Three patients with cancer who developed rapid-eye-movement sleep behavior disorder.

This article discusses the clinical significance of differentiating parasomnia, such as rapid-eye-movement (REM) sleep behavior disorder (RBD), from delirium in patients with advanced cancer. We describe three patients with advanced cancer who presented with aberrant behavior at night. All three patients developed violent behaviors when they were administered opioids and/or chemotherapy. Polysomnography (PSG) showed REM sleep with tonic electromyography. Previous treatment with neuroleptics had failed to improve their problematic behaviors. Diagnosis was made using criteria for REM behavior disorder of the International Classification of Sleep Disorders, 2nd edition, and PSG. Clonazepam (0.5 mg/day) was administered orally once at night. After treatment with clonazepam, aberrant and violent behaviors were improved. It should be noted that it is not rare for patients with advanced cancer to present with parasomnia, such as RBD, although organic brain syndrome, such as delirium, is more prevalent. Therefore, it is necessary to provide adequate assessment and treatment of aberrant behaviors in cancer patients.

Synthetic Smac peptide enhances the effect of etoposide-induced apoptosis in human glioblastoma cell lines.

Smac/DIABLO is a mitochondrial protein released into cytosol during the progression of apoptosis. Smac/DIABLO promotes apoptosis by neutralizing the inhibitory effect of the inhibitor of apoptosis proteins (IAPs) on the processing and activity of the effecter of caspase. Here, we generated synthetic Smac peptide which possesses an IAP-binding domain and Drosophila antennapaedia penetration sequence, and examined whether it enhances the effect of the chemotherapeutic agent etoposide in the human glioblastoma cell line. Cellular uptake of Smac peptide in several glioma cell lines was most prominent at 6-12 h after addition. Caspase activity assay showed that our peptide successfully increased the activity of caspase-3 and caspase-9 in etoposide-induced apoptosis. In addition, Smac peptide increased the amount of cleaved PARP (poly ADP-ribose polymerase), but control peptides did not. Moreover, the addition of z-VAD-fmk, a caspase inhibitor, counterbalanced the effect of Smac peptide. Finally, we demonstrated that Smac peptide could enhance the growth inhibition effect of etoposide compared with control peptides. These results suggest that synthetic Smac peptide may be a new molecular targeting anti-tumor therapy for human glioblastoma.

Moyamoya syndrome after prophylactic cranial irradiation for acute lymphocytic leukemia.

A 9-year-old boy presented with an episode of syncope, and MR imaging revealed bilateral internal carotid artery stenosis with moyamoya vessel formation. He had had prophylactic cranial irradiation at a total dose of 24 Gy for the treatment of acute lymphocytic leukemia at the age of 4. Following this, he was in a complete state of remission for 6 years. During an observation period of a year after the onset of syncope, MR imaging showed development of multiple ischemic lesions in both hemispheres. He developed a transient ischemic attack of mild motor weakness in his arm and an indirect anastomosis was performed on the severely affected side at the age of 10. Radiation-induced vasculopathies are known to be associated with primary diseases of intracranial tumors, but the frequency is unclear. Ours is the third case in whom prophylactic cranial irradiation for a hematological disorder might have induced cerebral vasculopathies.