7^th International Conference on Brain Injury and Neurological Disorders April 10-12, 2018 Amsterdam, Netherlands

Biography:

Lena Ehrhard successfully completed her apprenticeship as Occupational Therapist at the Rhön-Akademie in Schwarzerden/Germany in 2002. She also finished her professional training on Psychic Trauma Therapy in 2012. As a co-partner of the health care center in Rotenburg an der Fulda/Germany, she is currently working as a Neurofeedback Therapist, using a 19-channel-discovery-system, trained by IFEN, Munich/Germany.

Abstract:

New techniques make writing Q-EEG possible, especially ambulant treatment for severe affected patients in hospitals or at home. On this foundation is a grounded and progressive neurofeedback therapy in nearly everywhere possible. Patients who couldn't take part in treatments due to mobility reasons can now do so. Case by case examples (locked-in, stroke, pain disorders) will demonstrate appraisal, methods and the betterment of the patient during the ambulant neurofeedback therapy

Biography:

Adrián Gaitán Fariñas is a PsyD professional who conducts the first clinic specialized in QEEG and Neurofeedback treatment in the area of Cadiz (South of the Spain). He is a QEEG and Neurofeedback Instructor at the IFEN Institute, and European Institution devoted to train professionals in Neurofeedback therapy. He is also a QEEG and Neurofeedback Treatment-Planning Consultant of several clinics in Spain.

Abstract:

Neurofeedback is a form of neuromodulation that uses brainwave conditioning to modify aberrant neural functioning and optimize brain functioning, leading to emotional and cognitive improvements. It has also been proposed to provide benefits in brain insults like traumatic brain injuries and stroke; through training the damaged networks and facilitating cognitive remediation. A recent evolution of Neurofeedback known as sLORETA neurofeedback uses an inverse problem algorithm solution to identify and train activity of specific Brodmann areas instead of EEG activity detected at the scalp, and it is believed to provide faster and better outcomes than classic neurofeedback due to the superior precision. We will review the case of a patient suffering from alexia following a left hemisphere stroke. QEEG and sLORETA brain imaging showed dysregulation in Brodmann areas linked to reading, and neuropsychological examination revealed profound impairment in reading function. After a relatively short, combined treatment with cognitive stimulation and sLORETA z-score neurofeedback of the damaged networks, patient experimented a significant improvement in reading and cognitive functioning. QEEG and sLORETA imaging demonstrated enhanced regulation of electrical activity in the areas trained, suggesting that sLORETA neurofeedback helped to recover the function impaired due to the brain damage. Implications of sLORETA neurofeedback in the cognitive remedation and brain insult treatment will be discussed

Biography:

Hashim Hasan Balubald has been graduated from the Medical College at King Abdulaziz University-Jeddah in 1995 and completed his Internship at King Abdulaziz University- Hospital from 1995 to 1996 to 2001. He has joined the residency program in Internal Medicine at King Fahad National Guard hospital in Riyadh, Saudi Arabia.

Abstract:

Stroke is a chronic disease that affects the functional, cognitive and psychosocial status of the patient. Post stroke, the patient needs extensive medical, physical and psychosocial interventions. Rehabilitation to get the patient back into the community is essential. Things that need to be addressed and assessed post stroke include the following: social reintegration, depression, cognition, sexuality and care giver burden.

Biography:

Raed M Aljubour, MD, FEBNS, is a Consultant Neurosurgeon at KHMC, Jordan. He has completed his Fellowship in Skull Base from INI Hannover, Germany. He is a Member in European Board of Neurological Surgery, Arab Board of Health Specializations. He pursued his Diploma in EuroSPIN.

Abstract:

Objective: Severe brain injury is defined as a brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8. Patients in this condition need endotracheal intubation and mechanical ventilation, the main cause of secondary brain injury is increase in intracranial pressure which is preventable when it is detected and can decrease mortality and morbidity rate.

Method: This study focused in management of severe head injury and of intracranial pressure monitoring to decrease the morbidity and mortality, multi-centric study compares the outcome between patients with same GCS in hospital with intracranial pressure monitor versus patients in hospital without intracranial pressure monitor.

Results: We took 2 groups with same GCS, first group patients in hospital with intracranial pressure monitor and second group patients in hospitals without intracranial pressure monitor. Compare the mortality rate in both groups, with same GCS which shows less mortality and morbidity rate is more significant in GCS 7 and 8.

Conclusion: Hospital with intracranial pressure monitor especially intra-ventricular had less mortality and morbidity rates in patients with severe head injury with GCS 7 and 8, no difference in GCS below 6.

Biography:

Reza Amani is the academic member at Isfahan University of Medical Sciences (IUMS), Isfahan, Iran. He received his PhD and MSc in Nutrition Science from Tabriz University of Medical Sciences, Tabriz, Iran. He has obtained his fellowship in Clinical Nutrition. He has also worked at the University of Sydney, Australia as Visiting Scholar. He has published more than 120 scientific papers in Persian and English academic journals and has supervised above 50 Post-graduate theses and research projects. Currently, he is working as the Head of Food Security Research Center at IUMS. He has been awarded as eminent Researcher at Ahvaz Jundishapur University of Medical Sciences for five years.

Abstract:

Background & Aim: Stroke is the second cause of death among elderly people and oxidative stress plays important role in brain damage after stroke. The aim of this study was to evaluate the status of Vitamin D, antioxidant enzymes, and the relation between the ischemic stroke patients.

Materials & Methods: This case–control study was carried out on 36 patients with ischemic stroke patients and 36 matched subjects as controls. Intake of fruits and vegetables, exposure of sunlight, serum lipid profile, concentrations of serum Vitamin D, activities of serum superoxide dismutase, and glutathione peroxidase enzymes were determined.

Results: Severe Vitamin D deficiency was seen in 30% of the patients versus 11% of the controls (P<0.05). Consumption of fruits and vegetables was lower in patients than that of controls (P<0.05). Activities of antioxidant enzymes and intake of fruits were positively correlated in stroke patients (P=0.02). The most potent predictors of stroke risk were hypertension, high levels of low-density lipoprotein cholesterol (LDL-C) and history of cardiovascular disease (CVD) (odds ratios: 3.33, 3.15, and 3.14, respectively, P<0.05 for all). There was no association between 25(OH) D levels with activities of serum antioxidant enzymes and lipid profile in the two groups.

Conclusion: Ischemic stroke patients have higher prevalence of severe Vitamin D deficiency and lower intakes of fruits and vegetables. Intake of fruits was positive correlated to higher antioxidant enzyme levels. High levels of blood pressure, history of CVD, and high LDL‑C levels are the strongest predictors of ischemic stroke.

Biography:

Anatoly Uzdensky has completed his PhD in 1980 from Rostov State University (Russia). He is the Principal Investigator and Head of the Laboratory of Molecular Neurobiology in the Sothern Federal University (Rostov-on-Don, Russia). He has published more than 120 papers in reputed journals.

Abstract:

In focal ischemic stroke, vessel occlusion rapidly induces local infarct of the brain tissue. During next hours, injurious factors (glutamate, Ca²⁺ and others) propagate to surrounding tissue and form the transition zone, penumbra, where both, neurodegeneration and neuroprotection processes are developed. Cell protection in penumbra is the aim of neurologists, but effective neuroprotectors are not found yet. So, deeper studies of biochemical processes in penumbra are needed. Neuronal and signaling antibody microarrays (Panorama, Sigma-Aldrich) were used to study changes in expression of >400 signaling and neuronal proteins in penumbra surrounding photothrombotic infarct core in rat cerebral cortex 1, 4 or 24h after impact comparing with untreated contralateral cortex. The greatest changes were observed at 4h after photothrombosis. They included simultaneous upregulation of proteins involved in diverse subcellular systems: proapoptotic (caspases 3, 6 and 7, Bcl-10, AIF, SMAC/DIABLO, p53, E2F1, p38, JNK, NMDAR2a, c-myc, Par4, p75, GADD153, GAD65/67, PSR) and anti-apoptotic (Bcl-x, p63, p21WAF-1, MDM2, ERK5, MKP-1, NEDD8, estrogen receptor) proteins. Various signaling proteins (calmodulin, CaMKIIα, CaMKIV, ERK1/2, MAKAPK2, PKCα, PKCβ, PKCμ, RAF1, protein phosphatase 1α, ATF2, EGF receptor, DYRK1A) were upregulated, whereas others (phospholipase Cγ1, S-100, GSK-3, Axin1, NUMB, TDP-43, FRAT1) - downregulated. Proteins involved in mitochondria quality control (Pink1, parkin), proteolysis (ubiquilin-1, UCHL1), intercellular interactions (N-cadherin, PMP22), neurite integrity and guidance (Nav3, CRPM2, PKCβ2) were overexpressed. Proteins associated with actin cytoskeleton (cofilin, actopaxin, p120CTN, α-catenin, p35, myosin Va and pFAK) were upregulated, whereas other cytoskeleton components (ezrin, tropomyosin, spectrin (α+β), β_IV-tubulin, polyglutamated β-tubulin, doublecortin, neurofilaments 68 and M, cytokeratins 7 and 19) - downregulated. Downregulation of syntaxin, synaptophysin, synaptotagmin, VILIP, ALS2, and adaptin β1/2 indicated impairment of vesicular transport and synaptic processes. Enzymes that mediate dopamine biosynthesis (tyrosine hydroxylase, DOPA decarboxylase, dopamine transporter) were downregulated, whereas proteins involved in biosynthesis of serotonin and GABA (tryptophan hydroxylase, MAO-B, glutamate decarboxylase) - upregulated. Down-regulation of CDK6, CDC7 kinase, TRF1, and topoisomerase-1 suppressed proliferation. Levels of mitochondrial antioxidant protein AOP-1, chaperons Hsp70 and Hsp90 were reduced. Amyloid precursor protein, nicastrin and β-amyloid were upregulated. These data provide the integral view on neurodegeneration or neuroprotection processes in penumbra after photothrombotic infarct. Some of these proteins can be considered as potential targets for anti-stroke therapy. Supported by Russian Science Foundation (14-15-00068) and Russian Ministry of Education and Science (6.4951.2017/6.7).

Biography:

Anthony Lee has received his Bachelor of Science Degrees in Mechanical Engineering and in Biology with a minor on Music. He pursued his MD from The College of Physicians and Surgeons at Columbia University. He has completed his Internship at New York Hospital Queens and his residency training at NYU in Physical Medicine and Rehabilitation. He has obtained his Fellowship training at New England Baptist Hospital in Spine Medicine. He is a Faculty Physician at Harvard Medical School, directly responsible for training future pain physicians in one of the top pain fellowship programs in the United States. His expertise is in complex spinal disorders, headaches and general rehabilitation. He divides his clinical work between the Department of Anesthesia and the Department of Orthopedic Surgery at Beth Israel Deaconess Medical Center.

Abstract: