Major Depression with Catatonic Features in a Child Remitted with Olanzapine

Introduction

C atatonia was first described by Karl Ludwig Kahlbaum in 1874 and includes a set of psychomotor symptoms that appear in several medical and psychiatric conditions. It does not imply a specific diagnosis because of these associations. Catatonia has been observed rarely in children and adolescents (Cohen et al. 1999; Thakur et al. 2003). Evidence-based treatment of catatonia is also lacking especially for children and adolescents (Dhossche and Bouman 1997; Taylor and Fink 2003). However some treatments are reported to be effective in relieving catatonic symptoms despite the fact that they were not formulated based on its pathophysiology.

In the following case report, the authors present a 12-year-old girl diagnosed with major depressive disorder with catatonic features, which remitted following treatment with olanzapine.

Patient

The patient was a 12-year-old Caucasian female brought to the child and adolescent psychiatry clinic by her parents with complaints of frequent crying, withdrawal, loss of interest in friends and enjoyment of activities, speaking less, sleeplessness, loss of appetite, weight loss, and a depressive mood that started 20 days before and worsened in the 5 days prior to their visit. Further symptoms were described by her parents as loss of spontaneous speech, marked psychomotor retardation, staying in the same posture for long periods of time, and needing to be fed.

During the psychiatric evaluation, she demonstrated mutism, negativism, blunted affect, marked psychomotor retardation, stuporousness, posturing, waxy flexibility, and catalepsy. She was uncooperative and did not complete the childhood depression scales. The physical examination of this 40-kg child was otherwise unremarkable. Her psychiatric history was negative for prior traumatic experiences, repeated hospital admissions, stressful life events, or substance use. Peer relationships were good and cognitive and social maturation was at the expected level for her age. Her family history was negative for psychiatric disorders.

Results of cranial magnetic resonance imaging, computerized tomography, electroencephalography, electrocardiography, complete blood count, blood biochemistry, thyroid function tests, and markers for systemic lupus erythematosus, Epstein–Barr virus, and hepatitis viruses were unremarkable or negative. She was diagnosed with a major depressive disorder with catatonic features (American Psychiatric Association 2000).

The patient was not hospitalized due to the absence of parental consent; she was followed with weekly visits as an outpatient. Five mg/day of olanzapine was prescribed. When reevaluated 1 week later, the patient's symptoms had diminished. She cooperated with the interviewer, was less stuporous, responded to questions, but still had no spontaneous speech. The family reported that she was eating and sleeping better. The dosage of olanzapine was increased to 10 mg/day. During the third visit, it was found that her catatonia and vegetative symptoms had remitted; she was only slightly depressed. Her Childhood Depression Inventory score of 10 was below the cutoff for depression. With remission of the catatonic symptoms, her olanzapine dosage was decreased to 5 mg/day, and, after observing a euthymic mood, the olanzapine was stopped at a later visit. The patient was followed through monthly visits for the first 3 months at which point the visit intervals were increased to 6 months. The patient has continued to visit for the last 18 months without a recurrence or any psychiatric symptoms.

Discussion

Catatonia is a condition characterized by a group of psychomotor symptoms, (i.e., mutism, echolalia, mannerism, grimacing, echopraxia, stereotypy, negativism, blunted affect, marked psychomotor retardation, stuporousness, posturing, waxy flexibility, and catalepsy) that cannot be explained by neuropathology or neurochemistry (Fink and Taylor 2001; Taylor and Fink 2003). In addition to psychiatric disorders, it can occur with central nervous system infections, head trauma, epilepsy, metabolic and endocrine disorders, hepatic insufficiency, hepatic encephalopathy, systemic lupus erythamatosis, infections (Epstein–Barr, hepatitis B/C), and adverse drug reactions (Madan and Lantz 2003). In the differential diagnosis, laboratory tests may clarify some underlying etiologies; however, catatonia secondary to a mood disorder or a schizophreniform disorder has no pathognomonic laboratory correlate. Therefore, in our case, we relied on the personal and family history of the patient, which was mainly derived from the parents. Another issue in the diagnosis was the absence of specified criteria for children and adolescents. The criteria of the Diagnostic and Statistical Manual of Mental Disorders, 4^th edition, Text Revision (DSM-IV-TR) (American Psychiatric Association 2000) are also used to describe catatonia in children and adolescents (Takaoka and Takata 2003). In DSM-IV-TR, catatonic features are included under the headings of schizophrenia, bipolar disorder (BD), and catatonic disorder related to a medical condition. In our case, there were symptoms of depression lasting for 20 days, and catatonic features were added to the clinical picture within the 5 days prior to the visit. In the examinations, no medical pathology was diagnosed. There was no previous manic, depressive, or mixed episode. On the basis of these findings, the patient was diagnosed with a major depressive disorder with catatonic features. It is known in the literature that mood disorders are the most frequent psychopathology associated with catatonia in children and adolescents (Taylor and Fink 2003). Early diagnosis and treatment may be important in the case of catatonia, due to its complications. Prolonged immobility and starvation may generate malnutrition, dehydration, weight loss, muscle wasting, contractures, and bedsores. Death may ensue from venous thrombosis and pulmonary emboli. For these reasons, a delay in the diagnosis and treatment intervention for treating catatonia in mood disordered patients clearly can increase morbidity and mortality (Williams 2007).

The underlying pathophysiology of catatonia has not been explored; however, some hypotheses have been suggested (Northoff 2002). The most commonly accepted hypothesis is related to γ-aminobutyric acid (GABA), which is a major inhibitor neurotransmitter in the central nervous system, and it is hypothesized that orbitofrontal, premotor, and motor cortices have decreased GABA activity in the case of catatonia (Northoff 2002). Remission achieved with benzodiazepines, e.g., lorezepam, which are GABA agonists, is accepted as evidence for this hypothesis (Greenfeld et al. 1987; Salam et al. 1987; Rosebush et al. 1990; Marneros and Jager 1993; Van Dalfsen et al. 2006). It has been shown that some patients with catatonia also respond to amantadine, which is a weak antagonist of N-methyl-D-aspartic acid (NMDA) receptors (Babington and Spiegel 2007). Additionally anticonvulsives, bromocriptine, and electroconvulsive treatment (ECT) have been reported as effective in the treatment of catatonia (Mahmood 1991; Cizadlo and Wheaton 1995; Yeung et al. 1996; Kritzinger and Jordaan 2000; McDaniel et al. 2006; Esmaili and Malek 2007; Chung and Varghese 2008). Among them, ECT has been found to be effective in treating children and adolescents (Cizadlo and Wheaton 1995; Yeung et al. 1996; Esmaili and Malek 2007; Chung and Varghese 2008). Another hypothesis related to pathophysiology of catatonia is the inhibition of the D2 receptors (Philbrick and Rummons 1994).

Catatonia can be induced with atypical antipsychotics, although they have actually been found to be effective in the treatment of catatonia (Kopala and Caudle 1998; Duggal and Gandotra 2005; Babington and Spiegel 2007; Guzman et al. 2008). These studies suggest that dopamine regulation can be important in the treatment of catatonia. Atypical antipsychotics, e.g., olanzapine, may be safer in the case of catatonia, due to their lower D2 receptor blockade (Weller and Kornhuber 1993). For these reasons, we used olanzapine in the treatment of this specific case. In the literature, cases diagnosed with major depression with catatonic features are scarce and they are mainly treated with ECT (Mahmood 1991; Cizadlo and Wheaton 1995; Esmaili and Malek 2007). Although the response to the treatment has been found to be successful in most cases, the prognosis is strongly related to that of the underlying etiology. In our case, although the symptoms of catatonia were improved during the treatment with olanzapine, spontaneous remission or recovery from the underlying etiology may be another explanation.

The risk of developing BD due to a personal history of major depression is known to be significant in children and adolescents when compared to adults. It has been observed that between 20% and 40% of children and adolescents with major depression develop BD later in life (Kovacs 1996; American Academy of Child and Adolescent Psychiatry 1998). In our case, the early occurrence of depression and psychomotor retardation can be considered risk factors for BD later in this patient's life. After remission, the patient was followed with regular visits because of the risk of BD. To date, she has not developed any psychiatric recurrence. This case is being brought to the attention of clinicians working with children and adolescents due to its significance as an early onset catatonia and an example of the treatment of catatonia with an atypical antipsychotic, olanzapine. This case suggests that olanzapine can be an appropriate choice in the treatment of catatonia, especially when a mood disorder is determined as the underlying etiology.