FEATURE ARTICLE

m Psychiatry. 20lO:17(4):41-47

The Pharmacotherapy of Catatonia

Brendan T. Carroll, MD, Joseph W.Y. Lee, MBBS, MRCPsych, FRANZCP, Francisco Appiani, MD,
and Christopher Thomas, PharmD, BCPP

ABSTRACT
FOCUS POINTS
Catatonia is an important clinical syndrome that occurs in affec-
Multiple pharmacologie agents have been used in the
tive, psychotic, autistic, developmental, and medical disorders. treatment ot catatonia,
The pharmacotherapy of catatonia is complex because of multiple The proposed pattiophysiology nt catatona involves gab-
aergic, dopaminergic. glutamatergic, and other neiiro-
and varied ttierapeutic agents. The proposed pathophysiology of
chemical systems.
catatonia includes: y-aminohutyric acid (GABA)/^ hypoactivity dopa- The primary treatments tor catatonia have mechanisms
mine-2 hypoactivity. glutamate W-methyl-o-aspartate hyperactivity. of action that involve one or more of these neurochemical
systems,
serotonin-2 hyperactivity. and choiinergic hyperactivity. The pharma-
The alternative pharmacologie treatments ot catatona are
cotherapy of catatonia includes henzodiazepines. CABA promoters. important when benzodiazepmes and electroconvulsive
certain anticonvulsants. glutamate inhibitors, and second-generation therapy are not ettective treatment options.

antipsychotics. The role of first-generation antipsychotics remains The application of pharmacologie treatment tor catatona
is illustrated in case vignettes.
unclear Catatonia. a treatable syndrome, occurs in a variety of psy-

chiatric, medical, and neurologic illnesses. Physicians may benefit

from learning about these pharmacologie treatment options.
INTRODUCTION
The clinician should approach cataronia as a diagnosable
;iiid treatable disorder. One approach is that catatonia is a
psychiatric disorder and the clinician should treat the primary
psychiatric disorder.' However, another view is that, since cata-
tonia \s found in non-psychiatric medical disorders, it is a
neuropsychiatrie illness and treatment should focus on the
medical disorder' The authors of this article favor the concept
of catatonia as a neuropsychiatrie syndrome with an identified
set of etiologies, core features, pathophysiology, and treatment
response.* Catatonia constitutes a neurobiologie syndrome
and is a constellation of symptoms reliably associated with
disturbance that Is functional, structural, neurochemical, or
neuropathologic in a circumscribed structural location or
neural circuit. The clinician is charged with the detection and
diagnosis of catatonia. Thus, when catatonia becomes the focus
oi treatment, there is an urgent need to explore the different
pharmacologie treatments. This heuristic approach may be
helpfiil in many ca.ses where the clinician begins with treatment
and works baekwards toward diagnosis.
MECHANISMS OF CATATONIA
There are multiple theories rq^arding the neuroehemical
etiology for catatonia. This article provides a brief mechanistic

Or Carrol! is clinical assistant professor of Psychiatry 3t Ohio University College ot Ostopathie Medicine in Athens, arjd chief of Psychiatry Service at the Chlllicnthe Veteran's Aftairs (VA) Medical Center in Ohio,
Or I ee IS clinical associate pmfessoi al the University ct Western Australia m Perth. Or. Appian is assistant prnfessor ol Pharmacology at Universiriad de Buenos Aires. Facultad de Medicina, and Oirectai ot Ihe
Association tor the Study and Develogment of the Neumsciences m Buenos Aires. Afgentma Dr Thomas is clinical pharmacy specialist m Psychiatry at the Chillicothe VA Medical Center.
Oisnlosun;: Df Carroll is a consultant to Neurotepltc Malignant Syndrame tniormation Service; is on the speaker s bureaus ot AhbotI, AslraZeneca, Bnstol-Mycrs Squibb, Eli Lilly, Forest Laboratories, Pfi?er, and
tanssen. and leceives granl support from Ptizef. Or, Lee is consultant to EJi Lilly and Plizer. and is on the speaker s bureaus and receives grartt support tn3m Janssen-Cilag. Or. Appiani reports no attiliation mth
Of ttnancial interest m any organisation that ma/ pose a conflict of interest, Dr Thomas is on the speaker's bureau of AstraZeneca.
Please direct all correspondence tO: Brendan T Carroll, MO, Chief, Psychiatiy Service, MHCL, ChiKicothe VA Medical Center, 116A, 17273 State Route 104, Chillicothe, OH 45601, Tel 740-773-1141 i;7871:
Fax 740-772-7179; E-mail, btcartollI0cs.com.

Prtmary Psychiatry 41 AprtI 2010

 B.T. Carroll, J.W.Y. Lee, F. Appiani, C. Thomas

overview of catatonia; a tnore cotnprehensive review of specific
theories of catatonia can be found elsewhere.' In general, there
ate three major theories, naJiiely, dopaminc hypoactivity, y-aini-
nobutyric acid {GABA) hypoactivity, and glutamate hyperactiv-
ity,'' along with the two minor theories of serotonin hyperactivity
and cholinergic hyperactivity.'^ Dopamine (D) hypoactivity,
specifically at the Di receptor, is thought to be the predomi-
nate niechatiism that leads to catatonia. To flirther support the
hypoactive D-> receptor theory, several case reports exist that
demonstrate a relationship with high-potency typicaj antipsy-
chotics either causing or worsening catatonia. This phenomenon
is ioiown as neuroleptic-induced catatonia (NIC). The decrease
in activity at the Di receptor then causes an abundajit release
of glutamate, the major excitatory neurotransmitter, hence, the
physiologic attempt to increase dopamine activity via glutamate.
Glutamate is known to regulating the catecholamine release and
is directly involved in dopamine regulation. ' However, glutamate
is known to be excitotoxic, thereby, causing neuronal damage,
and may produce symptoms similar to catatonia.'"' GABA, the
major inhibitory neurotransmirter in the central nervotis system,
has an inverse relationship wirh glutamate. In environments
with high glutamate, GABA acts ro shur down glutamate release.
Therefore, to further support the high glutamate activity and
hypodopamine receptor theory, drugs that potentiate GABA
(benzodiazepines) or act as GABA agonists (anticonvtilsants) will
have a benefit in treating catatonia.
These general neurochemicai theories are supported by
pharmacologie treatment because clinical studies of neuro-
chemicai mechanisms are difficult to obtain in these patients.
These mechanisms will be reviewed further in the pharmaco-
therapy section of this article. Animal studies of catalepsy do
provide some information on the actions of pharmacologie
agents. However, there is no suitable model for catatonia in
humans. Electroconvulsive therapy has been a very important
treatment for catatonia and also contributes to these neuro-
chemicai theories.
Ftirthermore, catatonia is not a unitary syndrome and there
may be subtypes that respond favorably to one type of medi-
cation. Gatatonia is probably a heterogeneous condition with
subtypes different in treatment responses and pathophysiol-
ogy. Therefore, multiple agents may be required to not only
treat acute catatonia, but maintain or prevent the reoccur-
rence of chronic catatonia.
types. Patients who present in an acute psychiatric setting and
fora follow-up appointment in an outpatient clinic may both
meet Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition," criteria for the catatonia specifier. However,
there are differences in the level of functional impairment and
the severity of the syndrome (Table I). This separation may
help in selecting treatment for patients with catatonia.'
RATING SCALES FOR CATATONIA
Glinicians detect and diagnose catatonia with greater fre-
quency with the use of a larger number of catatonic signs and
a rating scale for catatona.'" " Furthermore, the treatment of
caratonia is enhanced by the use of a rating scale handled by
an experienced clinician with skill in administering the cho-
sen rating scale. Rating scales include: one by Rosebush and
colleagues,'- the Modified Rogers Scale,'* the Bush-Francis
Gatatonia Rating Scale,'' the Northoff Gatatonia Scale,''^
the Braunig Gatatonia Rating Scale,"' and the KANNER
Gatatonia Rating Scalc.'^ Garroll and colleagues' provide a
review of catatonia rating .scales. In North America, the Bush-
Francis Gatatonia Rating Scale is used most frequently.''
THE CATATONIC DILEMMA
Gatatonic signs may appear or worsen with antip.sychotic
pharmacotherapy."* This "catatonic dilemma" illustrates the
role of dopamine blockers on the pathogenesis of catatonia.
NIG has been described with Hrsr-generation antipsychotics
(FGAs) and, albeit less frequently, with second-generation
antipsychotics (SGAs). SGAs tend not to worsen catatonia
and have been recommended. NIG may emerge during
pharmacologie treatment and can mimic acute or chronic
catatonia. Thus, the physician may need to obtain a history
TABLE 1
ACUTE VS. CHRONIC CATATONIA
Measure of moairment Acute Chronic
Catatonic signs Greater Fewer
Nutritional compromise More likely Less likely
Dehydration More likely Less likely

Autonomie instability More common Less common

TYPES OF CATATONIA Urgent status Inpatient Outpatient or residential

Gatatonia is derived from a term for "tension insanity" Medical complications More likely Less likely
by Kahlbaum and colleagues.*' Since this original descrip- Recent diagnostic procedures More likely Less likely
tion, additional signs have been observed and described by
Impairment in ADLs More severe Less severe
Dhossche and colleagues.^ Physicians working in different
settings may encounter different forms of catatonia. A heu- AOLs=activ!ties ot dailiy living.
ristic approach is to classify catatonia into acute and chronic Carroll BT. Lee JWY, Appiani F, Thomas C. Primary Psychiatry. Vol 17, No 4.200,

P^vchi^trv 42 April ?010


of all mods administered and even toxicology for occult HGAs
and SCiAs.''' This modetn "catatonic dilemma" must be con-
sidered by the clinician in a case by case basis.
PHARMACOTHERAPY
Carroll and colleagues-^" and Lee and Carroll'' reviewed
several authoritative texts and review articles on the subject
of catatonia response. They divided the drugs into their
known classes and identified their mechanism of action. They
also reviewed 49 cases that were rated with the Bush-Francis
Rating Scale as part of clinical care at a neuropsychiatrie
institution between iyy5 and 2005/ Thirty-five patients
(66%) met the de.scription of schizophrenia with catatonic
features, l'en patients (19%) had catatonia due to a general
medical condition. Bipolar and unipolar mood disorders were
a minority (fout patients; 9%). Some improvement in catato-
nia and function occurred with medication treatment in 16
of the 49 cases. This included: SGAs (two), clozapine (two),
lorazepam (iour), broinocriptine (one), memantine (adjunct;
six), and memantine (monotherapy; one).*"
Meanwhile, Lee and CarrolH' reviewed treatments used in
71 episodes of catatonia (58 acute, 13 chronic) with schizo-
phrenia (according to the DSM-IV; most of them were seen in
two psychiatric intensive care facilities respectively irom 1996
lo 2002).' All met restrictive criteria \ox catatonia according to
Rosebush and colleagues" and Lohr and Wisenewski.'' They
were first treated with benzodiazepines {oral lorazepam or
inrianiuscular clona/.epani). I hose who failed benzodiazepines
icceived other treatments for their catatonic symptoms. The
efficacy of benzodiazepines in acute catatonia in schizophre-
nia was seen in 40 of 58 episodes (69%). [Respite the decent
icsponse In acute catatonia, this response was not sustained and
catatonia returned in the majority of patients. The response
TABLE 2
TREATMENT OF SCHIZOPHRENIA ANO CATATONIC FEATURES'^
Use Rationale
FGAs Often usedtor Sciizopirenia Controls positive sympfoms,
such as hallucinations and
delusions
SGAs Beneficial in catatonia Low D^ blockade is less likely
to worsen catatonia
BZDs Lrazepam and other 62Ds are Can be added to FGAs or SGAs
helpful in acute catatonia
ECI Beneficial in malignant catatonia Effective in catatona and
FGAs=first-gefieration antipsychotics; NMS=neuroleptic malignant syndrome; NIC=neuroleptic-induced catatonia; SGAs=second-generation a nti psychotic s ; D=dopamine;
BZDs=benzod3zepines; ECT=e!ectroconvulsive therapy,
Carroll BT, Lee JWY, Appiani F, Thomas C. Primary Psyctiiatry. Vol 17, No i. 2010,
imary Psychiatry 43
The Pharmacotherapy of Catatonia
rate in chronic catatonia in schizophrenia with benzodiazx'pines
was 8%, thus, a much lower response rate versus response in
acute catatonia. Response rates with amantadine, selegeline,
lithium, and SGAs occurred in nine of 13 (69%), yielding a
response rate similar to benzodiazepines in acute catatonia/'
These diverse medications have been reported to help improve
catatonia ('lables 2-6; Figures 1-4). Ixirazepam and other
GABA,\ promoters (ie, benzodiazepines, zolpideni) increase
GABA activity as their mechanism of action. Anticoiivulsants
may be helpful by increasing activity at GABA or modest anti-
gkitaminergic effects witb some reports of benefit from carbani-
azepine ;md valproic acid. In neuroleptic-induced catatonia an
anticholinergic might be helpful, suggesting a role for the choHn-
ergic system in catatonia. Clozapine and other SGAs have been
reported to improve catatonia in psychosis, perhaps via a greater
"pass-though" of dopamine to the D? receptor. Perhaps the most
promising finding is that M methyl-D-aspa rtate antagonists may
improve schizophrenia with catatonic featiLres.
CASES
Case 1
Ihe authors describe the case ot a 64-year-old female
patient who came for psychiatric treatment accompanied
by her son. According to her son's description, the patient
became mute. She could not perform her usual activities, and
spent [learly the whole day in bed with akinesia. During this
time the patient lost 15 Ib and ate once a day and only if she
was assisted. The patient had a history of two depressive epi-
sodes that, according to clinical records, were mild and pro-
duced by family conflicts. She was diagnosed by her former
psychiatrist with dysthymia and was treated with vcnlafaxiiie
Benefits Risks
Well-established and less The catatoriic dilemma Catatonia is
expensive difficult to distinguish from NMS and may
worsen catatonic symptoms (NIC)
Some series suggest greater The metabolic syndrome and agranulocyto-
efficacy sis with clozapine
Safe, first line treatment fof Respiratory compromise, incoordination,
catatonia sedation, potential for abuse
Less risk of NMS, useful lor Concerns with anesthesia, informed con-
treatment refractory catato- sent and availability
nia, rapid onset of action
April 2010
 B.T. Carroll. J.W.Y. Lee, F. Appiani, C. Thomas

75 mg/day with partial response. At this time she was also arms. Head computerized tomography scan showed an old
under psychotherapy treatment. She had one venlafaxine- small infarct in the subcortical zone of the riglit frontal lobe,
induced manic episode. the diagnosis of NIC was made. After rhe initial evaluation,
This catatonic syndrome developed 10 days after the patient risperidone was stopped. Treatment with lorazepam began at
was started with risperidone 3 mg/day. In the clinical examina- 2.5 mg/day gradually titrated to 2.5 mg Bll). After 48 hours oi
tion, the patient had immobility, she answered questions only this pharmacologie treatment the catatonic symptoms began to
with 'yes" or "no", and she had a marked delay of many sec- resolve. This was especially seen in an increase on verbal fluency
onds to answer. Physical examination revealed no fever, blood and feeding habits. After 2 weeks of treatment, the patient was
pressure ot 125/75 Hg mm, and cardiac frequency oi 85 beats almost without catatonic symptoms, and in the physical exami-
per minute. She had catalepsy and cogwheel rigidity in both nation she had mild cogwheel in hoch arms. She was started on
quetiapine 25 mg/day titrated to 150 mg/day in a month. This
drug was given to treat bipolar disorder. W i tti tliib regitnen or
TABLE 3
Ul/l/f AUT
OTHER TREATMENTS FOR CATATONIA
TABLE 5
Anti- Anti-
GABA glutamate glutamate
OTHER TREATMENTS FOR CATATONIA: DOPAMINERGIC
Medication DOtenc\ f BABA effects potency effects Anti-
rlillr
Valproic Acid Strong + GABAB-P Modest Cerebral DA glutamate Anti-glutamate
a s prtate Medication potency DA effects potency effects
- GABAB - T/0
Carbidopa/ Strong DA precursor None None (worsens
-- GABA oy levodopa psychosis)
GAD, synthesis.
release and Bfomocriptine Strong D^ agonist None None (worsens
transaminase psychosis)
inhibition Amantadine Modest -t- DA trans- Weak NMDA antagonism
Carbamazepine Modest + GABAg - P Modest Inhibition ot mission (non-competitive)
glutamate (worsens psychosis)
release Memantine None None Modest NMDA antagonism
Top ira mate Modest Potentiates Strong Inhibition ot (non-cmpetitive)
GABA AMPA recep- Seiegeline Modest -t-DA Weak Possible NMDA
tors (possible via MAO-B attenuation
NMDA attenu-
ation) DA=dopamine and D? receploi subtype; -(--mcrease, NMDA=/i(-niethyl-D-aspartate (ylu-
tamate receptor subtype); MAO-B=monamine o)(idase-8 enzyme.
GABA=Y-aminobutyric acid (A and B receptor subtype); +=increase: ---decrease;
P=pfomotof. T/O=turnyEf. GAD=v-amJno decarboxylase^ AMPA=amino-3-hydroxy-5 Carroll BT, Lee JWY, Appiani F, Thomas C. Primary Psychiatry. Vol l No i. 210.
methyl-4 isoazole (glutamate receptor); NMDA=A'-mettiyl-D-a s prtale (glutamate recep-
tor subtype).
TABLE 6
Carroll BT. Lee JWY, Appiani F, Thomas C, Primary Psychiatry. Vol 17. No 4. 2010. OTHER TREATMENTS FOR CATATONIA: SGAs
Anti-Glutamate
TABLE 4 Medication OABinding DA Effects Anti-5-HT Effects
OTHER TREATMENTS FOR CATATONIA Clozapine Loose 5-HT22A Unclear
Medication GABA GABA effects Anti- Anti- Ouetiapine Loose 5-HT2,, Uncleai
notenc}! glutamate glutamate
Olanzapine Loose 5-HT22A Unclear
potency effects
Risperidone Tight 5-HT2,, Unclear
Lorazepam Strong -1- GABAA - P None None
Ziprasidone Tight 5-HT22S Unclear
Zolpidem Strong + GABAA None None
- a subunit Ar i pip razle Tight with partial 5-HT2,i Unclear
pass through agonist
Memafitri ' None ' None Modest NMDA antag-
onism (non- Amisulpride Loose D^, D3 None Unclear
competitive) (low dose)
GABA=Y-aminobutync acid (A and B receptor subtype); -(-=incr8ase; -=decfease; SGAs=secofid-genefation antipsychotics; DA-dopamirte and 2, D3 and Oj receptor sub-
P=promotor; NMDA=A(-methyl-D-aspanate (glutamate receptor subtype). type; 5-HT;,A-serotiim receptor (5-HT? subtype).
CarrollBT, Lee JWY. Appiani F, Thomas C. Primary Psychiatry. M 17. No 4 2010. Garroll BT, Lee JWY. Appiani F. Thomas C. Primary Psychiatry. Vof 17. No 4. 2010.

Primary Psychiatry 44 April 2010

 The PharTTiacotherapy of Catatonia

qiietiiipinc 150 mg/day and lorazepam 5 mg/day the patient
ifniained aiyiiipu)m.itic Un 6 months until she decided to stop
taking lorazepam. Immediately after lorazepam discontinua-
tioti the patient developed a clinical state ot mutism, akinesia
with a narked anxiety state. Lorazepam was administered again
and symptom.s resolved in hours. The diagnosis of this episode
wa.s catatonic symptoms due to benzodiazepine withdrawal.
After this episode the patient remained sthle and continued
with lorazepam S mg/day and quctiapine I "^O mg/day, witliout
catatonic symptoms. Lithium 600 mg/day was added tor the
ireatment of the bipolar disorder, with a favorable response.
Case 2
A 31-year-old female was admitted to a general hospital
with immobility, waxy flexibility, negativism, mutism, rigid-
ity, and decreased blinking. Her husband had reported that
10 days prior to the admission her behavior changed, she
acted with increased suspiciou.sness, auditory hallucinations,
and mystical delusions. She refused to drink and eat and had
episodes of impulsivity without provocation. Weight loss was
evident. The patient had no prior history of psychiatric disor-
der. She lived with her husband and three sons.
Laboratory studies were normal range except for a mild
anemia with hemoglobin 9.2 g/dl and hematocrit 32.1 %.
A slow intravenous dose of lorazepam 2 mg was initiated.
After 20 minutes of lorazepam administration the patient
started to give brief delayed responses, with perseveration,
movement improvement, exhibiting facial gestures, and giv-
ing minimal response to external stimuli.
FIGURE 3
GABA GLUTAMATE HYPOTHESIS THREE
Glutamate

FIGURE 1
Beiizodtazepmes
GABA GLUTAMATE HYPOTHESIS ONE Zolpidem
Valproate
^ Memantine

H_
CarbamazepinE ^,,-^ Amantadme
lopiramate ^,,,-^'^t Topi ram ate
L Clozapine

According to this hypothesis, pharmacologie treatment tend to restore GABA-glutamate

In non-catatonic brain there is an equilibrium between GABA and glutimate concentrations.
GABA-y-ammobutyric acid: CNS-central nervous system.
Carroll BT, Lee JWY, Appiani F. Thomas C, Primary Ps^iiiatiy. Vol 17, No 4.2010.
imbalance, decreasing glutamate transmission or increasing GABA transmission.
Decrease of dopaminergic transmission may act indireclly, increasing GABA-glutamate
imbalance.
GABA-f-aminobutyric acid; CNS=ceniral nervous system.
Caffoll BT. Lee IWY. Appiani F, Thomas C. Primary Psychiatry. Vol 17, No 4. 2010.

FIGURE 2 FIGURE 4
GABA GLUTAMATE HYPOTHESIS TWO THE GABAA-GABAB CATATONIA HYPOTHESIS

In 3 catatonic bfain, the equilibfium between GA6A and glutamate is broken and there is According to this hypothesis, ttie GABA^-GABAB imbdlance Lould be restored by agonists of GABA^
a relative decrease of gabaergic transmission and a relative increase ot glutamate. receptor like lorazepam and zolpidem. or exacerbated y GABAu antagonists like bacioferi.

GABA-Y-aniinobu(yfic acid; CNS=central nervous system, GABA^-ammobutyric acid; CNS=central nervous system,

Carroll BT. Lee JWY. Appiani F, Thomas C. Primary Psychiatry. Vol 17, No 4. 2010. Carfoll BT. Lee JWY, Appiani F. Thomas C. Primary Psychiatry. Vol 17, No 4. 2010,

'rimary Psychiatry 45 April 2010

 The Pharmacotherapy of Catatonia

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Primary Psychiatry 47 April 2010

 The Pharmacotherapy of Catatonia

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