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ORI GIN AL PA PER
Delirious Mania and Malignant Catatonia: A Report of 3Cases and Review
Mark B. Detweiler Æ Abhishek Mehra Æ Thomas Rowell ÆKye Y. Kim Æ Geoffrey Bader
Published online: 6 February 2009� Springer Science+Business Media, LLC 2009
Abstract Delirious mania is often difficult to distinguish from excited catatonia. While
some authors consider delirious mania a subtype of catatonia, the distinction between the
two entities is important as treatment differs and effects outcome. It appears that as
catatonia is described as having non-malignant and malignant states, the same division of
severity may also apply to delirious mania. Non-malignant delirious mania meets the
criteria for mania and delirium without an underlying medical disorder. The patients are
amnestic, may lose control of bowel and bladder, but still respond to atypical antipsy-
chotics and mood stabilizers. However, with increasing progression of the disease course
and perhaps with an increasing load of catatonic features, delirious mania may convert to a
malignant catatonic state (malignant delirious mania) which is worsened by antipsychotics
and requires a trial of benzodiazepines and/or ECT. Three case reports are presented to
illustrate the diagnostic conundrum of delirious mania and several different presentations
of malignant catatonia.
M. B. Detweiler (&) � K. Y. Kim � G. BaderPsychiatry Service, Veterans Affairs Medical Center, 1970 Roanoke Boulevard,Salem, VA 24153, USAe-mail: [email protected]
K. Y. Kime-mail: [email protected]
G. Badere-mail: [email protected]
M. B. Detweiler � K. Y. Kim � G. BaderDepartment of Psychiatry and Neurobehavioral Sciences, The University of Virginia,Charlottesville, VA, USA
A. Mehra � T. RowellCarilion-University of Virginia Roanoke-Salem Psychiatric Medicine Residency Program,University of Virginia, 1970 Roanoke Boulevard, Salem, VA 24153, USA
A. Mehrae-mail: [email protected]
T. Rowelle-mail: [email protected]
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Psychiatr Q (2009) 80:23–40DOI 10.1007/s11126-009-9091-9
Keywords Delirious mania � Catatonia � Malignant catatonia �Neuroleptic malignant syndrome � Atypical antipsychotics
Introduction
The syndrome of delirious mania may often present with puzzling symptoms and etiologies
that can delay appropriate and timely treatment, increasing the risk of mortality. The North
American and voluminous international literature include a confounding variety of
nomenclatures that began in 1832 with the first reported description of the syndrome by
Calmeil in France in 1832 [1]. Delirious mania consists of a constellation of symptoms that
can arise from both psychotic and affective psychiatric diseases as well and from many
medical diseases [2]. It has been described as a subtype of the catatonia syndrome having a
rapid onset with signs of mania, delirium and catatonia [2–4]. Manic signs include
insomnia, acute excitement, grandiosity, emotional lability, delusions, altered conscious-
ness, disorientation characterized by delirium often accompanied by posturing, stereotypy,
mutism, negativism and echo-phenomena suggesting catatonia [2, 3]. An additional
recently described symptom of delirious mania is pouring water over the head or on the
floor [5].
In a case series of 16 delirious mania patients, Karmacharya et al. [5] summarized their
patient demographics. Aside from two older outliers of 43 and 64 years of age, the average
age was 21 years. Women (13/16) suffered more frequently than men. A majority (10/16)
had prior histories of bipolar disorder and seven patients had histories of drug and alcohol
abuse. Other prior diagnoses included depression (2/16), anxiety disorder (1/16), PTSD
(1/16) and psychotic episode (1/16). Only one patient had no previous psychiatric history.
Luther Bell is acknowledged to be the first author in the North American literature to
describe delirious mania [6]. Since that time the syndrome has had a confusing variety of
names including: ‘‘acute delirious mania’’ [7]; ‘‘specific febrile delirium’’ [8], ‘‘delirium
acutum’’ [9–11]; ‘‘manic-depressive psychosis’’ [12]; ‘‘benign stupors’’ [13]; ‘‘hyperactive
or exhaustive mania’’ [14]; and ‘‘lethal catatonia’’ [15]. In the North American literature,
Kraines [16] suggested that this syndrome be designated ‘‘Bell’s Mania’’ after Luther Bell.
Despite the diversity of nomenclature in different countries, the delirious mania syndrome
symptomatology has been fairly consistently described in the clinical reports [2]. There has
been an increased discussion in the North American and International literature regarding
the nosology of delirious mania and catatonia [2, 3, 17–21].
Fink [2] has described delirious mania as ‘‘a syndrome of acute onset of excitement,
grandiosity, emotional lability, delusions and insomnia characteristic of mania, and the
disorientation and altered consciousness characteristic of delirium. Almost all patients
exhibited signs of catatonia’’. Fink and Taylor [3] have published a concise and definitive
discussion of the various clinical presentations of catatonia including delirious mania,
NMS, serotonin syndrome, excited catatonia, and periodic catatonia in the effort to stan-
dardize the description and diagnosis of what are posited to be subtypes of a broad
catatonic syndrome. They propose a new DSM classification of catatonia with 3 subtypes
and four specifiers [21]. These authors emphasize that the multiple presentations of cat-
atonia need to be delineated for both clinical and neuroscience research ends. The critical
objective of their nomenclature proposal is the rapid diagnosis and treatment of delirious
mania and catatonia to prevent syndrome progression from reaching a malignant state
where mortality risk is increased.
24 Psychiatr Q (2009) 80:23–40
123
The syndrome of catatonia featuring a cyclic mixture of mood and motor signs was first
described in 1874 by Kahlbaum [22, 23]. Fink [2] reported that approximately 6%–9% of
new inpatient psychiatric admissions exhibit catatonic features. Some studies suggest that
7.6%–40% of catatonias are idiopathic while approximately 14% of catatonias are sec-
ondary to a general medical condition [6–14, 16, 20–22]. Recently, there have been more
reports of catatonia associated with mood disorders than with schizophrenias [23]. The
development of catatonia rating scales [24–26] has improved clinical recognition [2].
Three or more signs on the Peralta et al. [25] catatonia diagnostic scale have a sensitivity of
100% and a specificity of 99% [23]. Catatonia can be broadly divided into two variants,
excited-delirious and retarded-stuporous [20]. The principal signs of catatonia include
mutism, stupor, negativism (Gegenhalten), posturing (catalepsy), waxy flexibility, ste-
reotypy, automatic obedience, echopraxia, echolalia, and mannerisms [2]. Over 40
catatonic phenomena have been identified in the literature [20, 27]. Some authors suggest
that the presence of any two signs of catatonia for 24 h or more justifies the diagnosis of
catatonia [28, 29].
In the past and in DSM III, catatonia was principally associated with schizophrenia,
despite reports of catatonia being associated with mood disorders (e.g., depression, bipolar
disorder) and medical maladies (e.g., infections, toxic states) [2, 30]. Like delirious mania,
catatonia may be non-malignant or malignant [2, 23, 31]. Malignant catatonia differs from
non-malignant catatonia with the former exhibiting autonomic instability consisting of an
elevated fever ([38�C), tachycardia and hypertension. Speech and thoughts are disorga-
nized, accompanied by intense excitement, cataplexy, mutism, rigidity, stereotypy and
posturing. This syndrome has also been referred to as Bell’s Mania and delirious mania due
to overlapping symptoms [2].
We present three cases of catatonia to illustrate the similarities and differences in the
varied subtypes including non-malignant delirious mania, malignant catatonia associated
with schizophrenia and a case of catatonia secondary to varying medical etiologies that
evolved into two other catatonia forms. The clinical features of each case are described
according to the criteria of DSM IV TR, Peralta et al. [25] and Fink and Taylor [3].
Case Reports
Case 1
Mr X is 47-year-old male with no former psychiatric history who was transferred to our
hospital after recent admissions at two other hospitals where he had presented with
insomnia, sexual disinhibition, liability, and generally disorganized behavior accompanied
by neglected hygiene, inappropriate behavior and paranoid thoughts. He was reported to
have stopped taking his mediations following discharge from the first hospital.
Prior to the recent hospitalizations, the patient was described as being exceptionally
hardworking, preoccupied with his health, for example taking his blood pressure multiple
times a day. His concern about body fat contributed to daily runs of 12 to 15 miles, while
working two shifts at work and getting an estimated 1–2 h of sleep per night. Family and
friends had noticed an increasing trend of hyperactivity with increasing confused and
disinhibited speech. His family also reported his activities to include, working 27 straight
days, working two shifts daily, daily long runs while averaging 1 h of sleep per night plus
non stop volunteering to help church families. He had no history of drug or tobacco use.
Psychiatr Q (2009) 80:23–40 25
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On the acute psychiatry ward, the patient demonstrated extreme fluctuations of mood and
cognition with visual hallucinations resulting in behavior of plucking ‘‘flying insects’’ and
objects out of the air and off the walls and furniture. Periods of agitation included pushing
staff, pounding on doors and demanding to be released. When conversant he showed no
insight about his recent past or present situations, cognition or functional state. Despite
autonomic instability with elevated temperature (37.8�C/100.04�F), pulse (93), respirations
(24) and reported pain (10/10), his physical examination was non focal. Electrocardiogram
(EKG) and chest X-ray were unremarkable. Normal laboratory results included TSH, CBC,
PT/PTT, Troponin I, hepatitis C, RPR and urinalysis. Abnormal labs included mildly
decreased serum protein (5.8 g/dl), serum albumin (3.0 g/dl) alkaline phosphatase (32 U/l)
and RBC (4.48 9 106/ll) with a marginally increased SGOT (43 l/l). The urine drug
screen was negative, the serum alcohol level and GGT were normal.
After admission he tried to elope and required sedation and physical restraints. His
delirious state was marked by grimacing and motoric agitation including disrobing,
removing the mattress from his bed and crawling on the floor. In addition to the visual
hallucinations he appeared to be responding to auditory hallucinations. He would march
around his bed, alternating with sitting on the bed while performing repetitive hand
movements as if performing a manual task. Speech ranged from mute to delusional
ramblings. Staff initiated questions were often met with echolalia during the several days
of acute mania with delirium. He lost bowel and bladder control requiring diapers for
several days. His CLOX test and MMSE were zero as the patient could not participate and
was oriented to person only.
Intake medications included levetiracetam 50 mg twice daily, citalopram 40 mg once
daily and ziprasidone 60 mg twice daily. Levetiracetam was stopped, citalopram was held
due to the mania, ziprasidone 60 mg twice a day was continued and olanzapine 20 mg was
added for mood stabilization and psychosis. Haloperidol and lorazepam were ordered on an
as needed basis. On day three the patient had decreased disorganized behavior and a taper
of the ziprasidone was started. Increased confusion and disorganization followed this. The
ziprasidone dose was returned to 60 mg twice a day and olanzapine was increased to
30 mg at night. On day seven the delirium had subsided, however the patient was amnestic
to his symptoms and behavior for the week of delirium in the hospital and for at least one
week prior to admission.
The patient gradually improved with a stepwise decreased agitation and catatonic
symptoms. By day 12, cognition had markedly improved (CLOX1 = 13/15,
CLOX2 = 11/15, MMSE = 30/30). The patient became depressed when hearing about his
activities during the manic and delirious episodes, worrying about losing his job, marriage
and respect in his church community. Citalopram was restarted for depression. Lamotrigine
25 mg daily was initiated for bipolar depression and titrated to 50 mg bid. Ziprasidone was
cross tapered to quetiapine 150 mg twice a day for psychosis and olanzapine 30 mg qhs
was continued. He was also referred for marital and job counselling. The patient left the
acute service and his care was transferred to the outpatient service at another hospital.
There have been no additional episodes of acute mixed mania with catatonia (delirious
mania) for the past 4 years, with present medications including aripiprazole 10 mg and
venlafaxine HCL 75 mg daily.
Case 2
A 62-year-old male with a 40 year history of paranoid schizophrenia was transferred to our
acute inpatient service as a result of him kicking a hole in a hospital wall and threatening to
26 Psychiatr Q (2009) 80:23–40
123
kill the staff at another hospital where he had been admitted for acute exacerbation of
paranoid schizophrenia. He had been committed, placed in restraints and transferred. The
patient had started showing signs of mania, insomnia, hypersexuality and aggression
several months prior to his admission following the death of one of his daughters and with
the subsequent assumption of care of her five children.
On admission he had a reduced hemoglobin of 9.0 (baseline 12.5 g/dl) and a positive
hemoccult. He was admitted to the step-down unit for hypotension and to rule out a lower
GI bleed. The patient became verbally abusive and threatening to the staff resulting in
being placed in 4-point restraints. He was deemed inappropriate for colonoscopy, was
considered hemodynamically stable and he was transferred to psychiatry.
On transfer to the acute psychiatric unit the patient attempted to assault the officer who
escorted him to the ward. He was largely incoherent, not redirectable and demonstrated
severe psychomotor agitation. He had marked sexual disinhibition including verbal
aggression towards female staff, plus disrobing and masturbation when not in restraints. He
exhibited inappropriate and bizarre postures with grimacing and guttural vocalizations. At
times he was mute aside from making the guttural sounds. His level of aggression required
continual restraints. Intake laboratory abnormal values included albumin (2.4 g/dl), protein
(5.8 g/dl), iron (23 lg/dl), RBC (3.86 9 106/ll), hemoglobin (9.0 g/dl), hematocrit
(27.5%), platelets (407/mm [3]), magnesium (2.8 mEq/l), Westergren (36 mm/h). Tem-
perature increased to 38�C (100.4�F), pulse to 116, and blood pressure to 178/56. Chest
X-ray was normal and the head CT demonstrated no changes incongruent with the patient’s
age.
The patient refused to take any oral medications, food or fluids. He was started on
scheduled intramuscular olanzapine. Daily olanzapine doses exceeding 40 mg a day and
intramuscular diazepam, with doses up to 125 mg a day, had no effect in controlling the
delirium. With increasing CPK (high 1714.0 U/l), thought to be principally due to his
agitation in restraints, in addition to increasing WBC (12.8 9 106/ll) with minimal fluid
and food intake, he was transferred to the ICU for intravenous medications, fluids and
nutrition. He failed intramuscular haloperidol and benzodiazepines, therefore, these were
discontinued and ECT was initiated on day 12. With each ECT there was a direct decrease
in motoric and verbal agitation in addition to increased compliance with fluids, food and
medications. He was transferred back to the acute psychiatric unit midway through the
ECT course. He was restarted on olanzapine which was titrated to 20 mg at night and he
returned to his quiet, courteous baseline with no overt signs of mood or psychotic
symptoms. The patient was found to have underlying cognitive impairment (MMSE 11/30,
CLOX1 3/15, CLOX2 13/15). The patient was discharged on omeprazole for GERD and
olanzapine 20 mg at night. An out patient colonoscopy was scheduled at primary care
clinic. It was recommended that he be followed in a memory disorders clinic. After
3 years, the patient remains on the olanzapine 20 mg and he has had no acute episodes of
schizophrenia with excited catatonia (malignant catatonia).
Case 3
A 61-year-old female with a history of bipolar disorder, diabetes mellitus type II, hyper-
tension, hyperlipidemia, hypothyroidism and gastroesophageal reflux was admitted to the
ER for right arm pain. It was reported that she had stopped taking her trifluoperazine for an
indeterminate time prior to admission and she had been having increasing falls. She was
also prescribed escitalopram and lithium. The patient was found to have an elevated
troponin I and elevated creatinine kinase. She also presented with slurred speech and
Psychiatr Q (2009) 80:23–40 27
123
altered mental status described as ‘‘pleasantly demented’’. Significant positive signs
included elevated blood pressure (174/80), temperature (37.8�C), pulse (100 bpm), and
respirations (20). Oxygen saturation was 94% on room air, there was a grade II systolic
murmur at the left base, bilateral ?1 pitting edema and marked ecchymoses. An extended
bladder contained one liter of urine. EKG showed nonspecific ST wave changes. Head CT
and chest X-ray were noncontributory. Her lithium level was 0.64 mEq/l. Significant
laboratory values included increased WBC (15.3 9 106/ll), AST (127 U/l), ALT (61 U/l)
and decreased sodium (129 mEq/l). The patient was restarted on trifluoperazine 25 mg,
lithium 225 mg in the morning and 450 mg in the evening. Haloperidol 1 mg IV every 4 h
was ordered for agitation. Mental status waxed and waned with periods of unresponsive-
ness. EEG showed slowing secondary to muscle tension. Temperatures reached 38.3�C and
an LP done on day 5 showed one WBC/ll, 17 RBC/ll and a protein of 32 mg/dl. CSF
cryptococcal antigen was negatives and the CSF VDRL was nonreactive. Transesophageal
echocardiography revealed aortiosclerosis, mild left ventricular hypertrophy, a
0.8 9 0.4 cm left ventricular calcification and a calcified left aortic valve.
One week after admission, the patient was incoherent, had cogwheel and nuchal
rigidity and a head MRI revealed small vessel disease. Trifluoperazine was discontinued
and the olanzapine was started, however, the patient continued to demonstrate dysarthria
and psychotic symptoms. Ziprazidone 80 mg twice a day was added on day nine with
lithium continued. On day 10 the patient was still incoherent with her eyes closed. The
olanzapine and ziprazidone were stopped and replaced with trifluoperazine 5 mg in the
morning and 20 mg in the evening. Haloperidol 2 mg every 4 h was ordered for agitation.
Lithium was continued. On day 11 the patient became unable to recognize her long term
psychiatrist. She was disoriented, incoherent, physically and verbally agitated, exhibiting
negativism by refusing to follow commands or open her eyes. Significant rigidity was
noted. Suspecting NMS the trifluoperazine and lithium were discontinued. Urinalysis
showed an E. coli infections and ceftriaxone 1 mg/24 h was initiated. When blood cul-
tures were positive for coagulase positive Staphylococcus, vancomycin 1250 mg was
given. White blood cell count remained in the 10–15 (9106/ll) range throughout the
hospitalization.
Antibiotic therapy ended on day 21, however, patient’s clinical condition continued to
deteriorate with the patient becoming unable to take oral food or fluids. The patient
developed a significant hypokalemia which was stabilized by day 28. The patient remained
in a delirious state and unable to feed or hydrate herself. Intravenous hydration was
continued and ECT was initiated on day 28. There was a gradual improvement in mental
status and with slow resumption of oral fluids, food and medications. A total of six ECT
sessions were employed. As the patient had a history of poor response to atypical anti-
psychotics, she was discharged on haloperidol 10 mg at night, escitalopram 10 mg daily
and benztropine 1 mg three times a day.
Discussion
The three cases all meet criteria for delirious mania and catatonia according to Fink [2]
(Table 1), in addition to meeting DSM IV TR criteria for schizophrenia catatonic type
(295.20) and for the mood disorders with catatonia features specifier (Table 2). Moreover,
the three cases also meet catatonia criteria according to Peralta et al. [25] (Table 3). The
first two cases meet criteria for DSM IV TR delirium criteria due to a general medical
condition without having an identified contributing general medical condition (Table 4).
28 Psychiatr Q (2009) 80:23–40
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The third case had underlying medical conditions on hospital admission, thus meeting
DSM IV TR criteria for delirium due to a general medical condition (293.0) (Table 4).
These three cases represent patients frequently seen in ERs and on medical and acute
psychiatric units. There are two fundamental questions for the clinician. First what is the
correct diagnosis and second what is the appropriate treatment?
Table 1 Catatonia subgroups delirious mania and catatonia [3]
Symptoms Delirious mania Symptoms Catatoniaa
Case 1 Case 2 Case 3 Case 1 Case 2 Case 3
Sudden onset X X X Acute onset of excitement X X X
Intense excitement X X X Grandiosity X
Hyperthermia X Emotional lability X
Catalepsy X Delusions X X
Mutism X X X Insomnia of mania X X
Rigidity X Disorientation X X X
Stereotypy X X X Altered consciousness X X X
Posturing X Negativism X X X
Tachycardia X X X Stereotypy X X X
Tachypnea X X X Posturing X X
Hypertension X X Pressured Speech and Mutism X X X
Disorganized thoughts X X X Flight of Ideas
Disorganized speech X X X Hyperthermia X X X
Refuse food and fluids X X X Tachycardia X X X
Cycle from excited stateto stuporous state
X Tachypnea X X X
Hypertension X X
a Requires 2 or more signs for 24 h or longer (See Ref. [3])
Table 2 Criteria for schizo-phrenia catatonic type (295.20);mood disorders with catatoniafeatures specifier (DSM IV TR)
Symptoms Case 1 Case 2 Case 3
Motoric immobility
Waxy flexibility
Stupor X
Excessive motor activity X X X
Extreme negativism
Rigidity X
Mutism X X X
Peculiarities of involuntary movement
Inappropriate postures X X X
Bizarre postures X
Prominent grimacing X X X
Echolalia X
Echopraxia
Psychiatr Q (2009) 80:23–40 29
123
Differential Diagnosis
Medical Etiology Rule Outs
The differential diagnosis of both delirium and catatonia may include head injury, seizures,
metabolic disorders, medication intoxication (NMS, serotonin syndrome), exacerbations of
medical conditions, mood disorders and psychotic disorders [4]. In the medical setting,
delirium from toxicity or withdrawal from recreational drugs (benzodiazepines, cocaine,
amphetamines, barbiturates, etc.) and alcohol are frequent findings and need to be ruled out
with appropriate history and laboratory tests. This is especially important in the psychiatric
setting considering the comorbidity of drug and alcohol use in patients with psychiatric
disorders [30]. Bowl and bladder incontinence as in case 1 is not a common clinical finding
other than in profound cognitive deterioration such as in moderate to severe dementia [32],
or in delirious mania with marked cognitive disorientation [2, 30].
Table 3 Catatonia diagnosticcriteria [25]a
a Requires 3 or more for positivediagnosis
Symptom (11 most sensitive signs) Case 1 Case 2 Case 3
Immobility/stupor X
Mutism X X X
Negativism X X X
Opposition X X X
Posturing X X
Catalepsy X
Automatic obedience
Echo phenomena X
Rigidity X
Verbigeration X X
Withdrawal/refusal to eat or drink X X X
Table 4 Delirium due to a gen-eral medical condition (293.0)(DSM IV TR)
Symptoms Case 1 Case 2 Case 3
Disturbance of consciousness X X X
; awareness of environment X X X
; ability to focus X X X
; ability to sustain attention X X X
; ability to shift attention
Change in cognition X X X
Memory deficit X X X
Disorientation X X X
Language disturbance X X X
Perceptual disturbance
Short onset X X
Daily fluctuating course
Evidence of a General medical condition X
30 Psychiatr Q (2009) 80:23–40
123
In these case reports, the patient in case 3 presented in the ER with slurred speech, right
should and right arm pain, recent falls, hyperthermia (38.9�C), autonomic instability (BP
174/80), a systolic grade 2 murmur, disorientation, agitation, ongoing UTI, pulmonary
hypertension on CXR and small vessel disease on head MRI. She had significantly altered
blood chemistries including AST (127 U/l), ALT ((61 U/l), WBC (15.3 9 106 /l),
CK-MB (52 U/l), troponin (0.48 ng/dl), BUN (32 mg/dl), creatinine (11.3 mg/dl), glucose
(327 mg/dl), low serum sodium (129 mEq/l) with an EKG showing a non-specific ST
change. The patient had also stopped taking her conventional antipsychotic and lithium.
Thus, the role of a multiple destabilizing general medical conditions needs to be investi-
gated and a delirium of mixed etiologies, more probably to general medical conditions,
should be considered at first presentation in the emergency room.
In case 3, after first presenting in an agitated state, the patient’s behavior was subse-
quently described as having episodes of waxing and waning mental status unresponsive to
medications, accompanied by temperatures of 38.4–38.9�C and by periods of unrespon-
siveness or stupor. On some examinations she would moan and she was reported to be
unaware of her examiners. A UTI with gram positive clusters was treated with ceftriaxone.
When blood cultures were positive, suggesting septicemia, and vancomycin was started.
This suggests that the poorly controlled diabetes mellitus may have altered the patient’s
immune response leading to a concurrent local and then a systemic infection. It can be
argued that the patient’s failure to take her antipsychotic and mood stabilizer contributed to
not taking her medications for diabetes and hypertension. Thus, case 3 appears to be
initiated by a delirium secondary to hyperglycemia, hypertension with progressing local
and systemic infections compounded by medication noncompliance.
Delirious Mania vs Other Forms of Catatonia
Once identified as probably not having an organic etiology, the diagnosis of delirious
mania versus another form of catatonia is the next step. The first question is whether the
presenting symptoms were predominantly delirious or catatonic (Tables 1, 2 and 3)? In the
DSM IV TR, delirium is attributed to states resulting from medical conditions or substance
use. Delirium is not recognized as being associated with either schizophrenia or mood
disorders. Catatonia on the other hand, has both states of motoric immobility and states of
excessive motor activity. Catatonic features may appear during an episode of delirium [2].
According to DSM IV TR criteria, catatonic features may also accompany schizophrenia or
a mood disorder. If the predominant features were those of delirium with minor catatonic
features, the diagnosis would probably be delirious mania. This does not imply that the
catatonic features will remain minor compared to the delirious mania features as the
disease progresses and perhaps become predominant as in case 3.
Delirious mania has no DSM IV TR or ICD classification. Until the classification
scheme of Fink and Taylor [3], delirious mania was considered by many to be an acute
exacerbation of bipolar disorder as it has responded to antipsychotics and mood stabilizer
therapy in some reports [33]. Clinicians are aware that whenever there are clinical signs
of delirium and catatonia in the presence of antipsychotics, serotonergic agents and
multiple psychiatric medications, NMS should also be included the differential diagnosis
[2, 20].
Both cases 1 and 2 meet DSM IV TR criteria for delirium due to a medical condition
without having an identifiable acute medical condition. All 3 cases meet criteria for
delirious mania (Table 1) and catatonia according to the DSM IV TR (Table 2) in addition
to the catatonia criteria of Peralta et al. [25] (Table 3). Both patients in cases 1 and 2 first
Psychiatr Q (2009) 80:23–40 31
123
presented with elevated mood, grandiosity and disinhibition. As stated above, patient 3 was
initially agitated with slurred speech on admission, however, she lapsed into episodes of
stuporous catatonia. The cluster of catatonic signs seems to have increased as the disease
course progressed in all three cases.
Non-Malignant vs Malignant Catatonia
The next step is to differentiate between non-malignant and malignant catatonia as this
distinction guides treatment. As a result of the development and implementation of stan-
dardized examinations and rating scales, catatonia has been more frequently documented to
be associated with affective disorders and neurotoxic states [2, 33]. Exhibiting a notable
diversity of symptoms including motoric signs, excitement or stupor, bizarre and repeti-
tious behavior, it has been suggested that in the absence of autonomic instability and
hyperthermia, the catatonia be termed ‘‘simple or non-malignant catatonia’’. In the pres-
ence of autonomic instability and hyperthermia, the syndrome becomes ‘‘malignant
catatonia’’ [18, 28, 34]. Taylor and Fink [20] suggest that the nonmalignant forms of
catatonia be referred to as the Kahlbaum syndrome.
In case 1, a 47-year-old male with no prior psychiatric history until the events that lead
to his three consecutive hospitalizations. By his third admission, he presented with pre-
dominantly delirious symptoms and he exhibited progressing catatonic symptoms as the
delirium worsened. There was mild hyperthermia (37.8�C) and mild autonomic instability.
Notably, the patient responded to atypical antipsychotics and mood stabilizers which
generally are not effective in cases of malignant catatonia [2, 31]. These factors suggest
that the threshold for malignant delirious mania/catatonia was not reached in this case.
In case 2, a 62-year-old male with a history of paranoid schizophrenia, presented with
signs of mania, insomnia, hypersexuality, aggression and delirium accompanied by
extreme excitation, hyperthermia (38�C, more significant in an older patient) and with
moderate autonomic instability. He refused food and liquids during the excited phase
requiring continual 4-point restraints and required several sessions of intravenous hydra-
tion. He was unresponsive to atypical antipsychotics and benzodiazepines and only
responded to ECT. These clinical characteristics would qualify the case as a malignant
form of delirious mania or malignant catatonia.
The patient in case 3 entered the hospital in an agitated state with hyperthermia and
autonomic instability seemingly from several medical conditions (acute sub staphylococcal
coagulase negative infection, acute E. coli UTI, electrolyte imbalance, hypertensive car-
diovascular disease). As the medical problems were resolved, the patient continued to have
signs of delirium and stupor unresolved with the reintroduction of her outpatient trifluo-
perazine and lithium. She improved marginally on olanzapine and ziprazidone, but she had
some residual dysarthria and psychosis. Change to trifluoperazine, lithium and haloperidol
as a PRN produced increased agitation, disorientation, muscular rigidity and amnesia. At
this stage the diagnosis of NMS could be considered. However, it probably was not the
initial etiology of the malignant catatonia, rather a result of treatment employing a rapidly
changing regimen of conventional and atypical antipsychotics, in addition to lithium. NMS
has been associated with trifluoperazine [35], trifluoperazine with lithium [36], lithium and
haloperidol [37], ziprazidone [38], ziprazidone and lithium [39], olanzapine [40], and
olanzapine and lithium [41]. Regardless of the initial etiology in this case, the disease
course progressed from delirium due to a several general medical conditions, to NMS and
finally to malignant catatonia.
32 Psychiatr Q (2009) 80:23–40
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DSM IV TR vs Fink and Taylor Classifications
Diagnostic clarity is difficult for the clinician who sees only several cases of delirious
mania, exited catatonia or malignant catatonia each year. This is compounded by some
confusion in the literature secondary to authors using a diversity of competing classifi-
cation schemes [2, 20, 21]. Diagnostic clarity may be further confounded by the DSM IV
TR classification as the clinician will not find an appropriate code for ‘‘delirious mania’’ or
‘‘malignant catatonia’’ with either an apparent organic or functional etiology. Taylor and
Fink [20, 21] have presented a thorough discussion of the DSM IV TR limitations and their
suggestions for a new catatonia classification system. With the present DSM IV TR system,
delirious mania (case 1) or malignant catatonia (case 2) associated with psychotic or
affective disorder could be diagnosed as a mood disorder with catatonic features (DSM IV
TR page 417) and schizophrenia catatonic type (DSM IV TR 295.20) respectively. Cat-
atonia due to general medical conditions would be acceptable for phase one of case 3 as the
patient was not taking her antipsychotics or mood stabilizer and had numerous active
medical problems on admission. During phase two of her disease course, she was being
started and stopped on multiple antipsychotics combined with lithium and haloperidol
PRN, which may have initiated a NMS syndrome. In an early stage, the NMS would be
probably be classified as a drug induced form of non-malignant catatonia by Fink and
Taylor [3]. With increasing switching of conventional and atypical antipsychotics, in
addition to lithium, the NMS became malignant, which would be classified as a drug
induced form of malignant catatonia by Fink and Taylor [3]. DSM IV TR makes no
distinction between the non-malignant and malignant stages of NMS.
When delirious mania is diagnosed, the differential diagnosis would include delirious
mania versus excited catatonia, excited catatonia versus catatonia dominated by inhibition,
mania with psychotic features versus delirious mania and catatonia versus NMS [2]. Also,
the question for all the possibilities, is whether the presenting disease state is a non-
malignant or malignant form? The predominance of evidence supporting catatonia,
delirium or NMS may be the deciding factor. If there is a predominating cluster of signs
supporting either delirium or catatonia, this may be the deciding diagnostic element. NMS
would be suspected if the catatonic signs followed the introduction of an antipsychotic. Or,
the diagnosis may depend on when the disease was first observed. Evidence of the pre-
ceding phase or phases may not be available to the treating clinician.
In case 1, the delirious mania was the patient’s first psychiatric episode and could be
classified as a mood disorder with catatonic features using DSM IV TR. However, this does
not indicate the difference between a nonmalignant and malignant episode. The delirium
does not qualify for the DSM IV TR diagnosis of delirium as there is no underlying
medical condition. The proposed DSM addition by Fink and Taylor of catatonia as a
separate entity with subtypes (nonmalignant, delirious and malignant) in addition to 4
specifiers (mood disorders, general medical conditions or toxic states, neurological dis-
orders, psychotic disorders) [21] would classify case 1 as delirious catatonia secondary to a
mood disorder.
In case 2, the delirious mania or excited catatonia that progressed to a malignant state
was associated with a re-exacerbation of paranoid schizophrenia. DSM IV TR would
classify this as schizophrenia catatonic type. As in case 1, there is no qualifier for non-
malignant or malignant catatonia. Employing the Fink and Taylor diagnostic suggestions
[21], case 2 would be labeled as malignant catatonia secondary to a psychotic disorder.
In case 3, the patient seems to have had the initial symptoms of delirium secondary to
underlying medical conditions at intake, resulting from the patient failing to take her
Psychiatr Q (2009) 80:23–40 33
123
medications for hypertension and diabetes with eventual infections. This could be classi-
fied by DSM IV TR criteria as a ‘‘delirium due to general medical condition (poorly
controlled diabetes, hypertension and with urinary tract and eventually systemic infec-
tions). However, more appropriately, as there is a delirious mania accompanying the
medical conditions, a more appropriate DSM IV TR diagnosis would be ‘‘catatonic dis-
order due to a general medical illness’’ (DSM IV TR 293.89). It would not meet criteria for
DSM IV TR ‘‘mood disorder with catatonic features’’ as the medical problems were more
prominent in contributing to the delirium than the bipolar symptoms at admission. This
does not discount the signs of catatonia. Also, none of these diagnoses account for the signs
of non-malignant catatonia versus malignant catatonia. With progression of the disease and
the resolution of the initial medical problems, the patient appears to have entered into a
delirious mania that was treated with a multitude of medications (conventional and atypical
antipsychotics were added to lithium) that eventually precipitated a NMS state which
subsequently progressed to malignant catatonia.
Depending on the classification criteria, case 3 in the early phase could be classified as
having delirious catatonia due to general medical conditions [21], or delirium secondary to
general medical conditions (DSM IV TR), or catatonia [25]. The second phase could be
diagnosed as NMS in either the non-malignant or malignant form depending on the day of
illness, with a final presentation of malignant catatonia. Fink and Taylor [21] probably
would have classified phase 2 as non-malignant catatonia due to a toxic state (NMS), and
finally malignant catatonia due to a toxic state (NMS) in the final phase. In the third phase
DSM IV TR would have described the clinical presentation as NMS or bipolar disorder
with catatonic features.
In such complex cases as case 3, it can be observed that an initially nonmalignant
syndrome can rapidly progress to malignant catatonia having both signs of organic and
functional impairment. If the clinician does not have a thorough understanding of delirious
mania/excited catatonia and malignant catatonia, the reported etiology may reflect the
clinician’s orientation [5]. The diagnosis may also be missed as earlier treatment of the
delirious mania and malignant catatonia syndromes may reduce the number of cases in
which a case of nonmalignant catatonia progresses to the stuporous phase. It has been
suggested that the earlier treatment in recent years has resulted in the failure to recognize
an underlying catatonic syndrome in many more cases since the advent of ECT in 1934.
Regardless of the initial etiology, once fully developed, malignant delirious mania and
malignant catatonia syndromes have a high mortality if appropriate treatment is delayed
[2, 17, 19, 31].
Treatment
Historical
Perhaps the most critical clinical question is whether the delirious mania or catatonia is
non-malignant or malignant [2, 31]. Prior to the introduction of ECT in 1934, over 80% of
persons afflicted with delirious mania (or delirious catatonia) died in hours to days fol-
lowing stuporous exhaustion, coma and cardiovascular collapse [17, 19]. In Bell’s historic
review of 1700 admissions to his hospital from 1836–1849, 75% of the 40 patients
identified as having delirious mania died [2, 6]. In the early neuroleptic era, medications
were largely ineffective once the delirious mania and nonmalignant catatonia progressed to
malignant forms [42–44]. A few authors reported the success of utilizing ACTH and
34 Psychiatr Q (2009) 80:23–40
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corticosteroids in the early 1940s [45, 46], however, some cases also employed ECT in
addition to the corticosteroids thus improving treatment efficacy [17, 47]. The treatment of
choice in 1980 was a combination of haloperidol and lithium [33]. The use of neuroleptics
for malignant catatonic syndromes is still rarely effective [17–19, 48].
The advent of ECT markedly improved prognosis. Early reports describe treatment with
an average of 25–40 ECT sessions with an extreme case requiring 200 sessions [17]. One
technique, the ‘‘shock block’’ technique, employed three to five ECT sessions with 15 min
intervals followed by three more during the following 12 h [17, 49]. Improved and earlier
diagnosis with support from intravenous fluids reduced the number of ECT sessions to two
to 14 daily bilateral sessions [2, 3, 17, 50, 51]. It is notable that one form of catatonia has
been reported to have a familial link [52–54] that portends a poor prognosis as it seems to
respond poorly to benzodiazepines and ECT [20].
Treatment for Non-Malignant Delirious Mania/Catatonia
It may be prudent to initiate treatment for delirious mania while continuing a medical
work-up. If one utilizes the nosological system of Fink and Taylor [3, 21] delirious mania
is a variant of catatonia. Thus, it follows that some authors suggest that benzodiazepines
are the first treatment choice regardless of phase [2, 3, 20, 48, 55]. However, case reports
and retrospective studies have shown that there are alternative and perhaps second line
treatments for the non-malignant stages of some of the catatonic variants. For non-
malignant catatonic schizophrenia, atypical antipsychotics and mood stabilizers have
proven effective [31, 33, 56]. In a review of 16 cases of delirious mania Karmacharya el al.
[5] identified clozapine, olanzapine and quetiapine as effective atypicals. Ziprasidone was
successfully employed in case 1. Successful mood stabilizers have included lithium, val-
proate and oxcarbazepine [5].
The non-malignant stages of delirious mania may correspond to Kraeplin’s [57]
‘‘manic-depressive psychosis’’ that had a less severe course, including a lower fever,
insomnia, shorter duration, hypomania or mania and delusions. The malignant phase of
delirious mania appears similar to Kraeplin’s ‘‘collapse delirium’’ with a high fiver, con-
fusion, flight of ideas, extreme excitement and hallucinations.
Atypical antipsychotics were effective in case 1, congruent with the retrospective
studies and case reports cited by Van Den Eede et al. [31] in their discussion of the use of
antipsychotics for nonmalignant catatonia. In case 1, the patient responded to two atypical
antipsychotics with mood stabilizing properties (ziprasidone, olanzapine). Tapering the
ziprasidone made the symptoms worse. If the symptoms are primarily secondary to a
medication induced toxic states (e.g., NMS), then stopping the medications should improve
the symptoms [56, 58].
Treatment for Malignant Delirious Mania/Catatonia
Benzodiazepines
If delirious mania evolves into malignant catatonia, use of neuroleptics are ineffective and
should be discontinued [2, 31, 44]. In this situation, the only treatment modalities recom-
mended by most authors are benzodiazepines or ECT with use of conventional or atypical
neuroleptics only worsening the disease course [2, 31, 44, 48]. The malignant patient may
have a high fever, tachycardia, elevated blood pressure and be dehydrated if not having
received continuous intravenous fluids as in cases 2 and 3. While ECT is the most frequently
Psychiatr Q (2009) 80:23–40 35
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reported curative measure both in the pre-neuroleptic and neuroleptic eras [2, 19, 31, 42, 59,
60] a new early benzodiazepine early intervention has been proposed [55].
Some authors suggest using benzodiazepines in both non-malignant and malignant
states of delirious mania and catatonia. Lorazepam 6–20 mg/day appear to be effective up
to a certain malignant threshold, after which ECT is more effective [30]. Bush et al. [48]
employed a 5-day oral or parenteral benzodiazepine challenge (1 mg given every 5 min for
two doses, maximum 8 mg/day) with reduction in symptoms as measured by Bush-Francis
Catatonia Rating Scale (BFCRS) [24]. The greater the drop in BSCRS scores on the first
day following the second lorazepam dose, the better the response to the benzodiazepine.
It is notable that American Psychiatric Association recommends that benzodiazepines
be avoided in cases of delirium. With the current understanding of delirious mania, this
guideline may need modification for the treatment of delirious mania [5]. Effective ben-
zodiazepine dosing has been reported for delirious mania in a pediatric patient [61], for
idiopathic catatonia [62] and for catatonia associated with schizophrenia [55].
Pommepuy and Januel [23] have proposed a five step treatment protocol for catatonia
which would also include delirious mania: (1) stop medication(s) suspected of symptom
production; (2) test for and treat underlying physical disease states (include standard
chemistries, urine drug screen, EEG, head CT); (3) trial of lorazepam 2.5 mg; rate cata-
tonic signs after 1 h; with partial or total response, start 3 mg/for 6 days followed by a
tapering dose; (4) for the 20% that may not respond to lorazepam, employ ECT; if
malignant catatonia is suspected by the presence of and/or autonomic instability go directly
to ECT.
Huang [55] reported a 100% response rate on day one when the patients were treated
with lorazepam 2 to 4 mg im. If the response is not sufficient, intravenous diazepam
10 mg/2 m/l in 500 m/l is infused with normal saline every 8 h. Other authors have not
reported success with benzodiazepine use once the disease progresses to malignant cata-
tonia. When the delirious mania progressed to a malignant phase, lorazepam doses as high
has 10 mg/day have failed [2] as did a midazolam drip of 8 mg/h [44]. If the delirious
mania progresses to a malignant phase, ECT may need to be employed as it has been
reported to be effective in reducing mortality regardless of the etiology of the syndrome
[2, 19, 31, 44].
ECT
Most cases of malignant delirious mania have responded to ECT and it is the consensus
treatment of choice with the majority of malignant cases requiring two-12 ECT sessions
[2, 5, 31, 44]. Some authors recommend every other day ECT [44], while others suggest
daily ECT treatments to hasten recovery [2, 3]. A more conservative ECT protocol than
‘‘shock block’’ [49], is the ‘‘en bloc’’ ECT regimen consisting of daily ECT on two or more
consecutive days. In the 13 cases of malignant catatonia cited by Philbrick and Rummons
[18], six of the eight patients receiving ECT survived. Karmacharya et al. [5] in their
retrospective series of 16 delirious mania cases reported that the last effective treatment in
10 cases was high dose benzodiazepines (4 cases), lithium and valproate (2 cases) and
clozapine (2 cases). In six cases ECT was the last effective treatment choice with clinical
improvement noted after one to four ECT sessions.
We propose that delirious mania (or delirious catatonia) may have a less acute stage that
responds to mood stabilizers and antipsychotics in addition to benzodiazepines as sug-
gested by Van Den Eede et al. [31] and as illustrated in the cases series of Karmacharya
et al. [5]. However, like other forms of malignant catatonia, once the threshold is reached
36 Psychiatr Q (2009) 80:23–40
123
for severe malignant delirious mania (or malignant catatonia), benzodiazepines or ECT are
the treatment of choice. The malignant phase of delirious mania may be identified by
having a predominance of catatonic signs as opposed to the nonmalignant phase of
delirious mania when delirium signs predominate. These phases can be documented by
employing serial catatonia rating scale [24, 25] scores during the disease course. As the
clinician observes increases in catatonic signs, the suspicion of an impending progression
into a malignant state should be expected. Once malignant catatonia is suspected, failure to
respond to benzodiazepines with a concurrent continued increase in catatonic signs might
be an index of having breached the malignancy threshold. Thus, we suggest that delirious
mania, like other forms of catatonia, can be divided into non-malignant and malignant
forms. These nonmalignant forms seem to be responsive to atypical antipsychotics and
mood stabilizers, which are not effective in the malignant catatonic stage. A limitation of
atypical antipsychotics and mood stabilizers is that they may not resolve the non-malignant
symptoms as rapidly as benzodiazepines and mood stabilizers [5].
Conclusions
Delirious mania and excited catatonia are often difficult to distinguish. More than 25% of
manic patients have catatonic features and meet criteria for catatonia. Also, more than 50%
of catatonic patient have features of mania. Delirious mania seems to be a more acute form
of mania that will respond to antipsychotics and mood stabilizers in the nonmalignant
stage, but not when it has progressed to malignant delirious mania. Delirious mania
patients may have catatonic features that increase with disease progression. It is unclear if
the threshold for converting from non-malignant delirious mania to malignant delirious
mania is quantitative, based on the number of catatonic features as measured by appro-
priate scales and/or on quantitative thresholds for hyperthermia and autonomic instability.
The possibility of quantifiable thresholds for the conversion from non-malignant delirious
mania to malignant delirious manic (or malignant catatonia) would benefit from future
studies. This delineation might be helpful to clinicians in assuring appropriate treatment
and it might reduce the risk of progression from non-malignant to malignant delirious
mania syndromes as classified by Fink and Taylor [3, 21]. By aiding the clinician in
achieving an early diagnosis and appropriate treatment, the prognosis of delirious mania
may be improved.
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Author Biographies
Mark B. Detweiler, MD, MS is a Staff Psychiatrist at the Salem Veterans Affairs Medical Center and anAssistant Professor of Psychiatry and Neurobehavioral Sciences at the University of Virginia.
Psychiatr Q (2009) 80:23–40 39
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Abhishek Mehra, MD is PGY-4 psychiatric medicine resident of the Carilion-University of VirginiaRoanoke-Salem Psychiatric Medicine Residency Program, Salem, Virginia.
Thomas Rowell, MD is PGY-4 psychiatric medicine resident of the Carilion-University of Virginia Roa-noke-Salem Psychiatric Medicine Residency Program, Salem, Virginia.
Kye Y. Kim, MD is the Director of the Memory Disorders Clinic at the Salem Veterans Affairs MedicalCenter and a Professor of Psychiatry and Neurobehavioral Sciences at the University of Virginia.
Geoffrey Bader, MD is the Director of the Consult Liaison Service at the Salem Veterans Affairs MedicalCenter and an Assistant Professor of Psychiatry and Neurobehavioral Sciences at the University of Virginia.
40 Psychiatr Q (2009) 80:23–40
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