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Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320
Plasma homocysteine levels and cognitive status in patients with ischemic cerebrovascular disease
Legal aspects of dementia assessment expertise: Croatian experience
N. Sternica, A. Pavlovica, T. Pekmezovica, J. Zidverc-Trajkovica, Z. Jovanovica, M. Mijajlovica, A. Radojicica, G. Tomica, I. Novakovicb, R. Obrenovica, V.S. Kostica a Institute of Neurology, Clinical Center of Serbia, Belgrade, Serbia b Institute of Biology and Human Genetics, School of Medicine, Belgrade, Serbia
V. Seric, I. Martinic Popovic, M.J. Jurasic, V. Demarin Clinical Department of Neurology, Zagreb, Croatia
Background and aims: Hyperhomocysteinemia is an important and independent risk factor for vascular disease, including stroke. The relationship between plasma homocysteine levels and cognitive status in patients with different types of ischemic cerebrovascular disease has been explored. Methods: Plasma homocysteine levels were determined in 95 patients with ischemic cerebrovascular disease. All patients underwent vascular RF assessment, neuropsychological testing and brain MRI scanning. Total Age Related White Matter Changes (ARWMC) scale score was obtained. Score on modified Rankin scale (mRS) was determined in all patients. Results: Group comprised 55 (57.9%) men, 40 women (42.1%), mean age 55.6 ± 14.9 years. Mean group homocysteine level was 14.3 ± 5.03 μmol/L. Univariate analysis showed that higher homocysteine levels were associated with an increased risk of cognitive decline (OR 1.14; 95% CI 1.04–1.25, p = 0.005), higher score on mRS (OR 1.1; 95% CI 1.01–1.21, p = 0.050), and higher ARWMC total score (OR 1.14; 95% CI 1.04–1.25, p = 0.006). In multivariate model, higher homocysteine levels were independently associated with an increased risk of cognitive decline (OR 2.71; 95% CI 1.12–6.54, p = 0.026). Conclusions: There is an association between higher plasma homocysteine levels and cognitive decline in patients with ischemic cerebrovascular disease. doi:10.1016/j.jns.2009.02.037
Natural course of melas in Japanese cohort study
Medical care and legal system are two different scientific disciplines with different sets of knowledge and a different approach to the same problem: understanding the human being and its behavior in the interest of a just approach to its actions. Social, legal and moral norms regulate relationships and coexistence in the community. In most countries, an increase in elderly criminality is difficult to prove implying the existence of “dark figures”, probably showing a strong public emotion that legal sentence is not the proper means of treatment of the elderly and feeble persons. Thus, legal norms do not explicitly address the elderly and their older age changes opposed to underage delinquency that constitutes a separate legal status. The law does allow acknowledgment of phenomenological and etiological specificities of criminal acts performed by the elderly implying milder sentences, an individual approach and adjustments to specificities and differences of such age. A frequent daily legal problem is: what can be done with the elderly delinquents? Questions of competency to stand trial, legal responsibility and competency to be sentenced can be approached differently. The expertise process should determine whether aging is physiological or if dementia exists. In the case dementia is established, specific type and cause, course and prognosis of the disease should be assessed. The influence of social factors, possible alcohol abuse or other influences should be estimated as well. Such individuals are usually labeled as partially or completely incompetent. In cases of crime or felony by perpetrators incompetent because of advanced dementia or mental deficiency due to older age, or if a social danger is present, he or she may be confined to a secured medical facility or placed in an institution for long-term medical care. An increased number of elderly prisoners in Croatia and in other countries with individuals who develop dementia whilst in custody, raises other ethical implications. doi:10.1016/j.jns.2009.02.039
Y. Koga, S. Yatsuga, Y. Akita, J. Nishioka, K. Katayama, N. Povalko, T. Matsuishi Department of Pediatrics and Child Health, Kurume University, Kurume, Fukuoka, Japan Background and aims: Natural course of MELAS has not been clarified. The specific aim of the present study is to estimate the incidence, natural course, and severity of the disease based on Japanese cohort study. Methods: Demography of MELAS is collected by a questionnaire retrospectively. The questionnaire was constructed based on Japanese mitochondrial disease rating scale. We analyzed the age, symptoms of onset, survival rate, and clinical progression of MELAS. Results: We found 233 MELAS patients in Japan. The population based prevalence is 0.18/100,000 in Japan. Since there is a bimodal distribution in the onset of the disease, we divided MELAS into two sub-groups; juvenile and adult type. First symptoms were noted at the mean age of 9 years in the juveniles and of 32.2 years in the adult type. Death described at mean age of 15 years in the juveniles and 40 years in the adult type. Convulsion, strokelike episodes, headache and muscle weakness was the most frequent first symptoms in both forms. Short stature and developmental delay was significantly higher in juveniles than those seen in the adult type. On the other hand, deafness and diabetes mellitus were significantly more recognized in the adults than in the juvenile type. Using Japanese mitochondrial disorders' rating scale, some juvenile types showed a rapid increase their exacerbation within 5 to 9 years after the onset of disease. However, adult type showed slow increase in their exacerbation during the entire course of the disease. Using Kaplan–Meier survival analysis, juvenile type has 3.2 times more chance of death than that seen in the adult type. Seventy eight percent of MELAS has an A3243G mutation and all showed abnormality in muscle biopsy. Conclusions: MELAS is the most common clinico-pathological entity among mitochondrial disorders, shows the vascular dementia in the progressive stage, and turns out to be a rapidly progressive degenerating disorder in Japan. doi:10.1016/j.jns.2009.02.038
Aromatase and C/EBP expression after global ischemia/reperfusion injury in rat hippocampus P. Kelicena, N. Burul-Bozkurta, M. Cincioglua, M. Dagdevirenb, C. Pekinera Department of Pharmacology, Faculty of Pharmacy, Hacettepe University, Sihhiye-Ankara, Turkey b Department of Biochemistry, Institute of Natural and Applied Sciences, Middle East Technical University, Balgat-Ankara, Turkey
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Background and aims: Global ischemia after cardiac arrest, intraoperative hypoxia/hypotension, or hemorrhagic shock is one of the causes of brain injury, resulting in severe neurological and neurobehavioral deficit. Since neurodegeneration can be protected from by local aromatase expression and estrogen synthesis can be neuroprotective in the ischemia/reperfusion process, aromatase may be a potential target to study reperfusion injury after brain ischemia. We investigated the expression of aromatase and C/EBP by using Western blotting in rat hippocampus after transient global ischemia+ hypotension (CAO + jvht). Methods: Transient two vessel occlusion global ischemia plus hypotension was produced. Briefly, animals were anesthetized and body temperature maintained within the normal range (37.0–37.5 °C), throughout the experiment. The femoral artery was exposed and catheterized to allow continuous recording of arterial blood. Bilateral common carotid arteries were temporarily occluded (CAO), and blood was gradually withdrawn from the jugular vein to reduce the mean arterial blood pressure (MABP) to 35– 45 mm Hg (ht). After 10 min of ischemia, the withdrawn warmed shed blood was reinfused to restore normotension and animals monitored during 3 h. Rats were decapitated, hippocampi were removed and homogenized and then immunoblotting was applied. Results: Protein expression of aromatase and C/EBP was observed after 10 min, 3 h and 24 h reperfusion period at the same level in both control and damaged tissues. These protein expressions peaked at 1 week and decayed at 2 weeks in damaged hippocampi after global ischemia-hypotension.