The role of deprivation, abuse, and trauma in pediatric catatonia without a clear medical cause


D. M. Dhossche, Department of Psychiatry, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA.


Dhossche DM, Ross CA, Stoppelbein L. The role of deprivation, abuse, and trauma in pediatric catatonia without a clear medical cause.

Objective:  Catatonia is considered a unique syndrome of motor signs, at times life-threatening when aggravated by autonomic dysfunction and fever, but eminently treatable with specific medical treatments, if recognized early. Catatonia commonly occurs in children and adolescents with a wide range of associated disorders. The role of deprivation, abuse, or trauma in the development of pediatric catatonia is examined.

Method:  Reports considering deprivation, abuse, or trauma as precipitants of catatonia in pediatric cases are culled from the classic writings on catatonia and from a selective review of modern contributions.

Results:  Kahlbaum gave trauma a central role in catatonia in many young adult cases. Kanner described children with psychogenic catalepsy. Anaclitic depression, a condition found by Spitz in deprived institutionalized children, strongly resembles stuporous catatonia. Leonhard considered lack of communication with the mother or substitute mother as an important risk factor for childhood catatonia. Children including those with autism who experience emotional and physical trauma sometimes develop catatonia. The clinical descriptions of children with classic catatonic syndromes and those of contemporary refugee children with a syndrome labeled Pervasive Refusal Syndrome are similar.

Conclusion:  The literature supports the view that deprivation, abuse, and trauma can precipitate catatonia in children and adolescents.

Clinical recommendations

  •  Children with symptoms of catatonia should be assessed for traumatic and abusive events in family and broader environments in addition to medical causes for catatonia
  •  Pediatric catatonia, especially in the more severe forms, is an urgent indication for medical intervention, regardless of purported etiology
  •  If traumatic or abusive events are suspected or ascertained, specific preventive actions are indicated, and social or psychotherapeutic interventions may be appropriate when the acute symptoms have abated

Additional comments

  •  Catatonic symptoms may be falsely attributed to other disorders or syndromes related to deprivation, abuse, or trauma and labeled as anaclitic depression, quasi-autism, reactive psychosis, and pervasive refusal syndrome
  •  Lack of systematic studies precludes estimates of the number of cases of pediatric catatonia in which deprivation, abuse, or trauma play a role
  •  The usefulness of benzodiazepines and ECT in pediatric catatonia needs to be further assessed


Catatonia is a unique syndrome of motor signs, at times life-threatening when aggravated by autonomic dysfunction and fever, but treatable if recognized early with specific medical treatments. Identifiable motor signs are immobility, sometimes alternating with excessive motor activity that is apparently purposeless and not influenced by external stimuli, extreme negativism or muteness, peculiarities of voluntary movement, echolalia, or echopraxia. Catatonia was originally described in adults by Kahlbaum in 1874 (1). Kraepelin incorporated catatonia as a type of schizophrenia (2) although subsequent studies have shown that the syndrome occurs in adult patients with affective, drug-induced, stress-induced, and medical disorders (3, 4). Unfortunately, catatonia is often erroneously perceived as uniquely associated with schizophrenia (5) and therefore is missed as a distinct treatable syndrome. Clinical reports find benzodiazepines and electroconvulsive therapy (ECT) effective treatments for catatonia.

The study of pediatric catatonia has not received much attention but, during the last few years, progress has been made in delineating this syndrome in children and adolescents across a wide range of disorders (6–8). Catatonia not only occurs in children and adolescents with associated psychotic, affective, drug-induced, or medical disorders, but also in patients with autistic, developmental, and tic disorders, and occasionally in children with no identifiable medical or psychiatric conditions (9, 10). Catatonia is poorly recognized and maybe particularly so in children and adolescents, owing to many factors, including its lack of independent status in psychiatric classification (8), the effects of overshadowing (i.e. the falsely attributing of catatonic symptoms to another disorder) both in children with autistic or other developmental disorders and in children with complex and poorly defined medical or neurological disorders, such as idiopathic encephalopathy or aseptic encephalitis (10, 11). Pediatric catatonia occurs fairly commonly and is treatable as it is in adults, although the number of prepubertal cases in whom catatonia is diagnosed and treated with benzodiazepines and ECT is small (12, 13).

Exhaustive searches for medical causes of pediatric catatonia usually eclipse the assessment of environmental, social, and psychological risk factors despite the absence of medical causes in many cases and the existence of competing theories supporting psychogenic factors in catatonia. Moskowitz (14), for example, has summarized competing theories supporting psychogenic factors in catatonia where catatonia is seen as a fear response, akin to the animal defense strategy of tonic immobility, in which catatonia represents a common end state to impending doom across a wide range of medical and psychiatric disorders.

There is increasing evidence that deprivation, abuse, and trauma in childhood and adolescence are risk factors for the later development of affective and psychotic disorders (15, 16). Their effects are usually not immediate but delayed with a time lag of years between exposure and the onset of psychosis. Therefore, they may be markers for other and more important risk factors for psychosis. Child abuse in itself is difficult to ascertain both in clinical situations and in research. Yet, its importance is paramount owing to the possibility of preventive and therapeutic actions once deprivation, abuse, or trauma is ascertained.

Aims of the study

In this report, the role of deprivation, abuse, or trauma in the development of catatonia is examined.

Material and methods

Reports supporting the view that deprivation, abuse, and trauma may precipitate pediatric catatonia are culled from the classic writings of Kahlbaum and Leonhard on catatonia and from a selective review of pediatric contributions on catatonia, malignant catatonia, catalepsy, stupor, immobility, withdrawal, and muteness as they relate to loss, trauma, deprivation, institutionalization, abuse, and other psychogenic factors.


Specific studies assessing deprivation, abuse, and trauma as risk factors for pediatric catatonia are not found in the literature. Several accounts find catatonia to develop in children, adolescents, and young adults after severe deprivation, abuse, and trauma.

Psychogenesis in Kahlbaum’s catatonia

In Kahlbaum’s 1874 original monograph (1), catatonia is described mainly in adults following a consistent sequence of depression, immobility, mania, and deterioration with terminal dementia. Some people recovered spontaneously and fully after long periods of immobility. Concerning etiology, Kahlbaum says that, ‘In most cases catatonia is preceded by grief and anxiety and in general by depressive moods and affects aimed against the patient himself. Very common are anguish related to unhappy love, or self-reproach resulting from secret sexual misdemeanors; this will be further discussed with the etiology. Next in frequency are financial troubles and injured respect (shame), which constitute the makeup of the initial symptoms’. His general impression of catatonic patients was ‘one of profound mental anguish, or an immobility induced by severe mental shock’.

Catalepsy in childhood

In 1934, Kanner reported six new cases of pediatric catalepsy (i.e. waxy flexibility) (17). Consistent with his time in which all catatonia was not viewed as a separate entity but only in relation to schizophrenia, children with catatonia but without signs of schizophrenia were described as cataleptic or stuporous depending on their main presenting symptom. The children that Kanner described ranged in age from 16 months to 9 years and suffered from infectious and toxic conditions. In one case, he noted ‘pseudocatalepsy’ (‘in which the patient helps the examiner actively in placing the limb in the position which seems to be intended’) which suggested to him the presence of ‘definite hysterical features’. Kanner’s review of the literature contains several cases of catalepsy associated with medical diseases, mainly typhoid fever and rickets, but also a case from 1854, described by Hirigoyen, of an 11-year-old boy who remained cataleptic for eight hours with arms lifted, the position that he took in defense at the moment when his father made a move to beat him, and another case from 1857, described by Schwartz, concerning a 7-year-old boy who developed a choreic condition in consequence of ‘rough maltreatment’ that was followed by a short period of catalepsy.

Stuporous catatonia in anaclitic depression

In the 1940s, René Spitz described a severe syndrome in infants admitted to institutions and separated from their mothers. He coined the term anaclitic depression, referring to psychoanalytic thinking on the effects of loss of a love object (18). Separation occurred because of incarceration of the mothers or inability to support themselves and their children (19). After 4 to 6 months in the nursery, some infants as young as 6 months would become weepy then withdraw, lose weight despite adequate hygiene and physical care, and become sleepless. After a few months, ‘...the weepiness subsided, and stronger provocation became necessary to provoke it. A sort of frozen rigidity of expression appeared instead. These children would lie or sit with wide-open, expressionless eyes, frozen immobile face, and a faraway expression as if in a daze, apparently not perceiving what went on in their environment. This behavior was in some cases accompanied by autoerotic activities in the oral, anal, and genital zones. Contact with children who arrived at this stage becomes increasingly difficult and finally impossible. At best, screaming was elicited’. Spitz observed that the syndrome developed in 19 of 123 unselected cases but quickly reversed on restitution of the mother provided the separation lasted <3 or 4 months.

In other cases with longer periods of separation from the mother, the condition worsened and extreme cases ‘varied from stuporous deteriorated catatonia to agitated idiocy’. In these children, unresponsiveness to social contacts, stupor, ‘combined with certain unusual postures of hands and fingers which seemed to us the precursors of the extremely bizarre hand and finger movements composing the total activity in those infants of Foundling Home whom we described as presenting a picture of stuporous catatonia’. At 2-year follow-up, the mortality rate was 37%, mostly owing to infections or cachexia (20). Twenty-one surviving children between ages 2 and 4, who were originally at the institution 2 years earlier, were found to be grossly underdeveloped both physically and mentally, with five children ‘incapable of any locomotion’, 12 who ‘cannot eat alone with spoon’, and six without speech. Spitz assessed irreparable damage because of the prolonged period of social and emotional deprivation.

Quasi-autism or pediatric catatonia?

Few images in child psychiatry are as unsettling as those of Spitz’s deprived and institutionalized infants. His findings have been instrumental in improving care in institutionalized infants and children, stimulating further research on the effects of maternal deprivation (21), and formulation of the attachment theory (22) by Bowlby, a British psychoanalyst. It has been elaborated by others (23) focusing on the quality of the relationships with one or more caregivers starting from birth and documenting mediating factors leading to the wide range of outcomes following early deprivation.

Strikingly, and following Spitz, the subsequent literature (24, 25) on the effects of severe deprivation in infants and young children is devoid of symptoms such as stupor, immobility, unresponsiveness, stereotypy, other oddities of speech, motor and social function, echolalia, and echopraxia that may be considered catatonic. Instead, these symptoms are considered as autistic but nonetheless reversible after intervention or diminishing in intensity with age.

In a study of 111 Romanian institution-reared children who were adopted into UK families before the age of 3.5 years, and evaluated at ages 4 and 6, seven children showed a syndrome that resembled typical autism yet was different because of a higher degree of social responsiveness, diminishing symptoms over time, normal head circumference, and equal sex ratio with age (26). One child was diagnosed with severe cognitive deficits. None of the controls of within-UK adoptees showed this syndrome. The authors called the syndrome ‘quasi-autism’. In a follow-up study when subjects were 12 years of age, three quarters of those with ‘quasi-autism’ were unchanged. In the recovered group, some difficulties with unsolicited spontaneous comments and intrusive physical contact were found, but no autistic symptoms.

At the time that Spitz conducted his studies, the view of autism as a unique syndrome was just being described (27, 28). It is not surprising, therefore, that Spitz recognized catatonia in his most severe cases and that, after the diagnosis of autism became widespread, similar cases were described as autistic or ‘quasi-autistic’. Attention has been called previously to the overlap between catatonic and autistic symptoms (29, 30), and the ensuing diagnostic confusion occurring when pediatric catatonia is mistaken for autism (31). We suggest that severe infant deprivation syndrome and its sequelae should best be viewed as examples of pediatric catatonia rather than autism.

Lack of communication and risk of pediatric catatonia

In the 1960s, Karl Leonhard reported high rates of stereotypical, impulsive, aggressive, self-injurious and disruptive behaviors, lack of expression, negativism, excitement, ambivalence, counter-grasping, mannerisms, echolalia, and neologisms in a sample of 117 catatonic children with onset of illness in the first years of life (32). These symptoms were not present in patients with developmental delay but without catatonia. Seventy-six of the 117 children were placed in long-term homes or stayed in the hospital during the first 3 years of life, because of the inability of the mother, for various reasons, to care for the child. Leonhard did not find any evidence for abnormalities in the child before placement or separation from the primary caregiver, and he considered the role of heredity to be low. This suggested to Leonhard that lack of communication with the mother or substitute mother during the first 3 years of life was an important risk factor for early childhood catatonia. He found that many children were exposed to neglect within their original families (although he does not report on clear abuse or other precipitating traumas). The similarities between Leonhard’s cases of childhood catatonia and Spitz’s cases of anaclitic depression, both thought to ensue after separation from the mother or main caregiver, are so far insufficiently acknowledged as supportive of the role of social deprivation and traumatic events in the development of catatonia in very young children.

Catatonia in autistic children following loss and trauma

Over the past 15 years and throughout the world, catatonia has been increasingly recognized as a syndrome that becomes engrafted on autism (33). Wing and Shah (34) report that 17% of a large referred sample of adolescents and young adults with autism satisfied criteria for catatonia and that stressful events often preceded the onset of catatonia.

A case-in-point is an 11-year-old boy with high-functioning autism, previously well adjusted and verbal, who developed catatonia characterized by psychomotor retardation, muteness, food refusal, incontinence, and withdrawal, following the sudden death of his father (35). The boy was treated with antidepressant and antipsychotic medications without benefit, but responded, with full resolution of catatonia, to a test dose of 1 mg of lorazepam after which he was able to return to school. He was maintained on 1 mg of lorazepam daily.

A 16-year-old adolescent with a diagnosis of Asperger syndrome and long history of being abused by his mother developed catatonia characterized by muteness, immobility, catalepsy, and mannerisms after the illness of his grandfather (36). The authors discuss the positive response of catatonia to diazepam in their patient, the importance of assessing catatonia in patients with autism spectrum disorders, who present with motor disturbances in the presence of abusive or traumatic events, and possible diagnostic confusion with catatonic schizophrenia or reactive attachment disorder. The patient’s catatonic reaction struck the authors as ‘death mimicry owing to the subjective perception of a life-threatening situation’ for which treatment with benzodiazepines and ECT should be considered.

Reactive catatonia in childhood

In 1972, Bemporad and Dunton (37) reported two new cases of catatonia in a 10-year-old girl and an 8-year-old boy, showing symptoms similar to those in adults with catatonia. They concluded that in some children, full-blown catatonia develops in response to severe emotional or physical trauma. Both children were negativistic and oppositional. Poor familial circumstances and parental rejection were regarded by the authors as contributory to the illness in both cases.

Previous research on acute stress symptoms has emphasized symptoms such as distortion of consciousness, depersonalization, derealization, automatic movements, flashbacks with illusions or hallucinations, panic attacks, acute depression, conversion reaction, excessive emotional expression, and psychotic reactions, but rarely catatonia (38). Cases of pediatric catatonia are labeled brief reactive psychosis (DSM-IV) (39) or acute, transient psychotic disorder (ICD-10) (40).

The use of anxiolytics including amytal and benzodiazepines as diagnostic tools and treatment is well known in catatonia but also in conversion disorders, psychogenic amnesia, and fugue states (41–45), suggesting a common basis for these conditions. Many reports describe intense anxiety in catatonia (46, 47). Several patients claim complete amnesia for the period of catatonia. Delusional thinking and command hallucinations during catatonia are reported by some patients once recovered. All of these features provide indirect support for the traumatic origins of catatonia in these cases.

Pervasive refusal syndrome in refugee children

The number of asylum seekers, refugees, and internally displaced people worldwide is rising. Asylum-seeking children are among the most vulnerable groups of displaced persons. Many children and their family members have been exposed to severe physical violence, death and murder, sexual abuse, persecution, and threat of kidnapping in their country of origin. Many flee to Europe and North America where they are detained before final determinations are made about asylum.

An epidemic of ‘apathetic’ asylum-seeking children has been reported in Sweden over the last decade (48, 49). Although similar influxes of refugee children with their families have occurred in other countries, where they have been detained in similar circumstances, the development of this particular disturbance has not been reported or, alternatively, may not have been recognized, in refugee children outside of Sweden.

The clinical presentation is as follows (48): ‘The child is totally passive, immobile, lacks tonus, withdrawn, mute, unable to eat and drink, incontinent, and not reacting to physical stimuli or pain. Periods of panicky refusal and anxiety can precede or intervene with the stuporous state. Secondary symptoms may appear, such as tachycardia, rise in temperature, edema, profuse sweating, reactivation of latent viral infection, skin ulcers and muscular atrophy. No evidence of underlying medical diseases is found. Many children need nasogastric tube feeding and others supportive medical care. The mean time from onset to recovery is 6 months. Often, the first sign of recovery is the resumption of non-verbal communication, through touch and eye contact, followed by the return of gross motor skills, then fine motor skills (including self-feeding), and finally verbal communication’.

The condition meets criteria for catatonia and particularly malignant catatonia when autonomic dysfunction and fever aggravate the syndrome. However, the authors suggest that the condition is a type of pervasive refusal syndrome (PRS) (48), a syndrome first described in 1991 (50) by Lask in four girls aged 9–14 as a potentially life-threatening condition characterized by refusal to eat, drink, walk, talk, or care for themselves over a period of several months. There is no evidence of organic illness. All children need hospital care. The recommended treatment is supportive involving the ward milieu, physiotherapy, individual therapy, parental counseling, and family therapy. Medications are deemed ineffective although controlled trials are lacking; sedatives are used sparingly and reserved for situations in which the child is inordinately distressed by such necessary procedures as nasogastric tube feeding or physiotherapy. The recovery process is slow (average duration of therapy, 12.8 months), but most children recover fully (complete recovery in 67% of known cases). To date, 24 cases of PRS have been described in the English literature (51). Reports on PRS are absent from the American literature.

Pervasive refusal syndrome or reactive catatonia?

The clinical descriptions of these refugee children and those of children with classic catatonic syndromes are strikingly similar, suggesting that catatonia in the aftermath of trauma and abuse is poorly recognized. Following a description of PRS (52), Fink and Klein (53) pointed out that it would be better to consider PRS as catatonia for treatment purposes.

Lask believes that PRS is different from catatonia (54), because ‘the immobility of PRS is not associated with generalized psychomotor retardation, nor increased motor tone, and movement still occurs in sleep and when physical contact is attempted by those caring for the child. The social withdrawal (of PRS) is not associated with hypervigilance, hallucinations, delusions, or thought disorder. The mutism is either selective or becomes so as recovery occurs’.

A review of catatonia studies (3, 4) qualifies these purported differences and shows that immobility alternates with agitation and that immobile episodes are present without sustained psychomotor retardation. Increased motor tone or rigidity, which is not listed as a symptom of catatonia in DSM-IV, is not an obligatory symptom of catatonia as erroneously implied in Kahlbaum’s image of catatonia as ‘Spannungsirresein’ or tension insanity, but does occur in about 40–70% of patients with catatonia (3, 39, 55, 56). Patients with catatonia move during sleep. Catatonic patients display movements during social interactions, although some movements may be abnormal reflecting negativism, echopraxia, or stereotypy. Catatonia occurs in patients without hallucinations, delusions, or thought disorder being present (these features may be present but cannot be assessed in mute patients). Muteness fluctuates in catatonic patients.

Lask (54) also distinguishes PRS from stupor because ‘although akinesis and negativism are common to both conditions, the willful negativism of children with pervasive refusal syndrome, as well as the very gradual return of function over many months, make this diagnosis unlikely’. However, negativism is considered a hallmark of catatonia by classic authors (4, 57) and prominent in pediatric cases (37). It is not uncommon for catatonic patients with unresponsiveness or stupor to display subtle signs of resistance to passive movement, for example when they resist their eyelids being opened (58), nor is it uncommon for recovery from catatonia to be slow when inadequately treated. Indeed, Kahlbaum described a series of cases that remitted fully after a year or more of severe catatonia (1).

The claim that PRS and catatonia are different conditions is questionable and may be due to misunderstanding the symptoms and signs of catatonia. The similarities outweigh the number of purported differences (4, 53). Unfortunately, treatment studies in PRS of benzodiazepines and ECT are lacking. Similar treatment responses to these interventions would validate PRS as catatonia.


Although the literature supports the view that deprivation, abuse, and trauma can precipitate pediatric catatonia, there are no systematic studies thereby precluding estimates of the number of cases in which these factors play a role. Underreporting of traumatic and abusive events and poor recognition of pediatric catatonia in children with autistic, developmental, medical, and neurological disorders are challenging clinical and research issues. The effects of diagnostic overshadowing of pediatric catatonia, or the falsely attributing symptoms of catatonia to another disorder, extend to syndromes related to deprivation, abuse, or trauma, labeled as anaclitic depression, quasi-autism, reactive or brief psychosis, and pervasive refusal syndrome. Catatonia and the efficacy of benzodiazepines and ECT need to be assessed in these conditions.

The finding that deprivation, abuse, and trauma may be risk factors for catatonia raises questions about mechanisms by which these factors lead to catatonia or other disorders. The biological pathways of early deprivation, stress, and trauma leading to psychiatric and medical disorders are thought to encompass endocrine, immune, electrophysiological, and neuropsychological factors as well structural changes in the developing brain (59–63). A recent review of mechanisms of catatonia has offered different models of motor circuitry dysfunction, abnormal neurotransmitters (especially GABA), seizure activity, genetic risk factors, endocrine dysfunction, and abnormal immune response (64). The likely involvement in catatonia of central GABA function that has a major role in central integration of HPA stress responses in the basal forebrain and hypothalamus (65) is an important lead for further clinical and experimental studies assessing early deprivation, stress, and trauma as contributing to the development of pediatric catatonia.

Findings support the clinical corollary of assessing every child with symptoms of catatonia for traumatic and abusive events in family and broader environments, in addition to medical causes. The same applies to young children with onset of autistic symptoms, given the overlap between autistic and catatonic symptoms. Catatonia, especially in the more severe forms, is an urgent indication for medical intervention, regardless of purported etiology. Clearly identifiable medical or drug-induced disorders may require separate treatment. If traumatic or abusive events are suspected or ascertained, specific preventive actions are indicated, and social or psychotherapeutic interventions may be appropriate when the acute symptoms have abated.



Declaration of interest

Dirk Dhossche has received research grants from the Thrasher Pediatric Research Fund, the American Foundation for Suicide Prevention, and the University of Mississippi Medical Center. Colin Ross and Laura Stoppelbein have no declarations of interest.