Biography:

Ettore Di Scipio is an MD and Clinical Neurophysiologist at San Filippo Neri Hospital in Rome. He is shifting his focus from neurological investigation to nervous system protection. He treats both inpatients and outpatients, and has expertise in electromyography, intraoperative neurophysiological monitoring, electroencephalography and polysomnography. Currently, he is studying new applications of "CE-Chirp® BAEP's stimulus" in Neurology.

Abstract:

CE Chirp© LS is a new acoustic stimulus designed to provide faster detection of larger amplitude BAEP's waves. CE Chirp LS BAEP's are performed in the same way as click BAEP's. Surface electrodes are placed at the vertex (Cz) and on each earlobe (A1 and A2). Filters bandwidth are 150-1500 Hz. Two channels are used: A1-Cz and A2-Cz. Stimuli are presented by inserting earphones with alternate polarity at 41.1 Hz, but can also be presented at higher frequencies. Sound pressure range is 80 to 100 dB nHL, choosing the sound pressure level giving the clearest waves. Controlateral ears are masked by white noise at 50 dB nHL. CE Chirp© LS stimulus has the same spectrum and the same calibration as a usual square wave click stimulus. Acoustic energy from low, mid and high frequency components of CE Chirp© LS stimulus reaches all the regions of the cochlea at the same time. This allows neurons in the cochlea to fire synchronously. This change in stimulus presentation results in a CE Chirp© LS BAEP's wave V of double amplitude than click BAEP's wave V. Double amplitude of wave V translates in a reduction of test time. SNR improvement is equal to the square root of the number of trials averaged. If we want to achieve the same Signal/Noise Ratio (SNR) of click ABR, if the response is 2 times bigger, then we need 1/(2)2 of sweeps, that means only 25%. So, instead of 2000 sweeps we need only 500. This is a quarter of test time. Combined with high frequency of stimulation, e.g. 63 Hz, we can have a very clear BAEP's in 5-15 seconds. In our experience, CE Chirp© LS BAEP's monitoring can be performed up to four times faster than click BAEP's. Neurophysiologists can be able to inform neurosurgical equipe in few seconds about variations of wave V parameters.

Biography:

Sadaf Mohtashami is a Master’s student in the Division of Experimental Medicine in the Faculty of Medicine at McGill University. She is pursuing her research under the supervision of Dr. Guy Rouleau who has contributed to the identification of over 20 disease-causing genes and new mutational mechanisms. The laboratory team of Dr. Rouleau is focused on identifying genes involved in neurological and psychiatric diseases and on understanding the biological function of those genes.

Abstract:

Hereditary sensory and autonomic neuropathies form a group of genetic disorders characterized by variable sensory and autonomic dysfunctions. HSAN type II (HSANII) is a debilitating subtype manifesting in early childhood with distal numbness and loss of pain, temperature and touch. The first cluster of HSANII cases was reported in eastern Canada, with half the patients of French-Canadian descent. Our laboratory has reported truncating mutations in a nervous-tissue-specific exon (HSN2) of the WNK1 gene. The WNK1 isoform containing the alternatively spliced exon (HSN2) is referred to as the WNK1/HSN2 isoform. Interestingly the protein region encoded by the alternatively spliced exon was found to interact with a particular isoform of another HSANII causative gene, KIF1A. The HSANII-causing KIF1A isoform is referred to as KIF1A/25B since disease-causing mutations were exclusively found in the alternative exon “25B”. KIF1A belongs to a superfamily of microtubule-dependent proteins that mediate specific and diverse motile processes within the cell.

Materials & Methods: The expression profile of KIF1A/25B across the nervous system is determined by performing WB immunodetection using tissues from wild-type mice and a rabbit antiserum. The function of the protein encoded by exon 25B is assessed through a profiling of its interacting partners by performing co-immunoprecipitation for full-length KIF1A/25B protein, full-length KIF1A/25B minus exon 25B, the protein that correspond to exon 25B and EGFP protein as a negative control. Positive interactions are confirmed using liquid chromatography–mass spectrometry.

Results: KIF1A/25B is the transit system through which WNK1/HSN2 traffics within the cells and offers the two proteins an opportunity to interact with other cellular elements relevant to the sensory and nociceptive aspects of HSANII.

Conclusions: This study answers fundamental questions regarding the molecular pathophysiology of HSANII, though our findings have an impact on the understanding of other neuropathies and of normal neuronal processing.

Biography:

Abstract:

Introduction: Sleep as a widespread physiological phenomenon is seen in all vertebrates. In primates as human, the sleep consists of two components REM & non-REM. One of the major centers involved in the control of REM sleep is Locus Coeruleus. REM sleep deprivation causes neural death in the LC. In the present study, we administered melatonin as an antioxidant factor and neuroprotective agent to prevent neural death.

Material & methods: In this study, the Flowerpot approach has been used to induce RSD. Melatonin was administered for 7 days, the count & the volume of the LC neurons examined due to stereology methods. The enzymatic test for GSH & measurement of Caspase-3 & C-Fos was done to assess the antioxidant property and apoptosis process and neural activity respectively. Immunohistochemistry of Anti-TH factors was done to assess the noradrenergic neurons and the Iba-1 test was also done to show the microglial migration.

Results: According to the papers the RSD cause neural apoptosis in LC. Melatonin leads to a reduction in the level of apoptotic factor Caspase-3 expression followed by RSD. According to stereology analysis, the count of adrenergic neurons & the volume of the nucleus reduces after RSD & in the administered-melatonin group the apoptotic protein Caspase-3 reduces to prevent neural death. Microglial migration to the LC occurs after neural death and the melatonin increases GSH levels in RSD group finally.

Conclusion: Melatonin with neuroprotective property can be used to treatment of adrenergic-depended sleep disorders & prevention of neural apoptosis in LC

Keywords: Locus Ceoruleus, Melatonin, RSD, apoptosis, oxidative stress

Biography:

Abstract:

In the columns of one paper of the World Health Organization published on 16th May, 2002, it appears that in the developing countries, over 80% of the population lives in rural areas. Generally, the content of the exchange of these populations is insufficient to help all the needs of daily life including access to modern medicines already very expensive in large cities. To solve the problems of health, these populations use medicinal plants. Often the therapeutic properties of these plants remain hypothetical or just placebos. Currently in Cameroon and elsewhere in Africa, Asia and South America, government efforts are growing in the direction of more rational and scientific use of medicinal plants. Mimosa pudica Linn. (M. pudica) is a plant empirically used in some countries to treat anxiety and depression. In the present study, two months old mice, Mus musculus Swiss were acutely treated by different doses of M. pudica (3, 10 and 30 mg/kg) and anxiety related responses evaluated by analyzing Stress-Induced Hyperthermia (SIH), Elevated Plus Maze (EPM), Elevated T Maze (ETM), open field and hole board parameters. The horizontal wire and rota-rod tests were then used to highlight possible myorelaxant properties of M. pudica. Finally, we investigated the effect of aqueous extract of M. pudica on regulation of Dorsal Raphe Nucleus (DRN) 5-Hydroxytryptamine (5-HT) neuronal activity using an in-vitro mouse brain slice preparation providing from adult male C57/BL6 mice. The decrease of SIH was observed with M. pudica (30 mg/kg) treatment. In the EPM, significant increase of open arms entries and percentage of time spent in the open arms with M. pudica (10 mg/kg) was observed. Neither diazepam (3 mg/kg) nor M. pudica (3 and 10 mg/kg) produced changes of motor activity. However the change of motor activity was observed with M. pudica (30 mg/kg). In the hole-board test, M. pudica (3 and 10 mg/kg) significantly increased the number and duration of the head-dips respectively. The anxiolytic properties of M. pudica as assessed using the EPM test were abolished by flumazenil (3 mg/kg), by bicuculline (5 mg/kg), and FG 7142 (10 mg/kg). Acute treatment with M. pudica extract also had an anxiolytic effect on behaviour in the ETM, specifically on inhibitory avoidance behaviour. In the horizontal wire test, both M. pudica (3 and 10 mg/kg) and distilled water allowed animals to grasp within 30 s. M. pudica (3 and 10 mg/kg) did not impair the duration of the time spent on the rota-rod. However at the dose of 30 mg/kg, up to 60 min, the M. pudica significantly reduced the time that animals remained on the rota-rod. Acute application of the extract alone had no effect on the activity of DRN 5-HT neurones. However, when co-applied with the GABAA receptor agonist THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c] pyridin-3-ol), the extract enhanced the inhibitory effect of the THIP on DRN 5-HT neurones. This study indicates that M. pudica contains an effective psychotropic agent that acts via the benzodiazepine site of the GABAA receptor complex as an anxiolytic at low doses and as a muscle relaxant at higher doses. These results in part could justify and confirm the use of this plant extract as an anxiolytic agent.

Biography:

Adam D. Swanson is a nationally awarded public speaker dedicated to equity in public and health care systems. He assists state governments, universities and other organizations improve quality of care for people in crisis at the Suicide Prevention Resource Center in Washington, DC. He has served on national and international expert panels to advise organizations in addressing minority health disparities. He previously led LGBTQ initiatives and oversaw national efforts to implement innovative first-episode psychosis treatment services at the National Council for Behavioral Health. In the U.S. Senate, he helped advance anti-bullying legislation and Ryan White HIV/AIDS Care Act reforms. He is a former Mental Health America fellow.

Abstract:

For more than a decade, studies have shown that Americans of minority status face remarkable disparities when it comes to preventable illnesses, mental health and addicition conditions, and overall mortality. The statistics speak for themselves: Black babies are almost 5 times more likely to die before reaching their first birthday than white babies; suicide attempts for high school-aged Hispanic girls are 70 percent higher than for white girls in the same age group; lesbian, gay and bisexual (LGB) adults are about 5 times more likely than heterosexual men and women to have a mental illness in their lifetime such as those related to mood, anxiety or substance use; and nearly 40 percent of all transgender people report that they have faced harassment or discrimination when seeking routine health care. Explainations of this phenomna from researchers and policymakers varies across issues of access, poverty, and biology. But the less talked about root cause of health dispairities— discriminiation—is all too often glossed over. Adam D. Swanson, a nationally awarded public speaker and health equity advocate, will share his harrowing life story about crisis health care interactions to help demostrate the impact of discrimination as a major root cause of systemic health disparities within clinical care settings. His story and supporting data about the vulnerablities facing minority populations will help providers of all levels and researchers think more broadly about how to improve health outcomes, eliminate health disparities, and achieve health equity.

Biography:

Abbas A Shakir Alnaji has completed his degree in Neurosurgery from University of Baghdad in 1999. He is interested in research work and has 12 papers published in the field of Surgical Pathology Causations.

Abstract:

Head injury is often associated with vomiting, which varies in frequency and severity with the magnitude of the injury. In this article, we want to throw some light on the nature of this phenomenon from social and medical visions. It is really of benefit to the patient. It should not be inhibited, the expelled fluid not replaced but assure the patient, vomiting is a regulatory neurophysiologic event that occurs to assist the body to accommodate itself against the changes inside the brain after being injured; hence it is not considered as a harmful reaction. The vomitus mainly is water with some hydrogen ion as HCl from the gastric content, which is a natural regulatory step taken by the body to bring a relative dehydration, for which, some use diuretics. Secondly, this hydrogen ion, however little in percentage, brings about smooth metabolic alkalosis; the third benefit of vomiting is the accompanying valsalva maneuver which is associated with sympathetic activation (fear) which brings for spontaneous hyperventilation then respiratory relative alkalosis. So the metabolic alkalosis caused from losing hydrogen ion with vomited water, along with the sympathetic hyperventilation alkalosis, decreases the blood acidity similar to what is practiced by some neurosurgeons to subject head injured patients to mechanical hyperventilation in ICU to wash CO2 (decrease blood acidity), so that cerebral vasoconstriction is attained