Neuroimaging studies in patients with Charles Bonnet Syndrome

Charles Bonnet Syndrome (CBS) is characterized by complex formed and recurrent visual hallucinations in psychologically normal people, and is often associated with eye pathology. Many psychiatrists have taken an interest in CBS because this syndrome could provide clues to the mechanisms underlying visual hallucinations. In the present paper, we review previous neuroimaging studies in patients with CBS and summarize the results of these studies. There could be a fundamental dysfunction in the primary and secondary visual cortices in some patients with CBS, and transient cortical activation occurs in the inferior lateral temporal cortex during the appearance of visual hallucinations in CBS patients. External visual stimuli are perceived in the retina and are transmitted to the primary visual cortex (Brodmann area (BA) 17). The stimuli are transmitted from BA 17 to the secondary visual cortex (BA 18) and then to the visual association cortices (BA 19 and BA 37). In general, our perception of external visual stimuli normally has an inhibitory effect on the endogenous activation of the visual cortex. Visual loss due to certain conditions, of which eye pathology is the most commonly postulated in CBS patients, produces a state of sensory deprivation that releases the visual cortex from regulation by external stimuli, resulting in visual hallucinations (cortical release phenomenon). The results of previous neuroimaging studies suggest that the cortical release phenomenon hypothesis for the occurrence of visual hallucinations in patients with CBS is plausible. In addition, the results indicate that not only eye pathology, but also dysfunction in the primary and secondary visual cortices could result in deprivation of external visual stimuli.     

Stepped care medical treatment for cirrhotic ascites: Analysis of factors influencing the response to treatment

Abstract Thirty-two patients with liver cirrhosis and ascites were treated by stepped care diuretic treatment as follows: step 1, placed on a 35 mEq sodium diet; step 2, given 400 mg/day of potassium canrenoate in addition to step 1 treatment; step 3, given 40-80 mg/day of furosemide in addition to step 2 treatment. Eleven out of 32 patients (34.4%, group 1) and 12 of 21 patients (57.1%, group 2) lost their ascites at step 1 and step 2, respectively. The remaining nine patients (group 3) required step 3 treatment. Basal urinary sodium excretion and creatinine clearance were significantly lower and β₂-microglobulin was significantly higher in group 3 than those in groups 1 and 2. Elevation of basal plasma renin activity and norepinephrine was evident only in group 3. In group 1, urinary sodium excretion decreased after the treatment. In group 2, plasma α-atrial natriuretic polypeptide was lowered and plasma renin activity and norepinephrine were elevated after the treatment. These results suggest that basal renal function and plasma renin activity and norepinephrine levels are useful indices to predict the effect of ascites treatment and that responders to sodium restriction or potassium canrenoate may be in the state of vascular overflow, while non-responders to potassium canrenoate may be in the state of vascular underfilling. In summary, this stepped care treatment is safe without any side effects, although the diuretics themselves may lead to relative vascular underfilling.     

Plasma endotoxin concentration and endotoxin binding capacity of plasma acute phase proteins in cirrhotics with variceal bleeding: An analysis by new methods

Plasma endotoxin levels in 12 cirrhotics with bleeding from oesophageal varices and 50 cirrhotics without bleeding were measured by the chromogenic assay after the pretreatment of sample by perchloric acid (HClO₄) and triethylamine. Endotoxin in cirrhotics with bleeding from varices was significantly higher than those without bleeding. In patients with bleeding, endotoxin increased for 3 days after the bleeding, first in the supernatant fraction and then in the precipitate fraction by HClO₄ treatment. Peak plasma α₁-acid glycoprotein and haptoglobin were observed 3 days after the bleeding. Alpha 1-antitrypsin gradually increased for 14 days. Transferrin did not markedly change. The endotoxin-binding capacity of transferrin and α₁-acid glycoprotein increased immediately after bleeding and thereafter decreased, but that of α₁-antitrypsin tended to increase in the recovery period. In summary, the plasma endotoxin concentration and endotoxin-binding capacity of α₁-acid glycoprotein and transferrin were shown to have increased after bleeding from varices by this new method. There may be a close relationship between endotoxaemia and acute phase reaction in this situation.     

Macrophage colony-stimulating factor-producing malignant histiocytosis

Summary. We describe a patient with malignant histiocytosis who had a prominent neutrophilia uncommonly observed in this disease. Serum concentration of macrophage colony-stimulating factor (M-CSF) was markedly elevated, and correlated with clinical symptoms and neutrophil counts during clinical course. Moreover, M-CSF was detected in the cytoplasm of malignant histiocytes of the lymph node and bone marrow by immunohistochemical staining. These results indicate that the neutrophilia observed in this patient was caused by M-CSF produced by the malignant histiocytes.