Education modifies the relation of vascular pathology to cognitive function: cognitive reserve in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

A clinical impact of cognitive reserve (CR) has been demonstrated in Alzheimer's disease, whereas its role in vascular cognitive impairment (VCI) is largely unknown. In this study, we investigated the impact of CR in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a genetic variant of pure VCI. A total of 247 NOTCH3 mutation carriers from a two-center study were investigated using detailed neuropsychological and neuroimaging protocols. CR was operationalized as years of formal education. Brain pathology was assessed by MRI using normalized brain volume and lacunar lesion volume as proxies. Multivariate analyses were done for each structural measure with scores of processing speed, executive function, and memory as dependent variables. Additional linear regression models were conducted with interaction terms for education × brain volume and education × lacunar lesion volume. Education had an independent impact on cognitive performance in subjects with mild and moderate degrees of brain pathology, whereas there was no significant influence of education on cognition in patients with severe MRI changes. This interaction was found for processing speed, the cognitive domain most impaired in our patients. Our findings demonstrate an interaction of education and brain pathology in regard to cognitive impairment: the effect of education seems most pronounced in early disease stages but may ultimately be overwhelmed by the pathological changes. The results extend the concept of CR to VCI.     

White matter abnormalities in Parkinson's disease patients with glucocerebrosidase gene mutations

Glucocerebrosidase gene mutations represent a genetic risk factor for the development of Parkinson's disease. This study investigated brain alterations in Parkinson's disease patients carrying heterozygous glucocerebrosidase gene mutations using structural and diffusion tensor magnetic resonance imaging. Among 360 Parkinson's disease patients screened for glucocerebrosidase gene mutations, 19 heterozygous mutation carriers (5.3%) were identified. Of these, 15 patients underwent a neuropsychological evaluation and a magnetic resonance imaging scan. Sixteen age‐ and sex‐matched healthy controls and 14 idiopathic Parkinson's disease patients without glucocerebrosidase gene mutations were also studied. Tract‐based spatial statistics was used to perform a white matter voxel‐wise analysis of diffusion tensor magnetic resonance imaging metrics. Mean fractional anisotropy values were obtained from white matter tracts of interest. Voxel‐based morphometry was used to assess gray‐matter atrophy. Cognitive deficits were found in 9 mutation carrier patients (60%). Compared with controls, Parkinson's disease patients carrying glucocerebrosidase gene mutations showed decreased fractional anisotropy in the olfactory tracts, corpus callosum, and anterior limb of the internal capsule bilaterally, as well as in the right anterior external capsule, and left cingulum, parahippocampal tract, parietal portion of the superior longitudinal fasciculus, and occipital white matter. Mutation carrier patients also had decreased fractional anisotropy of the majority of white matter tracts compared with Parkinson's disease patients with no mutations. No white matter abnormalities were found in Parkinson's disease patients without glucocerebrosidase gene mutations. No gray matter difference was found between patients and controls. In Parkinson's disease patients, verbal fluency scores correlated with white matter abnormalities. Parkinson's disease patients carrying glucocerebrosidase gene mutations experience a distributed pattern of white matter abnormalities involving the interhemispheric, frontal corticocortical, and parahippocampal tracts. White matter pathology in these patients may have an impact on the clinical manifestations of the disease, including cognitive impairment. © 2013 Movement Disorder Society     

A common polymorphism in the brain-derived neurotrophic factor gene in patients with adult-onset primary focal and segmental dystonia

Brain-derived neurotrophic factor (BDNF) modulates neuroplasticity. A functional polymorphism [Val66Met (G196A)] in BDNF has been reported to modify cortical plasticity in humans. Physiologic investigations have revealed that dystonia might be a consequence of the pathologic plasticity of the sensorimotor cortex. We aimed to investigate the role of the Val66Met polymorphism in a cohort of Serbian patients with adult-onset primary focal and segmental dystonia (PTD). One hundred and forty-nine patients with primary adult-onset PTD, 194 patients with Parkinson’s disease (PD), and 366 healthy control subjects were recruited for the study. Patients with PTD and PD, as well as healthy controls had a similar distribution of genotypes and allele frequencies. There was no any significant difference in the allelic distribution at the Val66Met SNP of the BDNF gene among patients with adult-onset PTD, PD, and healthy volunteers from the same geographic areas. In addition, the presence of the Met allele did not influence the clinical characteristics of PTD patients. Patients with the Met variant did not differ by age at onset, number of affected regions, and efficacy of a sensory trick. Met66Met is not associated with an increased risk of dystonia.     

Illness perceptions predict exercise capacity and psychological well-being after pulmonary rehabilitation in COPD patients

Objective

Patients' beliefs about their disease have been associated with emotional adjustment and outcomes in several severe illnesses. The aim of the present study was to investigate whether illness perceptions before pulmonary rehabilitation influence exercise capacity and quality of life after rehabilitation in patients suffering from chronic obstructive pulmonary disease (COPD).

Methods

Ninety-six patients with COPD (GOLD III/IV) were approached on admission to rehabilitation and reassessed before discharge. Assessment included medical measures of FEV?% predicted, and exercise capacity (6 min walk test). Additionally, depressive symptoms (Hospital Anxiety and Depression scale), anxiety (COPD specific anxiety questionnaire) and quality of life (Short Form 36 health survey (SF-36)) were assessed. Illness beliefs were measured by the Revised Illness Perception Questionnaire (IPQ-R).

Results

Exercise capacity and psychological well-being (SF-36) of patients improved after rehabilitation programme, while physical functioning (SF-36) did not change. Additionally, patients showed significantly lower levels of depressive symptoms, COPD specific anxiety and negative perceptions of their illness after pulmonary rehabilitation compared to baseline. In the hierarchical multiple regression analyses, after controlling for socio-demographic data, psychological variables, illness severity and baseline scores of the corresponding variables, it was shown that illness perceptions before rehabilitation predicted exercise capacity and psychological well-being, both assessed at the end of treatment.

Conclusion

COPD patients' perceptions about their illness before rehabilitation influence exercise capacity and quality of life (psychological well-being) after treatment. Therefore it might be relevant to identify and change maladaptive illness perceptions in order to improve medical and psychological outcome in COPD.     

Nonsurgical Endodontic Treatment of Necrotic Teeth Resolved Apical Lesions on Adjacent Implants with Retrograde/Apical Peri-implantitis: A Case Series with 2-year Follow-up

Retrograde (or apical/periapical) peri-implantitis (RPI) presents with radiographic signs of bone loss at the periapical area of endosteal implants and may also present with clinical signs of abscess formation or a sinus tract traceable to the implant periapex. The lesion may form days up to several years after the initial implant placement. In contrast to marginal peri-implantitis, which has a prevalence of 19.83%, RPI may be underreported because many clinicians are currently not aware of this type of lesion. The etiology, although not fully understood, may be attributed to endodontic infection of an adjacent tooth or residual microorganisms present after the extraction of an infected tooth at the implant site. There are several treatment modalities available for the management of RPI. Nonsurgical root canal treatment may be an option if the implant RPI etiology is suspected to be related to an adjacent endodontically involved tooth. In a previous report, surgical treatment modalities to correct RPI were described. This current case series presents 2 cases of RPI in which nonsurgical treatment of the necrotic adjacent teeth resulted in full radiographic and clinical resolution of the adjacent apical peri-implant lesions with 18-month and 2-year follow-ups, respectively. RPI may be prevented by evaluating the endodontic status of natural teeth adjacent to the implants and by addressing endodontic infections near the implant sites. Certain types of implant RPI may successfully be resolved nonsurgically by addressing adjacent endodontic infections as shown by this case series.     

Disorders of protein metabolism in neonatal hyperbilirubinemia and their correction by extracorporeal detoxification

A close relationship was established between the gravity of bilirubin intoxication, dysproteinemia and hyperpeptidemia in neonates. It is shown that accumulation of peptides belonging to the medium molecule group and associated pathophysiological manifestations may account for a graver course and less favourable prognosis of hemolytic disease of the newborn as compared to conjugation hyperbilirubinemia. It is suggested that the measures aimed at bilirubin removal by the control of the medium molecule effects should be supplemented. The results of hemosorption (51 sessions in 42 children) and substitution transfusion (27 operations in 24 children) were subjected to clinical and laboratory comparisons. In addition to bilirubin removal from the body, hemoperfusion permits the correction of protein metabolism abnormalities occurring in hemolytic disease.