[Catatonia in a 14 year-old girl: treatment with clorazepam and carbamazepine, a 10-year follow-up].

Child and adolescent catatonia has been poorly investigated. Moreover, diagnosis criteria only exist for adult psychiatry, and there are no therapeutic guidelines. The aim of this paper is to describe the case of a 14-year-old girl presenting an overlap between psychogenic and neuroleptic induced catatonia, acute treatment and ten year's follow-up. A 14-year-old Caucasian French girl, Elsa, was admitted in February 1998 to a University adolescent mental health center with an acute psychotic disorder. She showed agitation, impulsivity (sudden engagement in inappropriate behaviour), paranoid delusions, visual and auditory hallucinations, diurnal and nocturnal urinary incontinence, lack of self-care, inadequate food intake because of fear of poisoning, and vomiting after meals leading to rapid weight loss of 5 kg. Clinical examination, laboratory tests, EEG and RMI were normal. Toxicological tests were negative. Her IQ, assessed six months before admission, was in the dull average range (70-75). Elsa was treated with loxapine 150 mg per day for one week without improvement and this was then replaced by haloperidol 30 mg per day. One week after the start of haloperidol her agitation, impulsivity, and hallucinatory symptoms decreased. Twenty four days after loxapine introduction and 17 days after the haloperidol, her condition deteriorated rapidly over less than 48 hours. She exhibited immobility, minimal response to stimuli, staring and catalepsy with waxy flexibility. The diagnosis of catatonia was established. Examination revealed tremulous extremities, tachychardia (110 pm) and apyrexia. Creatine phosphokinase levels were 106 UI/l (normal range 0-250). Human immunodeficiency virus, hepatitis, listeria and Lyme serology were negative. Cerebrospinal fluid analysis was normal. Haloperidol was stopped and intravenous clonazepam 5mg/kg was begun. It was not possible to obtain signed consent from the two parents for Electroconvulsive therapy. The patient was transferred to a pediatric intensive care unit. The treatment was standard parenteral nutrition, nursing, intravenous clonazepam 0.05 mg/kg, with regular attendance by a child psychiatrist. Elsa stayed three weeks in this condition. She then began to notice the child psychiatrist, and a few days later she was able to carry out simple requests. Elsa was transferred to an adolescent psychiatric unit. As soon as she could eat by herself again, carbamazepine 400mg per day was begun. Her agitation reduced at a carbamazepine level of 7 mg/l. One month later her condition was stable. However, language difficulties persisted for a further six months. One year after the episode she scored 66 on a repeat IQ test and her RMI was normal. She exhibited no significant residual symptoms except some cognitive impairment. She integrated into a special education facility. These attempts to stop the carbamazepine were followed by depressed mood, aggressiveness and impulsivity; carbamazepine was finally stopped successfully after seven years. Ten years later, Elsa is the mother of two young children and is able to take care of them. She has never had a relapse of her psychotic disorder or catatonic state. The etiopathogenic diagnosis is problematic. Some indices in the familial history may suggest a traumatic event. But one to the total residual amnesia it was never confirmed, and traumatic catatonia are extremely rare. Normal CPK levels, with autonomic disturbance limited to tachycardia and the lack of resolution after discontinuance of medication, argues against a diagnosis of neuroleptic malignant syndrome (NMS). But CPK levels are non specific, and NMS without pyrexia has been described. The occurrence of the catatonic syndrome 21 days after the first dose of a neuroleptic could be diagnostic. This case involved a non organic catatonic psychosis followed by neuroleptic induced catatonia. Catatonia is described as a risk factor for the development of NMS and some consider NMS to be a variant of malignant catatonia. The interest of this report is (1) it reinforces the need to be cautious before prescribing neuroleptics in adolescents presenting with symptoms of catatonia; (2) the complete recovery from catatonia after treatment with intensive care and more than three weeks of intravenous clonazepam without the use of ECT and (3) the effectiveness of carbamazepine over a long period of follow-up. Although trials on carbamazepine in catatonia are published, there are no data available for the control of residual symptoms or the long term prognosis, especially in child and adolescent psychiatry.

Askenazy F ，Dor E ，Benoit M ，Dupuis G ，Serret S ，Myquel M ，Seddiki Y ... -  《ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE》

[Catatonia de novo, report on a case: immediate vital prognosis and psychiatric prognosis in longer term].

Patry L ，Guillem E ，Pontonnier F ，Ferreri M ... -  《ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE》

[Acute catatonia and neuroleptic malignant syndrome. A case of infantile psychosis].

Revuelta E ，Bordet R ，Piquet T ，Ghawche F ，Destee A ，Goudemand M ... -  《ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE》

[A study of neuroleptic malignant syndrome in the presenium and senium].

Suzuki I ，Honma H ，Watanabe N ，Matsubara S ，Koyama T ... -  《-》

[Follow-up of a 16-year-old adolescent with early-onset schizophrenia and catatonic symptoms].

The aim of this paper is to underline the need of a systematic monitoring (1) of atypical antipsychotics and (2) of catatonic symptoms in child psychiatry. We present in this paper the clinical history of a 16-year-old adolescent inpatient needing a prescription of atypical antipsychotic drug. We present the most relevant results of our clinical monitoring over 7 months. A 16-year-old Caucasian male adolescent, by the name of Paul, was admitted in August 2009 to an Adolescent University Psychiatry Unit for an acute psychotic disorder. On admission, he presented paranoid delusion, auditory hallucinations and impulsive movements. The score on the Bush-Francis Catatonia Rating Scale (BFCRS) was 17 (the threshold score for the diagnosis of catatonic symptoms is 2). Laboratory tests showed the lack of blood toxic levels, creatine phosphokinase (CPK) level was 684 IU/L. Paul was treated with clonazepam (0.05 mg/kg/d). This particular day was considered to be day #1 of the clinical drug monitoring. Immediately after, regular follow-up of catatonic symptoms was performed. On day #15, the CPK level returned to normal with improvement of clinical catatonia but with still a score of 4 on the BFCRS scale. Auditory hallucinations and delusion persisted. Risperidone treatment was begun (1mg/d and 1.5mg/d after 24 hours), associated with oral clonazepam (0.05 mg/kg/d). On day #17, after 48 hours of improvement of delusion, the catatonic symptoms rapidly worsened. Risperidone was stopped; Paul was transferred to intensive care where he was treated with clonazepam IV (0.1mg/kg/d). The score on BFCRS scale was 20, Paul presented no fever and the CPK level was below 170 IU/L. The diagnosis was a relapse of the catatonic episode, which was caused by the administration of risperidone. On day #24, no improvement in the state of catatonia was obtained. The treatment was changed with the following combination of medicine: clonazepam (0.1mg/kg/d)-lorazepam (5mg/d)-carbamazepine (10mg/kg/d). With this combination, the state of catatonia improved quickly and on day #31, he was transferred to the adolescent psychiatry unit. However, delusion and hallucinations persisted; a treatment with olanzapine was started at 5mg/d and then progressively increased to 20mg/d for 10 days. On day #115, after 3 months with olanzapine, no improvement of the hallucinatory and delusional symptoms was observed; the diagnosis of early-onset refractory schizophrenia was established. The Therapeutic Drug Monitoring (TDM) confirmed the good compliance; clozapine was introduced and progressively increased up to 250 mg/d. On day #199, after 3 months under clozapine (250 mg/d), the speech was coherent and delusion was rare. During this period, no relapse of the catatonic state was observed. In this case, the BFCRS scale was sensitive to catatonic symptom diagnosis. CPK levels vary differently for each atypical antipsychotic and are not a specific complication indicator. In complex cases, the TDM seems useful when choosing atypical antipsychotics. The association of two benzodiazepines (clonazepam-lorazepam) with carbamazepin allowed the improvement of catatonic symptoms. Plasma levels of atypical antipsychotics helped the practitioner in deciding the type of care required: plasma levels confirmed the patient's treatment adherence and thus reinforced the choice of clozapine.

Menard ML ，Yagoubi F ，Drici M ，Lavrut T ，Askenazy F ... -  《ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE》