Andrew Francis, MD, PhD

 has been recognized and described since antiquity. It is a brain disturbance manifested by a syndrome of diverse neuro­­psychiatric symptoms. Various terms have been used for delirium, such as acute brain disorder, metabolic enceph­alopathy, organic brain syndrome, and ICU psychosis. The DSM-IV model views delirium as an acute reversible neuropsychiatric syndrome caused by general medical conditions and/or  exogenous substances.

 DSM-IV criteria for delirium require a disturbance of consciousness or atten­tion and a change in cognition that de­velops acutely and tends to fluctuate in severity. Lipowski

 characterized de­lir­ium as a disorder of attention, wakefulness, cognition, and motor behavior.

Here we discuss the various subtypes (hypoactive, hyperactive, and mixed) of 

 and review the cases of 16 patients who met criteria for concurrent delirium and catatonia. These cases support the concept of a catatonic subtype of delirium. Our findings may have treatment implications that are yet to be determined.


 Studies of noncognitive features of delirium, such as motor activity, have led to the conceptualization of hypo­active, hyperactive, and mixed subtypes based on the salient activity pattern.

 Numerous studies over the past 20 years have attempted to define these motor subtypes of delirium. These studies show various rates of the hypoactive, mixed, and hyperactive forms using differing criteria and definitions. Some studies have found that these subtypes predict etiology, clinical course, morbidity, presence of psychosis, and other factors.

Other studies of delirium have shown evidence for neurochemical differences according to motor subtype. For example, in a study of delirium tremens, elevated cerebrospinal fluid concentrations of homovanillic acid (HVA, a metabolite of dopamine) correlated with the degree of agitation.

 A more recent study examined urinary excretion of 6-sulfatoxymelatonin (6-SMT, a metabolite of melato­nin) in patients with hypoactive delir­ium.

 Levels of 6-SMT were markedly elevated in patients with hypoactive delirium, and were reduced during recovery.

Patients with the hyperactive subtype of delirium showed an opposite pattern, with initially low levels that increased with recovery.

In addition to etiology and clinical features, the motor subtype of delirium may affect treatment response. This view is supported by an open pro­spective study of delirium treatment in 79 patients with cancer.

 The study used rating scales to monitor severity of delirium after treatment with olanzapine for 7 days. Patients with the hypoactive form of delirium showed a significantly reduced response rate (48%) compared with those who had the hyperactive subtype (83%). However, an earlier smaller study with 24 patients found no difference in the efficacy of haloperidol and chlorpromazine for delirium according to motor subtype.

 A recent review supports the concept that motor subtypes in delirium may differ and that subtyping may prove useful for clinical and research goals.

The most comprehensive recent synthesis of strategies for motor subtyping of delirium used a factor analysis to define the motor subtypes.

 The resulting hypoactive motor factor included 

•  A reduced awareness of one’s  surroundings

• Reduced alertness, withdrawal, or both

The presence of at least 2 items from this list identified the hypoactive subtype. Delirium or catatonia?


 Our hypothesis is that hypoactive (or hyperactive) forms of delirium may also be conceptualized as motor signs of catatonia. Sporadic reports suggest that signs of catatonia can be seen in delirium, but there has been no attempt to examine this question systematically using defined criteria for catatonia.

Catatonia is a well-characterized but often unrecognized syndrome with motor and behavioral signs. Among the most common signs are immobility, withdrawal, posturing, mutism, and negativism, which could be identified in hypoactive delirium. Similarly, impulsivity, mannerisms, excitement, and combativeness are signs of catatonia that may be associated with hyperactive delirium. Establishing the existence of a catatonic subtype of delirium may have implications for treatment, since patients with catatonia respond well to high-potency benzodiazepines, which are generally avoided in the treatment of delirium.

 Catatonia may worsen or progress to neuroleptic malignant syndrome with butyrophenones (such as haloperidol), which are frequently administered for delirium.

In the DSM schema, delirium requires the recent onset of disturbed consciousness with altered cognition, a fluctuating course, and a medical cause.

 While these criteria do not overlap with catatonia, other nondiagnostic motor and behavioral aspects of delirium appear in rating scales and models of hypoactive and hyperactive subtypes. Some of these parallel the Bush-Francis Catatonia Rating Scale (BFCRS) signs of catatonia of which 2 are required for diagnosis: excitement, stupor, mutism, staring, catalepsy, grimacing, echolalia/echopraxia, stereotypy, mannerisms, verbigeration, rigidity, negativism, “waxy flexibility,” and withdrawal.

 The Table summarizes this concordance for hypoactive delirium.


 We recently encountered 3 hospitalized medical patients who had delirium with signs of catatonia. We reported these cases and reviewed earlier reports and available literature that addresses instances in which catatonia accompanied delirium. We sought to determine whether the episodes of delirium would meet clinical (DSM-IV) or research criteria using the BFCRS for catatonia.

 DSM-IV criteria for catatonia secondary to a medical condition (293.89) require an identified medical or toxic cause as well as presence of at least 1 of 12 signs of catatonia. According to DSM guidelines, recognition of catatonia is not allowed in the presence of delirium. However, we have found no empirical basis for this exclusion, which has been refuted.

Research criteria based on the BFCRS require presence of at least 2 signs of the initial 14 from among 23 possible signs, which are operationally defined by this anchored scoring instrument. This rating scale is well validated, has high interreliability, and is sensitive to treatments.

Our method was based on 3 approaches to identify delirium with catatonic features: use of the BFCRS on published case reports of delirium, reassessment of our earlier review of 20 clinical reports of drug-induced catatonia for signs of concurrent delirium, and summation of our 3 recent cases of delirium with the BFCRS.

The literature review yielded 6 case reports of delirium with sufficient detail to determine the presence of multiple signs of catatonia on the BFCRS (mean 4.7, range 2 to 7). In all 6 cases, catatonia was attributed to recent benzodiazepine cessation: symptoms improved with drug repletion. Reanalysis of our review of 20 published cases of drug-induced catatonia yielded 7 additional cases in which delirium and catatonia co-occurred. Of these, 6 were induced by disulfiram and 1 by corticosteroids. For these 7 cases, ratings with the BFCRS showed a mean of 5.3 signs of catatonia (range  2 to 12).

Finally, the 3 recent medical patients seen on our psychiatry consultation service who had DSM-IV delirium were concurrently rated using the Delirium Rating Scale-Revised (DRS-R), Mini-Mental State Examination (MMSE), and the BFCRS.18,19 The 3 patients met DSM-IV criteria for delirium simultaneously with the DSM-IV and Bush-Francis criteria for catatonia. They showed 5, 7, and 11 BFCRS signs of catatonia, respec-tively. The DRS-R, MMSE, and BFCRS scores are summarized in Figure 1.

A summary of the 13 cases from the literature along with the 3 new cases reveals the frequency distribution of catatonic signs of retarded catatonia typical of that seen in psychiatric in­patients without delirium (shown in Figure 2).

We previously reported the emergence of simultaneous catatonia and delirium in 2 patients who had received electroconvulsive therapy (ECT).10

The first patient was a 41-year-old woman with schizoaffective disorder, who had been treated with several psychi­atric medications (including haloperidol decanoate) and who had had a recent epi­sode of pneumonia.

Her presenting symptoms were auditory hallucinations and suicidal ideation. Dosages of sodium divalproex, paroxetine, and benztropine were tapered in preparation for ECT. Clonazepam was also tapered off and discontinued over 2 weeks. Ris­peridone was started and titrated to 4 mg daily; mirtazapine was added at 15 mg daily. The interval between the last benzodiazepine dose and the start of ECT was  16 days.

A day after the fourth ECT session, the patient was found immobile, confused, and disoriented. She was rigid, mute, stared vacantly, and refused to eat or drink. She had ambitendency and cata­lepsy. She was afebrile but tachycardic. She was incontinent of urine and feces. Clinical diagnoses of catatonia and post-ECT delirium were made. Risperidone was discontinued.

The catatonia resolved with multiple 
 1-mg doses of lorazepam IM. ECT was discontinued. The patient reported a decrease in the auditory hallucinations, and olanzapine was prescribed at 5 mg daily. She was discharged from the hospital 1 week later after symptoms had resolved.


 To date, we have identified 16 patients who met criteria for concurrent delirium and catatonia. Their cases support the concept of a catatonic subtype of delirium. All 16 met DSM-IV and Bush-Francis criteria for catatonia, and they showed a mean of 5.5 (range 2 to 12) signs of catatonia on the BFCRS. The number of BFCRS signs and the severity scores were well within those typical of hospitalized psychiatric patients who present with catatonia.

In cases where benzodiazepine cessation was implicated, resumption of therapy resulted in resolution of the catatonia among these patients with concurrent delirium and catatonia.

Insufficient data are available about the frequency of catatonic features in delirium, or the treatment implications of this co-occurrence. Based on the case series of 3 new patients, there may not be a relationship between severity of the delirium (MMSE or DRS-R-98 score) and the severity of catatonia (BFCRS score). We are planning a study of prevalence of signs of catatonia among medical patients with delirium. Meanwhile, we seek to alert clinicians to the preliminary findings that some patients with delirium may show prominent catatonic features. These findings have treatment implications that are yet to be determined.

Drugs Mentioned in This Article
Benztropine mesylate oral (Cogentin)
Chlorpromazine (Largactil, Thorazine)
Clonazepam (Klonopin, Rivotril)
Disulfiram (Antabuse)
Divalproex (Epival, Depakote)
Haloperidol (Haldol)
Lorazepam (Ativan)
Olanzapine (Zyprexa)
Paroxetine (Paxil)
Risperidone (Risperdal)

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2. Lipowski ZJ. Delirium: Acute Brain Failure in Man. New York: Oxford University Press; 1990.
3. Meagher D, Moran M, Raju B, et al. A new data-based motor subtype schema for delirium. J Neuro-
psychiatry Clin Neurosci. 2008;20:185-193.
4. Banki CM, Molnar G. Cerebrospinal fluid metabolites in delirium tremens. Psychiatr Clin (Basel). 1981; 14:167-177.
5. Balan S, Leibovitz A, Zila SO, et al. The relation between the clinical subtypes of delirium and the urinary level of 6-SMT. J Neuropsychiatry Clin Neurosci. 2003;15:363-366.
6. Breitbart W, Tremblay A, Gibson C. An open trial of olanzapine for the treatment of delirium in cancer patients. Psychosomatics. 2002;43:175-182.
7. Breitbart W, Marotta R, Platt MM, et al. A double-blind trial of haloperidol, chlorpromazine and lorazeÂ­pam in the treatment of delirium in hospitalized AIDS patients. Am J Psychiatry. 1996;153:231-237. 
8. Stagno D, Gibson C, Breitbart W. The delirium subtypes: a review of prevalence, phenomenology, pathophysiology, and treatment. Palliat Support Care. 2004; 2:171-179.
9. Hauser P, Devinsky O, De Bellis M, et al. Benzodiazepine withdrawal delirium with catatonic features. Arch Neurol. 1989;46:696-699.
10. Malur C, Francis A. Emergence of catatonia during ECT. J ECT. 2001;17:201-204.
11. Alilci-Evcimen Y, Breitbart W. An update on the use of antipsychotics in the treatment of delirium. Palliat Support Care. 2008;6:177-182.
12. White DA, Robins AH. An analysis of 17 catatonic patients diagnosed with neuroleptic malignant syndrome. CNS Spectr. 2000;5:58-65.
13. Bush G, Fink M, Petrides G, et al. Catatonia, I: rating scale and standardized examination. Acta Psychiatr Scand. 1996;93:129-136.
14. Francis A, Malur C. Delirium or catatonic disorder due to a medical condition: reply to Dr Conrad Swartz. J ECT. 2002;18:168.
15. Francis A. Update on catatonia. Psychiatric Times. 2006;23:23-24.
16. Lopez-Canino A, Francis A. Drug-induced catatonia. In: Caroff S, Mann S, Francis A, Fricchione G, eds. Catatonia. Washington, DC: American Psychiatric Press; 2004:129-140.
17. Lopez-Canino A, Garro B, German M, et al. Delirium With Catatonic Features: A New Sub-Type? Washington, DC: American Psychiatric Association; 2008. 
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 20. Clarifying confusion: the confusion assessment method. A new method for detection of delirium. Ann Intern Med.1990;113:941-948.
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Articles

Delirium has been recognized and described since antiquity. It is a brain disturbance manifested by a syndrome of diverse neuro­­psychiatric symptoms. Various terms have been used for delirium, such as acute brain disorder, metabolic enceph­alopathy, organic brain syndrome, and ICU psychosis.

Delirium With Catatonic Features: A New Subtype?

Since its initial description by Kahlbaum (1828-1899)

 over a century ago, catatonia has been associated with psychiatric, neurologic, and medical disorders. Contemporary authors view catatonia as a syndrome of motor signs in association with disorders of mood, behavior, or thought. Some motor features are classic but infrequent (eg, echopraxia, waxy flexibility) while others are common in psychiatric patients (eg, agitation, withdrawal), becoming significant because of their duration and severity. Catatonia may be subtle and overlooked, which perhaps accounts for former reports suggesting a declining incidence. With renewed recent attention, catatonia is increasingly recognized; several reports of systematic screening in psychiatric admissions find an incidence of 7% to 17%.

After Kahlbaum, catatonia was associated with schizophrenia by Kraepelin (1855-1925) and Bleuler (1857-1939). This notion continued in the 

 series, despite reports linking catatonia to affective disorders

 now recognizes catatonic schizophrenia (295.3x), catatonia due to a general medical condition (293.89), and catatonia secondary to mania or major depression (these lack specific diagnostic codes).

Some authors have advocated a separate nosology for catatonia.

 This argument is based on the provisional nature of a diagnosis of catatonia, since it can be associated with metabolic, toxic, neurologic, or psychiatric conditions while appearing similar in features. In addition, the treatment of catatonia is different from that of other major psychiatric disorders. It typically responds well to lorazepam and related benzodiazepines as well as electroconvulsive therapy (ECT), and it may be precipitated or worsened by antipsychotic medications.

 nosology is that catatonia due to a general medical condition (293.89) is disallowed for an episode that occurs exclusively during the course of a delirium. The 

 requisite of assessing consciousness/attention and cognition is problematic in the usually mute catatonic patient.

Another nosologic debate is whether neuroleptic malignant syndrome (NMS) and serotonin syndrome are forms of malignant catatonia.

 These syndromes share many clinical features with catatonia, and recent reports show autonomic disturbances in catatonia, highlighting the clinical overlap. A systematic review of defined NMS cases showed 15 of 16 with catatonia, and severity ratings of NMS correlated with the number of catatonic signs.

 may treat both catatonia and NMS. The advent of specific rating scales for NMS should allow for systematic research as to its treatment and clinical similarity with catatonia.

The relationship of catatonia to other motor disorders, particularly Parkinson disease, has also been addressed. Two reports found catatonia could be separately identified by divergent scores on parallel ratings of Parkinson disease and catatonia scales in elderly patients with either schizophrenia

 Of note in the latter study, apomorphine improved symptoms of Parkinson disease without affecting catatonic symptoms.

In routine practice, the diagnosis of catatonia can be difficult. Operational definitions for catatonic phenomena have not been well described. In addition, there is debate in the research literature about the number of signs necessary and sufficient to diagnose catatonia, with a range of 1 to 4 signs.

, the number of motor signs required to meet criteria for catatonia varies with the primary diagnosis. For catatonia secondary to a general medical condition, only 1 motor sign is needed; for the other diagnoses, 2 signs are required.

 does not define these signs well, lacks guidelines about the severity required, and offers a probably incomplete list of signs (only 12 signs are given in the criteria for catatonic schizophrenia). Our group developed a 23-item rating scale (Bush-Francis Catatonia Rating Scale [BFCRS]) that operationally defines each catatonic sign, rates its severity, and provides a standardized schema for clinical examination. A case is defined by the presence of at least 2 of the first 14 items from this scale as shown in the 

Reliability of the BFCRS depends on the use of its companion standardized examination procedure.

 This protocol allows rapid and systematic examination, which facilitates monitoring treatment response, which may occur within hours or less. This scale has been confirmed as highly reliable and sensitive to clinical change.

 Other catatonia rating scales have been published and generally correlate well.

 Although the BFCRS has proved useful and practical for clinical and research purposes, the comparative clinical use of these scales is not well established.

Once catatonia is recognized, the clinician should consider psychiatric catatonia as a matter of exclusion, especially with unfamiliar patients or new onset. A variety of systemic, neurologic, and toxic conditions may produce a catatonic syndrome. Catatonia arising from psychiatric illness and that secondary to general medical conditions or toxicities shows a similar pattern and severity of catatonic signs.

The laboratory workup should vary based on clinical factors. Brain imaging is encouraged, since strokes, hematomas, and space-occupying lesions can all present with new-onset catatonia

 and such patients may worsen if exposed to prolonged treatment with benzodiazepines. Other tests to consider include blood chemistries, hematology, electroencephalography, toxicology, and possibly lumbar puncture. The scope of investigation will depend on the age of the patient, psychiatric history, severity and duration of the catatonic state, and the promptness of response to initial treatment.

No specific genetic, pathologic, neurochemical, or structural mechanisms have been elucidated in catatonia, although promising information is becoming available.

Familial clustering of catatonia suggests a genetic component that lacks classic Mendelian inheritance. For example, in a study of 25 catatonia patients, Barnes and colleagues

 found familial clustering in probands with overt psychiatric disorders as well as in patients whose catatonia appeared idiopathic or associated with a general medical condition. Molecular studies of periodic catatonia show familial aggregation and initial evidence for genetic linkage to chromosome 15.

Neurochemical studies in catatonia have focussed primarily on dopamine and -aminobutyric acid (GABA).

 Attention has been directed to these systems because of clinical similarities between catatonia and basal ganglia disorders in which these transmitters are implicated. In addition, effective biologic treatments, such as amobarbital, benzodiazepines, and ECT, have direct or indirect actions on these neurochemical systems. Northoff

 found elevated levels of the dopamine metabolite homovanillic acid in a series of inpatients with catatonia, and higher levels predicted a positive initial response to lorazepam during the first 24-hour period of treatment. Anecdotal reports of a positive treatment response to zolpidem, which shares strong GABA-A agonism with lorazepam, led Carroll

 to hypothesize a role for GABA-A receptor dysfunction in catatonia.

The treatment response in catatonia is typically one of complete resolution. Benzodiazepines and ECT are the most recommended modalities in current usage. Amobarbital has a longer history of clinical use, dating from the early 1930s. Only 1 randomized placebocontrolled double blind trial for initial treatment has been published.

 This study of 20 mute patients compared intravenous amobarbital with saline infusions in a crossover design. There was no change among 14 saline trials, but 10 of 20 patients responded to amobarbital (scores on a 5-point arousal scale improved 56% within 10 minutes).

In an open trial with 13 acute catatonic patients, Bush and colleagues

 reported that 2 mg of intravenous lorazepam reduced catatonia scores on the BFCRS by 60% within 10 minutes. Numerous case series and prospective open trials over the past 20 years with parenteral or oral benzodiazepines such as lorazepam show a response rate of 60% to 80% within hours or days, but there are no published randomized controlled trials for acute catatonia.

 Despite this, the consistent response in these studies along with extensive clinical experience has led to a consensus favoring benzodiazepines as initial treatment. A parenteral benzodiazepine challenge has been encouraged as initial treatment for catatonia.

Although amobarbital has not been directly compared with benzodiazepines for initial treatment of catatonia, arguments favoring benzodiazepines include familiarity in contemporary psychiatric practice, a favorable therapeutic index, and the availability of flumazenil, a specific antagonist for benzodiazepines. (Of note, the salutary effect of lorazepam was reversed by flumazenil in a case of catatonic stupor and mutism.

Recent prospective open trials show that marked improvement or complete resolution of catatonia will occur in 60% to 80% of cases within hours or a few days with lorazepam and related benzodiazepines. Initial dosages of 2 to 6 mg of lorazepam per day are recommended by any route of administration, but some patients may require titration to higher doses ranging from 12 to 16 mg daily. Prolonged trials of benzodiazepines are not advised for severe catatonia, since complications such as dehydration, decubitus ulcers, and embolic events have been reported in this situation.

Benzodiazepines appear effective for catatonia attributed to psychiatric illness, neuroleptic toxicity, and a variety of other conditions. Age, sex, and severity of catatonia do not appear to predict treatment response,

 but comorbid schizophrenia may predict a less robust effect.

 Since these comorbid disorders cannot be reliably assessed in mute catatonic patients, specific treatment may be delayed until resolution of the catatonic state. Chronic catatonia associated with schizophrenia may be poorly responsive to lorazepam added to antipsychotics.

Convulsive therapy has both a historical tradition and modern support as a treatment for catatonia. In the 1930s, the use of both chemically induced and electroconvulsive seizures was described. Since then, clinical experience and case series have shown that ECT produces remission of catatonia even when other treatments such as amobarbital or lorazepam have failed.

 An additional advantage of ECT is its effectiveness for both the catatonic syndrome and the frequently associated affective or psychotic disorders. Clinical reports suggest that ECT and lorazepam are synergistic in the treatment of catatonia.

The available literature on antipsychotics in the treatment of catatonia is inconsistent and suggests caution. Several clinical reports show that the older highpotency agents, such as haloperidol or second-generation antipsychotics, failed to improve catatonia, induced or worsened catatonia, or led to progression from catatonia to NMS.

 In contrast, other case reports suggest risperidone or other second-generation antipsychotics may be beneficial.

 One report reanalyzed data from clinical trials of schizophrenia, using 3 items from the Positive and Negative Symptom Scale as a retrospective proxy for catatonia, and suggested modest treatment benefit of olanzapine after 6 weeks.

Only 1 randomized double-blind study involving antipsychotics in catatonia has been published.

 In this study, 14 of 68 nonaffective catatonic patients in whom a trial of lorazepam failed were randomized to receive risperidone plus sham ECT (n = 6) or bilateral ECT plus placebo (n = 8). Scores on the BFCRS declined more than 90% with ECT and approximately 50% with risperidone after 3 weeks.

The inconclusive literature on antipsychotics has led to an expert consensus favoring initial treatment with lorazepam and consideration of ECT for refractory or severely compromised cases if lorazepam fails after a period of days. Unfortunately, ECT may not be available, leading the clinician to consider use of second-generation antipsychotics. In this situation, Rosebush and Mazurek

 envision a cautious trial of these agents with continued benzodiazepines and careful monitoring for worsening catatonia or signs of NMS.

Use of antipsychotic agents in the treatment of malignant catatonia (an uncommon severe variant characterized by extreme agitation, fever, and other autonomic disturbances) is also not recommended because of the risk of exacerbation. In this setting, prompt use of ECT has been advocated.

Catatonia is a distinct neuropsychiatric syndrome that is becoming more recognized clinically and in ongoing research. It occurs with psychiatric, metabolic, or neurologic conditions. It may occur in many forms, including NMS. Treatment with benzodiazepines or ECT usually leads to a dramatic and rapid response, although systematic randomized trials are lacking. An important unresolved question is the role of antipsychotic agents in treatment and their potential adverse effects.

Dr Francis is professor of psychiatry in the department of psychiatry and behavioral science at the health sciences center of the State University of New York at Stony Brook.

Dr Francis reports that he has no conflicts of interest concerning the subject matter of this article.

Amobarbital (Amytal) 
Apomorphine (Apokyn) 
Flumazenil (Romazicon) 
Haloperidol (Haldol) 
Lorazepam (Ativan) 
Olanzapine (Zyprexa) 
Risperidone (Risperdal) 
Zolpidem (Ambien)

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Since its initial description by Kahlbaum (1828-1899) over a century ago, catatonia has been associated with psychiatric, neurologic, and medical disorders. Contemporary authors view catatonia as a syndrome of motor signs in association with disorders of mood, behavior, or thought. Some motor features are classic but infrequent (eg, echopraxia, waxy flexibility) while others are common in psychiatric patients (eg, agitation, withdrawal), becoming significant because of their duration and severity.

Author | Andrew Francis, MD, PhD

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