SUMMARY Catatonia is common, and has an incidence in psychiatric A catatonic patient is more likely to be suffering from a bipolar disorder than any other

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391 ISSN 1758-2008 10.2217/NPY.13.41 © 2013 Future Medicine Ltd Neuropsychiatry (2013) 3(4), 391Œ399 SUMMARY Catatonia is common, and has an incidence in psychiatric inpatients from the USA, UK and other western countries of 10%. Half of the patients with catatonia su˜er from bipolar disorder and approximately 10% have a diagnosis of schizophrenia. With multiple possible etiologies, a unifying pathogenesis of catatonia that explains all motor and autonomic symptoms remains elusive. Early recognition is of utmost importance in order to provide optimal treatment and to decrease morbidity and mortality. Benzodiazepines are the ˚rst treatment of choice and yield high response rates, especially in the context of mood disorders. Should a treatment with benzodiazepines fail, electroconvulsive therapy should be started without delay. 1Department of Psychiatry, University Psychiatric Center Œ Catholic University of Leuven, Campus Kortenberg, Leuvensesteenweg 517, 3070 Kortenberg, Belgium 2Department of Psychiatry, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA 3Center for Psychiatry & Addiction Medicine, Szent István & Szent Laszló Hospitals, Gyali Utca 17Œ19, 1097 Budapest, Hungary 4Department of Psychiatry & Psychotherapy, Faculty of Medicine, Semmelweis University, Balassa Utca 6, 1083 Budapest, Hungary *Author for correspondence: Tel.: +32 2 7580511; REVIEW Pascal Sienaert* 1, Dirk M Dhossche 2 & Gabor Gazdag 3,4 Adult catatonia: etiopathogenesis, diagnosis and treatment Practice points Catatonia is common in psychiatric inpatients. A catatonic patient is more likely to be su˜ering from a bipolar disorder than any other disorder. Prompt recognition and treatment with benzodiazepines or electroconvulsive therapy decreases the lethality of the catatonic syndrome. Speci˚c catatonic signs should be elicited during a neuropsychiatric clinical examination. The use of a screening instrument improves the detection of catatonia. The lorazepam test validates the diagnosis of catatonia. Lorazepam 2Œ16˛mg/day is the ˚rst treatment of choice. Should lorazepam fail, electroconvulsive therapy should be started without delay.

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Neuropsychiatry (2013) 3(4) 392 The evolution of a diagnosis Catatonia is common in psychiatric inpa -tients. Prospective studies report an incidence of the catatonia syndrome among hospitalized psychiatric patients of approximately 10% [1] . Kahlbaum, in 1874, described it as a set of motor symptoms that were not tied to a speci˜c disease, but was seen both in psychotic and in mood dis -turbed patients [2] ; however, years later, Krae -pelin classi˜ed it as a form of dementia praecox [1,3] . In the ˜rst four editions of DSM, catatonia is classi˜ed as a subtype of schizophrenia. This historical decision partly explains the neglect of the catatonic syndrome and its dramatic under -diagnosis [4] . It has become clear, however, that most patients with catatonic symptoms prob -ably have medical and neurological disorders [5] . These insights have led to the addition of ‚cata -tonia secondary to a general medical condition™ in DSM-IV. Catatonic symptoms are observable in most patients diagnosed with anti-NMDAR encephalitis [6,7] , after surgical procedures [5,8] , during drug intoxication and withdrawal, and in patients with epilepsy and abnormal meta -bolic states [9] . Patients developing catatonia from a psychiatric disorder will probably suf -fer from a mood disorder, but practically any kind of psychiatric disorder can be associated with catatonia, including schizophrenia, obses -siveŒcompulsive disorder, post-traumatic stress disorder and autism [10Œ12] . Since catatonia is eas -ily recognizable and distinguishable from other conditions, pleas to the DSM-5 Work Groups for its classi˜cation as an independent, distinct syndrome have been published [1] . Catatonia has a characteristic course, as already described by Kahlbaum [2] , and an effective treatment response [13,14] . In DSM-5, the divorce between catatonia and schizophrenia is ˜nalized with the deletion of catatonia as a schizophrenia subtype. Catatonia can now be classi˜ed either as a coded speci˜er ‚with catatonia™ for all psychotic dis -orders and mood disorders, or as ‚unspeci˜ed catatonia™. The latter diagnosis means that cata -tonia can be classi˜ed as an independent syn -drome, which will hopefully fifoster recognition of the catatonia syndrome and permit research on nosology, treatment and outcomefl [1] . Catatonia in mood disorders Half of the patients with catatonia suffer from bipolar disorder [9,15] . It is not uncommon that a catatonic attack is a ˜rst episode of a bipo -lar disorder [16] . This preferential link between catatonia and mood disorders was already observed by Kahlbaum, who wrote that in most cases catatonia manifests itself in the ˜rst stages with an easily recognizable clinical pic -ture of melancholia, often preceded by mania [2] . According to Fink and Taylor, recovery occurred most often in Kraepelin™s catatonic patients in whom the episode started with a depressive phase [9] . A similar favorable outcome of a fibenign stuporfl, a finew manic-depressive reaction typefl, was observed by August Hoch in 1921 [17] . Bleuler wrote that catatonic symp -toms were, as a rule, intertwined with manic and melancholic conditions, and that they often dominate the clinical picture, in which case he spoke of a manic or melancholic catatonia [18] . Kirby observed that a catatonic phase fimay replace the depression in what appears to be a circular attackfl [16] . In more recent studies [19] , it was shown that in patients presenting with catatonic symptoms, schizophrenia is overdiag -nosed. A quarter of the patients diagnosed with the catatonic subtype of schizophrenia ful˜ll research criteria for an affective disorder. This overdiagnosis probably results from a failure to recognize mania and from a belief that cata -tonic symptoms occur only in schizophrenia [20] . In an early prospective trial of 55 consecu -tive admissions exhibiting one or more catatonic signs, only four (7%) had a diagnosis of schizo -phrenia, ˜ve (9%) had depression, whereas 34 (62%) ful˜lled research criteria of mania [21] . Approximately a third of patients presenting with manic or mixed episodes will exhibit a range of catatonic symptoms, as assessed with the Bräunig Catatonia Rating Scale [22] . Whether or not a subset of catatonic symptoms is more frequently observed in mood disorders than in other conditions remains debatable [23] ; although it has been suggested that catatonia in manic patients is typically associated with excitement [24] , whereas depressed catatonic patients present with profound motor retarda -tion and catatonic inhibition, automatic obedi -ence, and, less frequently, waxy ˚exibility [9] . The prognosis of catatonia is good, regardless of the underlying cause and the number or pat -tern of catatonic features, but it is even better in mood disorders [9] . Conversely, the presence of catatonic symptoms may indicate a more severe course of the bipolar disorder as cata -tonia is associated with longer hospital stays, more comorbidities and more suicide attempts in manic patients [22] .

PAGE – 3 ============ 393Catatonia in schizophrenia Approximately 10Œ20% of patients with catato -nia meet the criteria for schizophrenia [9,15] . In a Croatian sample of 402 schizophrenic patients, 15% had a diagnosis of schizophrenia, catatonic type [25] . In a random sample of 225 Chinese patients with chronic schizophrenia, a third met stringent criteria for catatonia [26] , and 80% of patients exhibited at least one catatonic symp -tom [27] . Some authors suggest that abnormal movements, mannerisms, stereotypes, catalepsy, negativism, automatic obedience and waxy ˚ex -ibility are, more than other catatonic signs and symptoms, associated with schizophrenia [24] , but con˚icting results show that there is no clear and distinct catatonic picture accompanying schizophrenia [26,28] . Catatonic features indicate a generally poor prognosis in the chronic phase of schizophrenia [26] . Catatonic subjects have a signi˜cantly earlier age of onset [25,26] , more negative symptoms [26] , exhibit more aggressive behavior and are more often hospitalized [25] . Moreover, the catatonic type of schizophrenia seems to be more genetically determined than other subtypes [25,26] . Huang and colleagues have postulated the existence of an acute and chronic type of catatonia [29] . The acute form is linked to mood disorders, and has a mean dura -tion of less than 2 weeks; whereas the chronic form lasts longer than 3 weeks and suggests an underlying schizophrenic condition. Malignant catatonia The most severe form of catatonia is malig -nant catatonia [30] . Although already observed in the ˜rst half of the 19th century [31,32] , the ˜rst widely known description of the syndrome originates from Stauder in 1934, who deemed it to be always fatal, calling it ‚lethal catatonia™ [33] . Although malignant catatonia is a serious medical condition, mortality is reduced with adequate treatment. Malignant catatonia is a hetero geneous syndrome. Psychomotor excite -ment, fever, altered consciousness, muscle rigid -ity and disturbance of autonomic regulation are the most characteristic symptoms. The excited phase usually results in exhaustion, stupor, cardio vascular collapse and death. In some cases psychomotor excitement alternates with stuporous episodes. This was the typical course of malignant catatonia described in reports from the preantipsychotic era [34] . Less frequently, in approximately 10% of reported cases, the course is primarily stuporous, without a preceding phase of motor excitement. This form is very close to what is observed in neuroleptic malignant syn -drome, which is considered by several experts to be a drug-induced form of catatonia [35] . The widespread use of antipsychotics from the 1950s seemed to have decreased the frequency of malignant catatonia in general, but gave birth to a new subtype, an antipsychotic drug-induced stuporous form of malignant catatonia [36] . An extensive review of all published cases revealed that malignant catatonia can appear in asso -ciation with diverse psychiatric, neurological and medical conditions, such as paraneoplastic conditions and autoimmune diseases [37] . The syndrome is, however, most frequently associ -ated with schizophrenia and bipolar disorder. The mortality rate of malignant catatonia, which was above 75% in the preantipsychotic era [38] , has decreased to 14% in the last 25 years. The most important step in decreasing the lethal -ity of the syndrome is its prompt recognition and early effective treatment of the severe auto -nomic imbalance, as well as the frequent medical complications. Etiopathogenesis of catatonia The occurrence of catatonia in such a wide variety of conditions and its unique response to benzodiazepines and electroconvulsive therapy (ECT) supports the theory that catatonia may have unique biological correlates separate from other syndromes and disorders [39,40] . With mul -tiple possible etiologies, a unifying pathogenesis of catatonia that explains all motor and auto -nomic symptoms remains elusive; although there are several models of catatonia [39,41] that should be used and expanded in future research to assess possible biomarkers of catatonia and predictors of treatment response and outcome. Motor circuitry model Dysfunction of the motor system involving frontal lobe basal ganglia circuitry or interfer -ence with this system (through thalamic, pari -etal lobe, cerebellar or limbic abnormalities) has been described as a possible mechanism of catatonia [9,42] . Epilepsy model The symptom overlap between psychomotor seizures and catatonia and the high prevalence of seizures in patients with catatonia lend strong face validity to the model in which seizure-like activities manifest clinically as catatonia. The

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Neuropsychiatry (2013) 3(4) 394 frontal lobes and anterior limbic systems are likely sites of abnormal electrical discharges in this model that also provide a rationale for the ef˜cacy of anticonvulsants, benzodiazepines and ECT through their common mechanism of increased seizure threshold. Neurotransmitter model The often dramatic response to treatment with benzodiazepines, positive modulators of the benzodiazepine/GABA A receptor complex, is a crucial observation supporting the role of GABA dysfunction in catatonia [43,44] . Tolerance of high doses of benzodiazepines in catatonic patients without ensuing sedation is another clue pointing to alterations in GABA A receptor func -tion. Several authors have discussed the role of neurotransmitters and synaptic transmission in catatonia usually involving GABA [45,46] , gluta -mate (the biological antagonist of GABA) [47,48] and dopamine (hypoactivity) [49,50] . Genetic model Studies show an increased familial transmission in ˜rst-degree relatives for periodic catatonia [51,52] , a type of psychomotor psychosis in the classi˜cation system of endogenous psychoses of Leonard [53,54] . These ˜ndings await replication. Endocrine model Several lines of evidence suggest the impor -tance of neuroendocrine abnormalities in cata -tonia. The early studies of periodic catatonia by Gjessing suggested thyroid abnormalities [55] and hypothalamic dysfunction [56] . Case reports associate catatonia and endocrinopathies such as hypoparathyroidism, thyrotoxicosis and pheochromocytoma [57,58] . Immune model Catatonia has been reported in patients with infections of the CNS, as in herpes [59] , HIV [60] , cerebral malaria [61] and typhoid fever [62] . In these examples, catatonia is probably caused by neuroinvasion of the infectious agent or parasite. Aseptic or autoimmune encephalitides such as antiphospholipid syndrome [63] , lupus cerebritis [64] , pediatric autoimmune neuropsy -chiatric disorders associated with streptococcal infections [65] and anti-NMDAR encephalitis have also been associated with catatonia [66Œ68] , supporting involvement of autoimmunity and cerebral antibodies in the mechanism of catatonia. Fear model The ˜nding that severe trauma and anxiety may precipitate catatonia [69,70] raises questions about mechanisms by which trauma leads to catato -nia or other disorders. The biological pathways of trauma leading to psychiatric and medical disorders are thought to encompass endocrine, immune, electrophysiological and neuropsycho -logical factors, as well structural changes in the brain [71Œ73] . Autonomic nervous system model Although catatonia is considered to be pri -marily a motor syndrome, 40% of catatonic patients show autonomic symptoms including abnormalities of temperature, blood pressure, pulse rate, respiratory rate and perspiration [74] . Autonomic dysfunction is the hallmark of malignant catatonia [75] , its drug-induced variant neuroleptic malignant syndrome [76] and aseptic encephalitis with catatonic symptoms, including the recently coined anti-NMDAR encephalitis [40,66] . Early studies support that there is auto -nomic dysfunction in catatonia [77] . Autonomic dysfunction in catatonia implies involvement of the autonomous nervous system that consists of the parasympathetic subsystem, mediated by the vagus nerve, and the sympathetic subsystem, medicated by sympathetio-adrenal circuits in the spinal cord [78] . Diagnosis of catatonia Early diagnosis is of utmost importance in order to provide optimal treatment. Delaying diagnosis, and thus treatment, puts the patient at considerable risk for major adverse events, including mortality [5,79] . There is no consensus on what constitutes a diagnosis of catatonia, nor is there an agreed threshold for the number or the duration of symptoms that should be present to justify a diagnosis of catatonia [80,81] . Several authors have suggested various diagnostic crite -ria. Barnes and coworkers de˜ne catatonia as the presence of the combination of at least one motor symptom and at least one symptom of psycho -social withdrawal, excitement and/or bizarre repetitive movements [82] . Rosebush and cowork -ers [83], and Peralta and Cuesta [84] require the presence of at least four out of 12, or three out of 11 criteria, respectively. Fink and Taylor sug -gest that in the presence of immobility, mutism or stupor lasting for at least 1 h, patients have to exhibit only one secondary criterium (catalepsy, automatic obedience and posturing) observed

PAGE – 5 ============ 395 or elicited on two or more occasions [9] . In the absence of immobility, mutism or stupor, a diag -nosis can be con˜rmed when at least two other symptoms are present. In DSM-5, the presence of any combination of at least three symptoms out of a set of 12 (Table˜1) de˜nes the diagnosis of catatonia. In rating scales, a total of 42 different symp -toms are examined. What the scienti˜c basis is for the selection of 12 in DSM is not entirely clear. The DSM-criteria narrow the de˜nition of catatonia, placing an unreasonable emphasis on symptoms such as echophenomena (two of 12 symptoms), stupor and mutism (if stupor is present, it is highly likely that mutism will also be present), and postural immobility (three symptoms), while omitting important and fre -quent symptoms such as automatic obedience and ambitendency (Table˜2) . Given the fact that the 12 DSM-5 symp -toms are all included in, and comprise ten of the 14-items of, the screening instrument of the BushŒFrancis Catatonia Rating Scale (BFCRS) [85] (posturing and catalepsy are sepa -rate symptoms in DSM-5, while seen as one in BFCRS, as are echolalia and echopraxia; and the BFCRS items staring, rigidity, verbigera -tion and withdrawal are not in DSM-5 criteria), DSM-5 criteria are probably a useful screening tool and can indeed help to detect catatonia. One might argue that it is advantageous that the catatonic symptoms in DSM-5, apart from waxy ˚exibility and catalepsy, are all obvious on observation and do not necessitate a clini -cal examination. Nevertheless, observation and psychiatric interview will not suf˜ce to detect the catatonic syndrome, since the most strik -ing symptoms, such as posturing, are present only in a minority of the cases. It is of impor -tance to elicit speci˜c catatonic signs during a neuro psychiatric examination. A rating scale or checklist can guide the clinician and improve detection. A number of catatonia rating scales have been published, and have recently been extensively reviewed [80] . The systematic use of these rating scales has been found to improve rates of identi˜cation of the catatonic syndrome [4,85] . Of 139 patients screened, clinicians diag -nosed catatonia in 2%, whereas a systematic screening using the BushŒFrancis Catatonia Screening Instrument diagnosed catatonia in 18% [85] . It is important to note that the choice of including certain symptoms in the de˜nition of catatonia, and excluding others, can empha -size overlaps of symptoms between catatonia and other disorders, such as Tourette™s syndrome. The presence of isolated catatonic symptoms, such as echophenomena in Tourette™s disorder, does not imply the presence of a catatonic syn -drome but should alert the clinician to the pres -ence of other catatonic symptoms that should be veri˜ed through a focused exam, use of a comprehensive rating scale and implementation of a lorazepam test. Table˜1. De˚nition of DSM-5 symptoms of catatonia. DSM-5 symptom Symptom de˚nition Catalepsy Maintains posture(s), including mundane (e.g.,˛ sitting or standing for hours without reacting) Waxy ˝exibility During reposturing, patient o˜ers initial resistance before allowing him-/her-self to be repositioned (similar to that of bending a warm candle) Stupor Extreme hypoactivity and immobility. Minimally responsive to stimuli Agitation, not in˝uenced by external stimuli Extreme hyperactivity, constant motor unrest that is apparently nonpurposeful Mutism Verbally unresponsive or minimally responsive Negativism Apparently motiveless resistance to instructions or to attempts to move/examine the patient. Contrary behavior, does the opposite of the instruction Posturing Maintains posture(s), including mundane (e.g.,˛sitting or standing for hours without reacting) Mannerisms Odd, purposeful movements (hopping or walking tiptoe, saluting passers-by and exaggerated caricatures of mundane movements) Stereotypies Repetitive, nongoal-directed motor activity (e.g.,˛˚nger-play, repeatedly touching, patting or rubbing˛self) Grimacing Maintenance of odd facial expressions Echolalia Mimicking of examiner™s speech Echopraxia Mimicking of examiner™s movements Symptom de˜nitions have been taken from [10] .

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Neuropsychiatry (2013) 3(4) 396 Possible laboratory tests, primarily to assess various underlying conditions, include a com -plete blood count and metabolic panel, erythro -cyte sedimentation rate, MRI, electroencepha -logram, cerebrospinal ˚uid ana lysis, antinuclear antibodies, and urine and organic metabolic testing [11,86] . A drug screen to detect com -mon illicit and prescribed substances is neces -sary. The fact that there is no biologic marker diagnostic of catatonia complicates an adequate differential diagnosis. A benzodiazepine chal -lenge of 1 or 2 mg of lorazepam administered per os (PO), intramuscularly or intravenously, can verify the diagnosis of catatonia [5,9,11] . If no change is observed, a second dose is admin -istered after 5 min intravenously, 15 min intra -muscularly or 30 min PO. When a single dose of lorazepam improves catatonia, lorazepam can be prescribed at regular intervals to maintain the improvement [11] . The use of the GABA recep -tor modulator zolpidem has also been developed as an alternative catatonia challenge test (5 or 10 mg PO) [87] . Treatment of catatonia As discussed, the most important argument in favor of classifying catatonia as a distinct syn -drome is its speci˜c response to benzodiazepines and ECT. Benzodiazepines The ef˜cacy of sedative drugs Œ that is, barbi -turates Œ in catatonia was discovered more than 80 years ago [88] . In the 1980s, benzodiazepines replaced the use of barbiturates. In catatonia, prospective studies found 70Œ90% response rates, irrespective of the excited or stuporous character of the state [43] . Some studies reported rapid and dramatic improvement of the catatonic symptoms, even after a single benzodiazepine dose [83,89] . As a result, lorazepam 2Œ4 mg was recommended as the ˜rst treatment of choice in catatonia. In case of nonresponse, after 1Œ2 days, the dose should be increased to 8Œ16 mg/day. It is suggested that response to benzodiazepines is particularly high in mood disorders. Studies in schizophrenia, catatonic type, have yielded low Œ below 50% Œ response rates to low doses of lorazepam [90] , and benzodiazepines were found ineffective in the long-term treatment of chronic catatonic schizophrenia [91] . In the absence of a sustained response, ECT is to be proposed without delay [9,92] . Antipsychotics Given the fact that catatonia often results in a diagnosis of schziophrenia, antipsychotics are used frequently, in spite of the fact that these drugs can induce or worsen catatonic symptoms. This unfavorable effect is especially character -istic for ˜rst-generation antipsychotics [93] . The role of the second-generation antipsychotics in the treatment of catatonia is more hetero -geneous, and several authors have reported a good response. Clozapine, olanzapine and ris -peridone were reported to be effective in the treatment of catatonia associated with schizo -phrenia [92] . Only one randomized controlled trial is available to date. In this study, 14 stu -porous psychotic patients were randomized to either ECT or risperidone (4Œ6 mg/day). The ECT-treated patients showed signi˜cantly Table˜2. De˚nitions of catatonic symptoms that are not included in DSM-5. Symptom De˚nition Ambitendency The patient appears stuck in indecisive, hesitant motor movements Automatic or passive obedience (mitgehen) Exaggerated cooperation with examiner™s request, or repeated movements that are requested once Raising arm in response to light pressure of ˚nger, despite instructions to the contrary Autonomic abnormality Abnormality of temperature (fever), blood pressure, pulse rate, respiratory rate and inappropriate sweating Combativeness Usually in an undirected manner, without explanation Gegenhalten/counterpull Resistance to passive movement that is proportional to strength of the stimulus; response seems automatic rather than willful Grasp re˝ex Strike open palm of patient with two extended ˚ngers of examiner™s hand. Automatic closure of patient™s˛hand Impulsivity Patient suddenly engages in inappropriate behavior (e.g.,˛runs down the hallway, starts screaming or takes clothes o˜) without provocation. Afterwards, behavior cannot be explained Perseveration Repeatedly returns to the same topic or persists with same movements Rigidity Maintenance of a rigid position despite e˜orts to be moved Staring Fixed gaze, little or no visual scanning of environment and decreased blinking Symptom de˜nitions have been taken from [10] .

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