Comparison and Analysis of Delirium Induced by Histamine H2 Receptor Antagonists and Proton Pump Inhibitors in Cancer Patients

Objective: H2 blockers have been reported to be responsible for drug-induced delirium. We compared the incidence of delirium between two groups of patients who were treated with H2 blockers (H2 group) or proton pump inhibitors (PPI group) for anastomotic ulcer prevention following surgical treatment of esophageal cancer. Method: The incidence and severity of delirium were retrospectively compared in patients of the H2 group (30 cases; age, 65.2 ± 8.1 years) and the PPI group (30 cases; 65.2 ± 6.5 years). The diagnosis of delirium was based on the Diagnostic and Statistical Manual of Mental Disorders-IV-Text Revision. Delirium severity was rated on the Delirium Rating Scale (DRS). Results: The incidence of delirium was significantly lower in the PPI group than in the H2 group (p = 0.047). In the 11 patients from the H2 group who developed delirium, discontinuation of H2 blockers resulted in a significant reduction in the DRS score (p = 0.009). In three patients for whom H2 blockers were discontinued, DRS scores decreased by 50% or more three days after discontinuation compared to the prediscontinuation score. Conclusions: These results suggested that switching antiulcer drugs from H2 blockers to PPIs reduced delirium and thus provided an appropriate coping method for drug-induced delirium from antiulcer drugs

Diagnosis and Surgical Management of Foramen Magnum Meningioma

Two cases of foramen magnum meningioma were successfully treated at early stage. The magnetic resonance imaging (MRI) played an important role for accurate diagnosis. The tumors were microsurgically removed and the patuents returned to socity in full capacity. The foramen magnum meningioma is rare, and potentially curable. The recognition of this entity is important for neurologists, orthopodists and neurosurgenos in the differential diagnosis of the craniocervical problems

Aneurysm Arising from the Junction of Internal Carotid Artery and Duplicated Middle Cerebral Artery

A case of an aneurysm arising from the junction of the internal carotid artery and duplicated middle cerebral artery was reported. A 77-year-old female was admitted to our hospital with complaints of headache, nausea, vomiting and disturbance of consciousness. CT scan showed a high-density area in the basal cistern and Sylvian fissure. Carotid angiography revealed saccular aneurysm arising from the junction of the right internal carotid artery and duplicated middle cerebral artery orginating from the internal carotid artery. The neck of aneurysm was clipped via the basal interhemispheric approach on the day of onset. Transient right oculomotor nerve palsy occurred in the postperative course. Normal pressure hydrocephalus was treated by ventriculoperitoneal shunt. The relationship between the genesis of aneurysms and the duplicated middle cerebral artery was discussed. From the location of these aneurysms associated with the duplicated middle cerebral artery, we suggested that congenital etiological factors were modified by the acquired hemodynamic factors

Casein kinase II is responsible for phosphorylation of NF-L at Ser-473

AbstractSer-473 is solely phosphorylated in vivo in the tail region of neurofilament L (NF-L). With peptides including the native phosphorylation site, it was not possible to locate responsible kinases. We therefore adopted full-length dephosphorylated NF-L as the substrate, and employed MALDI/TOF (matrix-assisted laser desorption and ionization/time of flight) mass spectrometry and a site-specific phosphorylation-dependent antibody recognizing Ser-473 phosphorylation. The antibody showed that casein kinase I (CK I) as well as casein kinase II (CK II) phosphorylated Ser-473 in vitro, while neither GSK-3β nor calcium/calmodulin-dependent protein kinase II did so. However, the mass spectra of the tail fragments of the phosphorylated NF-L indicated that CK II was the kinase mediating Ser-473 phosphorylation in vitro as opposed to CK I, because CK I phosphorylated another site as well as Ser-473 in vitro. The antibody also demonstrated that NF-L phosphorylated at Ser-473 was abundant in the neuronal perikarya of the rat cortex, indicating that phosphorylation of Ser-473 may take place there. This result may support the suggestion that CK II is the kinase responsible for Ser-473 phosphorylation. Despite many reports showing that CK I mediates phosphorylation of neurofilaments, CK II may phosphorylate NF-L in vivo