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Neuroleptic malignant syndrome and catatonic disorders
1. P R E S E N T E R : D R . M E L A K U . Y ( Y E A R I
M E D I C A L R E S I D E N T )
M O D E R A T O R : D R . M E S A L I
J E M A L ( P S Y C H I A T R I S T , A S S I S T A N T
P R O F E S S O R O F P S Y C H I A T R Y )
Adama Hospital Medical College
Department of Psychiatry
Seminar On
Neuroleptic malignant
syndrome and Catatonic disorders
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3. Introduction
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Catatonia is a neuropsychiatric syndrome that
appears in medical, neurological or psychiatric
conditions.
There are presentation variants: “malignant
catatonia” (MC) subtype shares many characteristics
with the neuroleptic malignant syndrome(NMS)
4. Neuroleptic Malignant Syndrome(NMS)
Introduction:
The neuroleptic malignant syndrome, or NMS, may have
been first described in 1959 by Walker
Reported a case of what appeared to be tetanus in a 19-
year-old man
After given trifluoperazine—fever and profound
parkinsonian rigidity that was partially relieved by
trihexyphenidyl
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5. NMS…
Epidemiology :
About 0.01 to 0.02 percent of patients treated with
antipsychotics develop neuroleptic malignant syndrome.
Men are affected more frequently than women, and
young patients are affected more commonly than elderly
patients.
The mortality rate can reach 10 to 20 percent or even
higher when depot antipsychotic medications are
involved
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6. NMS…
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Proposed Pathophysiology:
The precise cause of NMS is not well elucidated.
The most enduring proposal for the mechanism underlying the
symptoms observed during NMS is an excessive dopamine
blockade, most prominently at the D 2 receptor.
Antagonizing this receptor within the nigrostriatal, hypothalamic,
and mesolimbic/cortical pathways likely explains the rigidity,
hyperthermia, and AMS, respectively,
Furthermore, this proposed mechanism is supported by resolution
of symptoms on discontinuation of neuroleptics that cause
dopamine blockade, specifically those with potent D 2 affinity.
7. NMS…
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Proposed…
Moreover, removal of dopamine agonists can induce
NMS symptoms.
Atypical antipsychotics with less D 2 antagonist activity
can also cause NMS, which suggests that dopamine
blockade may not be the sole precipitator of NMS.
Increased catecholamines in the urine and plasma
support the sympathoadrenal hyperactivity hypothesis.
8. NMS…
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Proposed…
Abnormalities in this system would explain the lack of
tonic inhibition as well as autonomic instability, though
downstream effects of dopamine blockade may also
explain the sympathoadrenal dysfunction.
Unregulated sympathetic outflow can account for nearly
all the symptoms commonly seen in NMS.
Another possible mechanism that could contribute to
NMS presentation could be predisposition of the
patient’s musculoskeletal fiber, as seen in the
pathophysiology of malignant hyperthermia
11. NMS…
Clinical features:
The motor and behavioral symptoms include
muscular rigidity and dystonia, akinesia, mutism,
obtundation, and agitation.
The autonomic symptoms include hyperthermia,
diaphoresis, and increased pulse and blood pressure
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12. NMS…
Laboratory findings:
increased white blood cell count
increased levels of creatinine phosphokinase,
liver enzymes, plasma myoglobin,
and myoglobinuria, occasionally associated with renal failure
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14. NMS…
Diagnosis:
Diagnosed if a patient had three or more major criteria,
or two of the major criteria and four of the minor criteria
Other criterion sets, including one proposed by APA,
fever and rigidity as essential to the diagnosis and add
dysphagia, incontinence, mutism, and tremor to the
minor criteria.
The APA criteria require both severe rigidity and fever
(rather than accepting just one of the two if there is an
elevated creatine kinase); only two minor criteria must
be present
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18. NMS…
Course and Prognosis :
The symptoms usually evolve over 24 to 72 hours,
and the untreated syndrome lasts 10 to 14 days.
The diagnosis is often missed in the early stages, and
the withdrawal or agitation may mistakenly be
considered to reflect an exacerbation of the psychosis
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19. NMS…
Treatment:
Supportive medical treatment,
the most commonly used medications for the
condition are dantrolene and bromocriptine ,
although amantadine is sometimes used.
Bromocriptine and amantadine pose direct DRA
effects and may serve to overcome the antipsychotic
induced dopamine receptor blockade.
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20. NMS…
Treatment:
The lowest effective dosage of the antipsychotic drug
should be used to reduce the chance of neuroleptic
malignant syndrome.
High potency drugs, such as haloperidol, pose the
greatest risk.
Antipsychotic drugs with anticholinergic effects seem
less likely to cause neuroleptic malignant syndrome.
Electroconvulsive therapy (ECT) has been used
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24. Catatonia
Introduction:
Catatonia was first described by German psychopathologist Karl Kahlbaum
1874 as a motor syndrome in patients with behavioral disorders
Catatonia is a complex neuropsychiatric syndrome characterized by a broad
range of motor, speech and behavioural abnormalities
It is seen in the setting of psychiatric disorders, medical, neurological and
surgical conditions, as well as in the setting of certain drugs and toxins
Although it may become life-threatening, catatonia has an excellent
prognosis if recognized and treated early
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25. Catatonia…
Epidemiology :
Catatonia is an uncommon condition mostly seen in advanced
primary mood or psychotic illnesses.
Among inpatients with catatonia, 25 to 50 percent are related to
mood disorders (e.g., major depressive episode, recurrent, with
catatonic features), and approximately 10 percent are associated
with schizophrenia.
The percentage of catatonia due to a general medical condition is
reported to range from 20% to 39%.
.
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26. Catatonia…
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Pathophysiology:
The specific pathophysiological mechanisms underlying
catatonia are not well understood.
Neurochemical studies have focused on the inhibitory
neurotransmitter γ-aminobutyric acid (GABA) A
The role of GABA in catatonia is supported by the observation
of a dramatic response to treatment with benzodiazepines and
zolpidem
The GABAergic hypothesis is also supported by the
observation that ECT
27. Catatonia…
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Clinical features:
The catatonic syndrome is seen in two principal forms
hypokinetic (withdrawn type) or hyperkinetic (excited
type)
Some patients, however, may display features of both
types during the course of the illness
There is no difference in the expression of catatonic
symptoms based on the underlying cause, whether it is
psychiatric or medical
31. Catatonia…
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Clinical …Malignant catatonia
Malignant catatonia is characterized by sudden development
of intense excitement, delirium, high fever, hypertension,
catalepsy, mutism, rigidity, stereotypies and posturing.
Because of accompanying marked autonomic instability and
hyperthermia this form of catatonia is potentially fatal.
Numerous medical conditions leading to malignant catatonia
have been reported.
Although randomised clinical trials are lacking,
electroconvulsive therapy (ECT) is effective in the treatment
of malignant catatonia
32. Catatonia…
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Clinical …Periodic Catatonia
Periodic catatonia has a rapid onset and consists of brief,
recurrent hypokinetic or hyperkinetic abnormalities with
episodes lasting 4–10 days which recur over a period of
weeks to years.
Patients are generally asymptomatic between episodes, but
may exhibit inter-ictal facial grimacing, stereotypies and
negativism, particularly late in the course of the illness.
Overall, periodic catatonia is considered to have a better
prognosis than the malignant form of catatonia
33. Catatonia…
Diagnosis:
There are no pathognomonic laboratory findings in
catatonia.
Appropriate medical tests may include complete blood
counts, electrolytes, brain imaging, and
electroencephalography (if seizures are suspected).
In addition, serum creatinine phosphokinase, white
blood cell count, and serum transaminases should be
checked because the results of laboratory tests are
elevated in patients with neuroleptic malignant
syndrome.
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36. Catatonia
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Assessment:
Several rating scales have been developed for the
assessment of catatonia.
The Bush-Francis Catatonia Rating Scale (BFCRS) is
the most widely used scale.
This includes 23 items and up to 30 signs
37. Catatonia
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Assessment:
There is also a screening version of BFCRS known as Bush-Francis
Catatonia Rating Screening Instrument (BFCSI), which contains 14
most common catatonic signs
(excitement, immobility/stupor, mutism, staring gaze,
posturing/catalepsy, grimacing, echopraxia/echolalia, stereotypes,
mannerisms, verbigeration, rigidity, negativism, waxy flexibility and
withdrawal).
If two or more of the BFCSI signs are present for 24 h or longer,
catatonia should be considered as a possible diagnosis.
To avoid overdiagnosis, signs such as ‘impulsiveness’ and
‘combativeness’ were excluded from the screening instrument
38. Catatonia…
Differential Diagnosis (DDX):
Hypoactive delirium,
End-stage dementia,
Akinetic mutism,
Catatonia due to a primary psychiatric disorder.
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39. Catatonia…
Course and Treatment:
Catatonia impairs a person’s ability to care for himself or
herself and therefore requires hospitalization.
In an excited state, the catatonic patient may represent a
danger to others; hence, close supervision is needed.
Fluid and nutrient intake must be maintained, often
with intravenous lines or feeding tubes.
The catatonic individual must be assisted with hygiene.
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40. Catatonia…
Course and Treatment:
The primary treatment modality is identifying and
correcting the underlying medical or pharmacological
cause.
Benzodiazepines can provide temporary improvement in
symptoms, and their use may improve patients’ ability to
communicate and to care for themselves.
ECT is appropriate for catatonia due to a general medical
condition, especially if the catatonia is life threatening
(e.g., inability to eat) or has developed into lethal
(malignant) catatonia.
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42. References
Kaplan and Sadock’s Synopsis of Pyschiatry,11th edition
European Journal of Psychiatry, Volume 33
British medical journal of neuropsychiatry
WWW.thelancet.com
WWW.researchgate.net
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