Risk of hip fracture can be reduced by hip protectors among elderly women with fall history and low BMI.

Thirty case reports published in Japan that refer to psychiatric symptoms accompanying interferon (IFN) therapy were examined. These papers covered a total of 49 cases. W e categorized these 49 cases into 35 cases of mood disorder, 10 of delirium and four of psychotic disorder. The key findings of our study of these cases are as follows: (i) in total, 11 patients had psychiatric past histories: five patients in the mood disorders group were susceptible to the influence of social or psychological factors; (ii) whereas the symptoms of mood disorder or delirium appeared soon after IFN was administered, the symptoms of psychotic disorders appeared later. The patients with delirium displayed many neurological abnormalities, which were reduced by suspending IFN therapy. This suggests the neurologcal toxicity of IFN; (iii) the outcome of most patients was good; and (iv) we suspect that IFN-induced psychiatric symptoms other than delirium are connected with psychoneuroimmunological functions.

Child and adolescent catatonia has been poorly investigated. A literature review was undertaken to clarify phenomenology, diagnosis, etiology, and treatment as well as ethical problems of catatonia in childhood and adolescence. Although there are no accepted standardized criteria for catatonia in childhood and adolescence, catatonic features described by child psychiatrists are similar to Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM-IV) criteria for catatonia. With respect to etiology, the motor and behavioral symptoms that are part of catatonia bear some similarities with those seen in autism. Several case reports suggest an association between catatonia and general medical conditions. Certain drugs abused by youngsters as well as prescribed medicine can induce catatonia. Regarding catatonic cases originally diagnosed as schizophrenia, it is unclear whether all of these cases should be identified as schizophrenia or whether some of them are pervasive developmental disorders that develop psychic features in adolescence. Environmental changes preceding the onset of catatonia in patients with mood disorder play a possibly important role. Examples that suggest stress-induced catatonia, although rare, also exist. A few patients exhibit features of malignant catatonia, some without taking neuroleptics and others having taken them. Benzodiazepines and electroconvulsive therapy are considered to be effective treatments for catatonic youngsters.

Catatonia in geriatric patients has been insufficiently investigated. We reviewed 71 case descriptions from 45 studies to clarify the phenomenology, diagnosis, etiology, and treatment of catatonia in the elderly. In elderly patients, catatonia is frequently observed in association with general medical conditions. In patients with a history of depression or schizophrenia, physicians occasionally overlook the medical conditions because they believe the previous psychosis to be the cause of the catatonic features. Despite historical discussions of a relation between the disorders, the number of patients with catatonia and a prior diagnosis of schizophrenia or another psychotic disorder is not large. A diagnosis of catatonia should be considered in cases of atypical "collapse" in elderly patients with a previous psychiatric history of mood disorder. Catatonia due to anxiety/adjustment disorder is quite rare, whereas catatonia in association with neuroleptic malignant syndrome is fairly common. For early commencement of treatment, early detection of catatonia in the elderly is important. In studies of psychotropic drug treatment, many authors observed a beneficial response to lorazepam in catatonic patients. For medication-refractory patients, electroconvulsive therapy should be considered. It is important to prevent the development of venous thrombosis as a serious complication in stuporous catatonic patients.

The present paper describes a patient who exhibited ‘Alice in Wonderland’ (AIW) syndrome as well as lilliputian hallucinations. The patient regularly consumed a cough syrup that contained dihydrocodein phosphate and dl-methylephedrine hydrochloride over 3 years. At the age of 46, he developed AIW syndrome. The patient ingested a large dose of triazolam and exhibited delirium. Even after the disappearance of symptoms associated with AIW syndrome and delirium, the patient continued to experience lilliputian hallucinations. We believe that these hallucinations were caused by some of the components of the cough syrup.