Abnormalities of cortical thickness, subcortical shapes, and white matter integrity in subcortical vascular cognitive impairment.

Subcortical vascular cognitive impairment (sVCI) is caused by lacunar infarcts or extensive and/or diffuse lesions in the white matter that may disrupt the white matter circuitry connecting cortical and subcortical regions and result in the degeneration of neurons in these regions. This study used structural magnetic resonance imaging (MRI) and high angular resolution diffusion imaging (HARDI) techniques to examine cortical thickness, subcortical shapes, and white matter integrity in mild vascular cognitive impairment no dementia (VCIND Mild) and moderate-to-severe VCI (MSVCI). Our study found that compared to controls (n = 25), VCIND Mild (n = 25), and MSVCI (n = 30) showed thinner cortex predominantly in the frontal cortex. The cortex in MSVCI was thinner in the parietal and lateral temporal cortices than that in VCIND Mild. Moreover, compared to controls, VCIND Mild and MSVCI showed smaller shapes (i.e., volume reduction) in the thalamus, putamen, and globus pallidus and ventricular enlargement. Finally, compared to controls, VCIND Mild, and MSVCI showed an increased mean diffusivity in the white matter, while decreased generalized fractional anisotropy was only found in the MSVCI subjects. The major axonal bundles involved in the white matter abnormalities were mainly toward the frontal regions, including the internal capsule/corona radiata, uncinate fasciculus, and anterior section of the inferior fronto-occipital fasciculus, and were anatomically connected to the affected cortical and subcortical structures. Our findings suggest that abnormalities in cortical, subcortical, and white matter morphology in sVCI occur in anatomically connected structures, and that abnormalities progress along a similar trajectory from the mild to moderate and severe conditions.

CSF and brain structural imaging markers of the Alzheimer's pathological cascade.

Cerebral spinal fluid (CSF) and structural imaging markers are suggested as biomarkers amended to existing diagnostic criteria of mild cognitive impairment (MCI) and Alzheimer's disease (AD). But there is no clear instruction on which markers should be used at which stage of dementia. This study aimed to first investigate associations of the CSF markers as well as volumes and shapes of the hippocampus and lateral ventricles with MCI and AD at the baseline and secondly apply these baseline markers to predict MCI conversion in a two-year time using the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. Our results suggested that the CSF markers, including Aß42, t-tau, and p-tau, distinguished MCI or AD from NC, while the Aß42 CSF marker contributed to the differentiation between MCI and AD. The hippocampal shapes performed better than the hippocampal volumes in classifying NC and MCI, NC and AD, as well as MCI and AD. Interestingly, the ventricular volumes were better than the ventricular shapes to distinguish MCI or AD from NC, while the ventricular shapes showed better accuracy than the ventricular volumes in classifying MCI and AD. As the CSF markers and the structural markers are complementary, the combination of them showed great improvements in the classification accuracies of MCI and AD. Moreover, the combination of these markers showed high sensitivity but low specificity for predicting conversion from MCI to AD in two years. Hence, it is feasible to employ a cross-sectional sample to investigate dynamic associations of the CSF and imaging markers with MCI and AD and to predict future MCI conversion. In particular, the volumetric information may be good for the early stage of AD, while morphological shapes should be considered as markers in the prediction of MCI conversion to AD together with the CSF markers.

Hemoperitoneum in cirrhotic patients without abdominal trauma or tumor.

BACKGROUND: Hemoperitoneum is associated with several emergency conditions and is especially evident when it occurs in patients with liver cirrhosis. This study aimed to assess the clinical characteristics of cirrhotic patients who did not have abdominal trauma or tumor but who developed hemoperitoneum. METHODS: We reviewed the clinical records of 1276 consecutive cirrhotic patients with hemoperitoneum at our center between January 2007 and December 2009. Hemoperitoneum was confirmed by abdominal paracentesis. RESULTS: Of the 1276 cirrhotic patients, 19 were found to have hemoperitoneum, but only 6 did not have abdominal trauma or tumor. The occurrence of spontaneous hemoperitoneum in the cirrhotic patients was therefore 0.5%. Hemoperitoneum can occur spontaneously in severely decompensated cirrhotic patients with intra-abdominal collateral vessels and high scores on the model for end-stage liver disease and Child-Pugh-Turcotte test. Most patients presented with abdominal distension, abdominal pain, increased abdominal girth and hemodynamic instability with a significant drop in the hemoglobin level. Three patients died of hemorrhagic shock within 24 hours, and the other 3 died of hepatic encephalopathy or spontaneous bacterial peritonitis after 5 to 10 days because of further decompensation of the liver. CONCLUSIONS: Hemoperitoneum can occur in cirrhotic patients who do not have abdominal trauma or tumor. It mainly occurs in severely decompensated end-stage cirrhotic patients. Cirrhotic patients with hemoperitoneum have a poor prognosis.

[Clinical features and outcome of infection of type 2 Streptococcus suis in human].

OBJECTIVE: To analysis the clinical features and efficacy of treatment for patients with type 2 Streptococcus suis (S. suis 2) infection, and to inform better diagnosis and treatment of S. suis 2. METHODS: Clinical data of 68 patients with S. suis 2 infection were retrieved retrospectively. The diagnoses were confirmed by clinical symtom or/and isolation of S. suis 2 from the infected sites in Shichuan province in the summer of 2005. The patients ranged from general type (simple sepsis) to septic shock type; meningitis type and mixed type. RESULTS: The outbreak of S. suis 2 infection occurred in June to August in 2005. The common source of infection came from pigs. The people in great risks were farmers who exposed to sick or dead pigs with S. suis 2 infection. Most infection occurred on the people who slaughtered infected pigs, followed by those who dressed infected meats. The prominent symptoms included fever with sharp chills, dizziness, headache, malaise and myalgia. Some patients had abdominal pain and diarrhea. Septic shock and coma often occurred in severe cases. According to the clinical manifestations, patients were categorized into four different clinical types: general type, septic shock type, meningitis type, and mixed type. S. suis 2 isolated from the patients were susceptible to most antimicrobial agents, except for tetracycline. All of the patients were treated with beta-lactam antibiotics (penicillins or cephalosporins). Some were given combined antimicrobial agents. Seventy seven percent (52/68) of patients survived. All of the general patients recovered completely. Fifty eight percent (15/26) of patients with septic shock died. The artificial ventilation and persistent blood filtering treatment played an important role for treating patients with septic shock. Although most patients with meningitis (97.5%) survived, a decrease in hearing or even hearing loss occurred to some of the survivors. CONCLUSION: Purulent meningitis and septic shock are the major clinical manifestations for S. suis 2 infection in human. The treatment for patients with meningitis is more effective than that for patients with septic shock.