Patients with schizophrenia often present sleep complaints, but its relationship with general satisfaction with life (SWL) and burden for caregivers has been understudied. We aimed to assess the differences in SWL between patients with and without self-reported sleep disturbances and that of their caregivers. In a noninterventional study, 811 schizophrenia adult outpatients were screened for their subjective perception of having (or not) sleep disturbances and evaluated with the Brief Psychiatric Rating Scale (BPRS) and the Pittsburgh Sleep Quality Index (PSQI). Patients self-reporting sleep disturbances were significantly more symptomatic (P < 0.001), presented significantly worse family support (P = 0.0236), and self-reported worse SWL in all domains. Caregivers of patients with schizophrenia self-reporting sleep disturbances also reported worse SWL in all domains, as compared to caregivers of patients without subjective sleep disturbances. Patient and caregivers' SWL was significantly correlated to patients' quality of sleep (P < 0.0001 for all domains). Patient' and caregivers' SWL was negatively affected by patients' poor quality of sleep. We found that patients self-reporting sleep disturbances showed greater symptom severity, worse quality of sleep, worse SWL, and less caregiver support. SWL was also worse for caregivers of patients with schizophrenia reporting sleep disturbances.
THE PATIENT WAS a 37-year-old married Caucasian woman, who had at least five episodes of catatonic stupor during the previous 10 years. The first episode occurred in 1995, when the patient presented with crisis of jealousy and paranoid suspiciousness. She complained that the water and food had been poisoned, and believed that someone was watching her movements inside the house via cameras. She reported auditory hallucination and was verbally and physically aggressive toward her family. Her first psychiatric diagnosis was paranoid schizophrenia and treatment was initiated with haloperidol (5 mg/day) and clonazepam (2 mg/day), with full symptomatic remission after 4 weeks. The second episode occurred 3 years later (1998), and she was admitted to the psychiatric ward with negativism, mutism, and stupor, for 3 weeks. Because the staff doctor believed that she was in a depressive stupor, the patient received four electroconvulsive therapy (ECT) sessions with very rapid response. Sertraline 50 mg per day was then prescribed for maintenance During the next episode (1999), she was admitted in a catatonic state, presenting extreme negativism, and mutism for 48 consecutive hours. Tube feeding was required on that occasion. The diagnosis of periodic catatonia was made. Dramatic response was observed with olanzapine (20 mg/day) and clonazepam (1 mg/day), and she was discharged with no psychotic movements or symptoms. The patient then relapsed after discharge, and underwent four ECT sessions. During follow up the patient had no psychotic or residual symptoms with complete restitutio ad integrum, and returned to her usual job, maintaining use of olanzapine (20 mg/day). Her last hospital admission was in 2005, after the patient voluntarily discontinued medication for 3 months, quit her job without a good reason, started to quarrel with her husband and became agitated. The patient described weight gain, constipation, and some episodes of nausea; for these reasons she voluntarily discontinued medication. The patient arrived at the hospital emergency unit in full mutism, with staring, waxy flexibility, negativistm, stupor, and ambitendency, scoring 30 (out of a maximum of 69) on the Bush–Francis Catatonia Rating Scale (BFCRS),1 with no evidence of recent drug or alcohol use. She had normal brain computed tomography, electroencephalography (EEG), magnetic resonance imaging, and blood work-up (including electrolytes, thyroid, liver and renal function test, and blood counts). In the ward she had three transient episodes of catatonic state, which lasted for a few hours. EEG was performed during one of the catatonic seizures with negative findings. She was discharged on the 40th day of hospitalization (July 2005), receiving olanzapine (20 mg/day), with full recovery, without negative or affective symptoms. Catatonia has been described as one of the most enigmatic phenomena in psychiatry and neurology.2 Catatonia is a rare psychomotor syndrome, which can be associated with psychiatric illnesses such as schizophrenia (catatonic subtype) and manic depressive disorder, as well as with neurological and medical diseases.3 Mostly studied by European psychiatrists, periodic catatonia is rare; the usual treatment is ECT or high doses of oral benzodiazepines. Therapeutically, 60–80% of the acute catatonic patients respond to lorazepam, a GABA-A receptor agonist.4 We report a case of periodic catatonia that responded well to olanzapine. Because the physiopathology of periodic catatonia is unknown, testing has been done on a mostly trial-and-error basis. Although the use of olanzapine is not fully justified, in contrast, patients who had not previously responded well to ECT and typical antipsychotic, recent report on the use of atypical antipsychotic (risperidone, ziprasidone and olanzapine) may indicate their utility in treating some varieties of catatonia.5–7 Atypical neuroleptics such as olanzapine have a broader range of affinity for neuronal receptors than typical neuroleptics, but it is not clear whether atypicals will prove to be a therapeutic option for catatonia. The use of atypical antipsychotics, as replacements for or in addition to benzodiazepines, ECT or conventional antipsychotics, should be considered as an alternative for patients whose symptoms do not improve with conventional therapy, although the systematic recommendation of olanzapine has not been justified by currently available data.
Catatonia is a rare psychomotor syndrome, which can be associated with psychiatric illnesses such as schizophrenia (catatonic subtype) and manicdepressive disorder, as well as with neurological and medical diseases. 2 Mostly studied by European psychiatrists, periodic catatonia is rare; their usual treatment of choice consisted of electroconvulsive therapy (ECT) or high doses of oral benzodiazepines. Therapeutically, 60-80% of the acute catatonic patients respond to lorazepam, a GABA-A receptor agonist. 3 We report a case of periodic catatonia that responded well to olanzapine. Patient A is a 37-year-old married Caucasian woman, who presented at least five episodes of catatonic stupor along the last 10 years. The first episode occurred in 1995, when the patient presented with crisis of jealousy and paranoid suspiciousness. She complained that the water and food had been poisoned, and believed that someone was watching her movements inside the house through cameras. She reported auditory hallucination and was verbally and physically aggressive toward her family. Her first psychiatric diagnosis was paranoid schizophrenia and treatment was initiated with haloperidol (5 mg/day) and clonazepam (2 mg/day), with full symptomatic remission after 4 weeks. During the next episode (1999), she was admitted in a catatonic state, presenting extreme negativism, and mutism for 48 consecutive hours. Tube feeding was required in that occasion. The diagnosis of periodic catatonia was made. Dramatic response was observed with olanzapine (20 mg/day) and clonazepam (1 mg/day), and she was discharged with no psychotic movements or symptoms. Indeed, she relapsed after discharge, and was submitted to 4 ECT sessions. During the follow-up, she showed no psychotic or residual symptoms with complete restitutio ad integrum, and returned to her usual job, maintaining use of olanzapine (20 mg/day). During her last hospital admission, no evidence of recent drug or alcohol use was found. She had a normal brain CT, EEG, MRI, and blood work-up (including electrolytes, thyroid, liver and renal function test, and blood counts). In the ward, she presented 3 transient episodes of catatonic state, which lasted for a few hours. EEG was performed during one of the catatonic attacks with negative findings. She was discharged on the 40th day of hospitalization, receiving olanzapine (20 mg/day), with full recovery, without negative or affective symptoms. Since the physiopathology of periodic catatonia is unknown, therapeutic efforts have been tested on a mostly trial-and-errors basis. Although this patient had previously responded to ECT and to typical antipsychotics, the use of olanzapine could be justified with basis on previous reports of atypical antipsychotic treatment for some types of catatonia. 4-6