Dr. Dhossche is professor and Dr. Wilson is resident in the Department of Psychiatry at the University of Mississippi Medical Center in Jackson. Dr. Wachtel is assistant professor in the Department of Psychiatry at Johns Hopkins University School of Medicine, Kennedy Krieger Institute, in Baltimore, Maryland.
Disclosure: The authors report no affiliation with or financial interest in any organization that may pose a conflict of interest.
Please direct all correspondence to: Dirk M. Dhossche, MD, PhD, Professor, Department of Psychiatry, University of Mississippi Medical Center, 2500 N State St, Jackson, Mississippi 39216; Tel: 601-984-5805; Fax: 601-984-6965; E-mail: firstname.lastname@example.org.
The study of catatonia in children and adolescents shows that its presentation is similar as in adults and, as such, is readily diagnosable. Catatonia occurs in children and adolescents with affective, psychotic, autistic, developmental, drug-induced, and medical disorders. Benzodiazepines and electroconvulsive therapy, the treatments that have historically proven to be effective in adults with catatonia, also improve catatonia in children and adolescents. These findings shed new light on the importance of catatonia in psychiatric impairments across the lifespan by loosening the purported link between catatonia and schizophrenia, and thereby supporting an independent category of catatonia in psychiatric classification. Catatonia, a treatable syndrome, occurs in children and adolescents, and warrants prompt identification and treatment.
• Catatonia occurs in children and adolescents with affective, psychotic, autistic, developmental, drug-induced, and medical disorders, but its prevalence is unknown due to lack of systematic studies.
• The symptoms of catatonia in youths are the same as in adults.
• Catatonia in youths is a treatable syndrome, regardless of any underlying disorders; its primary treatments, also effective in adults, are benzodiazepines and electroconvulsive therapy.
• Child psychiatrists and other pediatric specialists should be attentive to the diagnosis of catatonia in their patients given that effective treatment is available.
• The study of catatonia in youths supports an independent category of catatonia in psychiatric classification.
Systematic controlled studies of catatonia in childhood and adolescence are lacking in modern literature. Findings in this area are based on case reports and smaller studies1-8 supporting the occurrence of catatonia in children and adolescents diagnosed with affective, psychotic, autistic, developmental, drug-induced, and medical-neurologic disorders.
An overview of associated conditions of catatonia in children and adolescents is provided in Table 1.7-22 The frequencies of the most common catatonic symptoms in children and adolescents are shown in Table 2.8 Rates for urinary and fecal incontinence as a feature of catatonia are only available for pediatric patients.
These findings in pediatric patients mostly parallel findings of catatonia in adult patients. Between 10% and 15% of adult patients with catatonia meet the criteria for schizophrenia. Various neurologic, medical, and drug-related etiologies23 are also found in adult patients with catatonia. Although there are no controlled treatment studies in catatonia, the literature consistently shows positive effects of benzodiazepines and barbiturates, and of electroconvulsive therapy (ECT), regardless of the severity or etiology of catatonia24-26 or age of the patient.7,27-32
On a historic note, catatonia was originally described in 1874 by Kahlbaum33 as a separate brain disorder with a cyclic, alternating, and progressive course. It was incorporated as a type of dementia praecox or schizophrenia by Kraepelin34 in 1896. In the 1970s, various authors described catatonia to be a feature in affective disorders in adults, particularly mania.35-37
Recent reports contradict the rarity of pediatric catatonia. Approximately 33% (12 of 38) of children with schizophrenia exhibited catatonic signs in one report,38 although no formal diagnoses of catatonia were made. Another study13 of 198 child and adolescent psychiatric outpatients showed a 5% prevalence of catatonia, and 17% prevalence in the subgroup with psychotic disorders. Catatonia has been increasingly recognized as a comorbid syndrome of autism.11 Two systematic studies39,40 show catatonia to occur in 12% to 17% of adolescents and young adults with autism. A caveat in these studies is that medication status was not fully described. This should be addressed in future studies given the overlap between antipsychotic-induced parkinsonism and catatonia in some cases.
Is catatonia underdiagnosed in children and adolescents? In the early 1980s, catatonia was thought to be almost extinct. However, recent studies report prevalence rates of catatonia between 7% to 17% in acute adult psychiatric inpatients23,41 and show that, although its symptoms are easily recognized, catatonia is underdiagnosed42,43 in adults with affective and psychotic disorders, leaving specific anti-catatonic treatments like benzodiazepines and ECT underused. Underdiagnosis of catatonia may be due to the historic decision to classify catatonia as a type of schizophrenia, the segregation of severely ill psychiatric patients and patients with developmental disorders in long-term facilities, the perceived lack of anti-catatonic treatments, and the disparagement of physical and neurologic examination by psychiatrists.23
Diagnostic and therapeutic errors of omission may also be instrumental in poor recognition of catatonia in children and adolescents given the considerable stigma and ambivalence surrounding pediatric ECT in the general and medical community. While errors of commission, such as operating on the wrong knee, may be more visible and anxiety provoking, errors of omission undoubtedly have an enormous cumulative impact on patient outcomes including or especially in psychiatry in the United States and in other countries.44,45 Such errors in pediatric patients concern the failure to diagnose or avoidance of perceived high-risk diagnoses (ie, severe or lethal catatonia), or not providing appropriate perceived high-risk or controversial treatments (ie, high-dose benzodiazepines or ECT), leading to undertreatment or no treatment at all.
Catatonia should be considered in any pediatric patients when there is a marked deterioration in psychomotor function and overall responsiveness. Infectious, metabolic, endocrine, neurologic, toxic, and autoimmune conditions have been associated with catatonia and must therefore be ruled out. A drug screen to detect common illicit and prescribed substances is necessary. All prescribed medications should be evaluated for their potential to induce catatonic symptoms since many medical and psychiatric medications can cause catatonia or catatonia-like conditions.23,46 Antipsychotic agents should be discontinued as they are contraindicated in patients who exhibit the signs of catatonia because of the reported increased incidence of malignant catatonia or neuroleptic malignant syndrome (NMS) in patients with incipient signs of catatonia.
Although different criteria for a diagnosis of catatonia are used in clinical practice and research, the authors of this article find the criteria proposed by Fink and Taylor23 most relevant based on experience in pediatric populations. Diagnosis is based on the presence of immobility, mutism, or stupor of at least 1 hour duration, associated with at 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, which can be observed or elicited on two or more occasions: stereotypy, echolalia/echopraxia, waxy flexibility, automatic obedience, posturing, negativism, or ambitendency.
The proposed medical treatment Algorithm for catatonia reflects the cumulative experience in this area,11,23,26 and features the lorazepam test (by mouth, intravenous, or intramuscular administration of lorazepam 1–2 mg) for the rapid resolution of acute catatonia. If improvement is seen after the challenge test, treatment with increasing doses of lorazepam is recommended. The reports cite doses up to 30 mg as necessary in adults. The authors’ experience shows that in some adolescents with catatonia, doses up to 24 mg are tolerated without ensuing sedation and result in marked reduction of catatonic symptoms. This suggests that in some cases, catatonia may be associated with high tolerance to benzodiazepines. However, careful monitoring in a medical setting for excessive sedation, respiratory compromise, and other side effects is mandatory.
ECT is indicated in catatonia when increased dosages of lorazepam do not bring rapid relief. The efficacy of bilateral (bitemporal or bifrontal) electrode placement is better documented than is unilateral placement. The concurrent use of lorazepam and ECT is a useful treatment variant when lorazepam treatment brings benefits but not complete remission or return to baseline function. Intravenous administration of flumazenil, a benzodiazepine antagonist, can be used if lorazepam interferes with eliciting seizures during ECT. In a case series, synergy of lorazepam and ECT treatment using flumazenil was observed.47
The relief of catatonia requires more frequent seizures than does the relief of major depression. In severe or malignant catatonia, daily “en bloc” treatment for 3–5 days may be needed. The number of sessions needed before substantial improvement or remission occurs varies greatly per case.
Continuation treatment after an effective ECT course with lorazepam or maintenance ECT (M-ECT) is essential as relapse after short courses of treatment is common. A flexible approach to the frequency of treatments in M-ECT is preferable and should be guided by patient tolerability and clinical status. Several pediatric patients have maintained stable improvements with M-ECT but relapse if the intensity of M-ECT is decreased.
Case Vignette Of Adolescent Catatonia
M is a 16-year-old adolescent who was in a good state of physical and mental health until he became preoccupied with food and the sinfulness of eating. These obsessions increased for several months, and one morning, M was found rigid in front of his computer with his arms extended outwards above his lap. Parents were initially unable to move M at all. With much prompting he was able to ambulate with physical assistance, but moved very slowly with ongoing staring, mutism, unresponsiveness, and frequent posturing. M was admitted to a psychiatric facility, diagnosed with catatonia and psychosis, and started on olanzapine and lorazepam, but then developed food refusal with resultant need for intravenous hydration. Olanzapine was discontinued and risperidone was begun with lorazepam ordered only on a PRN basis. Catatonic symptoms worsened rapidly, including posturing, mutism, stupor, rigidity, food refusal, and incontinence. Risperidone was discontinued with improvement lasting for a few days only. M then presented again to the emergence room with reduced responsiveness and speech other than utterances, prominent waxy flexibility, and posturing, and was re-admitted.
During this admission, a neurologic work-up was conducted and found to be negative. magnetic resonance imaging and electroencephalogram were both within normal limits. The urine toxicology screen was negative. Catatonic symptoms in M waxed and waned during the next 6 weeks when he continued to be treated with various low doses of lorazepam and risperidone. Typically, when doses of lorazepam were increased, catatonic symptoms quickly resolved and M requested several food items and ate them, moved readily around his room, and was able to engage in normal conversation. M reported feeling “really weird” and remembering wanting to move his limbs but being unable to do such. He also reported remembering thinking that he “could not and should not eat.” Risperidone and lithium carbonate were also prescribed to target psychosis as evidenced by ongoing discussions of demons and auditory hallucinations telling M not to eat, and to target potential underlying mania. When catatonic symptoms remained absent for 2 weeks, lorazepam was decreased to 1 mg TID; within days, M became unresponsive and mute, with posturing and waxy flexibility, incontinence, and food refusal, laying in bed immobile and purring all day. Agitation, incoherent yelling, aggression and self-barricading in the bathroom followed, as well as ongoing posturing episodes and sudden bursts of self-slapping behavior.
At this juncture, ECT was finally pursued due to the severity of impairment and clear lack of efficacy of psychotropics. All psychotropics were stopped. M received seven bilateral ECT treatments over the course of 14 days, resulting in complete remission of all catatonic, psychotic, and affective symptoms. ECT was terminated after seven treatments, yet within 4 days M began again to report vivid thoughts of religious character, delusions related to devils, and disturbed sleep. Parents refused further antipsychotic trials based on past poor response, and elected to return to ECT. The patient received a second course of five ECT treatments, with complete resolution of symptoms. M was discharged and continued with four outpatient ECT treatments once weekly followed by an additional four ECT treatments every other week. M has remained without psychiatric symptoms since stopping ECT 6 months ago, and was able to return to school.
The case vignette is fictitious and intended to illustrate the convoluted diagnostic and treatment trajectory that follows when unequivocal catatonia currently presents in children and adolescents, as treatments targeting psychosis or depression are usually pursued more often and more vigorously than the treatment specifically targeting catatonia.
Typically, after considerable delay and ineffective trials of different classes of psychotropic medications, ECT is pursued and proves to be the definitive treatment for catatonia whose symptoms are clearly present in the early stages of illness. Continuation ECT consolidates the resolution of catatonia, and no further treatment is needed. Other patients need longer courses of maintenance treatment to avoid relapses, or treatment of symptoms that are independent of catatonia.
Lorazepam, sometimes prescribed as a PRN agent for “agitation” and not for catatonia, is found to improve catatonia allowing the patient to start communicating, eating, and drinking for a few hours. However, lorazepam is usually prescribed at low doses and is not continued, leaving catatonia only partially resolved and prone to relapse. Although antipsychotics should not be used or should be discontinued as there is a risk for precipitating malignant catatonia or NMS in patients with incipient signs of catatonia, trials of antipsychotics and antidepressants in patients with catatonia are a common strategy in an attempt to improve latent or possible underlying affective or psychotic disorders. However, catatonia often then remains the primary source of psychiatric impairment and is left untreated. Unfortunately, specific anticatatonic treatments are often not considered until catatonia worsens or only after considerable delay.
Catatonia In the DSM-5
One of the most important changes for clinical practice debated in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,48 work group responsible for psychotic disorders concerns the further separation of catatonia from schizophrenia. Catatonia is currently found in several categories of the DSM-IV,49 and this may add to diagnostic confusion and poor selection of effective treatment for catatonia. First, catatonia due to a general medical condition (code 293.89) is listed as a distinct entity in the section on medical conditions. Second, the catatonia subtype of schizophrenia (code 295.20) is one of the original Kraepelinian forms of schizophrenia listed since the DSM-I50 in 1952. Third, catatonia is an episode specifier for depressive disorder and bipolar disorder but without separate diagnostic codes. Fourth, the diagnosis of NMS, which some consider a form of malignant catatonia,51,52 is listed separately as a medication-induced movement disorder.
The degree of independence that catatonia should be allotted in DSM-5 is actively debated. Fink and colleagues53 and Rosebush and Mazurek54 believe that catatonia deserves a home of its own in psychiatric classification,23,53,55 and that catatonia’s divorce from schizophrenia and its recognition as an independent syndrome, akin to delirium, are needed in the next psychiatric classification. Independence of catatonia would increase timely recognition of its frequent comorbidity with affective disorders and general medical disorders, and increase attention to specific diagnostic and therapeutic measures (specifically high-dose benzodiazepines and ECT) that are commonly overlooked. Catatonia research would also benefit from greater convergence with the existing body of research on repetitive behavior disorders.
Ungvari and colleagues56 warn against completely severing catatonia from the major psychotic and mood disorders as this may lead to continued neglect of catatonia as a valid syndrome and to continued exclusion from vital research on the significance of psychomotor phenomena as a symptom dimension of psychotic and mood disorders. Heckers and colleagues57 ponder the use of specifiers to diagnose catatonia in three different patients groups (ie, schizophrenia, mood disorder, and general medical condition) versus the creation of an independent category of catatonia:
“The crucial step is a divorce of catatonia from schizophrenia. As divorces go, this is a nasty one… It appears problematic for catatonia to become a completely independent diagnostic class as it is not a single condition but an expression of several different disorders and because of the particular difficulties it would create for the nosology of schizophrenia… It may be justified to give catatonia more prominence in the next edition of the DSM, by consolidating catatonia across different diagnoses into one section. If such a consolidation does occur, it should likely be in the section on Psychotic Disorders because catatonia is a dimension of psychosis.”57
Despite warnings that a complete divorce between catatonia and psychosis would be nasty,57 the authors of this article believe it should be done, not only for the reasons already mentioned but also “for the sake of the children”. Separating catatonia from psychosis and schizophrenia would improve early diagnosis and treatment of catatonia in children and adolescents, especially those with autistic or developmental disorders, outweighing any negative or unintended consequences. The occurrence of catatonia in adolescents with a non-psychotic disorder like autism is an important finding that further loosens the historic link between catatonia and psychosis/schizophrenia. Systematic studies and treatment trials of catatonia are warranted in children and adolescents with affective, psychotic, autistic, developmental, drug-induced, and medical conditions.
ECT is likely to remain an essential component in the treatment of catatonia. Wider recognition of the benefits of ECT in pediatric catatonia will help to reduce stigma of ECT that is widespread when recommended for children and adolescents or patients with developmental disorders. To a lesser extent, this would also apply to the application of benzodiazepines that are frowned upon when prescribed in high doses, but often critical for treatment. PP
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