Effects of deep brain stimulation on cognitive functioning in treatment-resistant depression: a systematic review and meta-analysis.

Deep brain stimulation (DBS) is a promising intervention for treatment-resistant depression (TRD). Effects on cognitive functioning are unclear since they have been studied in small samples. We aim to estimate the impact of DBS on cognitive functioning in TRD with a systematic review and meta-analyses. After systematically searching PubMed we included 10 studies which compared standardized neuropsychological tests before and after DBS or between active and sham DBS in TRD. Different random-effects meta-analyses were done for different cognitive (sub-)domains and for different follow-up time windows (<6 months, 6-18 months, and >18 months). We found no significant differences in cognitive functioning up to 6 months of DBS. After 6-18 months of DBS small to moderate improvements were found in verbal memory (Hedge's g = 0.22, 95% CI = [0.01-0.43], p = 0.04), visual memory (Hedge's g = 0.37, 95% CI = [0.03-0.71], p = 0.04), attention/psychomotor speed (Hedge's g = 0.26, 95% CI = [0.02-0.50], p = 0.04) and executive functioning (Hedge's g = 0.37, 95% CI = [0.15-0.59], p = 0.001). Not enough studies could be retrieved for a meta-analysis of effects after >18 months of DBS or for the comparison of active and sham DBS. Qualitatively, generally no differences in cognitive functioning between active and sham DBS were found. No cognitive decline was found in this meta-analysis up to 18 months of DBS in patients with TRD. Results even suggest small positive effects of DBS on cognitive functioning in TRD, although this should be interpreted with caution due to lack of controlled data.

Three novel KCNA1 mutations in episodic ataxia type I families.

Hereditary paroxysmal ataxia, or episodic ataxia (EA), is a rare, genetically heterogeneous neurological disorder characterized by attacks of generalized ataxia. By direct sequence analysis, a different missense mutation of the potassium channel gene (KCNA1) has been identified in three families with EA.

Cerebrospinal fluid C-reactive protein in meningitis: diagnostic value and pathophysiology.

We examined the diagnostic value of C-reactive protein (CRP) in cerebrospinal fluid (CSF) on initial lumbar puncture in a prospective study including 126 patients (30 neonates, 96 infants and children) suspected of having meningitis. Twenty patients were considered to have bacterial and 25 were considered to have viral meningitis. In infants and children, a retrospectively chosen cut-off CRP titre of 4 (i.e. approximately equal to 0.4 mg/l CRP) had a sensitivity of 100% and a specificity of 94% for differentiating bacterial meningitis from both viral meningitis and normal. It was a more sensitive and selective test for differentiating bacterial from viral meningitis on initial CSF examination than was the CSF leucocyte count, glucose concentration or protein concentration. In neonates, no such cut-off CRP titre could be found, presumably due to the immaturity of the blood-CSF-barrier (B1-CSF-B) during the first weeks of life. In a parallel study including a non-selected group of 13 infants and children (4 without, 9 with bacterial meningitis), the serum/CSF CRP concentration ratios were determined and inserted in the individual B1-CSF-B diagrams according to Felgenhauer. The results were fully consistent with the hypothesis that the CRP concentration in CSF reflects the normal permeability characteristics of the B1-CSF-B, or the degree of its impairment. Based on our results, we recommend the CSF CRP estimation in the routine evaluation of infants and children suspected of having meningitis.

Factors determining the occurrence of serum agglutinins to eubacterium and peptostreptococcus species in patients with Crohn's disease and ulcerative colitis.

Recently, the demonstration of serum agglutinins to Eubacterium and Peptostreptococcus strains has been found to be useful as a diagnostic test for Crohn's disease. Therefore, conditions determining the occurrence of these antibodies were studied in patients with Crohn's disease and ulcerative colitis. Localization of Crohn's disease in the colon, the presence of fistulae and serum levels of immunoglobulins were found to be contributory determinants for the occurrence of the agglutinins.

Plasma lysozyme levels and decay of neutrophilic granulocytes in patients with Crohn's disease.

In patients with Crohn's disease, the lysozyme concentration in plasma was compared with the Crohn's disease activity index, the granulocyte lysozyme content, the number of circulating neutrophilic granulocytes in peripheral blood and the unsaturated vitamin B12-binding capacity of the plasma cobalophilins as an index for the granulocyte decay. There was no difference in the lysozyme content of granulocytes from patients and controls. Patients with increased plasma lysozyme levels suffered from a more active disease and had larger numbers of circulating granulocytes in their blood than those with normal plasma lysozyme levels. The plasma lysozyme levels correlated well with the cobalophilin levels, in patients with increased levels even more markedly than in those with normal levels. The results suggest that in patients with Crohn's disease increased plasma lysozyme levels are due to an increase in granulocyte decay.

A possible role of Eubacterium and Peptostreptococcus species in the aetiology of Crohn's disease.

The faecal flora of patients with Crohn's disease has been found to contain higher numbers of anaerobic gram-negative rods and gram-positive coccoid rods than the flora of healthy subjects. In a considerable percentage of sera from patients with Crohn's disease, agglutinating antibodies were found against four strains of the coccoid rods, in contrast to sera from patients with ulcerative colitis, other diseases and healthy subjects. In the present study, coccoid strains C18, Me46 and Me47 were found to activate complement by the alternative pathway. IgG antibodies to strains Me44, C18 and Me47 had opsonic properties but those to strain Me46 failed to induce phagocytosis. The data suggest an inadequate immune defence against strain Me46 in patients with Crohn's disease. The possible role of strain Me46 in the pathogenesis of Crohn's disease is discussed.