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AUTISM/AS AND CATATONIA

Although the co-occurrence of Catatonia and autism/AS is said to be low, it’s been increasingly recognized in adolescents and young adults on the spectrum over the last 15 years. The following article includes case studies, a book review, links for further reading/research, hopefully providing the reader with a greater understanding of what’s considered an enigmatic condition. Before we take a closer look at all aspects of this particular condition, it’s important to point out the dangers in regard medication, specifically neuroleptics. I’m familiar with autistic people who experience catatonia. They would tell you that the following information on neuroleptics cannot be emphasized enough.


Neuroleptics are a class of drugs often strongly not recommended for people with catatonia.


There is, among life-threatening reactions:

 

1. Neuroleptic malignant syndrome.
2. Tardive dyskinesia affecting the airway (through affecting swallowing or breathing).
3. Acute dystonic reaction affecting the airway.
4. Anaphylactic shock.

 

For further information on this particular class of drugs and autistic people, please refer to “APANA”:

http://www.dinahm.pwp.blueyonder.co.uk/

frozen in time

 

The following information was last updated April, 2008 courtesy of Research Autism.
It provides us with a fairly comprehensive yet concise overview of what precisely Catatonia is, its prevalence, its causes, effects, interventions and some excellent Research articles and reading materials for those with a specific interest in this area.

http://www.researchautism.net/asditem.ikml?t=3&ra=45&infolevel=4

 

Description

 

Catatonia is a complex disorder covering a range of abnormalities of posture, movement, speech and behaviour associated with over- as well as under-activity.

 

There is increasing research and clinical evidence that some individuals with autism spectrum disorders, including autism and Asperger syndrome, develop a complication characterised by catatonic and Parkinsonian features (Wing and Shah, 2000; Realmuto and August, 1991).

 

In individuals with autistic spectrum disorders, catatonia is shown by the onset of any of the following features:

  •  
  • *increased slowness affecting movements and/or verbal responses;
  • *difficulty in initiating completing and inhibiting actions;
  • *increased reliance on physical or verbal prompting by others;
  • *increased passivity and apparent lack of motivation.
  • *other manifestations and associated behaviours include Parkinsonian features including ‘freezing’, excitement and agitation, and a marked increase in repetitive and ritualistic behaviour.

 

When there is deterioration or an onset of new behaviours, it is important to consider the possibility of catatonia as an underlying cause.

 

Prevalence

 

Catatonia appears to be a relatively rare problem in people with autistic spectrum disorders.

 

For example, In a study of referrals to Elliot House who had autistic spectrum disorders, it was found that 17% of all those aged 15 and over, when seen, had catatonic and Parkinsonian features of sufficient degree to severely limit their mobility, use of speech and carrying out daily activities.

 

It was more common in those with mild or severe learning disabilities (ID), but did occur in some who were high functioning.

 

Causes

 

There is little information on the cause of catatonia. In the Eliot House survey, the development of catatonia in some people, seemed to relate to stresses arising from inappropriate environments and methods of care and management. The majority of the cases had also been on various psychotropic drugs.

 

Effects

 

Catatonia can have severe effects in people with autistic spectrum disorders. For example it can be very distressing for the individual concerned and it is likely to exacerbate the difficulties with voluntary movement and cause additional behavioural disturbances.

 

Interventions

Scientific evidence for interventions

There is no valid and reliable scientific evidence to show which interventions are effective in treating catatonia in people with autistic spectrum disorders.

There is very little evidence about effective treatment and management of catatonia. No medical treatment was found to help those seen at Elliot House (Wing and Shah, 2000). There are isolated reports of individuals treated with anti-depressive medication and electro-convulsive therapy (ECT) (Realmuto and August, 1991; Zaw et al, 1999).

 

Research

 

If you are a UK resident you may be able to obtain full copies of some of the items listed on this page from your local public library, your college library, or the National Autistic Society’s Information Centre. You may also be able to obtain copies of items from the publishers of those items.

  •  
  • *Brasic JR et al. (2000). Dyskinesias differentiate autistic disorder from catatonia. CNS Spectr, 5(12), pp. 19-22. Read Abstract
  •  
  • *Bush G. et al (1996) Catatonia. I. Rating scale and standardising examination. Acta Psychiatrica Scandinavica, 93 , pp. 129-136. Read Abstract
  •  
  • *Dhossche DM, Carroll BT, Carroll TD. (2006). Is there a common neuronal basis for autism and catatonia? Int Rev Neurobiol., 72, pp. 151-164. Read Abstract
  •  
  • *Gillberg C. and Steffenburg S. (1987) Outcome and prognostic factors in infantile autism and similar conditions: a population based study of 46 cases followed through puberty. Journal of Autism and Developmental Disorders, 17(2), pp. 273-287. Read Abstract
  •  
  • *Kakooza-Mwesige A, Wachtel LE, Dhossche DM. [Epub ahead of print]. Catatonia in autism: implications across the life span. Eur Child Adolesc Psychiatry. Read Abstract
  •  
  • *Neumarker KJ. (2006). Classification matters for catatonia and autism in children. Int Rev Neurobiol, 72, pp. 3-19. Read Abstract
  •  
  • *Ohta M, Kano Y, Nagai Y. (2006). Catatonia in individuals with autism spectrum disorders in adolescence and early adulthood: a long-term prospective study. Int Rev Neurobiol, 72, pp. 41-54. Read Abstract
  •  
  • *Realmuto G. and August G. (1991) Catatonia in autistic disorder; a sign of comorbidity or variable expressions? Journal of Autism and Developmental Disorders, Vol. 21 (4), pp. 517-528. Read Abstract
  •  
  • *Schieveld JN. (2006). Case reports with a child psychiatric exploration of catatonia, autism, and delirium. Int Rev Neurobiol., 72, pp. 195-206. Read Abstract
  •  
  • *Shah A, Wing L. (2006). Psychological approaches to chronic catatonia-like deterioration in autism spectrum disorders. Int Rev Neurobiol, 72, pp. 245-264. Read Abstract
  •  
  • *Stoppelbein L, Greening L, Kakooza A. (2006). The importance of catatonia and stereotypies in autistic spectrum disorders. Int Rev Neurobiol, 72, pp. 103-118. Read Abstract
  •  
  • *Takaoka K, Takata T. (2007). Catatonia in high-functioning autism spectrum disorders: case report and review of literature. Psychol Rep, Dec, 101(3), pp. 961-969. Read Abstract
  •  
  • *Wing L. and Shah A. (2000) Catatonia in autistic spectrum disorders. British Journal of Psychiatry, Vol. 176 , pp. 357-362. Read Abstract
  •  
  • *Wing L, Shah A. (2006). A systematic examination of catatonia-like clinical pictures in autism spectrum disorders. Int Rev Neurobiol, 72, pp. 21-39. Read Abstract
  •  
  • *Zaw F. K. et al (1999) Catatonia, autism and ECT. Developmental Medicine and Child Neurology, Vol. 41, pp. 843-845. Read Abstract

http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=2596

 

Reading

 

Publications on this issue, other than scientific trials which have been published in peer-reviewed journals:

 

If you are a UK resident you may be able to obtain full copies of some of the items listed on this page from your local public library, your college library, or the National Autistic Society’s Information Centre.

  •  
  • *Lishman W. A. (1998) Organic psychiatry: the psychological consequences of cerebral disorder pp. 349-356. Oxford: Blackwell.
  •  
  • *National Autistic Society. (200?). Mental health and Asperger syndrome. London: NAS. Read Full item
  •  
  • *Rogers D. (1992) Motor disorder in psychiatry: towards a neurological psychiatry. Chichester: Wiley.
  •  
  • *Shah A. and Wing L. (2006) Psychological approaches to chronic catatonia-like deterioration in autism spectrum disorders. In Dhossche D.M. et al (eds.) Catatonia in autism spectrum disorders pp. 246-260 Academic Press.


The following book review is provided courtesy of “Communication” – NAS Magazine Volume 40 Number 3 Autumn 2006.

Catatonia in Autism Spectrum Disorders

Edited by Dirk M. Dhossche, Lorna Wing, Masataka Ohta and Klaus-Jurgen Neumarker.

Published by Elsevier http://www.elsevier.com/wps/find/bookdescription.cws_home/707498/description


Autism and Catatonia


Judith Gould, Director of the Centre for Social and Communication Disorders, reviews the first-ever book published on the relationship between autistic spectrum disorders and catatonia spectrum disorders.

 

Autistic spectrum disorders (ASDs) and catatonia spectrum disorders (CSDs) are each associated with unusual patterns of behaviour and little is known of their underlying nature, so this book is speculative, emphasising how little is known for certain and putting forward hypotheses to stimulate future research.

 

Until recently, ASDs were considered to be the province of child psychiatrists and psychologists, whereas CSDs were seen in the context of psychiatric illnesses, such as schizophrenia, that affect adults but which could also occur in children. However, when all the features that can be found in ASD are compared with all those that can be found in the catatonia spectrum, the remarkable degree of overlap cannot be denied. Both sets of conditions manifest many similar peculiarities of speech, posture, movement and behaviour. The most severe form of catatonia is catatonic stupor, where the person is immobile, holds strange postures and is mute. This may alternate with periods of excitement and irrational behaviour. However, catatonic features include slow movements, tip-toe walking, difficulty crossing lines and thresholds, holding hands in odd postures, stereotyped movements, echolalia and many others very familiar in people on the autism spectrum. Catatonic stupor can occur in autism but seems to be rare. However, perhaps 10% of adolescents and adults on the autism spectrum show marked exacerbation of the catatonia-like features to an extent that interferes with everyday activities. This is referred to as ‘catatonia-like deterioration’.

 

The first three sections of the book concern theoretical and practical issues of classification, assessment and the underlying biology of autism and CSDs.

 

Further research needed

 

The fourth section concerns behavioural and medical treatments and tackles the controversial subject of the use of electro-convulsive therapy (ECT) in children and adolescents, which arouses strong feelings. Frank Zaw points out the safety and success of ECT in treating catatonia in adults, but acknowledges the lack of evidence for or against its use in children, and in catatonia associated with ASDs, calling for further research.

 

Amita Shah and Lorna Wing discuss the psychological dysfunctions that may underlie catatonia-like deterioration in people on the spectrum and suggest that an unknown number of people who, in the old mental institutions, were diagnosed as having catatonic schizophrenia, were actually on the autism spectrum. They give a detailed description of psychological methods of intervention, with emphasis on providing an organised, stress-free daily programme and the encouragement of movement through verbal or, if necessary, physical prompting and through activities enjoyed by the person concerned.

 

Section five suggests blueprints for the assessment, treatment and future study of catatonia in those ASDs, recommending an initial search for possible causes, such as anti-psychotic medications. Treatment choices are the psychological approach, outlined by Shah and Wing, treatment with high doses of medication, such as lorazepam, or ECT. The authors make suggestions for future research and, given the current dearth of knowledge in the area, the field is wide open.

 

Catatonia-like deterioration affects only a small minority of people on the autism spectrum, but it is a great burden on the person concerned and their family. Perhaps the co-occurrence of autism and catatonia will provide a new and revealing clue to the nature of both conditions and, if this book stimulates research in this field, it will have achieved its objective.

 

Inspiration

 

Lorna Wing’s contribution to the book reflects her special ability to make connections that others have not thought of. Her experience as a psychiatrist, and as the parent of a daughter with classic Kanner’s autism, brought home to her the remarkable degree of overlap between autistic and catatonic features. During her lifetime, Susie Wing was the inspiration for Lorna’s innovative ideas concerning the nature of autism and so it is appropriate that this book has been dedicated to her.

frozen in time

The following information includes news and findings from the most recent studies. We also take a look at 3 case studies, that of an adolescent male, a 35 year old man and a 9 year old boy. Shah and Wing’s invaluable contribution is duly recognized.


Source: http://www.psychiatrictimes.com/display/article/10168/51131


Catatonia


Catatonia is a complex disorder covering a range of abnormalities of posture, movement, speech and behaviour associated with over- as well as under-activity (Rogers, 1992; Bush et al, 1996; Lishman, 1998).


There is increasing research and clinical evidence that some individuals with autism spectrum disorders, including Asperger syndrome, develop a complication characterised by catatonic and Parkinsonian features (Shah and Wing, 2006; Wing and Shah, 2000; Realmuto and August, 1991).


In individuals with autistic spectrum disorders, catatonia is shown by the onset of any of the following features:


  • *increased slowness affecting movements and/or verbal responses;

  • *difficulty in initiating completing and inhibiting actions;

  • *increased reliance on physical or verbal prompting by others;

  • *increased passivity and apparent lack of motivation.

 

Other manifestations and associated behaviours include Parkinsonian features including freezing, excitement and agitation, and a marked increase in repetitive and ritualistic behaviour.


Behavioural and functional deterioration in adolescence is common among individuals with autistic spectrum disorders (Gillberg and Steffenburg, 1987). When there is deterioration or an onset of new behaviours, it is important to consider the possibility of catatonia as an underlying cause. Early recognition of problems and accurate diagnosis are important as it is easiest to manage and reverse the condition in the early stages. The condition of catatonia is distressing for the individual concerned and likely to exacerbate the difficulties with voluntary movement and cause additional behavioural disturbances.


There is little information on the cause or effective treatment of catatonia. In a study of referrals to Elliot House who had autistic spectrum disorders, it was found that 17% of all those aged 15 and over, when seen, had catatonic and Parkinsonian features of sufficient degree to severely limit their mobility, use of speech and carrying out daily activities. It was more common in those with mild or severe learning disabilities (ID), but did occur in some who were high functioning. The development of catatonia, in some cases, seemed to relate to stresses arising from inappropriate environments and methods of care and management. The majority of the cases had also been on various psychotropic drugs.


There is very little evidence about effective treatment and management of catatonia. No medical treatment was found to help those seen at Elliot House (Wing and Shah, 2000). There are isolated reports of individuals treated with anti-depressive medication and electro-convulsive therapy (ECT) (Realmuto and August, 1991; Zaw et al, 1999).


Given the scarcity of information in the literature and possible adverse side effects of medical treatments, it is important to recognise and diagnose catatonia as early as possible and apply environmental, cognitive and behavioural methods of the management of symptoms and underlying causes. Detailed psychological assessment of the individuals, their environment, lifestyle, circumstances, pattern of deterioration and catatonia are needed to design an individual programme of management. General management methods on which to base an individual treatment programme are discussed in Shah and Wing (2001).

Recent studies(as reported in Psychiatric Times) September 1, 2006. Vol. 23 No. 9:


Only 2 systematic studies of catatonia in autism have been reported.3,4 They suggest that catatonia-like features are present in about 1 of 7 (12% to 17%) adolescents and young adults with autism and constitute an important source of impairment in this population. In a recent study, 17% of a large referred sample of adolescents and young adults with autism satisfied modern criteria for catatonia.3 Thirty persons with autism aged 15 years or older met criteria for catatonia. Classic autistic disorder was diagnosed in 11 persons (37%), atypical autism in 5 (17%), and Asperger disorder in 14 (47%).


None of those under the age of 15 years had full catatonic syndrome, although isolated catatonic symptoms were often observed. In the majority of cases, catatonic symptoms started between the ages of 10 and 19 years. Five individuals had brief episodes of slowness and freezing during childhood, before 10 years of age. Schizophrenia was not diagnosed in any of the patients.


In a report based on a population study, 13 (11%) of 120 autistic persons aged 17 to 40 years (mean age 25.5 years) had clinically diagnosed catatonia with severe motor initiation problems.4 Another 4 had several catatonic symptoms but not the full syndrome. Autistic disorder was diagnosed in 8 of the 13 persons with catatonia; atypical autism was diagnosed in the remaining 5. The proportion of those with autistic disorder in whom catatonia was diagnosed was 11% (8 of 73); 14% of those with atypical autism (5 of 35) had catatonia.

 

An increasing number of case reports and case series on catatonia in autism that satisfy DSM-IVcriteria for catatonia have been published in the past 15 years.5-15 There is considerable overlap of psychomotor symptoms between the 2 disorders (eg, muteness, echolalia, stereotypical movements, and other psychomotor peculiarities).16 The diagnosis of catatonia in published cases was based on significant worsening of these symptoms and emergence of other catatonic symptoms. Some of the authors report that patients responded to treatment with lorazepam (the benzodiazepine most often used) and/or ECT. It should be noted that none of these studies were controlled and the number of cases was very small.

 

Case 1: Catatonia in an autistic adolescent

 

A boy in whom Asperger disorder had been diagnosed showed a decline in function at the age of 15 years when he stopped speaking except to family members. His posture deteriorated. He began to slump and would complain of back pain. At school, he refused to enter classrooms and would walk slowly through corridors with his head down. He was unable to retain food in his mouth. Eventually, he required support in order to stand. He showed poor fine and gross motor skills, with difficulty in holding and using implements (such as a knife to butter bread). His speech slowed excessively at home. He would not engage in activities other than those associated with his specific interest in transport, mostly aircraft. By the age of 17 years, it was very difficult to get him to leave the family home. He required assistance washing and dressing and stopped using the toilet. The psychiatrist considered a diagnosis of catatonia but demurred because of the seemingly selective occurrence of symptoms. During medical examinations, the patient was often uncooperative and unresponsive. He refused to take the prescribed diazepam and fluoxetine.


An intensive behavioral intervention was started using the framework set out by Shah and Wing15 for the treatment of catatonia in patients with autism. On evaluation 9 months later, he showed improvement, speaking more and walking almost everywhere independently. He was able to express a wider range of emotion verbally and nonverbally. Recent testing revealed an IQ of 89. Despite the progress made, he continues to show various motility problems across all circumstances, mainly slowness of movement, clumsiness, inability to control movement, poor coordination, freezing of movement, and awkward posture. The parents are pursuing other treatments for his condition.


Diagnostic considerations


A diagnosis of catatonia in this patient is likely. An algorithm for the assessment of catatonia in autism is shown in Figure 1.17 From the age of 15, the patient showed various catatonic symptoms, including mutism, stupor, and posturing, that have remained present although his level of function has recently improved. His symptoms satisfy criteria for catatonia in autism shown in the Table.17

 

TABLE Diagnostic criteria for catatonia in autism

 

Criterion A

 

Immobility, drastically decreased speech, or stupor of at least 1 day’s duration, associated with at least 1 of the following: catalepsy, automatic obedience, or posturing

 

Criterion B

 

In the absence of from baseline, for slowness of movement prompted, freezing stereotypy, echophenomena, ambitendency

 

The severity of catatonia should be determined by assessing the degree to which activities of daily living, occupational activities, and physiologic necessities (eating, drinking, and excretion) are affected. Definitions of mild, moderate, and severe catatonia can be found elsewhere.17 The level of impairment should guide the need for services and staffing levels, as well as the choice of available anticatatonic treatments. At his worst, the patient described above seemed to have severe catatonia–stupor, immobility for most of the day, and need of assistance with food intake–constituting a medical emergency. Patients with features of malignant catatonia (fever, altered consciousness, stupor, and autonomic instability as evidenced by lability of blood pressure, tachycardia, vasoconstriction, and diaphoresis) also fall in this category. Severe and malignant catatonia are indications for administration of lorazepam and ECT.


Does catatonia in autism respond to treatment?


An algorithm for the treatment of moderate catatonia in autism, as in the patient presented in the first case vignette, is shown in Figure 2.17 The proposed schedule relies on the recommendations of some catatonia researchers18,19 and some published case reports and case series.5-15 The psychological approach to treatment outlined below should be available for use in combination with medication or alone if medication fails.

 

Case 2: Lorazepam treatment


Severe psychomotor retardation developed over the last year in a 35-year-old man who was living in a residential treatment facility. His diagnoses included atypical autism, moderate ID, and seizure disorder. He stood motionless for hours, often in odd postures. His speech had decreased considerably, and he required assistance in daily living activities. The psychiatric examination did not reveal hallucinations or delusions. His medications included an antiepileptic agent for long-standing grand mal seizures and an atypical antipsychotic for a tentative diagnosis of psychosis not otherwise specified. Trials of antipsychotic medications have had no effect on his motor symptoms.


At this point, catatonia was diagnosed and a trial of lorazepam was started with the dosage titrated over the course of 2 weeks to 4 mg twice a day. The hospital administrators expressed concern that the patient might become dependent on benzodiazepines, but the psychiatrist assured them that lorazepam at the prescribed high dose is an accepted treatment for catatonia. The patient responded well to treatment, with decreased psychomotor slowness, fewer freezing episodes, and increased socialization. Three months after the start of lorazepam, catatonia had resolved. The patient functioned at baseline level again, and he had resumed work at a sheltered workshop. His medications include an antipsychotic, an antiepileptic, and lorazepam (4 mg twice a day). Lorazepam will be tapered and stopped if the patient continues to do well over the next 3 months.

 

Novel psychological treatment


A new addition to the anticatatonic armamentarium is the psychological method developed by Shah and Wing.15 In brief, the treatment involves keeping the person active, doing what he or she enjoys, using verbal or gentle physical prompts to overcome movement difficulties, and maintaining a predictable structure and routine for each day. The importance of educating caregivers to understand catatonic behavior and to realize that it is not under the control of the patient is paramount. Management techniques for specific issues such as incontinence, freezing in postures, eating problems, and episodes of excitement are specified. This approach can be used in conjunction with medical treatments or when medical treatments fail.

 

Case 3: Pediatric ECT


A 9-year-old boy with apparently normal development but high familial loading of psychosis was admitted for agitation, anxiety, perplexity, negativism, and psychomotor slowing. Stupor, mutism, fever, and facial flushing developed over the next 2 weeks. Results of extensive medical and psychiatric workups were negative. EEG recordings consistently showed overall slowing but no epileptic spikes. The symptoms satisfied criteria for CDD, which is characterized by massive regression after the age of 2 years but before the age 10 of years, followed by autistic symptoms. In the absence of recommended treatments for CDD, other medical and psychiatric diagnoses– including encephalitis and malignant catatonia–were considered. After failed trials with anticonvulsants, antiviral medications, and high-dose benzodiazepines, expert opinions regarding an ECT trial were sought; ECT consent was obtained from the caregiver. Stupor, muteness, and refusal to eat and drink improved rapidly during the first course of 7 treatments, but agitation, stereotypies, repetitive speech, and poor level of function remained.


Despite the widely different developmental and recent history, the symptoms of this patient were similar to those of other children with autism and conformed to the differential diagnosis of CDD. A second ECT course was given because the patient relapsed into stupor and immobility. Again, the most severe catatonic symptoms dissipated, but the patient remained impaired. The patient was discharged and continued with outpatient ECT (once every week or biweekly) for the next 5 months. During that time, the boy slowly returned to baseline function and now attends school and lives at home. There have been no relapses during the past 3 years.

 

Are autistic and catatonic regression related?


This case illustrates the importance of diagnosing catatonia amidst severe regression of unknown cause in prepubertal children in order to select effective therapies. CDD is considered rare, with a pooled estimate across 4 surveys of 1.7 per 100,000 subjects (95% confidence interval, 0.6-3.8 per 100,000).20 However, it is also likely that an unknown number of cases are not reported because neurologists and other pediatric specialists who are not familiar with the psychiatric classification of CDD label this condition differently (eg, as encephalitis). Textbooks describe CDD as sometimes being associated with known medical conditions, but usually no clear cause is found. Deterioration occurs over the course of weeks or months. Residual symptoms include impaired social interaction, restricted language output, and repetitive behaviors. Follow-up studies have suggested that older age at onset of autistic symptoms, as in CDD, may be associated with worse outcome.21 There is no recommended treatment.


Catatonia has also been reported infrequently in children,22,23 although no systematic studies in this age group have been done. The oldest description of catatonic symptoms (in a 3-year-old child) comes from de Sanctis (1908-1909).24 Lorazepam and ECT were reported to be effective in 2 more recently published reports.22,23

 

CDD and childhood catatonia are both poorly studied and probably poorly recognized. Catatonia should be studied systematically in children, adolescents, and young adults with psychiatric, neurologic, and developmental disorders–especially autism and Prader-Willi syndrome.25,26 The symptom overlap between autistic regression in CDD and catatonia should be further assessed, and the presence of catatonic symptoms should be assessed during regression in children with autism.27 Most important, catatonia in children seems to respond to the same treatments as in adults.


Recent accounts provide empirical evidence that catatonia is diagnosable in 7% to 17% of acute psychiatric inpatients and is treatable.18 This contradicts earlier comments that catatonia may have disappeared in adult psychiatry.28 Given these conflicting views and the ambiguous nosologic status of catatonia in DSM-IV,one could argue that catatonia has become like the elephant and the blind men. Many aspects of catatonia are described but the syndromal diagnosis is often not made, possibly leading to suboptimal therapy. The emerging evidence that a similar proportion of autistic adolescents and adults also meet criteria for autism has 2 major clinical implications.


First, catatonia should be considered in any autistic patient of any age when there is an obvious and marked deterioration in movement, pattern of activities, self-care, and practical skills. An outline for diagnostic evaluation in such cases is shown in Figure 1 and the Table. Researchers should seek further evidence that catatonia in autism responds to accepted anticatatonic treatments. Treatment responsiveness is key in clarifying the nature of the beast. Clinicians may find the proposed treatment algorithms for catatonia in autism, as in Figure 2, helpful in the treatment of the disorder in these challenging patients.


Second, autism should be considered as the underlying condition in patients presenting with catatonia, especially in those with histories of developmental problems. Psychiatrists working with adults are usually much more familiar with schizophrenia and other psychotic disorders than autism. Therefore, catatonia may be misdiagnosed as a feature of schizophrenia, and any underlying diagnosis of autism may be missed, leading to possible suboptimal treatment of both catatonia and autism.


Limitations


The lack of controlled studies and the very small number of published cases to date must be emphasized. It is not clear from the available evidence whether treatment with lorazepam and/ or ECT is helpful in all cases of autism in which catatonic features become exacerbated or only in those with very severe forms of catatonia. Another consideration is the likelihood that only examples of successful treatments will be published. These problems emphasize the necessity for more research in this field. Cooperation between centers would be particularly valuable because each clinician is likely to see only a few cases.


Evidence-based References


  • Dhossche D, Wing L, Ohta M, Neumarker K-J, eds. Catatonia in Autism Spectrum Disorders. International Review of Neurobiology, No. 72. San Diego: Elsevier Academic Press; 2006.Wing L, Shah A.

  • Catatonia in autistic spectrum disorders. Br J Psychiatry. 2000;176:357-362.

References
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21. Volkmar FR, Cohen DJ. Disintegrative disorder or “late onset” autism. J Child Psychol Psychiatry. 1989;30: 717-724.
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23. Dhossche D, Bouman N. Catatonia in children and adolescents. J Am Acad Child Adolesc Psychiatry. 1997; 36:870-871.
24. Neumarker KJ. Classification matters for catatonia and autism in children. Int Rev Neurobiol. 2006;72: 3-19.
25. Dhossche DM, Song Y, Liu Y. Is there a connection between autism, Prader-Willi syndrome, catatonia, and GABA? Int Rev Neurobiol. 2005;71:189-216.
26. Verhoeven WM, Tuinier S. Prader-Willi syndrome: atypical psychoses and motor dysfunctions. Int Rev Neurobiol. 2006;72:119-130.
27. Dhossche DM, Rout U. Are autistic and catatonic regression related? A few working hypotheses involving gaba, Purkinje cell survival, neurogenesis, and ECT. Int Rev Neurobiol. 2006;72:55-79.
28. Mahendra B. Where have all the catatonics gone? Psychol Med. 1981;11:669-671.


News Reports


11 April 2008  “Catatonia in childhood schizophrenia explored”:

http://schizophrenia.com:8080/jiveforums/message.jspa?messageID=14533

 

19 May 2008 “ECT:  Doctors don’t know how it works, so why use it?”:
http://www.telegraph.co.uk/health/main.jhtml?xml=/health/2008/05/19/hect119.xml


Further Reading Material:


“Catatonia  From Psychopathology to Neurobiology”

http://www.appi.org/SearchCenter/Pages/default.aspx?k=Catatonia%20%20From%20Psychopathology%20to%20Neurobiology


“It’s Ok, Eli by Carol Surber”

http://www.aspie-editorial.com/2011/01/18/book-its-ok-eli-by-carol-surber/

 

“Catatonia in Autism Spectrum Disorders”

http://www.abebooks.co.uk/servlet/SearchResults?tn=Catatonia+in+Autism+Spectrum+Disorders&x=87&y=13

 

“Psychiatry Weekly: Periodic Catatonic Schizophrenia in a 43-year-old Military Veteran”:

http://www.psychweekly.com/aspx/Article/articledetail.aspx?articleid=1361

 

“Psychiatry Weekly: Medical Aspects of Catatonia”:

http://www.psychweekly.com/aspx/Article/articledetail.aspx?articleid=899

 

“Psychiatry Weekly: Use of the Antibiotic Minocycline to Treat Catatonic Schizophrenia”:

http://www.psychweekly.com/aspx/Article/articledetail.aspx?articleid=394

 

“eMedicine – Catatonia: Article Excerpt by James Robert Brasic”:

http://www.emedicine.com/neuro/byname/catatonia.htm

 

“Jessica Kingsley Publishers” – For a wide range of publications on or including information relating to Catatonia:

http://books.google.com/books/jkp?hl=en&q=catatonia&btnG=Search+Books

rose frozen in time
Last Updated: Saturday 9th March, 2013.

comments (2)

 

1. carol left…

Saturday, 2 May 2009 12:06 am

My son, born with Downs syndrome, was diagnosed at the Ohio State University before age three as autistic. He attended early childhood education classes there for nearly 6 years. By age 16, he experienced a trauma at a new educational setting, unknown trauma, then developed severe, life threatening catatonia. He was mute, posturing, staring and stayed this way for nearly 8 months until….a catatonic specialist intervened and saved him. His name is Dr Brendan Carroll, and at the time, was working at the Neuropsychiatric part of the Ohio State University hospital. His work with catatonia is featured in the book, Catatonia-From Psychopathology to Neurobiology. He worked near 2 years to combine medications to keep Eli in the world..at a functioning level. Eli is now 32, and Dr Carroll stays active in his care. He has episodes of catatonia each day, but they last only minutes. The behavioral episodes of catatonia stay ever present. I kept journals from the time of my son’s birth, through 22 years of his life. Unknowing, I recorded all the pre-symptoms of the catatonia as it emerged and took Eli to another world. I also noted each treatment, medication and side effects. I published the unedited journal , Feb 2008. Titled– It’s Ok Eli– Autism and catatonia is more recognizable in Downs syndrome now…and possibly my book will help explain, accept and find treatment for those afflicted. At age 32, Eli has not regained the speech he lost at age two, his autistic rituals control his days, but he still functions at work, living with his autistic roommate for the past 6 years, and living his life! Love and sunshine to all, Carol and Eli http://stores.lulu.com/store.php?fAcctID=912333

 

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