndrome.
Organic Disorders – metabolic disorders (hyponatraemia, Tay-Sachs disease, Wilson’s
disease), infections, drugs.
Subarachnoid haemorrhages
Antiphospholipid syndrome
Systemic Lupus Erythematosus
1. Affective disorders
2. Increasing age
3. Postpartum disorders
4. Abrupt cessation of clozapine
5. Thrombotic thrombocytopenic purpura
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INVESTIGATIONS
First-line
Electrocardiography
Computed tomography
Magnetic resonance imaging
Electroencephalography
Urine culture
Blood culture
Test for syphilis
Test for HIV
Heavy-metal screen
Auto-antibody screen
Lumbar puncture
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Early treatment is important and clinical research has shown that electroconvulsive
therapy (ECT) and/or benzodiazepines are the recommended first-line choices for treating
catatonia. Combination therapy is clinically advantageous for increasing GABA
neurotransmission. [Escobar et al 2000]
Benzodiazepines
Electroconvulsive therapy
ECT has been used since 1934 with efficacy ranging from 53 to 100% with right
unilateral ECT reported to even be effective after one treatment. [Kugler et al 2015;
Medda et al 2015]
Often reserved for patients with treatment-resistant malignant catatonia
Treatment of choice in malignant catatonia (85 % response) which is less likely to
respond to BZDs (40%)
Consider sessions close to each other (three per week)
Alternative treatments such as aripiprazole (partial dopamine agonist), has the potential
to be marginally effective however more research is required as most of the data is based
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COMPLICATIONS OF CATATONIA
1. Dehydration and starvation
2. Increased risk of Deep vein thrombosis and death due to pulmonary embolism in
patients with persistent catatonia
3. Significant risk of harm to self or others in the phase of catatonic excitement
4. Progression to NMS with high mortality if untreated
CONCLUSION
Catatonia is a common syndrome in psychiatric patients and the symptoms and signs of
catatonia require careful assessment so that the correct treatment strategy is engaged
without delay to avoid precipitating neuroleptic malignant syndrome or severe medical
complications.
ECT and/or benzodiazepines are safe and effective interventions with the majority
responding to BZDs. Once catatonia is resolved, treatment of the underlying psychiatric or
medical illness should begin.
QUIZ
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RECOMMENDED BOOKS
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References
Catatonic Syndrome In A General Psychiatric Inpatient Population: Frequency, Clinical
Presentation, And Response To Lorazepam
Catatonia In Diagnostic And Statistical Manual Of Mental Disorders, Fifth Edition
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Dr. Sanil Rege is a Consultant Psychiatrist and
founder of Psych Scene and Vita Healthcare. He
currently practices on the Mornington Peninsula.
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