Catatonia is a syndrome involving motor disturbances and abnormal behavior. It can occur due to psychiatric conditions or physical illnesses. Diagnosis involves identifying catatonic signs and ruling out other potential causes through examinations and tests. Treatment depends on the underlying cause but commonly involves benzodiazepines, electroconvulsive therapy, or treating any identified medical conditions. Neuroleptic malignant syndrome is a potentially life-threatening reaction that can occur when taking antipsychotic medications. It involves symptoms like fever, muscle rigidity, and altered mental state. Treatment requires discontinuing the causative drug and providing supportive care.

1. 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
Malignant Syndrome

2.  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).

3. Diagnostic Criteria
 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
obedience).
 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
or hallucinations.
 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
catatonic disorder.

4.  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
293.89).

5. Mechanism of Action
 Deficits in fetal cortical development
 Developmental disorders
 Dopaminergic blockade - catatonia is caused by a
sudden and massive blockade of dopamine.
Antipsychotics may actually precipitate a worsening of
the condition.
 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.

6. Psychiatric condition
 Acute stress disorder
 Anorexia nervosa
 Autistic disorder
 Brief reactive psychosis with catatonia
 Conversion disorder
 Hysteria
 Major depression, single episode with catatonic features
 Mood disorders
 Neuroleptic malignant syndrome
 Posttraumatic stress disorder
 Schizophrenia
 Substance intoxication (3,4-methylenedioxymethamphetamine
[ie, "ecstasy"], alcohol, amphetamine, phencyclidine, substance
withdrawal, hypnotic-sedative, lorazepam

7. Neurologic conditons
 Administration of agents
that block postsynaptic
dopamine receptors
 Administration of
sibutramine.
 Akinetic-rigid syndrome
 Arachnoid cyst in right
parietal region
 Astrocytoma
 Atrophy of left amygdala
 Autistic disorder
 Basilar artery thrombosis
 Bilateral hemorrhagic
lesions of temporal lobes
 Cerebellar catalepsy
 Cerebral hemorrhage
 Cerebral infarct
 Cerebrovascular disease
 Cortical venous
thrombosis
 Central pontine
myelinolysis
 Cortical basal ganglionic
degeneration
 Dystonia
 Encephalitis
(herpes, Trypanosoma

8.  Encephalopathy (Borrelia
burgdorferi, human
immunodeficiency virus [HIV]
infection, Wernicke
encephalopathy)
 Familial fatal insomnia
 Fibromuscular dysplasia with
dissection of basilar artery
 Frontal lobotomy
 Head injury
 Huntington disease
 Hydrocephalus
 Hypopituitarism secondary to
postpartum hemorrhage
 Idiopathic recurring stupor
 Inherited neurometabolic
disorders
 Locked-in syndrome
 Meningitis, tuberculous
 Meningoencephalitis
 Multiple sclerosis
 Neurosyphilis
 Nonconvulsive status
epilepticus
 Pervasive developmental
disorders
 Pallidoluysian atrophy
 Paraneoplastic encephalitis
 Parkinsonism
 Postencephalitic parkinsonism

9.  Progressive multifocal
leukoencephalopathy
 Progressive supranuclear palsy
 Schizencephaly
 Seizures (complex with partial
symptomatology)
 Stiff-man syndrome
 Stroke
 Stupor
 Subarachnoid hemorrhage
 Subdural hematoma
 Substance intoxication
(alcohol, disulfiram, organic
fluorides, phencyclidine)
 Subthalamic mesencephalic
tumor
 Surgical removal of cerebellar
tumor
 Tay-Sachs disease
 Temporal lobe epilepsy
 Tuberous sclerosis
 Tumors
 Vegetative state
 Wilson disease

10. Clinical presentation
 typically episodic, with periods of remission
 presence of a variety of behavioral and motoric
traits – almost 2 dozen.
 Mutism
 Negativism
 Echopraxia
 Echolalia
 Waxy flexibility
 Withdrawal

11.  Excited state –
 people with catatonia may injure themselves and
assault others.
 autonomic instability manifested by
hyperthermia, tachycardia, and hypertension
 Exhaustion
 Immobile state
 Akinesia and stupor
 patient may appear unresponsive to external stimuli.
 unable to eat
 may exhibit catalepsy, the persistent maintenance of
spontaneous or imposed postures.

12.  Posturing
 The patient is able to maintain the same posture for
long periods. An extreme version of posturing is
catalepsy.
 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.

13. Negativistic Phenomena
 Gegenhalten
 Rigidity
 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
 Motor persistence
 The patient persists with a particular movement that
has lost its initial relevance.
 withdrawal from all usual activities and refusal to eat.

14.  Stereotypies - patient repetitively performs
apparently meaningless activities. Common motor
stereotypes include the following:
 Nose wrinkling
 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
rockin

15.  Preservation
 Ambitendency
 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.
 Echophenomena
 Echolalia - Echolalia refers to the repetition of the
examiner’s words.
 Echopraxia - The patient imitates the actions of the
interviewer.

16.  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
episode

17.  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

18. Work up
 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
syndrome.
 Serum ceruloplasmin.
 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.

19. Further investigations (depending on
findings on physical examination)
 Electroencephalography
 Urine culture
 Blood culture
 Test for syphilis
 Test for HIV
 Heavy-metal screen
 Auto-antibody screen
 Lumbar puncture

20. Differential diagnoses of catatonia
 Schizophrenia
 Depression
 Mania
 Organic disorders: e.g.
infections, epilepsy, metabolic disorders
 Drugs: prescribed or recreational
 Hysteria (psychogenic catatonia)
 Idiopathic

21. 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
increased.

22.  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

23. other treatment
 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.

25.  life-threatening neurological disorder .
 mortality rate is 10-20%
 adverse reaction to neuroleptic or antipsychotic
drugs.
 haloperidol or chlorpromazine have the greatest
risk.

26. Clinical presentation
 Hyperthermia
 Diaphoresis , tachycardia , elevated or labile blood
pressure
 Dysphagia , incontinence
 Tremor
 Changes in the level of consciousness , ranging from
confusion to coma
 Mutism
 Leukocytosis
 Lab evidence of muscle injury
 Liver enzyme elevation

27. pathophysiology
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)

28. treatment options and implications
 Aggressive use of supportive measures as well as
specific interventions.
 discontinue all antipsychotics
 Patients should receive circulatory and ventilatory
support as needed.
 Cooling blankets and antipyretics can be used to
control temperature
 Aggressive fluid resuscitation and alkalization of
urine can help prevent acute renal failure and
enhance excretion of muscle breakdown products

29. Lab findings
Increased LDH
Increased CK
Increased AST
Increased ALT
Increased alkaline
phosphatase
Hyperuricemia
Hyperphosphatemia
Myoglobinemia
Leukocytosis
Thrombocytosis
Proteinuria
Decreased serum
iron
Increased
cerebrospinal fluid
(CSF) protein
Hypocalcemia
Myoglobinuria

30. medications
 Dantrolene has been used when needed to reduce
muscle rigidity
 dopamine pathway medications such
as bromocriptine.
 Benzodiazepines may be used to control agitation.
 Amantadine
 Levodopa/ carbidopa
 ECT.

31. complications
 potential complications of neuroleptic malignant
syndrome includes the following:
 Rhabdomyolysis
 Renal failure
 Cardiac arrest
 Infection
 Aspiration
 Respiratory failure
 Seizure
 Pulmonary embolism
 Hepatic failure
 Uncontrolled psychoses