Cognitive impairment in patients with carotid artery occlusion and ipsilateral transient ischemic attacks

Abstract. Although transient ischemic attacks (TIAs) by definition do not cause lasting neurological deficits, cognitive impairment has been suggested in patients with carotid artery disease who have suffered from a TIA. The purpose of our study was to assess whether patients with carotid artery disease and TIAs are cognitively impaired, to describe the frequency, nature and severity of this impairment, and to search for associated patient characteristics.Thirty-nine consecutive patients with carotid occlusion and ipsilateral cerebral or retinal TIAs, and 46 healthy controls underwent extensive neuropsychological assessment. Performances were compared group-wise with analysis of variance. In addition, the presence of cognitive impairment in the individual patient was determined. Associations between illness characteristics and cognitive impairment were explored with regression analysis.Fifty-four percent of patients were cognitively impaired. Cognitive deficits were non-specific in nature and mild in severity. Impairment occurred also in patients with isolated retinal symptoms and in those without visible ischemic brain lesions on MRI. Neither the presence of any vascular risk factor, the side of the symptomatic carotid occlusion, the uni- or bilaterality of carotid occlusion, nor the number of cerebral ischemic lesions were predictors of cognitive impairment.We conclude that about half of the patients with carotid artery occlusion and ipsilateral TIAs are cognitively impaired. The presence of cognitive deficits in patients with isolated retinal symptoms and in those without cerebral ischemic lesions on MRI argues against an exclusive role for structural brain damage in the pathogenesis of these deficits.     

Pneumococcal vaccine in the elderly: the Norwegian experience

Pneumococcal infections have increased during the last 10 to 15 years in Norway. Their incidence is now about 20 per 100,000 population for all age groups, but is 2 to 3 times higher among the elderly. In 1996, the Advisory Board of Infectious Disease Control, National Institute of Public Health, Norway, recommended that pneumococcal polysaccharide vaccine should be administered to all individuals aged > or = 65 years. This recommendation has led to an increased use of pneumococcal vaccine, with a marked peak during the influenza vaccination season.     

Specific antibodies induce apoptosis in Trypanosoma cruzi epimastigotes

The susceptibility of Trypanosoma cruzi epimastigotes to lysis by normal or immune sera in a complement-dependent reaction has been reported. Mouse immune sera depleted complement-induced damage in epimastigotes characterized by morphological changes and death. The purpose of this work was to study the mechanism of death in epimastigotes exposed to decomplemented mouse immune serum. Epimastigotes were maintained in RPMI medium. Immune sera were prepared in mice by immunization with whole crude epimastigote extracts. Viable epimastigotes were incubated with decomplemented normal or immune sera at 37°C. By electron microscopy, agglutinated parasites showed characteristic patterns of membrane fusion between two or more parasites; this fusion also produced interdigitation of the subpellicular microtubules. Apoptosis was determined by flow cytometry using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and annexin V assays. Nuclear features were examined by 4′-,6-diamidino-2′-phenylindole diHCI cytochemistry that demonstrated apoptotic nuclear condensation. Caspase activity was also measured. TUNEL results showed that parasites incubated with decomplemented immune sera took up 26% of specific fluorescence as compared to 1.3% in parasites incubated with decomplemented normal sera. The Annexin-V-Fluos staining kit revealed that epimastigotes incubated with decomplemented immune sera exposed phosphatidylserine on the external leaflet of the plasma membrane. The incubation of parasites with immune sera showed caspase 3 activity. We conclude that specific antibodies are able to induce agglutination and apoptosis in epimastigotes, although the pathway is not elucidated.     

Cation exchange resins as pharmaceutical carriers for methylene blue: Binding and release

Methylene blue is a competitive inhibitor of the glutathione reductase of Plasmodium falciparum and is used in combination with other antimalarial drugs leading to a renaissance of methylene blue in malaria therapy. Its bitter flavour and tissue colouring property impair compliance, especially in children. These problems may be solved by binding the cationic methylene blue to cation exchange materials as pharmaceutical carriers in order to mask the undesirable properties. However, such carriers are only useful if the antimalarial is released under physiological conditions. The binding to seven cation exchange resins was studied. Ion exchangers on acrylic or methacrylic acid basis bound between 1.54 and 2.16 g methylene blue chloride trihydrate per gram ion exchanger. Polymers on divinylbenzene or styrene basis with sulphonic acid groups bound 306 and 384 mg of methylene blue chloride trihydrate per gram ion exchanger. In aqueous solution at pH of 1.5, nearly all bound methylene blue was released. The release of methylene blue from (meth)acrylic acid polymers in the presence of proteins and fat was not affected. From these data ion exchangers present a promising group of pharmaceutical carrier for the safe and compliant drug administration of methylene blue to children.     

Immunolocalization of dipeptidyl aminopeptidase (DAP IV) in the developing human brain

By means of immunohistochemical techniques we have investigated the presence of dipeptidyl aminopeptidase IV immunoreactivity in brain material derived from human fetuses, newborns and aged persons. It was revealed that the enzyme protein is abundantly present in the immature human CNS. On the contrary the adult human brain contains much less dipeptidyl aminopeptidase immunoreactivity. It is speculated that the enzyme might play an important role in neuronal proliferation and/or differentiation especially with regard to its possible action on certain neuronotrophic peptides (IGF II, growth hormone).     

Congenital disorder of glycosylation type Ia: benign clinical course in a new genetic variant

The congenital disorders of glycosylation (CDG) are autosomal recessive disorders of N-glycans processing. Several different subtypes have been identified in recent years. Cerebellar atrophy is a characteristic finding in subtype Ia. We report clinical, imaging and genetic findings in a patient with a particularly benign clinical course, who had a normal CT at the age of 9 months and a new, previously undescribed, combination of mutations of the PMM gene locus on chromosome 16p13 (647,691). The 691 mutation has been described only in severe cases so far. This could indicate that genotype-phenotype correlation is lower than expected.