Alper Ä°brahim Dai, graduated from Istanbul University, School of Medicine. He completed his paediatric residency at Jackson Memorial Hospital, University of Miami / Florida and Children's hospital of West Virginia at Morgantown. As a fellowship he had 3 years of paediatric neurology at SUNY, Children's Hospital at Buffalo / New York. He had 1 year of EEG / Epilepsy fellowship at Vanderbilt University, Nashville / Tennessee. He has been working at Division of Pediatrics Neurology at Gaziantep University Hospital, Gaziantep / Turkey for 15 years. His major interests are, phase III clinical trial in anti-epileptic medications and phase I and II clinical trials in stem cell therapy in children with neurological problems.

Purpose: Duchenne muscular dystrophy (DMD) is an X-linked recessive paediatric disorder that ultimately leads to progressive muscle degeneration. It has been known that cell-based therapies were used to promote muscle regeneration. The main purpose of this study was to investigate the effects of allogeneic Wharton jelly-derived mesenchymal stem cells therapy in Duchene muscular dystrophy.

 

Patients & Methods: Four ambulatory and five non-ambulatory male patients were assessed as having acceptance criteria. Gene expression and immunohistochemical analysis were performed for dystrophin gene expression. The fluorescent in situ hybridization method was used for detection of chimerism and donor–recipient compatibility. Complement dependent lymphocytotoxic crossmatch test and detection of panel reactive antigen were performed. All patients were treated with 2 × 106 cells/kg dose of allogeneic Wharton jelly derived mesenchymal stem cells via intra-arterial and intramuscular administration. Stability was maintained in patient follow up tests, which are respiratory capacity tests, cardiac measurements and muscle strength tests.

 

Results: The vastus intermedius muscle was observed in one patient with MRI. Chimerism was detected by fluorescent in situ hybridization and mean gene expression was increased to 3.3-fold. An increase in muscle strength measurements and pulmonary function tests was detected. Additionally, we observed two of nine patients with positive panel reactive antigen result.

 

Conclusion: All our procedures are well tolerated and we have not seen any application related complications so far. Our main purpose of this study was to investigate the effects of allogeneic mesenchymal stem cell therapy and determine its suitability and safety as a form of treatment in this untreatable disorder.

Kasid Ahmed Nouri is an adjunct Clinical Assistant Professor of Neurology at Mohammed Bin Rashid University of Medicine and Health Sciences (MBRU) College of Medicine, Dubai, UAE. He is also working as a consultant neurologist at Mediclinic City and Welcare Hospitals, Dubai, UAE.

Varicella- zoster virus (VZV) is an exclusively human neurotropic, double-stranded DNA alpha herpesvirus, primary infection causes varicella (chickenpox), with a decline in VZV-specific cell-mediated immunity in elderly and immunocompromised individuals and VZV reactivates to cause herpes zoster (shingles) with its complications. Varicella-zoster virus infections can produce multiple disorders of the central and peripheral nervous system and often without rash. The most common complication of herpes zoster is post herpetic neuralgia, pain that persists months to years after rash resolved. Herpes zoster may cause serious chronic complications, including PHN, cerebral arteritis and herpes zoster ophthalmicus. The important of early diagnosis with a rapid virology verification and early prompt treatment with antiviral agents can lead to complete recovery; even in patients with protracted disease. Herpes zoster vaccination significantly reduces the incidence of both Herpes zoster, post herpetic neuralgia and other complications. Given the limitations of existing zoster therapies, the prevention of VZV infection has gained overriding importance. VZV vaccinations can reduce both the health and economic eff ects of Herpes zoster. Although relatively costly, vaccinations not only reduce the risk of infection but may also preserve healthrelated QOL in the geriatric population. With seven cases studies presentation there will be a high light on different Varicella- zoster clinical presentations.

Wael Osman M Amer has completed his MD Al- Azhar University and Postdoctoral studies in Neuro intervention from School of Medicine, REIMS University, France. He is the Director of the stroke unit at Al-Azhar University School of Medicine. He has published more than 15 papers in reputed journals.

Objective: To investigate the relationship between silent brain infarcts and metabolic syndrome in middle aged patients with ischemic stroke.

 

Methods: We studied fift y middle aged patients between 40-59 years, (mean, 52.26 ± 5.29 years) with ischemic stroke who admitted to Al-Azhar University Hospitals or followed up in outpatient clinic. Metabolic syndrome was diagnosed according to the National Cholesterol Education Program Adult Treatment Panel III definition. Silent brain infarct was diagnosed using magnetic resonance imaging of the brain and without a history of corresponding neurologic symptoms or signs.

 

Results: Silent brain infarcts was diagnosed in 24(48%) patients (18 men and 6 women) while metabolic syndrome was diagnosed in 31(62%) patients of the 50 patients including (22 men and 9 women). There was a strong association

between metabolic syndrome and silent brain infarction in middle aged subjects with ischemic stroke. Among metabolic syndrome components elevated blood pressure and impaired fasting glucose were strongly associated

with the presence of silent lacunar infarction while hyper triglyceridemia, low high density lipoprotein cholesterol and large waist circumference were not significantly associated with silent brain infarction. Although, only elevated

blood pressure and impaired fasting glucose were found to be significant components, subjects with a greater number of metabolic syndrome components showed more prevalent silent brain infarctions.

 

Conclusions: Metabolic syndrome was significantly associated with the prevalence of silent brain infarction in middle aged patients with ischemic stroke. Independent risk factors for silent brain infarctions include elevated blood pressure and impaired fasting glucose. The clustering of metabolic syndrome components tends to increase the prevalence of silent brain infarctions as there is a dose response relationship between the number of metabolic syndrome components and the risk of having silent brain infarction.

Chika Okwuolisa is the Founder and Executive Director of Brain and Spine Foundation, Africa. Brain & Spine Foundation (BSFA) is an operational registered non-Governmental Organisation (NGO). It was established it following a first-hand traumatic experience during a harrowing pathological Brain event that has changed their lives forever. BSFA is founded to create awareness on the burden of Brain and Spinal conditions and all the variants there are of these in Nigeria and Africa. We also focus on ways to prevent, manage and reduce the burden of these illnesses which thrive on the general ignorance of individuals.

It’s a common knowledge that Africa has the least neurological services and African neurologists and neurosurgeons cannot match the rapid progress in the developed world. And this I write with extreme sadness. As the founder of The Brain and Spine Foundation Africa, it is no gain saying the fact I am coming from a background of diametric ramifications of health emergencies- ours is a harrowing experience and indeed, a sordid reality that no one can be proud of. Prominent among the challenges in the Nigerian health sector for example, is the escalation of various degrees of neurological emergencies. The world, especially European and American institutions/organizations  must rise to this urgency, and bring their technological edges to bear on this very challenging bracket, vis-à-vis the deployment of alleviative fiscal policies. Brain and Spine Foundation, Africa is from the grassroots; we are close to these unfortunate ones who are going through agonies everyday, never as a result of any fault of theirs. We hear their cries everyday, we see their despairs, because the cost of treatment is usually beyond their reach or there is no Neurospecialist available to attend to them. We render our helps which are usually grossly inadequate. Most importantly, we stay by their sides intentionally to be available for them, and serve as psychological reinforcements for their survival instincts. We watch them die sometimes owing to the lack of adequate facility for treatment and precarious volume of resources available to us, which often empty into paucity sooner or later. Neurological disorders as we all know are associated with high mortality, prolonged hospital stay and socioeconomic burden for the families. Unfortunately, in Sub-Saharan African countries, there’s a huge disconnect between where disease is and where experts are. We need you, most especially those of African descents to come and help us make changes to our national policies that could help our people. We need your help in working to build up the resources and networks necessary to conduct clinical trials in Africa, and to create education and training programs for health care providers and researchers. We as a Charity Organization are creating awareness, educating the public, providing support and hope, but we also work with the health care structure to ensure there are providers and treatment.

Katherine Radcliffe conducted this original research whilst incalating and studying MRes Translational Medicine at the University of Manchester. She has just graduated from Manchester Medical School and is due to start as an FY1 doctor in August. This research earned her the best poster prize within her course and she has presented posters at multiple conferences including a European Congress whilst studying.

A hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of frontotemporal dementia and motor neuron disease. Carriers present with both conditions concurrently, so they are considered a continuum. Th e RNA from the hexanucleotide expansion is translated by repeat associated non-ATG (RAN) translation; producing five dipeptide repeat (DPR) proteins. These are the alanine rich polyAP and polyGA, the arginine-rich polyGR and polyPR, and polyGP. Previous in vitro studies show that the arginine-rich DPRs are toxic because they localise to the nucleolus, causing nucleolar stress. However, preliminary research showed sequestration of polyGR by polyGA when they were co-expressed in HeLa cells, Drosophila and human neurons. Our aim was to determine whether alanine-rich DPR proteins sequester arginine-rich DPR proteins when the two are co-expressed in vitro. This was investigated using alternative coding sequences for the DPR proteins, cloned into mCherrytagged plasmids. Next, two DPR proteins with different fl uorescent tags were co-transfected into HeLa cells and the subcellular locations of the DPR proteins were visualised using immunofluorescence. Our results showed cytoplasmic co-localisation of the arginine-rich DPRs with polyGA. This was replicated 3 times in HeLa cells and once in SH-SY5Y cells. Co-transfection, but no colocalisation, was seen when two alanine-rich or two argininerich DPR proteins were co-expressed. Overall, our findings suggest that the arginine-rich DPRs are sequestered by polyGA in the cytoplasm, meaning they are unlikely to cause nucleolar stress. This demonstrates that single transfections of DPR proteins may not be a good model to study DPR protein function or toxicity.

Güllü Tarhan is a 26 year old and working as a Neurology resident in the Gaziosmanpasa Taksim Training and Research Hospital. She has completed Istanbul Faculty of Medicine two years ago.

KIF1C mutation is genetic defect which is observed with hereditary spastic paraparesis and cerebellar dysfuntion. In this report, we analyzed the Turkish family who had spastic paraparesis and cerebellar dysfunction with KIFC mutation. There were paraparesis, ataxia, dysarthria, tremor in brothers whom parents were second degree relatives and asymptomatic. Father and mother's ages were 65 and 62 and brothers were 44, 42, 36. Their complaints appeared

with tremor in their hands in childhood. In the following terms, the other complaints began to reveal. There were no point in family history. Patients' neurologic examination: their speech were dysarthric, biletaral dysmetria and

dysdiadokokinezi in all. Intention tremor could be seen in all brothers' heads and extremities. The patient's, who were 44 years old, spastic paraparesis is more serious than the other two and he were walking by using one crutch. The other two brothers', who are 42 and 36 years old, spastic paraparesis were less serious and they could walk without using any crutch. General medical tests such as routine biochemistries, hemograms, hormones, B12, VDRL, HIV, vitamin A and E, thyroid hormones, plasma ceruloplasmin and copper were normal. In Cranial-Spinal MR, there were remarkable cortical and cerebellar atrophie. Electrocardiographies, electromyographies and odiographies were normal. They had adequate IQ scores, which were among 80-100 scores. In whole exome sequencing two variant mutation were identified in their KIF1C genes. The parents are heterozygote and brothers are homozygote. On the basis of clinical and genetical analyzies, autosomal recessive spastic paraparesis and ataxia were considered due to mutation in KIF1C.