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J Can Acad Child Adolesc Psychiatry. 2010 May; 19(2): 138–140.
PMCID: PMC2868561

A Case of Adolescent Catatonia

Jonathan A. Brake, MD1 and Sabina Abidi, MD, FRCPC1,2

Catatonia is a motor dysregulation syndrome in which patients lose the ability to move normally despite having the full physical capacity to do so. It is a syndrome, a cluster of symptoms, and in itself is not a diagnosis. The syndrome was first described by the German psychiatrist, Karl Kahlbaum, in 1874 in his monograph, Die Katatonie oder das Spannungsirresein (Kahlbaum, 1874). Kahlbaum reported twenty-six cases of what he called tension insanity, of various etiologies. Its recognition in the following years rose dramatically in psychiatric populations, with prevalence estimates between 6% and 38% (Fink & Taylor, 2003). Its identification rose to such extents that Emil Kraepelin’s notion of dementia praecox considered catatonia to be a hallmark of the disorder. Others, such as Kleist, Wernicke, and Leonhard, noted catatonic features in patients with affective disorders (Shorter, 1997).

As a syndrome, there are a number of cardinal features which have been described (Fink & Taylor, 2003). Mutism refers to verbal unresponsiveness; alternatively, echolalia (repetition of the sounds and words produced by others) may also occur. Patients may also imitate physical gestures (echopraxia). Negativism refers to the process of actively resisting any efforts to be moved or failure to obey requests or commands; this process is involuntary. Conversely, patients may demonstrate automatic obedience, the inability to resist following commands. Other patients demonstrate waxy flexibility (cerea flexibilitas), allowing their limbs to be molded at the examiner’s will. Patients may exhibit catalepsy, maintaining abnormal and peculiar postures for an extended period of time; prior to the advent of adequate treatment, some patients would maintain these postures for days or months. Patients may also demonstrate stereotypies (purposeless, repetitive motor behavior) and mannerisms (odd, purposeful or exaggerated movements).

A wide variety of causes of catatonia have been reported (Takaoka & Takata, 2003). Psychiatric conditions, including schizophrenia, bipolar disorder, post-traumatic stress disorder, eating disorders, and depressive disorders have been associated with catatonia. Medical causes such as autoimmune disorders, paraneoplastic syndromes, and metabolic disturbances have also been identified. Catatonia also occurs in a variety of neurological conditions including encephalitis, stroke, and seizure disorders. Catatonia has been associated with ecstasy, phencyclidine, inhalant, steroid, and neuroleptic use, as well as the abrupt withdrawal of benzodiazepines.

A number of subtypes of catatonia have been described (Fink & Taylor, 2003). Kahlbaum’s instrumental role in delineating the entity led to a specific form of retarded catatonia (with rigidity, inhibition of movement, abnormal posturing, mutism, and failure to respond to painful stimuli) to be called Kahlbaum’s syndrome. In contrast, excited catatonia (delirious mania, Bell’s mania) involves restless movements, talkativeness, agitation, frenzy, disorientation, and confusion. Periodic catatonia, most frequently associated with bipolar disorder, involves fluctuations between stupour and excitement. Malignant catatonia (lethal, pernicious) is characterized by rigidity and an altered level of consciousness with hyperthermia and autonomic instability; this condition is potentially life threatening. Neuroleptic malignant syndrome and serotonin syndrome are considered forms of malignant catatonia.

Literature regarding catatonia in children and adolescents is sparse. Features particular to child and adolescent presentations have been described which include: (1) increased slowness affecting motor and verbal responsiveness, (2) difficulty initiating and completing actions, (3) increased reliance on cueing by others, (4) increased passivity and lack of motivation, (5) reversal of circadian rhythms, (6) Parkinsonian features, (7) excitement and agitation, and (8) increased repetitive and ritualistic behavior (Wing & Shah, 2000).

A number of rating scales have been developed to assist with its identification, including the Bush-Francis Catatonia Screening Instrument (BFCSI), the Bush-Francis Catatonia Rating Scale (BFCRS), and the Modified Roger’s Rating Scale (MRRS). The lorazepam challenge may also assist in evaluation. It involves the administration of 1–2mg of intravenous lorazepam. A positive test results in the rapid relief of catatonic symptoms, albeit usually transiently (Fink & Taylor, 2003). There is a high response rate, cited as typically between 75%–100% (Hawkins et al., 1995).

Admission to neurology or a medical intensive care unit is warranted for cases of catatonia associated with neuroleptic malignant syndrome, encephalitis, and non-convulsant status epilepticus. Atypical antipsychotics are preferred over typical agents due to the risk of precipitating or worsening a potential malignant state. If initially useful, regular doses of lorazepam (starting at 3mg per day) should be used to prevent relapse into catatonia. Parenteral nutrition and intravenous fluids should be considered for those with poor intake. Vitals should be monitored regularly for autonomic instability. If the above measures are unsuccessful, electroconvulsive therapy has been identified as the definitive treatment (Fink & Taylor, 2009).

Case

A 17 year old female with no previous mental health contact presented to the emergency department with her family. She had moved in with her grandmother several months prior, following an argument with her mother about her declining school attendance over the previous year. The family reported a rather abrupt onset over the previous week of unusual behavior. Prior to coming to hospital she spent over an hour in the shower standing naked, without running water. She slept in the bed with her grandmother at night, and required repeated reassurance that she and her family were safe. During the day she was uncharacteristically tearful, minimally communicative, and was mostly withdrawn to her room. She had reportedly taken a strong interest in religion, which was unusual for her. She expressed thoughts of being “damned.” Her boyfriend reported that over the previous several months she had become increasingly anxious about school and expressed a great deal of sadness about her family situation. He denied that she used any substances. She was on no medications prior to hospitalization.

In terms of her mental status on admission, she lay in a hospital bed and by facial expression and affect appeared significantly frightened and anxious. She was frequently tearful. She did not maintain eye contact, and appeared to resist any attempts to do so. She was rigid, with her arms held in flexion against her body. She demonstrated negativism, resisting any attempts to manipulate her extremities. She did not obey commands. She was largely mute; however, she did utter fragmented phrases of a religious nature, such as being “damned” and in “limbo.” She also frequently apologized for no apparent reason to her family members. It was difficult to assess whether she was experiencing perceptual disturbances.

She had a full medical evaluation, including a CT scan and lumbar puncture which were normal. As part of screening for structural anomalies, an MRI was ordered, which was subsequently normal. She was given lorazepam (2 mg parenterally) in preparation for this procedure. Approximately fifteen minutes after its administration, she demonstrated a profound change in her mental status. She began to respond appropriately to commands, the rigidity dissipated, and she began to verbalize appropriately, even demonstrating an appropriate sense of humour. She stated that she had been aware of the events and conversations that had occurred in her presence over the last several days.

Regular doses of lorazepam were initiated. It quickly became evident that she had significant nihilistic and religious delusions and was experiencing perceptual disturbances. She was treated with olanzapine and her psychosis resolved. She was discharged to outpatient follow up. On further investigation, there was a prominent low mood (which may have had its onset months prior); she was started on fluoxetine. Three months later, her depressive symptoms persisted, not having responded to the initial antidepressant. Throughout, she has demonstrated poor insight into her illness, particularly her mood state, yet has been agreeable to ongoing follow up and care.

Discussion

Although it has been suggested that advances in psychopharmacology are contributing to reduced rates of catatonic states (Mahendra, 1981), it remains an under-recognized phenomenon. One study demonstrated that while clinicians identified catatonia in 2% of 139 patients, researchers identified catatonia symptoms in 18% (van der Heijden et al., 2005). Part of its lack of recognition may be due to misinterpretation of symptoms. Cases of excited catatonia may be masked due to overlap with symptoms of mania. Negativism may be viewed as the patient simply not wishing to cooperate, dismissed as a behavioral problem rather than a true inability to cooperate. The shift towards outpatient care and the lack of emphasis on physical examinations may be contributory (Fink, 2009). Lack of education of medical and psychiatric residents may also play a role. Nevertheless, catatonia is not rare, and cases exist in child and adolescent populations. The astute clinician should evaluate for the presence of catatonic symptoms using the rating scales identified previously in this article, as well as a thorough medical examination. If catatonia is suspected, the lorazepam challenge should be considered an invaluable tool for confirming its presence.

We have presented a case of an adolescent female whose catatonic state was surreptitiously confirmed with the administration of benzodiazepines. Given the associated risks if left untreated, this case further outlines the need for clinicians to be vigilant for such presentations and cognizant of its various forms and etiologies, even in youth.

References

  • Fink M. Catatonia: a syndrome appears, disappears, and is rediscovered. Canadian Journal of Psychiatry. 2009;54(7):437–445. [PubMed]
  • Fink M, Taylor MA. Catatonia: a clinician’s guide to diagnosis and treatment. Cambridge, England: Cambridge University Press; 2003.
  • Fink M, Taylor MA. The catatonia syndrome: forgotten but not gone. Archives of General Psychiatry. 2009;66(11):1173–1177. [PubMed]
  • Hawkins JM, Archer KJ, Strakowski SM, Keck PE. Somatic treatment of catatonia. International Journal of Psychiatry in Medicine. 1995;25(4):345–369. [PubMed]
  • Kahlbaum KL. Die Katatonie oder das Spannungsirresein. Berlin: Verlag August Hirshwald; 1874.
  • Mahendra B. Where have all the catatonics gone? Psychological Medicine. 1981;11(4):669–671. [PubMed]
  • Shorter E. A history of psychiatry. New York, NY: John Wiley & Sons; 1997.
  • Takaoka K, Takata T. Catatonia in childhood and adolescence. Psychiatry and Clinical Neurosciences. 2003;57:129–137. [PubMed]
  • van der Heijden RM, Tuinier S, Arts NJ, Hoogendoorn ML, Kahn RS, Verhoeven WM. Catatonia: disappeared or under-diagnosed? Psychopathology. 2005;38(1):3–8. [PubMed]
  • Wing L, Shah A. Catatonia in autistic spectrum disorders. British Journal of Psychiatry. 2000;176:357–362. [PubMed]

Articles from Journal of the Canadian Academy of Child and Adolescent Psychiatry are provided here courtesy of Canadian Academy of Child and Adolescent Psychiatry