This document presents a case study of a 13-year old female patient who was admitted to hospital displaying symptoms of catatonia including psychomotor retardation, mutism, waxy flexibility, and staring episodes. The patient's symptoms and management are discussed in detail over her hospital stay. The document also provides background on catatonia as a historical concept, including its origins in the late 19th century and debates around its nosological status and relationship to other psychiatric conditions. Key figures who studied catatonia and helped develop understanding of the syndrome are also mentioned.

1. Catatonia: Breathing life
into an old concept
Dr. Vishnu Pradeep, Dr. Tareq Ghani, Dr. Louise Tansey
CAMHS/Intellectual Disability Services

2. TABLE OF CONTENT
• CASE PRESENTATION
• HISTORY
• SYMPTOMATOLOGY
• PATHOPHYSIOLOGY
• MANAGEMENT
• PROGNOSIS
• CONCLUSION

3. CASE PRESENTATION

4. INTRODUCTION
“The little patient lies perhaps for hours or days seemingly in a sort of
mystical contemplation, with limbs more or less rigid, or fixed in
strange postures; sometimes there is insensibility to impressions, while
in other instances vague answers are given, or there is actual
incoherent raving”
-Henry Maudsley on ‘cataleptoid insanity’ in children, 1867

5. BACKGROUND
Asked by the Paediatric team to review:
13 year old female with 4/52 history of psychomotor
retardation, recent discontinuation of Risperidone 0.25
mg, seen by the ID Services for management of
emotional and behavioural difficulties on the
background of Moderate Intellectual Disability and
ASD.

6. BACKGROUND
•13 year old female with Moderate Intellectual
Disability
• ASD
• No diagnosis of epilepsy
• No previous diagnosis of depression/psychosis
• Attends East Limerick Children’s Services

7. SOCIAL HISTORY
• Lives at home with Mother and two younger brothers (12 & 6)
• Father living abroad – moved out since 2006
• Attends St. Vincent’s school in Lisnagry – 5 days a week
• Gets respite with St. Joseph’s Early Intervention Team

8. PREVIOUS
ADMISSION/BACKGROUND HISTORY
• Previous admission (07.07.16) to paediatrics unit
• Presenting complaints
• Progressive regression in behaviour for past 2/12
• Since May/2016 – noticed to be intermittently staring into space
• Needed constant prompting to do things, such as dressing and self hygiene
• No prompting was needed prior
• Behavioural changes coincided with mother leaving (?PTSD)
• On admission:
• Noted periodic staring episodes
• Neurological Exam – Normal
• Bloods – Normal

9. PREVIOUS
ADMISSION/BACKGROUND HISTORY
• Social History on admission:
• Mom had to go to Ghana for 2 weeks as her mother had passed away
• Pt. had to go into respite (two different Places)
• Medication on Admission:
• Risperidone 0.25mg nocte - ? Compliance
• Withheld then D/C (8.7.16)

10. INITIAL MANAGEMENT - 12th
August,
2016
Management to-date:
Admitted under Paediatric team 09.08.16 with raised temperature,
labile BP and tachycardia. Covered for Encephalitis with Acyclovir and
Ceftriaxone for 3/7.

11. INITIAL MANAGEMENT
Investigations to-date:
• CT-Brain: high signal in sub cortical white matter in Left Frontal and
temporal lobe.
• MRI- Brain: focus of high-signal in the left frontal lobe and within the
left temporo-parietal lobe, broad differential: demyelination, micro
vessel ischaemic changes less likely.
• XR-Chest: Normal
• ECG: Sinus tachycardia rate 144
• EEG: No epileptiform changes (done 4 weeks ago)
• ABG: Normal findings
• LP: Not done

12. INITIAL MANAGEMENT
• WBC 15.32 (raised)
• Hb 14.1
• MCV, MCH, PV – Normal
• Neutrophil 9.61 (raised)
• U&E, LFTs – Normal
• Electrolytes – Normal
• Urine Dipstick/tox screen – Negative
• ASO – 319 (normal)
• RF <12 (normal)
• Prolactin – 180 (normal)
• Glucose 5.9
• CK -1993 (raised)  622
• TFTs – Normal
• CRP – unavailable

13. INITIAL MANAGEMENT
Additional team input:
• Neurology: Ruled out NMS or Encephalitis; thorough
infective/autoimmune/toxicology screen sent.
• Lyme – Negative
• ANCA, ANA – Negative
• HIV, Syphilis Serology – Negative
• Psychiatry-on-Call: Received stat dose 2 mg Lorazepam (the night
before)

14. BEDSIDE ASSESSSMENT
• Vitals: HR 141, O2 99%, BP 123/72 <-> 159/82, Temperature 36.9
• Appearance: young girl of Nigerian origin, casually dressed,
appropriately kempt, laying in bed, vacant gazing at the roof, laughing
intermittently, breath holding, significant psychomotor retardation
• Speech: muted
• Affect: flat, restricted
• Mood: (0bjectively) – ambivalent, stuporous
• Not responding to external stimuli (unable to establish if psychotic
features present)
• Waxy flexibility, Automatism

15. RECOMMENDATION
• Lorazepam Challenge
• 0.5 mg Lorazepam TDS to be increased to 1 mg TDS tomorrow
• Monitor closely for any excessive sedation/respiratory compromise
• Continue monitoring in Paediatric HDU
• DVT Prophylaxis
• Input/output monitoring; IV Fluids 1.5-2 L/day
• Risk of Silent Aspiration – SALT input
• Repeat CK , U&E, Electrolytes
• Daily Psychiatry Input

16. PROGRESS – 17th
August to 22nd
August, 2016
• Intervention:
• Lorazepam increased to 1.5mg TDS x 5/7
• Further increase to 2mg TDS x 2/7 (22/8/16)
• Observation:
• Vitals stable
• Able to answer simple questions – one word answer
• Lying in bed – watching TV; Intermittent staring
• Holding saliva – needs prompting to swallow
• Continues to require prompting for other activities

17. PROGRESS – VIDEO 18th
August, 2016
• Consent Obtained
• Recorded with Mom’s Permission

18. PROGRESS – 24th
August, 2016
• Intervention:
• Lorazepam increased to 2.5mg TDS x 2/7
• Observation:
• Mom – Not back to previous functional level
• No Significant improvement since admission
• Recommendation:
• Continue observation for over sedation

19. PROGRESS – 26th
August, 2016
• Intervention:
• Lorazepam increased to 3mg TDS x 6/7
• Observation:
• Observed in play room reading
• Engaging & Responding well to 1:1 attendance
• No over sedation
• Mom – noted slight improvement
• Intermittent smiling and response

20. PROGRESS – 1st
September, 2016
• Intervention:
• Lorazepam increased to 3.5mg TDS x 4/7
• Observation:
• Smiling more, more animated on commands
• Core features of Catatonia – resolved
• E.g. Mutism, Waxy flexibility
• Has tendency to stare into space
• Automatic obedience – e.g. Sings on request

21. PROGRESS – 2nd
to 5th
September, 2016
2/9/16
•Observation:
• Attending Ark School
• Engaging and enjoying being back to school
• Requires ongoing prompting with activities
5/9/16
•Intervention:
• Lorazepam increased to 4mg TDS x 2/52
•Observation:
• Bright and more aware of her surrounding

22. PROGRESS – 19th
September, 2016
• Observation:
• Maintaining improvement
• Increased awareness of surroundings
• Improved self care with less prompting
• Better communication
• Intervention:
• Began reducing Lorazepam by 0.5mg every 3/7
• 4mg BD & 3.5mg nocte

23. PROGRESS – 22nd – 26th
September,
2016
22/9/16
•Intervention:
• Increased reduction of Lorazepam by 1mg every 3/7
• 4mg mane & 3mg BD
26/9/16
•Observation:
• Continued improvement
•Intervention:
• Decided to reduce Lorazepam further to 3mg TDS

24. PROGRESS – 29th
September, 2016
29/9/16
•Observation:
• Doing well
• Spent weekend with Mom at home:
• noted improvement – more like her previous self
•Intervention:
• Decided to further reduce lorazepam to 3.5mg mane, 1mg tarde, 3.5mg
nocte

25. PROGRESS – 3rd
-4th
October, 2016
3/10/16
•Observation:
• Mixed statements re-progress
• Had a good day in school
• In play-room: Less engaging, Less animated, Holding saliva
• Monitor on current dose
4/10/16
•Observation:
• Unusual hand movement noted
• Not in good form & appeared in low mood (some what withdrawn)

26. PROGRESS – 6th
October, 2016
• Observation:
• Withdrawn, less interactive, not as bright
• School concerned
• Increased impulsivity
• Over activity
• Intervention:
• Decided to increase Lorazepam to 3mg TDS

27. PROGRESS – 10th
October, 2016
• Observation:
• Showing signs of improvement
• Remains somewhat overactive
• Sleep disturbance – early wakening
• Impulsive
• Observed to be elated
• Intervention:
• Commenced on Aripiprazole 2mg mane

28. PROGRESS – 13th
– 14th
October
13/10/16
•Observation:
• Remained Hyperactive
• Over-eating (looking for food everywhere both home and school)
• Sleep disturbed
14/10/16
•Intervention:
• Increased Aripiprazole to 5mg mane
• Began reducing Lorazepam by 0.25mg every 7/7 to 3mg BD & 2.75mg nocte

29. PROGRESS – 18th
October
• Observation:
• Impulsive behaviour subsided, No signs of agitation
• Positive feedback from school
• Sleep remains disturbed
• Intervention:
• Reduced lorazepam further to 3mg BD & 2.5mg nocte

30. PROGRESS – 21st
– 26th
October
21/10/16
•Observation:
• In much better form & Sleep has improved
•Intervention:
• Increased Aripiprazole to 7.5mg mane
26/10/16
•Observation:
• Continues to improve
• Engaging and needing less prompting
•Intervention:
• Further reduction in Lorazepam to 3mg BD & 2.25mg nocte

31. DISCHARGE PLAN – 1st
November,
2016
• Discharged on
• Aripiprazole 7.5mg mane
• Lorazepam 3mg BD and 2mg nocte
• Home care (Bluebird care) organized -
• Care staff to administer night medication and on weekends
• To organize additional activities
• School (East-limerick School Services)
• Staff to administer morning and afternoon doses
• Psychiatry team
• Home visits
• School visits

32. POST DISCHARGE
• School feedback
• Doing well
• Engaging
• Periodic saliva holding reported - ? Behavioural
• Home Feedback
• Doing well
• More talkative and engaging
• Mom says back to previous self

33. ADDITIONAL SUPPORTS IN PLACE
• Bluebird care
• Monday to Friday – 1 hr/day in the evening to give meds
• Weekends – 3 hrs/day (meds administration and social engagement)
• Respite
• D.O.C
• Overnight

34. MANAGEMENT CHALLENGES
• During hospital stay
• Pharmacological Management & Response
• 1:1 special
• Continues assistance
• Hospital environment – Social isolation
• Mom lack understanding – ? Cultural views

35. MANAGEMENT CHALLENGES
• Post discharge
• Mom lack of understanding of complexity
• Mom extremely dependent on external support re-management
• Ambivalence towards long term care
• Unavoidable need for shared care
• Difficulties in establishing aetiology:
• ? BPAD
• Increased risk of relapse with further reduction in medication
• Understanding Triggers

36. Catatonia: The past
and the present

37. INTRODUCTION
Photograph of a group of catatonic patients. This photograph appeared in the fifth edition of
Emil Kraepelin's Psychiatrie (Leipzig Johann Ambrosius Barth, 1896).

38. INTRODUCTION
“Ever since the introduction of the concept of catatonia,
it has been the focus of debate, a major point of
discussion being its nosological status. The question
rises whether it is to be considered a syndrome with a
wide variety of causes and clinical signs or a distinct
clinical entity”.
E. VANCAESTER and P. SANTENS Dept. of Neurology, University Hospital Gent,
Gent, Belgium

39. ORIGINS
The concept of catatonia, literally
meaning “to stretch tight”, goes back to
the original description by Karl Ludwig
Kahlbaum in 1874.

40. ORIGINS
In his research of catatonia, he
published the monograph, Die
Katatonie oder das
Spannungsirresein, in which he
characterizes the disorder as
• ‘disturbance in motor
functionality’ that represents a
phase in a progressive illness that
includes stages of
mania, depression and psychosis that
typically ends in dementia

41. ORIGINS
•Two major view-points emerged during the early 19th
century:
• one view supported the proposal of catatonia as a disease
of its own
• The opposing view was that it was a complication of
different pathophysiology's and not a distinctive disease

42. ORIGINS
• Karl Jaspers:
• portrayed catatonia as an illness with special characteristics like opposing
pairs of symptoms (negativism vs automatic obedience).
• Kurt Schneider:
• psychology of catatonia, which he found unknowable:
‘‘Sometimes it seems as though the patient is like a dead camera: He
sees everything, hears everything, understands everything and yet is
capable of no reaction, of no affective display, and of no action. Even
though fully conscious he is mentally paralyzed.’’
• He considered Catatoinia a complication of many illnesses and rejected
Kraepelin’s formulations

43. ORIGINS
• Mayer-Gross:
• Felt that catatonia was resolutely Kraepelinian that catatonia was a type of
schizophrenia.
• George Kirby (1913)
• pictured catatonia as typically occurring among patients with manic-
depressive illness
• August Hoch(1921)
• described 25 psychiatric patients in stupor. Thirteen with manic-depressive
illness had a favorable prognosis and 12 with general medical illnesses or
schizophrenia had a poor prognosis

44. ORIGINS
• Lange (1922)
• reported an experience with 200 patients found catatonia to be more
common among the manic-depressive patients than among those with
dementia praecox.
• Taylor and Abrams:
• 4 publications between 1973 and 1979, reported catatonia to be more
common among manic and depressed patients
• Gelenberg
• described catatonia among patients with neurologic and general medical
illnesses

45. CATATONIA AND ICD
• 6th
Ed. 1948: ‘‘catatonic type’’ among the ‘‘schizophrenic disorders.’’
• 10th
. Edition 1992: unchanged;
‘‘For reasons that are poorly understood, catatonic schizophrenia is now rarely
seen in industrial countries, though it remains common else where.’
• Catatonic schizophrenia (category F20.2)
• Pt. With severe depression is in a stupor- a diagnosis of ‘severe depressive episode with
psychotic symptoms’ (F32.3)
• manic stupor will be diagnosed as having ‘mania with psychotic symptoms’ (F30.2)
• Catatonia due to physical causes is diagnosed as ‘organic catatonic disorder’ (F06.1).

46. DEFINITION
• Catatonia is a syndrome that encompasses
more than two dozen signs that describes
in essence a “disturbance in motility”
• Stupor is the classic and most striking
catatonic sign. It is a combination of
immobility and mutism
• The patient is able to maintain the same
posture for long periods. An extreme version of
posturing is catalepsy (rigid; cant feel pain)
• highly uncomfortable postures, which are
maintained for a considerable period of time

47. FEATURES
• Stupor
• Posturing
• Waxy flexibility (cerea flexibilitas)
• Negativism (Gegenhalten)
• Automatic obedience
• Ambitendency
• Psychological pillow
• Forced grasping
• Obstruction
• Echopraxia
• Aversion
• Mannerisms
• Stereotypies
• Excitement
• Speech abnormalities
• Echolalia, logorrhoea and
verbigeration

48. RATING SCALES
• In general the syndrome is poorly
recognised, some of the commonly used
rating scales are as indicated below:
• Bush–Francis Catatonia Rating Scale (BFCRS)
• most widely used
• 23 items
• shorter, 14-item screening version
• Bush–Francis Catatonia Screening Instrument
(BFCSI)
• Modified Rogers Scale (MRS)
• Lorazepam Challenge Test (Fink & Taylor, 2003)
• Involves administering 1-2mg Lorazepam IV
• High response rate – 75-100% (Hawkins et al. 1995)

49. PREVALENCE
• Very rare
• Commonly under-recognised and under-diagnosed
•9%–15% of patients admitted to a typical acute care
psychiatric service meet diagnostic criteria for catatonia
(Rosebush, 2010)
• More common in mood disorders (28%-31% of catatonic
patients had mixed mania or mania) and only 10%-15%
had underlying diagnosis of schizophrenia

50. SUBTYPES
• Non-malignant
• Psychomotor retardation/withdrawn- appear awake and watchful, but with
minimal spontaneous speech and movement. Stupor, mutism, negativism, and
posturing are common signs
• Excited - excessive purposeless motor activity associated with disorganised
speech, disorientation, aggression, and violence
• Periodic – most frequently associated with Bipolar disorder. Involves fluctuations
between stupor and excitement (Fink & Taylor, 2003)
• Malignant catatonia- escalating fever and autonomic instability
• Resembles neuroleptic malignant syndrome (NMS)
• Some authors also consider toxic serotonin syndrome as a subtype of malignant
catatonia

51. ETIOLOGY
• Wide variety of causes reported (Takaoka & Takata, 2003)
• Psychiatric conditions:
• Schizophrenia, Bipolar disorder, PTSD, Eating disorder, Depressive disorder
• Medical conditions:
• Autoimmune disorders, Metabolic disturbance
• Neurological conditions:
• Encephalitis, Stroke, Seizure disorders
• Others
• Ecstasy, phencyclidine, inhalant, steroids, neuroleptics, abrupt withdrawal of BNZ

52. PATHOMECHANISM
• Exact cause of catatonia has not been
elucidated
• PET Scan has identified abnormalities in
metabolism bilaterally in the thalamus and
frontal lobes
• Moskowitz (2004) suggests that catatonia may
be understood as an evolutionary fear
response, catatonic stupor may represent a
common ‘end-state’ response to feelings of
imminent doom.

53. Catatonia in children & Adolescents
• Literature regarding catatonia in children & adolescents is sparse
• Wing & Shah, 2000. described Features particular to child and
adolescents presentation:
• Increased slowness affecting motor and verbal responsiveness
• Difficulty initiating and competing actions
• Increased reliance on cueing by others
• Increased passivity and lack of motivation
• Reversal of circadian rhythms
• Parkinsonian features
• Excitement and agitation
• Increased repetitive and ritualistic behaviour

54. INVESTIGATIONS
• Comprehensive physical examination,
with specific emphasis on neurological
signs
• Bloods- FBC, Renal, LFT, TFT, Glucose, CK
• Drug Screen
• ECG
• CT/ MRI
• EEG
• Culture
• LP
• Auto-Antibody Screen

55. MANAGEMENT
• Supportive care/ high level of nursing care
• Treatment with subcutaneous heparin, urinary catheterization
• May require IV fluids, Nasogastric tube feeds or PEG tube placement.
• Benzodiazepines are the drugs of choice for catatonia
• Lorazepam was the most commonly used treatment, resolving symptoms in 70% of
reported cases.
• Other benzodiazepines such as diazepam, oxazepam, and clonazepam have also been
reported to treat catatonia
• Zolpidem, like the benzodiazepines, is a GABA-A agonist and has been reported in one case
series to be effective in the treatment of catatonia
• continue the benzodiazepines until the causative illness has been fully treated

56. MANAGEMENT
• ECT
• ECT alone resulted in resolution of symptoms in
85%
• In malignant catatonia, the response to ECT was
89%,
• Emergency ECT is the treatment of choice for
malignant catatonia
• Identified as a definitive treatment (Fink & Taylor, 2009)
• NMDA Antagonists (Amantadine, Memantine)
• When ECT or Benzodiazepines fail
• Topiramate, Carbamazepine or combination of lithium
and an antipsychotic may be an option in treatment-
resistant catatonic stupor

57. ECT & ETHICS
• Although ECT has been reported to effective in treating catatonia,
several adverse affects are unavoidable (Takaoka & Takata, 2003)
• Several studies reported transient but frequent adverse effects:
• Post ECT asthenia
• Complaints of amnesia
• Memory loss
• Headaches
• Post ECT confusion
• Nausea, Vomiting & Vertigo

58. ECT & ETHICS
• In an article published by Cohen et al. he insisted that there no valid
grounds to banning ECT as a treatment for catatonia is adolescents
• Zaw et al., 1999. sought two independent second opinions in their
ECT treatment of a catatonic child. Proposed that:
• “For children aged 12 and under the evaluation and concurrence of two
psychiatrists who are experienced in the treatment of children and in ECT and
otherwise not involved with the treatment and care of the patient are
necessary”
• “For those aged 13 and above, one external reviewer should be involved”

59. MANAGEMENT – ANTIPSYCHOTIC
USE
• Not recommended during a catatonic phase
• Catatonia represents a highly significant risk factor for subséquent
neuroleptic malignant syndrome
• Atypical antipsychotics may have a role in the treatment of non-
malignant catatonia (Van Den Eede et al 2005)
• Multiple case reports and retrospective studies indicating the successful
treatment of catatonia with atypical antipsychotics (olanzapine,
risperidone, ziprasidone, aripiprizole, and clozapine)
• Few reports of atypical antipsychotics causing catatonia, though these
studies were largely in patients with schizophrenia and only one focused
on a patient with a medical illness

60. MANAGEMENT – ANTIPSYCHOTIC
USE
• During a prospective follow-up of 82 patients that had received
antipsychotics at some point when catatonic, NMS developed in three
cases (3.6%), a substantially higher incidence than the estimated
incidence of 0.07–1.8% in all antipsychotics-treated patients.
(Rosebush et. al 2010)
• The risk of worsening catatonia appears greater with neuroleptics and
antipsychotics with higher D2-blockade and a higher potential of
causing extrapyramidal side effects, but a worsening of catatonia and
precipitation of NMS has also been reported in association with, e.g.,
olanzapine.

61. PROGNOSIS
• Two-thirds show marked improvement or remission
• High incidence of recurrent catatonic episodes was
reported for idiopathic catatonia and catatonia due to
affective disorders
• Following ECT high relapse rate within a year
• continuation ECT is an efficacious treatment for
maintaining response (Suzuki et al 2005)
• “Chronic catatonia” in the context of schizophrenia is
phenomenologically different and less responsive to
either benzodiazepines or ECT

62. PROGNOSIS
• A longer illness duration, the presence of mutism, third-person
auditory hallucinations and ‘made phenomena’ (in which the
individual feels he is being made to do something) predicted a poor
response, whereas the presence of waxy flexibility predicted a good
response
• Van Waarde et. al have examined predictors of response to ECT in 27
catatonic patients and found improvement to be significantly
associated with younger age, and the presence of autonomic
dysregulation, especially higher body temperature

63. DIAGNOSTIC DIFFICULTIES
CATATONIA AND AUTISM
• Motor disorder
characterized by
stereotypy, rigidity,
mutism and posturing
• Rigidity is less in Autism
• Unable to clearly
delineate prodromal
features in Autism
CATATONIA AND NMS
• Life-threatening
• Antipsychotic can
worsen or trigger
NMS in Catatonia
• Rigidity in NMS
• Automatism in NMS

64. MENTAL HEALTH/CULTURAL IMPACT
• Mental health is a socially constructed and
defined concept, implying that different
societies, groups, cultures, institutions and
professions have diverse ways of conceptualising
its nature and causes, determining what is
mentally healthy and unhealthy, and deciding
what interventions, if any, are appropriate.
• Mental illness is a taboo subject that attracts
stigma in much of Africa. (Mary Amuyunzu-
Nyamongo, 2014)

65. MENTAL HEALTH/CULTURAL IMPACT
• A study conducted in Uganda revealed that the term ‘depression’ is
not culturally acceptable amongst the population.
• While another study conducted in Nigeria found that people
responded with fear, avoidance and anger to those who were
observed to have a mental illness.
• The stigma linked to mental illness can be attributed to lack of
education, fear, religious reasoning and general prejudice

66. MENTAL HEALTH/CULTURAL IMPACT
• Social stigma has meant that in much of Africa mental illness is a
hidden issue equated to a silent epidemic. Many households with
mentally ill persons hide them for fear of discrimination and
ostracism from their communities.
• Girls from homes known to have mental illness are disadvantaged
due to the fact that a history of mental illness severely reduces their
marriage prospects

67. CONCLUSION/TAKE AWAY POINTS
• Catatonia is a severe psychomotor syndrome with an excellent prognosis
if recognized and treated appropriately. The treatment of catatonia in
children and adolescents should follow the same principles as in adults.
• Great care should be taken to avoid (medical) complications.
• Although a number of pharmacological agents have been tried
successfully in catatonia, rarely, if ever, the effect is as immediate and
dramatic as seen with benzodiazepines.
• If benzodiazepines fail (inadequate or transient response, excessive
sedation), ECT should be started without delay. If the underlying
condition warrants ECT-treatment, or in life-threatening situations like
malignant catatonia or NMS, ECT is the treatment of first choice.

68. "You'll never find any gold if you don't go looking' for it”