27 Catatonia in Psychiatric Illnesses Dirk M. Dhossche, MD, PhD and Lee Elizabeth Wachtel, MD Abstract Catatonia challenges the validity of modern classification systems by cutting across its proposed boundaries. Contrary to earlier claims that catatonia is restricted to schizophrenia, and soon to be extinct, there is current evidence showing that catatonia is diagnosable in 7 to 17% of acute psychiatric inpatients. A similar proportion of autistic adolescents and adults also meet criteria for catatonia. Sedative treatment and electroconvulsive therapy, the treatments that have historically proven to be effective in catatonia, remain the therapeutic mainstay for catatonia. Evaluation and treatment algorithms that should be helpful when assessing and treating these challenging patients are presented, as well as a GABA-deficit theory of catatonia for guidance of future studies into this syndrome’s biochemical correlates. Further studies are needed to optimize the recognition and treatment of catatonia in a wide range of medical and psychiatric patients of different ages. Keywords Autism · Benzodiazepines · Catatonia · Childhood disintegrative disorder · Children · Delirium · Electroconvulsive treatment (ECT) · Gamma-aminobutyric acid (GABA) · Mood disorder · Movement disorders · Prader–Willi syndrome · Psychomotor abnormalities · Psychosis · Schizophrenia And the more you really see mental patients and get to know their symptoms, the more you will be convinced that finally nothing else can be found and observed but movements, and the whole pathology of mental patients consists of nothing else but the pecu- liarities of their motor behavior. —Carl Wernicke, 1900 (1) 1. Introduction The study of psychomotor abnormalities in psychiatric disor- ders requires considerable clinical acumen through direct observation combined with skills to elicit specific symptoms. Although some may interpret Wernicke’s quote as hyperbole, the salience of neuropsychiatric impairment manifesting as motor symptoms is nowhere clearer than in catatonia. Interest in this mysterious condition has been rekindled during the last decade. In this chapter, we cover classification issues of cata- tonia, differential diagnosis, evidence for catatonia as a neuro- biological syndrome, a gamma-aminobutyric acid (GABA) deficit theory of catatonia, pediatric catatonia, catatonia in autistic disorders, including childhood disintegrative disorder (CDD) or late-onset autism, and catatonia in Prader–Willi syndrome (PWS). At the end, algorithms for the evaluation and treatment of catatonia are presented. 2. Catatonia in DSM Catatonia was originally described in 1874 by Kahlbaum as a separate brain disorder with a cyclic, alternating, and ultimately progressive course (2). Kraepelin viewed cata- tonia as an exclusive subtype of dementia praecox or schizophrenia. In contrast, recent studies show the preponder- ance of underlying affective disorders, particularly mania, in adult catatonic patients (3–6). In the Diagnostic and Statis- tical Manual of Mental Disorders, 4th edition, text revi- sion (DSM-IV) (7), catatonia is a specifier of Schizophrenia, Primary Mood Disorder, and Mental Disorder due to a General Medical Condition. DSM-IV criteria for catatonia are given in Table 27.1, and definitions of specific catatonic symptoms in Table 27.2, with some illustrated by photos from Oswald Bumke’s 1924 textbook. Taylor and Fink (8,9) have recently proposed that catatonia should be viewed as a distinct syndrome in upcoming editions of DSM. Some consider catatonia as a loose constellation of psychomotor symptoms, that has almost disappeared because of obscure reasons (10) and that is usually associated with schizophrenia. However, empirical findings highlight its increased incidence in psychosis and validity as a syndrome and genetically determined phenotype (11, 12). For example, From: S. H. Fatemi and P. J. Clayton (eds.): The Medical Basis of Psychiatry c 2008 Humana Press, Totowa, NJ 455
Transcript
27Catatonia in Psychiatric IllnessesDirk M. Dhossche, MD, PhD and Lee Elizabeth Wachtel, MD
Abstract Catatonia challenges the validity of modern classification systems by cutting across its proposed boundaries.Contrary to earlier claims that catatonia is restricted to schizophrenia, and soon to be extinct, there is current evidence showingthat catatonia is diagnosable in 7 to 17% of acute psychiatric inpatients. A similar proportion of autistic adolescents and adultsalso meet criteria for catatonia. Sedative treatment and electroconvulsive therapy, the treatments that have historically provento be effective in catatonia, remain the therapeutic mainstay for catatonia. Evaluation and treatment algorithms that should behelpful when assessing and treating these challenging patients are presented, as well as a GABA-deficit theory of catatonia forguidance of future studies into this syndrome’s biochemical correlates. Further studies are needed to optimize the recognitionand treatment of catatonia in a wide range of medical and psychiatric patients of different ages.
And the more you really see mental patients and get to know theirsymptoms, the more you will be convinced that finally nothingelse can be found and observed but movements, and the wholepathology of mental patients consists of nothing else but the pecu-liarities of their motor behavior.
—Carl Wernicke, 1900 (1)
1. Introduction
The study of psychomotor abnormalities in psychiatric disor-ders requires considerable clinical acumen through directobservation combined with skills to elicit specific symptoms.Although some may interpret Wernicke’s quote as hyperbole,the salience of neuropsychiatric impairment manifesting asmotor symptoms is nowhere clearer than in catatonia. Interestin this mysterious condition has been rekindled during the lastdecade. In this chapter, we cover classification issues of cata-tonia, differential diagnosis, evidence for catatonia as a neuro-biological syndrome, a gamma-aminobutyric acid (GABA)deficit theory of catatonia, pediatric catatonia, catatonia inautistic disorders, including childhood disintegrative disorder(CDD) or late-onset autism, and catatonia in Prader–Willisyndrome (PWS). At the end, algorithms for the evaluationand treatment of catatonia are presented.
2. Catatonia in DSM
Catatonia was originally described in 1874 by Kahlbaumas a separate brain disorder with a cyclic, alternating, andultimately progressive course (2). Kraepelin viewed cata-tonia as an exclusive subtype of dementia praecox orschizophrenia. In contrast, recent studies show the preponder-ance of underlying affective disorders, particularly mania, inadult catatonic patients (3–6). In the Diagnostic and Statis-tical Manual of Mental Disorders, 4th edition, text revi-sion (DSM-IV) (7), catatonia is a specifier of Schizophrenia,Primary Mood Disorder, and Mental Disorder due to aGeneral Medical Condition. DSM-IV criteria for catatoniaare given in Table 27.1, and definitions of specific catatonicsymptoms in Table 27.2, with some illustrated by photos fromOswald Bumke’s 1924 textbook. Taylor and Fink (8, 9) haverecently proposed that catatonia should be viewed as a distinctsyndrome in upcoming editions of DSM.
Some consider catatonia as a loose constellation ofpsychomotor symptoms, that has almost disappeared becauseof obscure reasons (10) and that is usually associatedwith schizophrenia. However, empirical findings highlight itsincreased incidence in psychosis and validity as a syndromeand genetically determined phenotype (11, 12). For example,
Table 27.1. DSM-IV diagnostic criteria for the catatonic features spec-ifier (of schizophrenia, primary mood disorder, and mental disordercaused by a general medical condition).
The clinical picture is dominated by at least two of the following:
1 Motoric immobility as evidenced by catalepsy (including waxy flexibility)or stupor
2 Excessive motor activity (that is apparently purposeless and not influencedby external stimuli)
3 Extreme negativism or mutism4 Peculiarities of voluntary movement as evidenced by posturing, stereotyped
movements, prominent mannerisms, or prominent grimacing5 Echolalia or echopraxia
in recent samples of acute psychiatric inpatients, the preva-lence of catatonia was between 7 and 17% (13,14). Most cata-tonic patients were actually diagnosed with mood disorders,and many authors link catatonia to manic–depressive illness(4, 15). Twenty-five percent or more of manic patients haveenough catatonic features to meet the DSM criteria. Morethan half of catatonic patients have manic–depressive illness.Approximately 10 to 15% of patients with catatonia meet thecriteria for schizophrenia.
In a recent study (16), using a narrow definition of cata-tonia, i.e., the presence of four or more signs/symptoms withat least one having a score 2 or above on the Bush–Francis
Catatonia Rating Scale (BFCRS) (15), 72 subjects (32%)with chronic schizophrenia met the criteria for the catatoniagroup (mean number of catatonic signs/symptoms = 5.9F2.0;mean sum score of 8.7F3.4 on the BFCRS). The frequencydistribution of catatonic signs/symptoms in the catatonicgroup and in the whole sample was very similar, with manner-isms, grimacing, stereotypes, posturing, and mutism beingthe most frequent. Catalepsy, mannerisms, posturing, andmutism are the features traditionally associated with catatonicschizophrenia.
In another study (17), a large sample of schizophrenicpatients (n = 19,309) was studied. Although the diagnosis of
Table 27.2. Definition of catatonic symptoms.
Excitement Extreme hyperactivity, constant motor unrest that is apparently nonpurposefulImmobility/stupor Extreme hypoactivity, immobility. Minimally responsive to stimuliMutism Verbally unresponsive or minimally responsiveStaring (Fig. 27.1) Fixed gaze, little or no visual scanning of environment, decreased blinkingPosturing/catalepsy (Fig. 27.2) Maintains posture(s), including mundane (e.g., sitting or standing for hours without
reacting)Grimacing (Fig. 27.3) Maintenance of odd facial expressionsEchopraxia/echolalia Mimicking of examiner’s movements/speechStereotypy Repetitive, nongoal-directed motor activity (e.g., finger play, repeatedly touching, patting,
or rubbing self)Mannerisms Odd, purposeful movements (hopping or walking tiptoe, saluting passers-by, exaggerated
caricatures of mundane movements)Verbigeration Repetition of phrases or sentencesRigidity (Fig. 27.4 and 27.5) Maintenance of a rigid position despite efforts to be movedNegativism Apparently motiveless resistance to instructions or to attempts to move/examine the
patient. Contrary behavior, does the opposite of the instructionWaxy flexibility (Fig. 27.6, 27.7 and 27.8) During reposturing, patients offers initial resistance before allowing himself to be
repositioned (similar to that of bending a warm candle)Withdrawal Refusal to eat, drink, and/or make eye contactImpulsivity Patient suddenly engages in inappropriate behavior (e.g., runs down the hallway, starts
screaming, or takes off clothes) without provocation. Afterward, cannot explainAutomatic obedience Exaggerated cooperation with examiner’s request, or repeated movements that are
requested oncePassive obedience (mitgehen) Raising arm in response to light pressure of finger, despite instructions to the contraryGegenhalten/counterpull Resistance to passive movement that is proportional to strength of the stimulus; response
seems automatic rather than willfulAmbitendency The patient seems stuck in indecisive, hesitant motor movementsGrasp reflex Strike open palm of patient with two extended fingers of examiner’s hand. Automatic
closure of patient’s handPerseveration Repeatedly returns to the same topic or persists with same movementsCombativeness Usually in an undirected manner, without explanationAutonomic abnormality Abnormality of temperature (fever), blood pressure, pulse rate, respiratory rate,
catatonic schizophrenia dropped from 7.8% in 1980 to 1989to 1.3% in 1990 to 2001, a possible underdiagnosis of cata-tonic schizophrenia was found in an independent sample. In aconsecutive sample of patients admitted with psychosis, appli-cation of a systematic catatonia rating scale showed that 17%fulfilled criteria for catatonia (14).
Together, these studies (16, 17) suggest underdiagnosisand nonrecognition of catatonia both in patients withschizophrenia and bipolar disorder. The reasons are complex,but may include the historical decision to classify catatonia as
a type of schizophrenia, the segregation of severely ill psychi-atric patients in long-term facilities, and the perceived lackof anticatatonic treatments (13). Another author has positedthat, similar to hysteria, changing sociocultural circumstanceshave suppressed more obvious symptoms of catatonia, such aspervasive negativism, and that the symptom profile has shiftedtoward more subtle forms that require more clinical acumen todetect (18). This hypothesis assumes that some of the behav-ioral disturbances in catatonia are not only neurally but alsomentally driven. All of these factors may have decreasedinterest in and recognition of catatonia.
Although there are no controlled treatment studies in cata-tonia satisfying current standards for evaluating therapies, theliterature consistently shows positive effects of anticonvulsantdrugs, particularly benzodiazepines and barbiturates, and ofelectroconvulsive therapy (ECT), regardless of the severity oretiology of catatonia (19–21).
3. Differential Diagnosis
Catatonia needs to be distinguished through a detailed history,clinical examination, and application of diagnostic criteria,from other conditions, syndromes, or disorders featuringpsychomotor abnormalities that may overlap with the mani-festations of catatonia. The issue of differential diagnosisis separate from the presence in catatonic patients of anyunderlying psychiatric or medical disorder, or identification ofcatatonia-inducing substances. Psychiatric and medical inves-tigations are discussed in the section on the evaluation of cata-tonia. Making an adequate differential diagnosis of catatoniais compounded by the fact that there is no diagnostic biolog-ical marker of catatonia, and that the optimal definition ofcatatonia is not well established. The differential of catatonia
among hypokinetic and hyperkinetic conditions, syndromes,and disorders is reviewed.
Among the hyperkinetic states, acute dystonia (22) (asustained muscle contraction, frequently causing twistingand repetitive movements, or abnormal postures), tardivedyskinesia (a hyperkinetic involuntary movement syndromeprimarily affecting the mouth, lips, and tongue, but occa-sionally also the extremities and trunk), withdrawal-emergentdyskinesia (23), and akathisia (subjective sensation of motorrestlessness) are medication-induced conditions that may bemistaken for catatonia. Typical antipsychotics are the medi-cations that are usually associated with these movementdisorders, but atypical antipsychotics, tricyclic and tetra-cyclic antidepressants, selective serotonin-uptake inhibitors,monoamine oxidase inhibitors, antiemetics, calcium antag-onists, anticonvulsants, stimulants, and a variety of otherpsychotropics have also been implicated through alterations incentral dopamine metabolism (24). Antipsychotics may addi-tionally be a risk factor for the development of catatonia, asubject to be later reviewed.
Tic disorder, Gilles de la Tourette syndrome (characterizedby both motor and vocal tics), elective mutism, conversiondisorder, and compulsions in obsessive–compulsive disorder
(OCD) may also overlap with catatonia. An associationbetween catatonia and some forms of Tourette’s syndromeand OCD has been suggested based on cases with comorbidcatatonia and Tourette’s syndrome (25, 26), and comorbidcatatonia and OCD (27). In those patients, tics and explo-sive verbal behavior resolved with ECT (25, 26). In one casereport, obsessive–compulsive behaviors and catatonia devel-oped in a child after a streptococcal infection (28). Antistrep-tolysin O and DNAse B antibody titers were elevated. The
child improved rapidly with lorazepam treatment followedby plasmapheresis. The authors suggest that catatonia, likeOCD and tics, may be another manifestation of pediatricautoimmune neuropsychiatric disorders associated with strep-tococcal infections (PANDAS). Catatonia also needs to bedistinguished from the motor manifestations of hypocalcemia,tetanus, strychnine toxicity, and rabies.
Among the hypokinetic states, pseudo-parkinsonism (char-acterized by bradykinesia, rigidity, tremor, and gait andpostural disturbances singly or in combination) is amedication-induced condition resembling catatonia. Typicalantipsychotics are especially prone to cause pseudo-parkinsonism in a dose-dependent fashion, usually within the
first month of administration (29). Another group of disorderscharacterized by varying levels of hypokinesis and musclestiffness, in combination with altered levels of conscious-ness, also should be included in the differential diagnosis. Theboundaries between catatonia and conditions such as malig-nant hyperthermia, neuroleptic malignant syndrome (NMS),toxic serotonin syndrome, delirium, stiff-person syndrome,and locked-in syndrome are not well established, however(13). For example, there is discussion in the literature whetherNMS and toxic serotonin syndrome truly differ in key aspectswith catatonia, or, alternatively, if they should be regardedas medication-induced forms of catatonia (30, 31). The factthat NMS and toxic serotonin syndrome seem to respond tothe same treatments as catatonia strengthens the argument ofrelatedness.
In DSM-IV, it is acknowledged that catatonia can occurin association with various medical conditions of infectious,metabolic, endocrine, and neurological etiologies that mayalso be associated with delirium (7). However, the diagnosiscannot be made if catatonia occurs exclusively during thecourse of a delirium. The validity of this provision is uncertainbecause no recent studies that have assessed the importance ofcatatonia during delirium can be found in the literature. Theissue has therapeutic consequences because anticatatonic andantidelirium treatments are different, albeit with overlap. Theemergence of catatonia in delirium may also caution againstthe use of antipsychotic medications, because most cliniciansacknowledge that catatonia, at least in some patients, mayworsen with administration of typical and atypical antipsy-chotic medications (31–33). Future trials of lorazepam andECT treatment, the main treatments for catatonia, in patientswith comorbid delirium and catatonia, should be informativeabout the importance of catatonia in the course of delirium.
Another unresolved classification issue is whether catatoniashould be included in the differential diagnosis in patientswith coma (complete unresponsiveness) (34), and, in a similar
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vein, if stupor or profound unresponsiveness can be the solepresenting symptom of catatonia (34–36). Recent case reportshave shown that patients with levels of unresponsivenesssimilar to those in coma, and without other catatonic symp-toms (except resistance to eye opening) responded to ECT(37) and intravenous benzodiazepines (36). Freudenreich et al.(36) describe the challenge of prescribing high-dose benzo-diazepines to an unresponsive patient considered to havecatatonia. They also recommend the descriptive term “cata-tonic coma” to replace other terms that imply psychogenesis,such as psychogenic, conversion, dissociative, or hystericalcoma, that have no specific therapeutic consequences, oncemore common medical or neurological causes of coma areexcluded.
4. Catatonia as a Syndrome
Fujii and Ahmed (38) have proposed five criteria for a neuro-biological syndrome:
• A neurobiological syndrome is a constellation of symp-toms that are reliably associated with disturbance that isfunctional, structural, neurochemical, or neuropathologicalin a circumscribed structural location or neural circuit.
• Similar neurobiological disturbances (that is, in the loca-tion or in the neural circuit) that are secondary to differentetiologies would result in similar cognitive or behavioralsymptoms.
• Smaller amounts of similar neurobiological disturbancesare associated with milder symptoms.
• Additional symptoms such as cognitive, mood, psychiatric,or other associated neurological symptoms are relatedto other networks simultaneously affected by underlyingneurochemical or neuropathological processes.
• The treatment for the neurobiological syndrome is similaracross different underlying etiologies that may requireseparate treatment.
There are several candidate neurobiological syndromes,such as psychosis (e.g., hallucinations and delusions), cata-tonia, autism, and certain types of depression, e.g., melan-cholia. Although any attempt for validation of these putativesyndromes suffers from our limited knowledge of the relationbetween brain function and behavior, especially at the cellularand molecular level, this approach has heuristic value forrefining current classification systems such as DSM and Inter-national Classification of Diseases (ICD), focusing research,and tailoring treatments on an individual basis. Most impor-tantly, clinical presentation would be more firmly tied withneuropathology and etiology than in theoretical models suchas DSM or ICD.
Does catatonia qualify as a distinct neurobiologicalsyndrome according to the criteria of Fujii and Ahmed (38)?If so, this would be contrary to Kraepelin’s view of catatoniaas an exclusive subtype of dementia praecox or schizophrenia,
but in line with Kahlbaum’s original description of catatoniaas a separate brain disorder with a cyclic, alternating, and ulti-mately progressive course (2). Taylor and Fink (8, 9) haverecently made this argument. After reviewing the evidence forthe diagnostic validity of catatonia, they concluded (8):
Catatonia can be distinguished from other behavioral syndromesby a recognizable cluster of clinical features. Catatonia is suffi-ciently common to warrant classification as an independentsyndrome. It can be reliably identified, has a typical course whenappropriately treated, responds to specific treatments, and is wors-ened by other treatments. It is associated with many pathophysi-ologic processes and most often with mood disorder. These find-ings, which are consistent with established methods of definingdistinct diagnostic groupings, support consideration of catatoniaas an individual category in psychiatric diagnostic systems.
In support of the first criterion of Fujii and Ahmed (38),putative neural circuitries for catatonia have been describedby Northoff (39) and Carroll et al. (40), involving multiplefocal sites such as the anterior cingulate gyrus, the thalamus(mediodorsal), the basal ganglia, the medial frontal cortex, theinferior orbital frontal cortex, and the parietal cortex. Otherstudies also implicate the pons, upper brainstem, and cere-bellum (41). Neurochemical studies supported by functionalbrain imaging have provided insight into types of cerebraldysfunction responsible for producing the catatonic syndrome(42). Possible neurochemical etiologies for medical catatoniasinclude glutaminergic antagonism, GABA antagonism, sero-tonergic actions, and dopamine antagonism (43).
In support of the second criterion is the fact that catatoniahas been described as a feature of many psychiatric (Table27.3) medical and neurological conditions (44), includingmetabolic disturbances, endocrinopathies, viral infections(including HIV), typhoid fever, heat stroke, and autoimmunedisease. All of these conditions are commonly associatedwith both delirium and catatonia. Drug intoxications andwithdrawals may also induce catatonia. Neurological condi-tions associated with catatonia include postencephalitic states,parkinsonism, bilateral globus pallidus disease, thalamic andparietal lobe lesions, frontal lobe disease, and general paresis.Diffuse disease processes associated with medical catatonia
Developmental disordersAutistic disorder (classic or core autism)Asperger disorder (high-functioning autism)Childhood disintegrative disorder (late-onset autism)Pervasive developmental disorder not otherwise specified
(atypical autism)Prader–Willi syndrome
Mood disordersPsychosis not otherwise specifiedSchizophreniaMental disorders caused by a general medical conditionSubstance-induced disorders (including neuroleptic
malignant syndrome)
27. Catatonia in Psychiatric Illnesses 461
support the notion that pathway dysfunction rather than focal(site-specific) dysfunction causes catatonia.
The third criterion for a neurobiological syndrome statesthat milder neurobiological disturbances cause milder symp-toms. Transient drug intoxications with rapid resolution ofcatatonia support this criterion.
Fourth, catatonia is characterized by concurrent motor,emotional, cognitive, and behavioral symptoms as discussedby Northoff (39). Finally, several studies have found that cata-tonia responds to benzodiazepines and ECT, regardless ofetiology (13). Future research should continue to examine thevalidity of catatonia by expanding data on the pathophysi-ology, biochemistry, and treatment of catatonia.
5. Leonhard’s Psychomotor Psychoses
Nosology attempts to isolate syndromes that are optimal toguide treatment and prognosis. The classification system ofendogenous psychoses of Karl Leonhard (45), elaboratedby the group of Helmut Beckmann (46), deserves a specialmention. Patterns of psychomotor disturbances and cata-tonic symptoms are the basis for diagnosis in his system,which is highly standardized and which has shown reliability(46). Diagnostic categories are markedly different from DSMdisorders. Among the childhood psychomotor psychoses,Leonhard listed systematic catatonia (chronic catatonicschizophrenia with poor prognosis), motility psychosis (char-acterized by frequent hyperkinetic phases with psychosis),and periodic catatonia (catatonia with an intermittent courseof hyperkinetic and akinetic states) (47). Autism is not speci-fied in this classification.
Recent studies have shown that the age-specific morbidityrisk for periodic catatonia in first-degree relatives of probandswith periodic catatonia is 27% versus 5% for systematic cata-tonia in first-degree relatives of probands with systematiccatatonia (11). The pattern of familial transmission of peri-odic catatonia shows anticipation, i.e., the proband’s age atthe onset of disease was significantly earlier than that of theirparent, especially when the afflicted parent was the father(48). Linkage of periodic catatonia to the long arm of chro-mosome 15q15 has been shown in two studies by the sameresearch group (12,49). Heredity plays a minor role in system-atic catatonia (11).
Several DSM disorders may correspond with periodic cata-tonia that is classified as a subtype of schizophrenia by Leon-hard. Taylor and Fink (8) point out that some cases may alsofit DSM-IV criteria for bipolar disorder, catatonic subtype, orschizoaffective disorder. Because catatonia seems to be a late-onset complication in autism (50, 51), some patients in thiscategory may also suffer from an underlying autistic disorder.Systematic schizophrenia resembles DSM-IV schizophrenia,catatonic subtype. Family and genetic studies in DSM bipolardisorders do not typically have catatonic subtypes. An asso-ciation study in patients with affective disorders showed that
the distribution of allelic frequencies of a locus on the longarm of chromosome 15q11-13 differed significantly betweenbipolar patients and control subjects, but not between unipolarpatients and control subjects (52). The proportion of bipolarpatients with catatonia was not reported. Suspected loci forperiodic catatonia and bipolar disorder were found on the longarm of chromosome, although not on the exact same location.The relation between the two loci is unknown.
6. GABA Deficit Theory of Catatonia
A comprehensive biochemical theory of catatonia has provento be elusive to date (13, 21). In the next few paragraphs,the focus is on abnormalities of GABA function as theymay relate to catatonia. The single most important obser-vation leading to the thought that GABA dysfunction playsa role in catatonia is the often dramatic response to treat-ment with benzodiazepines, i.e., positive modulators of thebenzodiazepine/GABAA receptor complex (19, 53). Othereffective treatments for catatonia, i.e., barbiturates, zolpidem,carbamazepine, and ECT (54, 55), also enhance GABA func-tion. Efficacy of serotonergic and dopamine blocking agentsin catatonia has been less well documented, but seems lessconsistent.
Empirical evidence for GABA dysfunction in catatoniacomes from one single receptor-imaging study (56), inwhich a decreased density of GABAA receptors in the leftsensorimotor cortex was found in akinetic catatonia. Other,more circumstantial, evidence is found in a study in whichdecreased cerebrospinal fluid (CSF) levels of GABA werefound in 11 patients with NMS, a condition that may berelated to catatonia (57). In this study, levels of noradrenalinwere increased, but levels of 5-hydroxyindoleacetic acid (5-HIAA), the main metabolite of serotonin, were slightly, butnot significantly, decreased. Further evidence of impairedGABA function in catatonia must await future studies.
If one assumes a central role of GABA dysfunction incatatonia, the scope of GABA functions in the healthy brainshould allow the expression of catatonia when deficiencies inGABA function develop. Roberts (58) sees a central role ofGABA as neurotransmitter used by neurons that exert tonicinhibition of neural circuits for innate or learned behavioralsequences. In its extreme forms, catatonia is characterized byimmobility alternating with purposeless agitation. Althoughopposite in nature, both behaviors can be viewed as prim-itive reflexes in response to overwhelming stress or dangerthat are expressed when innate, genetically preprogrammedneuronal circuits are released from tonic inhibition. FollowingJohn Hughlings Jackson’s hierarchical concept of dissolution(59), immobility or hyperactivity are then “positive” symp-toms caused by the removal of the influence of higher centers.The neuronal circuitry that is involved in catatonia is not welldefined, but probably involves frontal cortex, parietal cortex,basal ganglia, and possibly the cerebellum (13).
462 Dhossche and Wachtel
A few general criteria for any viable GABA theory of cata-tonia are proposed:
• The theory has to accommodate findings from GABAergictheories of schizophrenia, affective disorders, autism, andPWS, because catatonia occurs in all of these disorders.
• Hypothalamic abnormalities of GABA function should bepresent and may account for severe autonomic dysfunctionin malignant catatonia, a severe type of catatonia with feverand autonomic instability.
• Treatments that relieve catatonia should enhance GABAfunction, directly or indirectly.
• Genetic studies in catatonia, schizophrenia, affective disor-ders, autism, and PWS, should provide support for involve-ment for genes affecting GABA function.
Evidence that GABA dysfunction in catatonia satisfiesthese criteria is summarized:
• GABA theories have been formulated for schizophrenia(60, 61), psychosis (62, 63), affective disorders (64–66)including bipolar disorder (67), autism (68–70), and PWS(71, 72).
• GABA is a prominent neurotransmitter in the hypotha-lamus (73). Hypothalamic GABAergic mechanisms areconsidered important for regulation of stress responses bythe hypothalamic–pituitary–adrenal (HPA) (74, 75).
• Most currently used psychotropic medications, includingbenzodiazepines, antipsychotics (76), selective serotoninreuptake inhibitors (77–79), phenelzine (80, 81), andanticonvulsants, seem to enhance GABA neurotransmis-sion, albeit through different mechanisms. A few studiessuggest a direct role of GABA in ECT. In a single-photon emission tomography (SPECT) study, increasedbenzodiazepine receptor uptake in cortical regions (excepttemporal cortices) was found 1 week after successfulbitemporal ECT (82). In a magnetic resonance spec-troscopy (MRS) study, twofold increased brain GABAlevels were found in depressed patients after a course ofECT (55). The small number of patients precluded conclu-sions regarding any correlation between clinical improve-ment and increased brain GABA levels. Previously, it wasreported that CSF GABA levels increased by 50% afterECT (83). In another study, cortical glutamate/glutaminelevels in the left anterior cingulum of depressed patientsnormalized after ECT, but only in responders (84). Innonresponders, levels remained low. Limitations in thisstudy’s MRS methodology did not allow obtaining sepa-rate measurements for GABA because of overlapping reso-nances of glutamate, glutamine, and GABA. In a studyof plasma GABA levels in depressed patients treated withECT, plasma GABA levels tended to decrease for approx-imately 1 hour after ECT (85). Limitations of this studyincluded variable storage times known to increase GABAlevels in plasma and CSF and as-needed administration ofchloral hydrate, which enhances GABA function similar tobarbiturates, during the ECT course.
• There is some evidence that GABA-related genes areinvolved in affective disorder and schizophrenia. GABRA5has been associated with bipolar disorder in two studies(52, 86). In a genome scan of catatonia, a linkage signal inthe region 15q11.2-q21.1 (where three GABA-A subunitgenes are located) was found (12). No (family-based)gene association studies in catatonia are available in theliterature. Findings from a family-based association studyin a sample of children and adolescents with childhood-onset schizophrenia (COS) (n = 72) suggested that thegene encoding GAD67 may be a common risk factorfor schizophrenia (87). Genetic studies have implicatedthe involvement of the proximal long arm of chromo-some 15 in autism (88–91) and catatonia (12, 49). ThreeGABAA receptor subunit genes (GABRB3, GABRA5, andGABRG3) are located at the chromosome location thatincludes the PWS/Angelman syndrome region. Animaland human studies have suggested a role for thesegenes in the phenotypic expression of PWS (92) andAngelman syndrome (93, 94). GABRB3 has been asso-ciated with autism in several studies (95–97), especiallyin patients with increased levels of “insistence on same-ness” (a composite score of difficulties with minor changesin personal routine or environment, resistance to trivialchanges in environment, and compulsions/rituals) (98)and with savant skills (97). Another cluster of GABA-Areceptor subunit genes located on the short arm of chromo-some 4 has recently been associated with autism through afamily-based association and linkage disequilibrium study(99). In another report, an inversion breakpoint disruptingone of the genes within this GABA-A receptor gene clusterwas discovered in two autistic brothers (100).
7. Catatonia in Children
In 1972, Bemporad and Dunton (101) reported the protractedcourse of illness in a 10-year-old girl and an 8-year-old boy.Both children were diagnosed with catatonia. Their symptomswere similar to symptoms in adult catatonic patients. Theyreviewed the literature and found only one other case in theliterature, which was published in 1926. The earliest descrip-tion of pediatric catatonia (in a 3-year-old girl) comes from deSanctis (102), as pointed out by Neumarker (103).
In a subsequent review (104, 105), from 1966 to 1996, 30cases of catatonia in children and adolescents were found. Themean age was 14.3 years (range, 8–18 years; standard devia-tion [SD], 2.7 years). There were 18 boys and 12 girls. All 30cases satisfied DSM-IV criteria for catatonia requiring two offive symptom clusters. Although not all cases had an episodeof complete immobility or stupor, all cases had a stupor-like phase with marked reduction of psychomotor activity.Only one case had predominant excitation. Two cases showedmixed features of retardation and agitation. Rates of indi-vidual catatonic symptoms in children and adults were similar,
27. Catatonia in Psychiatric Illnesses 463
except for urinary/fecal incontinence that was not systemati-cally reported in any of the adult studies. Incontinence is not aDSM-IV symptom of catatonia, but is frequently reported, atleast in children and adolescents. Diagnostic distribution wasalso similar with a preponderance of underlying neurologicalconditions and affective disorder.
Antipsychotic treatment was implicated in one case.Indeed, antipsychotic treatment is considered a risk factorfor catatonia in all age groups, especially if typical antipsy-chotics are administered in high doses (13, 33). The acuteonset of fever, autonomic instability, rigidity, and changes inmood and alertness after administration of antipsychotics arecardinal symptoms for NMS. This constellation of symptomswas described soon after the introduction of antipsychoticdrugs (106). However, a similar syndrome was describedbefore the introduction of these drugs and was referred to aslethal or malignant catatonia. The malignant form of cata-tonia is acute in onset, systematically devastating, and associ-ated with fever and autonomic instability. These patients lookas if they have an infectious disease, particularly an infec-tious encephalopathy. No specific infectious process is usuallyfound. Some are considered to suffer from a coma of unknownetiology. NMS and malignant catatonia overlap considerably,and some have concluded that NMS is an example of malig-nant catatonia triggered by exposure to antipsychotic drugs(30, 32, 107). The argument is supported by studies that showthat laboratory abnormalities are the same in both conditionsand, most importantly, that treatments for malignant catatonia,i.e., ECT and benzodiazepines, are equally effective in NMS(31, 108, 109).
What can be concluded from the sparse literature? First,a few studies suggest that the prevalence of catatonia isunderestimated. For example, more than one third of chil-dren (12 of 38 children) with schizophrenia had catatonicsymptoms (110). In a clinical survey of child and adoles-cent psychiatric outpatients, 5.5% of the sample and 17.7%of the patients with affective and non-affective psychoticdisorder met DSM criteria for catatonia (111). Second, despiteconcerns regarding the small number of cases, varying qualityof the reports, and publication bias, all reported cases satis-fied the DSM-IV criteria. Symptoms in childhood and adultcatatonia are similar. These findings support the validity ofchildhood catatonia. Third, catatonia in children and adoles-cents was associated with a variety of psychiatric and medicalconditions, including mental retardation and autism. Fourth,no biological or genetic marker for childhood catatonia isevident, a situation similar to that in adults. Fifth, benzodi-azepines and ECT are good candidate treatments for bothchildhood catatonia and adult catatonia. Although very littleis known regarding the use of ECT in adolescents, and(prepubertal) children especially (112), most published casesyounger than age 12 years in which ECT was used describethe presence of catatonia (113–115). There is also a recentDutch case report of successful ECT use in a 13-year-old girlwith malignant catatonia (116).
8. Catatonia in Autism
Hallucinations and delusions are relatively rare in peoplewith autism, but there is increasing evidence that catatonia isan important cause of impairment in adolescents and youngadults with autism (117). To date, there are two systematicstudies of catatonia in autism (50, 51) that show that cata-tonia occurs in 12 to 17% of adolescents and young adultswith autism. There are also personal accounts of people withautism with problems in this realm, as suggested by thefollowing description (personal communication, 2006, CoralHull):
I used to experience catatonic episodes in my early to mid twen-ties to the extent where I would stop moving. They would eithercome on gradually, slowly shutting down my ability to think,speak, and move or they would be sudden such as my bodyfreezing when involved in a decision making process that mybrain was unable to handle. Asking me something as simple aswhether I wanted pepper or salt on my meal could have me stopmoving in a haze of confusion and immobility where I became astatue. Sometimes I was able to make decisions and other times Iwas unable to.
Such accounts need to be interpreted within the limitationsof self-reporting, but, if studied in conjunction with concur-rent clinical–observational data, may be valuable for patientsand clinicians alike.
In the study of Wing and Shah (50), 17% of a large referredsample of adolescents and young adults with autism satis-fied modern criteria for catatonia. A semistructured inter-view was used to collect information from parents or othercaregivers. Patients were diagnosed with catatonia when anexacerbation of certain behavioral features occurred in suffi-cient degree to interfere with everyday functions of self-care, education, occupation, and leisure. Essential featuresof catatonia were increased slowness affecting movementsand verbal responses, difficulty in initiating and completingactions, increased reliance on physical or verbal promptingby others, and increased passivity and apparent lack ofmotivation. Other associated characteristics were reversal ofday and night, Parkinsonian features (tremor, eye rolling,dystonia, odd stiff posture, freezing in postures), excite-ment and agitation, and increase in repetitive, ritualisticbehavior.
Wing and Shah further reported that 30 individuals withautism aged 15 years or older met criteria for catatonia.Classic autistic disorder was diagnosed in 11 patients (37%),atypical autism in 5 patients (17%), and Asperger disorderin 14 patients (47%). All of those with catatonia were aged15 years or older. None of those younger than age 15 yearshad the full syndrome, although isolated catatonic symptomswere often observed. In the majority of cases, catatonic symp-toms started between 10 and 19 years of age. Five individualshad brief episodes of slowness and freezing during childhood,before age 10 years. Obsessive–compulsive and aggressivebehaviors preceded catatonia in some. Visual hallucinations orparanoid ideas were occasionally reported, but no diagnosis of
464 Dhossche and Wachtel
schizophrenia could be made. Referred patients with catatoniawere significantly more likely than patients without catatoniato have had impaired language and passivity in social interac-tion before the onset of catatonia.
In the second study (51), 13 (12%) of 120 autistic individ-uals between the ages of 17 and 40 years (mean age, 25.5years) had clinically diagnosed catatonia with severe motorinitiation problems. Another four individuals had several cata-tonic symptoms but not the full syndrome. Eight of the 13individuals with catatonia suffered from autistic disorder;the remaining 5 individuals were diagnosed with atypicalautism. The proportion of those with autistic disorder thatwere diagnosed with catatonia was 11% (8/73). Fourteenpercent of those with atypical autism (5 of 35 patients) hadcatatonia.
There are a few important limitations of these two studies.Important variables such as family history and treatment werenot recorded. The authors in both studies did not use DSM-IV criteria for catatonia. However, their definition of catatoniaincluded several DSM-IV core symptoms, including severepsychomotor retardation, decreased verbalizations, posturing,and agitated episodes. The high prevalence of catatonic symp-toms in autism suggests an intricate, but unaccounted for, rela-tionship between autistic and catatonic symptoms.
An increasing number of case reports and case seriesof catatonia in autism satisfying DSM criteria of catatonia(118–128) have been published during the last 15 years. Thereis considerable overlap of psychomotor symptoms betweenthe two disorders, e.g., muteness, echolalia, stereotypicalmovements, and other psychomotor peculiarities (129). Thediagnosis of catatonia in the published cases was made basedon significant worsening of these symptoms and emergenceof other catatonic symptoms. Some of the authors report thatpatients responded to treatment with lorazepam, the benzodi-azepine most often used, and/or ECT. It should be noted thatnone of these studies was controlled and the number of caseswas small.
Autism should be considered as the underlying conditionin patients presenting with catatonia, especially in those withhistories of developmental problems. Psychiatrists workingwith adults are usually much more familiar with schizophreniaand other psychotic disorders than autism. Therefore, cata-tonia may be misdiagnosed as a feature of schizophrenia, andany underlying diagnosis of autism may be missed, leading topossible suboptimal treatment of both catatonia and autism.
9. Catatonia and ChildhoodDisintegrative Disorder
An important clinical implication is the need to assess cata-tonia amid severe regression of unknown cause in prepubertalchildren, because effective anticatatonic therapies become a
treatment option once catatonia is diagnosed. Massive regres-sion, characterized by loss of language, social skills, adap-tive behavior, play, bladder or bowel control, and motor skills,in prepubertal children, followed by an autistic state is thehallmark of childhood disintegrative disorder (CDD). Thesymptom overlap between autistic regression in CDD andcatatonia has been noted, however, direct assessments of cata-tonia in children with CDD are not found in the literature. NoECT use in children with CDD has been reported.
CDD is considered rare, with a pooled estimate acrossfour surveys of 1.7 cases per 100,000 subjects (95% confi-dence interval, 0.6–3.8 per 100,000) (130). However, it isalso likely that an unknown number of cases are not reportedbecause neurologists and other pediatric specialists, whoare not familiar with the psychiatric classification of CDD,label this condition differently, e.g., as encephalopathy orencephalitis. Textbooks describe CDD as sometimes associ-ated with known medical conditions but usually no clear causeis found. Deterioration occurs over the course of weeks ormonths. Residual symptoms include impaired social inter-action, restricted language output, and repetitive behaviors.Follow-up studies have suggested that older age at onset ofautistic symptoms, as in CDD, may be associated with a worseoutcome (131). There is no recommended treatment. CDDand childhood catatonia are both poorly studied and prob-ably poorly recognized. The presence of catatonic symptomsshould be assessed in children with suspected CDD duringthe phase of massive regression (70). Lorazepam and/or ECTshould be considered once the diagnosis is confirmed.
10. Catatonia in Prader–Willi Syndrome
Prader–Willi syndrome (PWS) is a genetic disorder charac-terized by hypotonia at birth, small hands and feet, almondshaped eyes, hypogonadism, short stature, and diabetes (132).Most patients exhibit mild to moderate mental retardationand obesity. Obesity starts in infancy and is accompaniedby compulsive eating. The prevalence is estimated at one in16,000 to 25,000 live births (133–136).
This multisystem disorder occurs in all races and both sexesand arises from the lack of expression of genes on the pater-nally derived chromosome 15q11-13. Candidate genes forPWS in this region are imprinted and silenced on the mater-nally inherited chromosome. The genetic defect underlyingPWS is the absence of expression of one or more genes ofpaternal origin located on the long arm of chromosome 15(15q11-13). Several genetic mechanisms have been associ-ated with PWS, mainly paternal 4-Mb deletion (in ∼60% ofcases) and maternal uniparental disomy (UPD) (in ∼25% ofcases) (137). In a small number of patients (3%), imprintingerrors are found because of either a sporadic or an inheritedmicrodeletion in the imprinting center. There is a paternalchromosomal translocation in 1% of the cases. Imprinting
27. Catatonia in Psychiatric Illnesses 465
occurs partly through parent-of-origin allele-specific methy-lation of CpG residues, which is established either duringor after gametogenesis and maintained throughout embryo-genesis. Alternatively, if the deletion is maternal or there aretwo paternal copies of chromosome 15q, another syndromeis found, i.e., Angelman syndrome, characterized by severemental retardation, attention deficit, inappropriate laughter,ataxia, jerky gait, epilepsy, sleep disturbances, and craniofa-cial abnormalities (138).
Recent studies have shown that compulsions (132, 139)and psychotic disorders (140, 141) are associated with PWS.Compulsive behaviors in PWS are autistic-like and includeinsistence on sameness (142), perseveration, and ordering.Hand washing and checking, i.e., symptoms that are typi-cally found in OCD, are infrequent in PWS. Negativism andstereotypic movements of the self-injurious variety, particu-larly skin picking and scratching, have also been identifiedin PWS (143). Various psychotic symptoms, including para-noia, hallucinations, and bizarre behavior, have been reportedin PWS patients, usually in combination with affective symp-toms (140). The acute onset and mixture of affective andpsychotic symptoms suggest an atypical form of psychosis.
PWS patients with UPD seem particularly prone to developpsychosis (141, 144, 145). This suggests that an abnormalpattern of expression of sex-specific imprinted genes on15q11-13 is a risk factor for psychosis in PWS. Superiorvisual recognition memory is another feature in PWS thathas been associated with maternal UPD (146). The genesinvolved in the development of psychosis and superior recog-nition memory in PWS are unknown.
There is one detailed description in the literature of acute,full-blown catatonia that developed in an adolescent withPWS and that responded to lorazepam treatment (105). Cata-tonic symptoms have been described in other patients withPWS, but a formal diagnosis was not made. For example,Clarke (140) reported an acutely psychotic PWS patientwith significant psychomotor retardation, refusal of foodand fluids, and negativistic behavior. Abe and Ohta (147)described an adolescent with PWS who developed stupor,pallor, and delusional thinking. Bartolucci and Younger (148)observed, in four of nine youngsters with PWS, discreteepisodes of a refusal–lethargy syndrome, characterized by
akinesis, refusal of foods and fluids, incontinence, andself-neglect, which occurred independently from psychoticepisodes and lasted weeks up to several months. Thesedescriptions suggest the presence of catatonia. Catatoniamight have gone unrecognized, because some catatonic symp-toms are transient and need to be elicited by trained clinicians.Systematic studies are needed to assess the prevalence of cata-tonia in PWS. The clinician should consider a diagnosis ofcatatonia in people with PWS with onset of psychosis andpsychomotor abnormalities, and implement effective anticata-tonic treatments (149).
11. Evaluation of Catatonia
In Fig. 27.9, an evaluation algorithm for catatonia ispresented.
Catatonia should be considered in any patient if thereis an obvious and marked deterioration in psychomotorfunction and increase in unresponsiveness compared withprevious levels. This should prompt a thorough clinical assess-ment. Physical examination and laboratory investigationsare dictated by clinical assessment. Infectious, metabolic,endocrinological, neurological, and autoimmune diseaseshave been associated with catatonia and must, therefore, beexcluded. For an in-depth review, we refer to two recent publi-cations on this subject (13, 150).
All prescribed medications should be evaluated for theirpotential to induce catatonic symptoms because many medicaland psychiatric medications can cause catatonia or catatonia-like conditions (13, 151). Antipsychotic agents should bediscontinued because they are contraindicated in patients whoexhibit the signs of catatonia because of the reported increasedincidence of malignant catatonia or NMS in patients withincipient signs of catatonia. When the catatonia is resolved,antipsychotics may be useful for select indications, but anyreemergence of catatonic symptoms should prompt discontin-uation.
Illicit drugs (PCP, mescaline, psilocybin, cocaine,opiates, and opioids), disulfiram, steroids, antibiotic agents(ciprofloxacin), and bupropion have also been associatedwith the emergence of catatonia in case reports. Withdrawal
Figure 27.9. Algorithm for the evaluation and assessment of catatonia.
466 Dhossche and Wachtel
of benzodiazepines, gabapentin, and dopaminergic drugs,especially if done rapidly, has precipitated catatonia in somepatients (13). As with antipsychotics, antidepressants or anyother type of psychiatric medication may be indicated forselect indications, when the catatonia is resolved, but reemer-gence of catatonic symptoms should prompt discontinuation.
Different criteria for a diagnosis of catatonia are usedin clinical practice and research. It is unknown how thesedifferent criteria compare and which set of criteria is best,because there is no gold standard. Fink and Taylor (13)proposed to base the diagnosis on the presence of immobility,mutism, or stupor of at least 1-hour duration, associated withat least one of the following: catalepsy, automatic obedience,or posturing, observed or elicited on two or more occasions.Alternatively, in the absence of immobility, mutism, or stupor,the diagnosis is based on at least two of the following, whichcan be observed or elicited on two or more occasions: stereo-typy, echolalia/echopraxia, waxy flexibility, automatic obedi-ence, posturing, negativism, or ambitendency. These criteriaare less applicable to mute patients, or the majority of autisticpatients with baseline symptoms such as echophenomena,stereotypy, negativism, or other psychomotor abnormalities(129). Therefore, diagnostic criteria specific for catatonia inautism have been proposed in which drastically decreasedspeech replaces mutism and the duration of symptoms islonger (152). A rating scale or checklist may aid the quantifi-cation of catatonia. Several scales have been published duringthe last 10 years and have been discussed elsewhere (13, 21).None of these scales have been applied to autistic populations.
12. Medical Treatment of Catatonia
In Fig. 27.10, a medical treatment algorithm for catatonia ispresented based on the cumulative experience in this area (13,21, 153). The lack of controlled studies must be emphasized,as well as the limited number of published cases of catatoniain select disorders such as autism or PWS.
The algorithm features the lorazepam challenge test for therapid resolution of acute catatonia. The intravenous adminis-tration of amobarbital, lorazepam, or diazepam relieves cata-tonia in more than half of the patients. Specifically, an intra-venous line is established and a syringe containing 2 mg to
If positive result,Lorazepam Continuation
If negative result,Bilateral ECT
If positive, Lorazepam Trial If negative, Bilateral ECT
Lorazepam Challenge Test
Catatonia
Figure 27.10. Algorithm for the medical treatment of catatonia.
4 mg lorazepam in 2 ml (or larger volumes) of solution isprepared, and 1 mg is injected. In the next 2 to 5 minutes, anychanges are noted. If no change is observed, the second 1 mgof lorazepam is injected, and the assessment is repeated.
Lorazepam treatment in any mode of administration (intra-venous, intramuscular, oral) has a wide margin of safety.The most common side effect is sedation that may requirespecial attention in people with chronic obstructive pulmonarydisease, obstructive sleep apnea, or obesity. As with any medi-cation, appropriate safe guards should be in place for theoccurrence of allergic reactions.
If improvement is seen after the challenge test, treatmentwith increasing doses of lorazepam as high as 24 mg/day isrecommended. Improvement should be observed at least after3 days before considering bilateral ECT. Once the efficacyof lorazepam is demonstrated, a 6- to 12-month continuationphase commences. Although the usual dose range of 6 to 24mg/day is considered “high” in conventional psychopharma-cology, higher doses are reported to be helpful in catatonia.Lorazepam should be slowly tapered after the continuationphase to avoid withdrawal symptoms caused by tolerance.
ECT is indicated in severe catatonia when the lorazepamchallenge test fails or increased dosages do not bring rapidrelief. In such circumstances, ECT may be life-saving,and should be promptly considered, even in the face offrequent negative misconceptions regarding ECT in both theprofessional and lay communities. A few technical issuesconcerning electrode placement and concurrent medicationuse need to be considered to maximize the effect of ECT. Theefficacy of bilateral (bitemporal or bifrontal) electrode place-ment is better documented than is unilateral placement, andthe use of bilateral placement is, therefore, recommended. Allpsychiatric medications should be stopped before initiationof ECT, as well as any other nonpsychiatric medications, ifpossible.
The relief of catatonia often seems to require more frequentseizures than does the relief of major depression. In severeor malignant catatonia, daily treatment for 3 to 5 days maybe needed. The number of sessions that will be neededbefore substantial improvement or remission occurs cannot bepredicted. It seems reasonable to assess the patient’s overallresponse after the first 5 or 6 treatments, and then again after10 or 12 treatments. The cognitive and noncognitive sideeffects of ECT are well known and manageable (154).
Options for continuation treatment after an effective ECTcourse may include continuation of the lorazepam treatmentor continuation of ECT on an outpatient basis. Although theguidelines for frequency and number of ECT treatments arepoorly defined, weekly and biweekly ECT treatments may beneeded for up to 6 months to ensure a stabilized response.
27. Catatonia in Psychiatric Illnesses 467
Acknowlegment
The authors thank Edward Shorter, Hannah Professor in theHistory of Medicine at the University of Toronto, for valuablesuggestions and for lending a copy of Oswald Bumke’s 1924textbook.
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