Risk of ischaemic stroke in patients with transient global amnesia: a propensity-matched cohort study.

BACKGROUND: The exact pathophysiological mechanism of transient global amnesia (TGA) is unknown. It is debatable whether TGA is a risk factor for stroke. Therefore, here we investigated the possibility of TGA as a risk factor for stroke in a real-world setting using large-scale nationwide health claims data. METHODS: We used health claims data from the Korean National Health Insurance Service (NHIS). Patients diagnosed with TGA between 2007 and 2013 were selected. We initially extracted patients without TGA who were preferentially matched for age and sex with the patients with TGA at a ratio of 10:1 from the whole dataset. Further, we performed 1:2 propensity score matching analysis to balance the baseline characteristics between the two groups. In the propensity score-matched dataset, we performed multivariable Cox regression analysis to investigate the association between TGA and stroke type, including ischaemic, haemorrhagic and all stroke types. RESULTS: Patients with TGA (n=14 673) were selected from the NHIS database. After extracting from the whole database (n=140 486) and propensity score matching their data at a 1:2 ratio, a total of 10 448 and 20 442 patients were finally assigned to the TGA and control groups, respectively. The multivariable Cox regression analysis demonstrated that the TGA group had a higher risk of ischaemic stroke and all types of stroke (adjusted HR=1.194; 95% CI: 1.043 to 1.368; and HR=1.197; 95% CI: 1.056 to 1.357, respectively). CONCLUSIONS: Analysis of the nationwide claims database showed that TGA could be an important risk factor for stroke, especially for ischaemic stroke.

Latent gallbladder carcinoma in a young adult patient with acute cholecystitis: report of a case.

Acute cholecystitis associated with gallbladder carcinoma is very rare in young patients (younger than 30 years of age). Moreover, a definitive preoperative diagnosis is difficult. A 26-year-old man was referred to our hospital with a 5-day history of right upper quadrant pain. Computed tomography and ultrasonography demonstrated an enlarged gallbladder with a diffuse thick wall and a 2-cm gallstone obstructing the cystic duct. Magnetic resonance cholangiopancreatography showed no evidence of an anomalous pancreaticobiliary junction. The patient showed an elevation in the white blood cell count, serum C-reactive protein, and alkaline phosphate; however, total bilirubin, alanine aminotransferase, and tumor markers including carcinoembryonic antigen and carbohydrate antigen 19-9 were all within the normal ranges. The preoperative diagnosis of gallstone-induced acute cholecystitis was made and an open cholecystectomy was thus performed 2 days after admission. The macroscopic findings showed a necrotic enlarged gallbladder with a thick wall and a gallstone, but no intraluminal nodular lesion. Histologic examinations revealed well-differentiated focal adenocarcinoma in the gallbladder mucosa, but no venous, lymphatic, or perineural invasion. The postoperative course has been uneventful with no recurrence 18 months postoperatively.

Lithium enhances long-term potentiation independently of hippocampal neurogenesis in the rat dentate gyrus.

We measured the temporal and spatial profiles of neural precursor cells, hippocampal long-term potentiation (LTP), and signaling molecules in neurogenesis-induced adult rats. Chronic lithium treatment produced a significant 54% and 40% increase in the numbers of bromodeoxyuridine [BrdU(+)] cells after 12 h and 28 days, respectively, after treatment completion in the dentate gyrus (DG). Both LTP obtained from slices perfused with artificial cerebrospinal fluid (ACSF-LTP) and LTP recorded in the presence of bicuculline (bicuculline-LTP) were significantly greater in the lithium group than in the saline controls. Although the number of BrdU(+) cells, approximately 90% of which were double-labeled with a neural marker neuronal nuclear protein, were markedly increased in the granule cell layer (GCL) 28 days after the completion of the 28-day lithium treatment, the magnitude of LTP observed at this time was similar to that observed 12 h after completing the 28-day lithium treatment. However, protein levels of calcium and calmodulin-dependent protein kinase II, p-Elk and TrkB were highly elevated until 28 days after the 28-day lithium treatment. Acute lithium treatment for 2 days also enhanced LTP, which was accompanied by the elevated expression of p-CREB, but not by neurogenesis. Our results suggest that the enhancement of LTP is independent of the increased number of neurons per se and it is more closely associated with key molecules, which are probably involved in neurogenesis.