World Congress on Advances in Brain Injury, Disorders and Therapeutics October 21-22, 2019 | Tokyo, Japan

Woo Young Im is working at Konyang University and Yonsei University, South Korea.

Introduction & Objective: It is known that many of the cognitive and social deficits associated with autism can arise from abnormal functional connectivity between brain networks. This aberrant functional connectivity in Autism Spectrum Disorders (ASD) can be explained by impaired integrity of white matter tracts that link distant regions of the networks. Method: In the present study we investigated white matter in children and adolescents with High-Function Autism (HPA) compared to normal controls using diffusion tensor imaging (DTI). The aim of this research is to provide supporting evidence for abnormalities in neural connectivity as an underlying pathophysiology of the main characteristics of ASD. DTI was used to examine brain activations in 9 children with HPA and 13 typically developing controls. Results: We found impairment of neural connectivity, mainly in association fiber tracts, in individuals with high-function autism as evidenced by decreased Fractional Anisotropy (FA), the index of white matter integrity, of these tracts. Among them, Inferior Fronto-Occipital Fasciculus (IFOF), which connects the social brain, had a significant relationship with various domains such as social interaction, communication, repetitive behavior, verbal Intelligence Quotient (IQ), performance IQ, and functional IQ. The Inferior Longitudinal Fasciculus (ILF) and Superior Longitudinal Fasciculus (SLF) also showed decreased FA in individuals with HFA. FA of ILF and SLF had negative correlations with scores of social interaction and repetitive behaviors and positive correlations with IQ. Conclusion: These findings suggest that widespread abnormalities in association fiber tracts may contribute to both core and associated symptoms of ASD.

Nataliya Huseva is currently working at Belarusian State Medical University, Belarus.

Objective: To establish the histological and morphometric features of the human cerebral arterial circle as significant for cerebral circulation disorders development. Methods: The places of Willis circle vessels bifurcation were studied on 120 human brain preparations after staining with hematoxylin and eosin, Van-Gizon, orcein by Uann-Terzen, Sudan and with immunohistochemistry. Results: Reconstruction of cerebral vessels walls was determined inner layer growth (intimate thickenings), gradual thinning the middle layer till complete disappearance (p<0.05). The intimate thickenings growth was represented by 3 periods: (1) Formation (2-21 years); (2) slow growth (22-55 years); and (3) rapid growth (after 56 years). The medial layer in the first period of mature age (22-35 years) thinned by 53%; in the second period (36-55 years) by 59% and in the elderly age (56-74 years) by 79% or it was absent at all, that contribute to protrusion of the apical angle wall. Intimate thickenings were undergone an agerelated reconstruction caused by atherogenesis (appearance of lipid inclusions, moderate expression of Ki-67 protein). Conclusion: The histological and morphological features of human intimal thickenings were revealed. The following periods were distinguished as the crucial for cerebral circulation disorders development: The 1st period (30-35 years) - the medial layer thickness in branching vessel decreased significantly, that might contribute to the aneurysm formation; the 2nd period (after 56 years) - there was a significant increase in the height of intimal thickenings, that could lead to the vascular stenosis.

Giovanni Alano Vista has graduated from Cebu Institute of Medicine. Presently, he is a Resident in the Department of Internal Medicine in Perpetual Succour Hospital. He was recently offered a position of Research Subinvestigator for Perpetual Succour Hospital, Cebu Cancer Institute.

Spontaneous Acute Subdural Hematoma (ASDH) comprises 2.6% of all ASDH. In one recent study, only 178 cases of spontaneous ASDH were documented, however, only one of them was attributed to the presence of dural Arteriovenous Fistula (dAVF). Only less than 10% of all Subarachnoid Hemorrhage (SAH) are caused by vascular malformations. Spontaneous ASDH and SAH occurring together are extremely rare. There is a scarcity of literature on cases with dAVF of the occipital lobe as a cause of simultaneous spontaneous ASDH and SAH. A 44-year old Filipino male with no history of trauma, presented with severe headache, vomiting and decreasing sensorium; CT scan revealed acute parenchymal bleed in the left occipital lobe with subarachnoid extension and subdural hematoma in the left frontoparietotemporal convexity along the tentorium cerebeli and posterior interhemispheric falx. Due to the location of the lesion seen on CT scan and the gender distribution, arteriovenous malformation was initially considered, thus proceeded to CTA to establish the diagnosis of vascular anomaly, however, revealed dAVF instead. Four-vessel angiogram was done to assess the tributaries of the dAVF and confirmed the diagnosis. Complete obliteration of dAVF of the occipital lobe was done with Onyx Embolization in one session. This is the first case of Borden type II, Cognard type IIa+IIb dAVF, as reported in this institution. Although rare as a cause of SAH and ASDH, dAVF should be considered as a differential in patients with the absence of identifiable common cause of new onset of severe headache and poor neurologic status.

Yeliz Tasci is currently a PhD student at Erciyes University, Turkey.

Objective: A lot of evidence supports the hypothesis that the mechanism of memory trace formation at the cellular level is Long-Term Potentiation (LTP) and Long-Term Depression (LTD). LTP and LTD are initiated postsynaptically by the activation of N-Methyl-D-Aspartate (NMDA) receptors (NMDARs), resulting in Ca2+ influx and the subsequent activation of several kinases. Studies in which experimental animals were fed with fructose for a long time showed that insulin resistance occurred and this was associated with poor performance in hippocampus dependent learning. We therefore wanted to study that LTP/ LTD-related modifications of Tau phosphorylation could be, or not be, changed with High-Fructose Corn Syrup consumption (HFCS). Methods: The study was performed on 60 (100±15 grams; 20/group) 21-day old male Wistar Albino rats obtained from Erciyes University Experimental Animal Research Center. On the 21st day, the male rats leaving their mothers are fed with unrestricted standard rat chow and tap water, HFCS solution (8%; 0.24 Kcal/mL) or sucrose solution (10%, 0.4 Kcal/ mL) for at least 21 days. The field potentials were recorded from the right dentate gyrus with stimulation of the right medial perforant path. LTP and LTD were induced by High and Low Frequency Stimulation (HFS and LFS), respectively and total and phosphorylated forms of Tau was measured in the hippocampus at least 60 minutes after induction of plasticity. Results: The input/output curves of the study groups did not differ (P>0.05). After 1 hour of induction, LTD was 92±8% and 90±5% of the pre-LFS value in the control and sucrose groups, while LTP was 121±4% and 119±5%, respectively. There was no statistical significance between these groups (P>0.05). In the group fed with HFCS, the LFS and HFS did not induce LTP or LTD responses. In control and sucrose groups, it was found that the induced LTD was accompanied by spike potentiation (154±8% and 128±15%, respectively) and this potentiation was not observed in the HFCS group (P<0.01). Western blot experiments indicated that Tau protein was hyperphosphorylated at ser416 epitope upon LTP but rather hypophosphorylated at thr231 epitope upon LTP in the whole hippocampus of HFCS-fed rats. These changes concomitantly occurred with notable alterations in the levels of total Tau. Conclusion: These findings suggest that high fructose-containing diets may disrupt the balance between two forms of synaptic plasticity and thus adversely affect learning processes. Epitope specific Tau phosphorylation had been emphasized for Alzheimer’s disease-like learning deficit due to feeding with HFSC.