[Follow-up of a 16-year-old adolescent with early-onset schizophrenia and catatonic symptoms]. / Suivi thérapeutique d'un adolescent de 16ans souffrant de schizophrénie précoce avec symptômes catatoniques.

INTRODUCTION: 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. CASE REPORT: 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. DISCUSSION: 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. CONCLUSION: 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.

["Catatonic dilemma". Therapy with lorazepam and clozapine]. / "Katatones Dilemma". Therapie mit Lorazepam und Clozapin.

We are reporting on a patient with a schizoaffective disorder (ICD 10:F25.1), whose catatonic symptoms deteriorated while receiving high-potency neuroleptic drugs in combination with anticholinergic medication. Initially there was a "catatonic dilemma", i.e. it was not possible to differentiate between the morbigenous and pharmacogenic (malignant neuroleptic syndrome) etiology of the catatonic symptoms. Catatonic symptoms were successfully treated with a combination of lorazepam and clozapine. The severe catatonic syndrome was found to be a neuroleptic-induced deterioration of a primary morbogenous catatonic syndrome. Thus, this case also suggests that the malignant neuroleptic syndrome and neuroleptic non-responsive catatonia may not be two different disease entities but that catatonia under neuroleptic medication is caused by the interaction of individual disposition, morbigenous and pharmacogenic factors.

[Exacerbation of catatonic symptoms in neuroleptic therapy]. / Verstärkung katatoner Symptomatik unter Neuroleptikatherapie.

This paper deals with the worsening of catatonic symptoms in three schizophrenic patients treated with typical neuroleptics. The paranoid and/or hallucinatory symptoms were positively influenced, but all patients showed marked subjective and objective sensitivity to this treatment regimen. As demonstrated in the three case reports, the diagnostic assessment of catatonic motor expressions movement and speech before initiation of pharmacotherapy can facilitate the differentiation between morbogenic and pharmacogenic movement disorders.

[Severe hypernatremia within the scope of catatonic schizophrenia]. / Schwere Hypernatriämie im Rahmen einer katatonen Schizophrenie.

We report the case of a 57-year-old chronic schizophrenic patient who developed an acute catatonic stupor after postoperative withdrawal of neuroleptics with excessive and firstly therapy-resistant hypernatremia. Only after re-treatment with neuroleptics the hypernatremia could be compensated. A relationship between the catatonic schizophrenia and the electrolyte-disturbances can be supposed; probably in both diencephalic structures are involved. Therefore the syndrome of "acute life threatening catatonia" should be included into the differential diagnosis of uncertain metabolic disorders.

Primidone-induced catatonic schizophrenia.

The authors report the case of a severely retarded, 19-year-old female (treated with primidone 250 mg tid since age 12) who was admitted with visual and auditory hallucinations. After four days of continuing hallucinations, she went into classic catatonic schizophrenia. Upon examination, her primidone serum level was found to be well above the normal therapeutic range. The primidone dosage was decreased, and symptoms subsided as serum levels returned to normal.

Fever, tachycardia, and hypertension with acute catatonic schizophrenia.

Fever, tachycardia, and hypertension developed concurrently with the administration of thiothixene during an acute episode of agitation in a case of catatonic schizophrenia. No cause for the fever or hyperkinetic state was found, and the syndrome resolved spontaneously one week after antipsychotic drug therapy was halted. This case appears to be an example of "acute lethal catatonia" or the neuroleptic "malignant" syndrome, both of which may be due to disturbances of dopamine function within the CNS. Such cases are rare, but may be dramatic in their presentation; however, antipsychotic drugs must be withheld during the duration of the disorder.

Neurological complications of drug abuse.

Widespread drug abuse, a comparatively recent medicosocial phenomenon, presents protean clinical patterns and challenging diagnostic problems daily that mimic classical medical syndromes. However, few reports have delineated predominantly neurologic syndromes associated with drug abuse. Five patients were observed illustrating the critical importance of considering drug abuse in the differential diagnosis of neurologic disease, particularly in the young population. It has been found that attention directed to four sources of information will substantiate the diagnosis of drug abuse in the large majority, thus expenditing the prompt initiation of appropriately directed treatment. In addition careful history and neurologic examination, a routine screeen of blood and urine should be run for barbiturates, bromides, alcohol and salicylates. An electroencephalogram is highly recommended as an initial study. It is informative, non-traumatic and inexpensive. Low voltage fast activity is consistent with drug effect and usually rules out other metabolic causes of coma. Other diagnostic principles are enumerated and illustrative cases are cited.