D R S A L M A N K A R E E M
J U N I O R R E S I D E N T
D E P A R T M E N T O F P S Y C H I A T R Y
Catatonia and Neuroleptic
Catatonia is a state of apparent unresponsiveness to
external stimuli in a person who is apparently
awake, manifested by stupor.
First described by Kahlbaum (1874).
The ICD–10 diagnosis of catatonic schizophrenia (category
F20.2) requires that the patient prominently exhibits at
least one of the following catatonic features, for at least 2
weeks: stupor, excitement, posturing, negativism, rigidity,
waxy flexibility and command automatism (automatic
If a patient with severe depression is in a stupor, a
diagnosis of ‘severe depressive episode with psychotic
symptoms’ (F32.3) is made, even if there are no delusions
Similarly, a patient with manic stupor will be diagnosed as
having ‘mania with psychotic symptoms’ (F30.2).
Catatonia due to physical causes is diagnosed as ‘organic
In DSM–IV a diagnosis of ‘schizophrenia, catatonic
type’ (code 295.20) is made if the clinical picture is
dominated by at least two of the following: motor
immobility, excessive motor activity, extreme
negativism, peculiarities of voluntary
movements, and echolalia/echopraxia.
If a physical cause is identified the diagnosis is
‘catatonic disorder due to a medical condition’ (code
Mechanism of Action
Deficits in fetal cortical development
Dopaminergic blockade - catatonia is caused by a
sudden and massive blockade of dopamine.
Antipsychotics may actually precipitate a worsening of
Glutamatergic dysfunction - hyperactivity of glutamate,
the primary excitatory neurotransmitter, has also been
suggested as an underlying neurochemical dysfunction.
Clozapine-withdrawal catatonia is postulated to be due
to cholinergic and serotonergic rebound hyperactivity.
typically episodic, with periods of remission
presence of a variety of behavioral and motoric
traits – almost 2 dozen.
Excited state –
people with catatonia may injure themselves and
autonomic instability manifested by
hyperthermia, tachycardia, and hypertension
Akinesia and stupor
patient may appear unresponsive to external stimuli.
unable to eat
may exhibit catalepsy, the persistent maintenance of
spontaneous or imposed postures.
The patient is able to maintain the same posture for
long periods. An extreme version of posturing is
Waxy flexibility (cerea flexibilitas)
The examiner is able to position the patient in what
would be highly uncomfortable postures, which are
maintained for a considerable period of time.
demonstrate increasing resistance to passive
movement of the limbs
Automatic obedience (Mitgehen)
patient moving in the direction of a slight push from
the examiner in spite of the command to remain still
The patient persists with a particular movement that
has lost its initial relevance.
withdrawal from all usual activities and refusal to eat.
Stereotypies - patient repetitively performs
apparently meaningless activities. Common motor
stereotypes include the following:
Repetitive movements of the mouth and the jaw
Repetitive eye movements
Repetitive tapping of the foot, the finger, or the hand
Repetitive abdomen patting, shoulder shrugging, or body
The patient alternates between resistance to and
cooperation with the examiner’s instructions; for
example, when asked to shake hands, the patient
repeatedly extends and withdraws the hand.
Echolalia - Echolalia refers to the repetition of the
Echopraxia - The patient imitates the actions of the
comprehensive physical examination
specific emphasis on neurological signs, and a
thorough mental state examination, with special
emphasis on identifying catatonic signs
history of similar episodes of catatonia is important
to elicit. Determine whether the precipitating events
of the earlier episode are present in the current
emergency physician must quickly consider the
presence of neuroleptic malignant
syndrome,encephalitis, nonconvulsive status
epilepticus, and acute psychosis.
must identify comorbid disorders, including
schizophrenia, mood disorders, psychological
stressors, medical conditions.
Catatonia and the related condition, neuroleptic
malignant syndrome, may follow the administration
of neuroleptic medications
Complete blood counts (CBC)s, electrolytes, and
chemical analyses of blood.
Fibrin D-dimer greater than 500 ng/mL.
serum creatine kinase level and WBC count and perform
liver function tests, to rule out neuroleptic malignant
magnetic resonance imaging (MRI) or computed
tomography (CT) scanning is indicated to rule out
treatable mass lesion.
EEG is indicated to rule out a seizure disorder.
Further investigations (depending on
findings on physical examination)
Test for syphilis
Test for HIV
Differential diagnoses of catatonia
Organic disorders: e.g.
infections, epilepsy, metabolic disorders
Drugs: prescribed or recreational
Hysteria (psychogenic catatonia)
Treatment and management
Due to risk of serious complications of
catatonia, admission to an intensive care unit is the
treatment of choice for a patient with catatonia.
Benzodiazepines are the drugs of choice for catatonia.
unresponsive or in-sufficiently responsive to
benzodiazepines need electroconvulsive therapy (ECT) -
functional psychiatric disorders (including
schizophrenia) or organic causes.
Antipsychotics are generally not recommended during a
catatonic phase even if there is an underlying psychotic
illness such as schizophrenia, as the risk of precipitating
neuroleptic malignant syndrome is considerably
carbamazepine is effective in both the acute and
maintenance phases of catatonia.
Combination of lithium and an antipsychotic may be
an option in treatment-resistant catatonic stupor
NMDA antagonists: amantadine and memantine
Dopamine agonists (e.g. bromocriptine) and skeletal
muscle relaxants (e.g. dantrolene), especially if
neuroleptic malignant syndrome is suspected
refusal to eat requires parenteral nutrition.
Vitamin K deficiency must be identified and treated
in people with catatonia.
Autonomic instability requires intravenous fluids
and monitoring of vital signs.
life-threatening neurological disorder .
mortality rate is 10-20%
adverse reaction to neuroleptic or antipsychotic
haloperidol or chlorpromazine have the greatest
Diaphoresis , tachycardia , elevated or labile blood
Dysphagia , incontinence
Changes in the level of consciousness , ranging from
confusion to coma
Lab evidence of muscle injury
Liver enzyme elevation
Mechanism of action
Dopamine receptor blockade
Genetically reduced function of dopamine receptor D2.
Release of calcium is increased from the sarcoplasmic
reticulum with antipsychotic usage. This can result in
increased muscle contractility, which can play a role in
breakdown of muscle, muscle rigidity, and hyperthermia.
sympatho-adrenal hyperactivity (results from removing
tonic inhibition from the sympathetic nervous system)
treatment options and implications
Aggressive use of supportive measures as well as
discontinue all antipsychotics
Patients should receive circulatory and ventilatory
support as needed.
Cooling blankets and antipyretics can be used to
Aggressive fluid resuscitation and alkalization of
urine can help prevent acute renal failure and
enhance excretion of muscle breakdown products
Dantrolene has been used when needed to reduce
dopamine pathway medications such
Benzodiazepines may be used to control agitation.