Biography:

Dr. Sandro Iannaccone is a neurologist who received his medical training at the University of Milan (Italy) and completed his residency in Neurology in July 1986 and further specialized in Neuropathology in 1992. Since 1989, Dr. Iannaccone has been working as a contract Professor of Neurology at the Medical and Psychological Faculties of the University Vita-Salute San Raffaele of Milan. Dr. Iannaccone became Responsible of the Neurologic Unit of the San Raffaele Turro Hospital in 1999. In 2013, he became Director of the Neurorehabilitation Unit of the San Raffaele Hospital. Since 2014, Dr. Iannaccone is also the President of the Scientific Society entitled Association of Medical Rehabilitation Specialists of Private Hospitals (Associazione Medici Riabilitatori Specialisti dell’Ospedalità Privata). In a research point of view, Dr. Iannaccone is leading research and development of innovative rehabilitative strategies using new technologies based on virtual reality. He is also leading trials on new – pharmacological and non-pharmacological - therapies for Alzheimer’s disease. Dr. Iannaccone has also been involved in investigations in early detection of neurological degenerative disease biomarkers through neuropathological, proteomics and PET studies.

Abstract:

Over the last years, there has been increasing developments of new technologies to provide solutions to the limitations of standard rehabilitation (drop-outs, limited evaluation scores, or physical limitations of therapists) to enhance learning following neurological insults. To this aim, virtual reality (VR) settings provide an enriched environment able to generate augmented multisensory feedbacks (auditory, visual and proprioceptive). These settings, involving the mirror neurons system, help patients to develop a real-time "knowledge of results” and "knowledge of performance”, favoring the physiological mechanism of reinforcement learning. Such innovative strategies can be applied directly in the rehabilitation of motor, cognitive and speech functions, as well as in chronic pain treatment. Moreover, standard or virtual reality-based neurorehabilitation can be potentiated through the concomitant application of non-invasive brain stimulation, such as repetitive transcranial magnetic stimulation (rTMS) or transcranial direct current stimulation (tDCS). Indeed, the NeuroAD system offers the possibility of applying cortical stimulation during cognitive training. TDCS can also be applied on-line, during motor or cognitive rehabilitation. Moreover, as a portable device, it also brings the opportunity to the patient to be applied at home. Thus, the development of new technologies in NeuroRehabilitation is converging towards multimodal treatments offering the possibility of home-based monitoring.

Biography:

Joshua K. Underwood, ABD is the Head Athletic Trainer at Vermont Academy in Saxtons River, Vermont USA and is currently pursuing his doctorate of athletic training at the University of Idaho. He has worked in in a variety of clinical settings over the last 12 years including semi-professional football, summer collegiate baseball, adventure camps, secondary schools, and orthopedic clinics. He specializes in treating regional interdependent dysfunctions, concussions, orthopedic injuries, and fascia with a variety of treatments including Positional Release Therapy, Primal Reflex Release Technique, and Mulligan Concept. Mr. Underwood’s primary areas of research have focused on the treatment of concussions with manual therapy and the treatment of regional independent causation of pain or dysfunction.

Abstract:

Statement of the Problem: Due to the comparable somatic presentation and biomechanical nature of concussions, cervicogenic headaches (CGH), tension-type headaches (TTH), cervicogenic vertigo (CGV), and whiplash, it is conceivable that cranial and/or cervical-based dysfunctions can occur secondarily to concussions and increase somatic symptom presentation. Fascial restrictions found within cervical and cranial structures have been found to increase biotensegrital tensions along cranial nerves and vestibular systems; however, fascial release techniques like Positional Release Therapy (PRT) have been found to be an effective treatment in reducing symptoms related to CGH, TTH, CGV, and whiplash. The purpose of this study is to examine the post intervention effect of PRT in resolving somatic symptoms (i.e- headaches, vertigo, hyperacusis, and photosensitivity) associated with concussions in a secondary school setting. Methodology & Theoretical Orientation: An action research study utilizing numerical rating scale (NRS) and post-concussion symptom score (PCSS) to measure changes to headaches, vertigo, nausea, hyperacusis, and/or photosensitivity pre/post PRT interventions. Findings: The participants in this study were of an active population within a secondary school setting. Statistically significant decreases in intensity of headaches, nausea, vertigo, hyperacusis, and photosensitivity were witnessed by outcome measures between pre/post PRT interventions. Conclusion & Significance: Patients suffering from symptoms associated with concussions may additionally be affected by cervicogenic and cranial-based fascial restrictions which exacerbates headaches, nausea, vertigo, hyperacucis, and/or photosensitivity. Findings suggest concussion patients may benefit from PRT in reducing somatic symptoms during their recovery.

Biography:

Dr. Arshad Zaman is an experienced neuro specialist with over 15 years’ experience in developing and clinically applying functional Magnetic Resonance Imaging (fMRI) at international centers of excellence. Previous studies encompass a spectrum of clinical applications (epilepsy, oncology) to state-of-the-art applications (e.g. pain relief, mental health, brain training). Current commitments centre around further development and clinical utilisation of fMRI.

Abstract:

Functional magnetic resonance imaging or functional MRI (fMRI) is a state-of-the-art functional neuroimaging technique that measures brain activity by detecting associated changes in blood flow.

fMRI is increasingly playing a key role in providing a deeper insight into brain function and or functional brain networks. In fact, fMRI has matured over the last two decades from a research tool to a robust powerful clinical technique implemented in a wide spectrum of domains, from judicial, commercial to clinical. There are several new novel clinical applications of fMRI.

The session will cover an introduction to clinical fMRI, clinical and a wide spectrum of recent novel applications (in rehabilitation, neurobehavioural and cognitive disorders, neuropsychology, mental health and psychiatry). This session will spotlight what currently can and can't be done with fMRI.

Biography:

Abstract:

To study the ambulatory measured blood pressure (ABPM) profile in normotensive

patients with mild cognitive impairment (MCI). Patients and Methods: The study was designed as a case control study including 50male patients with mild cognitive impairment in the age group of 30 - 50 years old. The control group included 30 volunteers with no cognitive impairment and in the same age group (30 - 50 years old) and same gender. Mini-mental estate examination, office and ABP monitoring (ABPM) and brain MRI scans were done for cases and controls. Results: Thirty patients (60%) with MCI revealed a non-dipper blood pressure pattern. Sleeping systolic blood  pressure and sleeping systolic load were significantly higher in patients with MCI than in normal volunteers (p = 0.01). MRI brain showed more white matter lesions (WMLs) in patients with MCI than in normal volunteers; however, this didn’t reach significance level (p = 0.056). Conclusion: MCI in normotensive young adult patients could reflect an abnormal circadian blood pressure rhythm. Ambulatory blood pressure monitoring could be an essential investigation in young adult MCI patients.

Biography:

Finished her High School attended:  Khawla secondary girl’s school; 2003-2006. GPA= 99.3% Graduated from Medical university attended: Royal College of Surgeons in Ireland. 2006-2011 Completed internship  in Salmaneya Medical Complex- Bahrain Completed Bahrain licensure exam in June 2012 Completed Saudi licensure exam in June 2012. Previous job: ultrasound specialist and patient support consultant in Abbott laboratories from September 2012 to august 2013. Current Job: Slamaniya Medical Complex- Radiology Department.

Abstract:

Intracerebral hemorrhage (ICH) is described as spontaneous extravasation of blood into the brain parenchyma, presenting in 10% to 15% of all stroke cases in the Western population. It is also associated with a higher mortality rate compared with ischemic stroke . ICH is classified according to its primary (80% to 85%) or secondary (15% to 20%) causes.  More than 50% of primary ICH events are directly correlated with hypertension as a risk factor, whereas 30% are known to be associated with cerebral amyloid angiopathy (CAA). The causes of secondary ICH include hemorrhage conversion of Ischemiac stroke , amyloid angiopathy, stimulant drugs, vascular malformations (aneurysms, arterovenous malformations, venous angioma, cavernoma, dural arteriovenous fistula), coagulopathy (hereditary, acquired, induced by anticoagulants or antiplatelets), neoplasms, trauma, vasculitis, Moyamoya disease, or sinus venous thrombosis. A NEW  systematic stratification is proposed called,  (SMASH-U classification) , based on the underlying diseases of ICH:

1- Structural lesions (cavernomas and arterovenous malformations)

2- Medication (anticoagulation)

3- Amyloid angiopathy

4- Systemic diseases (liver cirrhosis, thrombocytopenia, and various rare conditions),

5- Hypertension, and Undetermined causes.

Biography:

Abstract:

The incidence of stroke is higher perinatally compared to any other time of life 1. Approximately 60% of children who suffer from perinatal stroke develop hemiplegic cerebral palsy 2. The impact on individuals and their families is substantial 3. The lack of bimanual dexterity in those affected has lifelong adverse effects on performance in activities of daily living. This in turn impacts significantly on mental health and quality of life4 despite the majority having cognitive capacities within the normal range 5.

The outcome after an adult onset stroke is largely determined by the extent of the initial brain injury and motor recovery occurs if a critical amount of corticospinal system function has been spared at the time of the lesion6.  However, this is not the case for a perinatal stroke and infants with a significant corticospinal projection from the infarcted cortex soon after the stroke, detected by transcranial magnetic stimulation, can still have a poor motor outcome7 . Early interventions that could provide trophic support to the infarcted motor cortex, or perhaps even replace lost corticospinal neurons, might help establish a more functionally active corticospinal projection from the infarcted side. However, the invasive nature of our proposed interventions requires that they are tested first in a rodent model.

Biography:

Abstract:

Neural cell death during cerebral ischaemia in neonates correlates with various significant pathological conditions, such as cerebral palsy in humans. Central white matter experiences irreversible injury when exposed to oxygen and glucose deprivation (OGD), a practical model of ischaemia. We collected evidence to examine that glutamate transporters have an essential role to perinatal white matter ischaemic injury. Several studies demonstrated that glutamate transport by oligodendrocytes maintains glutamate homeostasis in developing neonatal cerebral white matter. During ischaemia, functional activity of glutamate transporters may fail, leading to a lethal accumulation of glutamate.  Failures of glutamate transporters are responsible for excitotoxic cell injury during ischaemia with subsequent damage of white matter regions such as axons and glia. Our paper work aimed at demonstration of use of immunohistochemistry technique and examined the sub-cellular distribution of excitatory aspartate amino acid transporter (EAAC1), Glutamate–aspartate transporter (GLAST) and glutamate transporter (GLT1) proteins in the perinatal white matter using double labelling. The method using is: Immunohistochemistry technique and exposure of the optic rat nerves after dissection (RONs) to a practical model of ischaemia (OGD). The result demonstrated extensive expression of GLAST and GLT1 on the perinatal astrocyte processes while minor levels of EAAC1 expression were observed.  Although neurofilament-heavy (NF-H) axons express moderate levels of GLT1 & EAAC1 transporter proteins but they did not express GLAST transporter protein. The moderate levels of D-Aspartate uptake at NF-H and astrocyte processes confirmed the presence of functional Na+-dependent glutamate transporters. The expression of GLAST demonstrates the potential for transport mediated-glutamate release into the extracellular space result in necrosis of ischaemic white matter during the perinatal period. We have shown that high levels of glutamate transporter expression in NF-H +axons and astrocytes are consistent with a tight maintenance of extracellular glutamate in the zone where axons and glia meet. This work is consistent with several recent studies have revealed rapid astrocyte swelling will liberate astrocyte glutamate into the extracellular space in a glutamate dependent manner usually via GLAST and GLT1 transport result in necrosis of neonatal ischemic white matter. Understanding the pathophysiology in immature white matter will progressively lead scientists toward the further development of effective therapeutic interventions in the future.

Biography:

Abstract:

The incidence of stroke in Bahrain is rising in the Bahraini population and has nearly doubled over the last 16 years, while the incidence in the non-Bahraini population has not changed. Incidence of stroke in the Bahraini population (110/ 100 000) is now much greater than in the non-Bahraini population (27/100 000). The Bahraini stroke population is 10 years younger than Western comparators with a much higher prevalence of many of the risk factors for stroke, including diabetes (54%), hypertension (75%) and hyperlipidaemia (34%). The combination of an ageing Bahraini population alongside a high prevalence of risk factors suggests a ‘ticking time bomb’ that is likely to see a continuing rise in the incidence of stroke. The quality of risk factor prevention and hospital-based stroke care is therefore crucial in Bahrain. While 88% of patients were scanned within 24 h and 86% with non-haemorrhagic strokes were commenced on aspirin within 48 h, none of the patients received thrombolysis or were admitted to a stroke unit.

Improvement of stroke outcomes in Bahrain could be achieved through implementation of evidence-based measures, including improved risk factor management in primary care and stroke units and thrombolysis in secondary care.

 

Biography:

Mr. Varun Vikas Vij has done M pharmacy in Pharmacology and pursuing PhD from Baba Farid University of Health Sciences Faridkot Punjab India and currently working as a Pharmacy Executive in Dayanand Medical College and Hospital Ludhiana Punjab India. Mr. Vij has 11 years of experience in pharmaceutical industry (9 years in Pharmaceutical marketing and 2 years in Hospital pharmacy). He has 2 International publications. He has keen interest in Neuro Pharmacology.

Abstract:

Neuropathic pain (NP) is defined as pain associated with damage or permanent alteration of the peripheral or central nervous system. Current drug treatment for the management of neuropathic pain associated with various adverse effects. The present study was designed to investigate the combined effect of acamprosate and baclofen in experimental model of peripheral Neuropathic pain in wistar rats. Material and Methods: Neuropathic pain was induced by chronic constriction injured (cci) of sciatic nerve in rats. A camprosate (100 and 200 mg/kg p.o) and baclofen (10 and 20 mg/kg p.o) was given in different groups for 14 days starting on 7th day post sciatic nerve ligation. Further combination of acamprosate(100 mg/kg p.o) and baclofen (10 mg/kg p.o) was also given to one group. On 1th, 3rd, 7th, 14thand 21stday behavioral parameters like mechanical allodynia and thermal hyperalgesia were assessed. Then animals were sacrificed on 22nd day and biochemical parameters (gsh, lpo, catalase, nitrite, sod) were assessed. Results: ligation of sciatic nerve significantly induced mechanical allodynia and thermal hyperalgesia with increase in oxidative stress (increase in lpo and nitrite) and decline of anti-oxidant enzyme levels (catalase, sod, gsh) in sciatic nerve homogenate. A camprosate (100 and 200 mg/kg p.o) and baclofen (10and 20 mg/kg p.o) attenuated all the behavioural and biochemical parameters alone and/or combination.

Biography:

Abstract:

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.

Biography:

Abstract:

Spinal muscular atrophy (SMA) is a devastating childhood motor neuron disease caused by mutations in the survival motor neuron 1 gene (SMN1). SMN1 and SMN2 are nearly identical genes producing the survival of motor neuron (SMN) protein. SMN protein plays a crucial role in mRNA splicing and β-actin mRNA transport along the axons. In SMA the mutation leads to the loss of SMN1, which cannot be fully compensated by the SMN2 gene, which predominantly produces a truncated protein. The loss or reduction of SMN protein leads to motor axonal defects and motor neuron cell death. There are currently no treatments available but therapies have focused on increasing SMN through replacing SMN1 or increasing full length SMN from SMN2. The actin-binding protein Plastin 3 (PLS3) has been reported as a modifier for SMA, making it a potential therapeutic target. Recently, it was shown that the overexpression of the PLS3 gene improved axonal outgrowth in SMN- deficient motor neurons of SMA Zebrafish and cultured motor neurons from mouse embryos. Gene therapy using viral vectors was carried out in vitro and in vivo to assess whether the overexpression of PLS3 could rescue neuronal loss in SMA and be developed as a therapy. The SMNΔ7 mouse model produces low levels of SMN, modelling severe SMA disease with an average lifespan of 12 days and loss of motor neurons. This study has established that the SMNΔ7 mice have little or no detectable PLS3 from birth, making it a good model for developing PLS3 gene therapy. Lentiviral vectors were able to upregulate PLS3 expression in different cell lines. Transduction of NSC34 cells with LV-PLS3 vector led to a five-fold increase in expression of PLS3 compared to controls. In smn-deficient MNs, expression of PLS3 restored axonal length and showed a strong neuroprotective effect. Pre-clinical in vivo proof-of-concept studies using adeno-associated virus serotype 9 (AAV9) encoding PLS3 in SMNΔ7 mice showed high transduction efficiency and overexpression of PLS3 specifically targeted to neurons in the central nervous system (CNS). This led to a small but significant increase of lifespan by 54%. However, PLS3 was not able to prevent disease onset. Although there was no improvement of phenotype, this study has demonstrated the potential use of PLS3 as a target for gene therapy, possibly in conjunction with other modulators of disease