Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 26th European Neurology Congress Madrid, Spain.

Day 2 :

Keynote Forum

Dimitar Maslarov

Medical University of Sofia, Bulgaria

Keynote: Current therapy of Parkinson's disease

Time : 10:00-10:40

Conference Series Neurology Congress 2018 International Conference Keynote Speaker Dimitar Maslarov photo

Dimitar Maslarov PhD, DSC is a professor of neurology at the Medical University of Sofia. In the nineties, he was a research fellow at the Brain Research Institute, where he worked on the stress disorders. In 2017, he defended Doctor of Science thesis on "Cerebrovascular Diseases - Current Assessments and Ideas for Improving Public Health". Author of monographs, textbooks on neurology and a manual on nursing care. Have over 200 scientific publications and more than 150 congresses and conferences participations. He is a member of the Scientific Panels of Neurocritical Care and Palliative care at the European Academy of Neurology and Member of the International Scientific Committee of the SSNN. He is on the Management Board of the Bulgarian Society of Neurology and Chairman of the Sofia Branch. Member of the Editorial Board of Bulgarian Neurology and Deputy Director Editor-in-Chief of the Editorial board of the Health and Science Magazine.


Parkinson's disease (PD) is a disease, which encompasses the central nervous system. Symptoms start gradually, sometimes in just one hand. Th is condition usually is the reason for rigidity and tremor. Even though PD is not curable, some medicines could considerably improve the symptoms.
Medications: PD patients possess low levels of dopamine in their brains. The idea of medication is to increase or substitute for dopamine.
Levodopa-carbidopa: Th e drug that goes through the human brain barrier and turns into dopamine is levodopa which is combined with carbidopa.
Levodopa-carbidopa infusions: Patients with advanced PD disorder can still be influenced by Carbidopa-levodopa, however their response is variable. Yet, it's administered through a feeding tube that delivers the medication in a gel form directly to the small intestine. Dopamine agonists imitate the consequences of the dopamine on the brain. They consist pramipexole, rotigotine and
ropinirole. For fast alleviation can be used the Apomorphine, which is a short-acting injectable dopamine agonist. Monoamine oxidase B (MAO-B) Inhibitors contain selegiline, rasagiline and safi namide. Their function is to avoid the failure of the dopamine in the brain via constraining the MAO B enzyme of the brain. Catechol-O-methyl transferase (COMT) inhibitors – entacapone slightly extends the outcome of levodopa treatment through interlocking the enzyme which demolishes dopamine. One more COMT inhibitor is the Tolcapone, which can hardly be given to patients because of a danger of severe liver harm and liver failure.
Anticholinergics: Medicines used for decades to assist the tremor related with PD.
Amantadine: Amantadine alone provide short-term relief of symptoms of early PD. It could be combined with Carbidopalevodopa treatment throughout the advanced phases of PD to regulate the dyskinesias.
Surgical Procedures: In deep brain stimulation (DBS), are implant electrodes into the subthalamic nucleus or the globus pallidus
interna. DBS may steady the medicine variations, to decrease or stop dyskinesias, to diminish tremor and the rigidity. Also, can prevent slowing down patients’ actions. Treatment of PD should be personalized.
Recent Publications :
1. Connolly BS, Lang AE. Pharmacological treatment of Parkinson disease: A review. JAMA 2014; 311:1670.
2. Ferreira JJ, Katzenschlager R, Bloem BR, et al. Summary of the recommendations of the EFNS/MDS-ES review on therapeutic management of Parkinson's disease. Eur J Neurol 2013; 20:5.
3. Ferreira JJ, Lees A, Rocha J-F, Poewe W, Rakol O, Soares-da-Silva P. for the Bi-Park 1 investigators (Dimitar Maslarov, Bulgaria, First MHAT-Sofi a, Clinic of nerve diseases, 8 patients enrolled). Opicapone as an anjunct to levodopa in patients with Parkinson’s disease and end-of-dose motor fl uctuations: a randomized, double-blind, controlled trial. Lancet Neurol, 2015, published online Dec, 22 2015,
4. Olanow CW, Watts RL, Koller WC. An algorithm (decision tree) for the management of Parkinson's disease (2001): treatment guidelines. Neurology 2001; 56:S1.
5. Rogers G, Davies D, Pink J, Cooper P. Parkinson's disease: summary of updated NICE guidance. BMJ 2017; 358:j1951.


Keynote Forum

Avathvadi Venkatesan Srinivasan

Tamil Nadu Dr. M. G. R. Medical University, India

Keynote: 10:40-11:20

Time : 10:40-11:20

Conference Series Neurology Congress 2018 International Conference Keynote Speaker Avathvadi Venkatesan Srinivasan photo

Avathvadi Venkatesan Srinivasan, driven by his quest for excellence joined Madras Medical College (MMC) and received MD (General Medicine) in 1978. Later he pursued and received DM in Neurology from his alma mater. His thirst for research, skills and the latest development in Neurology made him fi nd his way to the National
Institute of Neurology and Neurosurgery, his pioneering research work on Neuroleptic Malignant Syndrome got him bestowed with the PhD degree in 2002. It made him the first ever recipient in Neurology from the Tamil Nadu Dr. M.G.R. Medical University, since its inception in 1988. His path breaking research (6 papers) in Phantom limbs, Stroke etc., with Padma Bhusan Dr. V S Ramachandran, Director, Center of Brain and Cognition, University of San Diego remain acclamatory to his undisputed authority in Behavioral Neurology and Movement disorders. He authored more than 100 scientifi c papers; dozens of his other work have found places in reputed medical journals and has published 12 chapters. His research papers presented, won acclaims in 60 National conferences and in 25 International conferences held in UK, USA, Japan, Australia, China, Europe and other countries. He is the only one from India to collaborate with Dr V S Ramachandran, who is the first recipient of Padma Bhusan for his contribution to Neurosciences.


Statement of the Study: The research question is whether the understanding of clinical conundrum of neuroleptic malignant syndrome (NMS) would become clearer when schizophrenia and affective disorders are studied separately.
Methods: Twenty schizophrenics and thirty aff ected disorder cases who developed NMS were studied between 1990 and 2001 prospectively. Modified criteria of Keck was used for the diagnosis of NMS. Only patients who developed fever, altered sensorium, extrapyramidal and autonomic symptoms are included, standard statistical analysis of the data which included factor analysis,
correlation analysis and discriminate analysis were performed.
Summary of Results: Mean age of onset in schizophrenia was 32 years (18-58 yrs.) and in aff ective disorders was 43 years
(15-73 yrs.). NMS developed within nine hours of starting therapy and lasted for a mean duration of 23 days. In the affective disorder group, NMS developed over a period 17 hours and lasted for a mean duration of 11 days. Fever occurred in all the cases and earlier is schizophrenia (11.9 hrs.) compared to aff ective disorders (16.8 hrs.). The altered sensorium occurred within 9.6 hours in schizophrenia and 25.69 hours in aff ective disorder. The  rigidity occurred in 38.8 hours in schizophrenia and 84.9 hours in aff ective disorder. Rigidity followed fever and altered sensorium in both the conditions. Autonomic symptoms occurred within 48 hours in schizophrenia and 107 hours in aff ective disorder. Th e correlation analysis showed signifi cant correlation between NMS onset with fever and altered sensorium. Cluster analysis indicated that autonomic and extrapyramidal symptoms cause for the evolution of NMS. The factor analysis of the parameter responsible for MNS in schizophrenics are extrapyramidal symptoms 0.913, autonomic symptoms 0.858, fever 0.779, altered sensorium 0.497, whereas in aff ective disorders extrapyramidal symptoms 0.931, autonomous symptoms 0.955, fever 0.200, altered sensorium 0.181. Four patients died in schizophrenic group.Our discriminant analysis clearly showed the importance of the parameters with the associated probability of discrimination; autonomic symptoms (0.9), extrapyramidal symptoms (0.7), altered sensorium (0.6) and fever (0.3). Th e misclassifi cation rate in the case of schizophrenia is 15% and aff ective disorder is around 7%. AVS-CUV criterion can be used confi dently in NMS. AVSCUV criterion; clinically defi ne autonomic symptoms and signs, extrapyramidal symptoms, altered sensorium, fever. Clinically probable: autonomic symptoms and signs, extrapyramidal symptoms. Clinically possible: altered sensorium with autonomic symptoms or extrapyramidal symptoms.
Conclusion: NMS developed earlier and look a longer time to resolve in schizophrenics compared with aff ective disorders. Mortality occurred only in schizophrenics. New AVS-CUV criteria have been added to the world literature.
Recent Publications :
1. Gurrera R J, Mortillaro G, Velamoor V and Caroff S N (2017) A validation study of the international consensus diagnostic criteria for neuroleptic malignant syndrome. Journal of Clinical Psychopharmacology 37(1):67-71.
2. Gurrera R J (2017) A systematic review of sex and age factors in neuroleptic malignant syndrome diagnosis frequency.


Break: Networking & Refreshment Break 11:20-11:40 @ Conference Centre lobby
  • Neurology | Central Nervous System | Advancements in Neurology
Location: Madrid, Spain


Birendra Kumar Bista

Neuro Cardio & Multispeciality Hospital Pvt. Ltd., India

Session Introduction

Bashir Ahmad Sanaie

Govt. Medical College Srinagar, India

Title: Transverse myelitis caused by varicella zoster virus in an immunocompetent patient – A case report

Time : 11:40-12:10


Bashir A Sanaie (DM, Neurology) is working as Assistant Professor and Head, Department of Neurology, Superspeciality Hospital of Govt. Medical College, Srinagar (J&K) India. Has expertise in dealing with patients of neuroinfections and is founder of Multiple Sclerosis Support Group of Kashmir. He has keen interest in patients’ awareness programs in addition to my own work as a consultant neurologist. Has been recently conferred Medical Excellence Award and Gold Medal by Indian Solidarity Council, International Award for Rising Talent in Nepal.


Varicella zoster virus infection causes chicken pox and herpes zoster. Varicella zoster virus can be latent in cranial nerve or dorsal root ganglia. Reactivation after several years/decades later produce rash and post herpetic neuralgia and severe neurological complications like cranial nerve palsies, zoster paresis, meningoencephalitis, cerebellitis, leukoencephalopathy, myelopathy, poly radiculoneuritis, ganglionitis, progressive outer retinal necrosis, stroke, necrotizing angitis etc. Herpes zoster myelitis usually occurs in immunocompromised and elderly patients and is very uncommon in immunocompetent patients. We report here a case of herpes zoster myelitis involving cervical and dorsal cord in an immunocompetent patient. A 55 years
old lady admitted in our department with insignificant past medical history with complaints of papulovesicular rash and pain along D4 and D5 distribution. Twelve days later, it was followed by pain, paresthesias, weakness left lower limb and bladder involvement. MRI showed evidence of myelitis in C6 to D11 region. Serum and CSF showed high levels of anti-varicella zoster
IgG levels. We treated patient with acyclovir for two weeks and methylprednisolone (1g) daily for three doses. Patient showed significant sensory, bladder and motor function improvement after two weeks. One month after treatment patient became steady and ambulatory. We suggest consideration of zoster myelitis in immunocompetent patient and early treatment with anti-virals and steroids.


Ramesh Bhattacharyya is a Consultant Neurologist and has avid interest in managing neurological pain disorders. He has established a reputed Neurological Pain Clinic in Tollygunge, Kolkata, W B, India. He regularly organizes medical camp and delivers lectures on neurological pain at various platforms. His aim in life is to give solace to the patient who suffers from this type of pain disorders.


Sterile inflammatory changes due to the release of neuropeptides, i.e. calcitonin gene related peptide (CGRP), neurokinin A and substance P in trigeminovascular system of brain stem is the likely mechanism of acute migraine attack. Recurrent attack of migraine sensitizes central and peripheral nervous system leading to chronicity. Although there are no structural changes occurs in brain stem but PET study proved several areas are activated during migraine attack like red nucleus (RN), substantia nigra (SN), dorsal raphe nucleus (DRN), periaqueductal grey (PAG) and locus caeruleus (LC). Pain initiated or caused by a primary lesion or dysfunction of brain including brainstem and spinal cord is called as central pain syndrome. As brainstem dysfunction also occurs in migraine it is likely that migraine can also produce central neuropathic pain. Sixteen cases of migraine have shown the features of central pain syndrome contralateral to the frequent hemicranial side and five
cases independent of headache side. Risk factors for developing neuropathic pain are same as that of migraine with nociceptive pain on the aff ected body parts like sprain or strain in ligament tendon and muscles. Majority of those cases has predominant limb and trunk pain (n=17) rather than headache. All the cases are of migraine without aura. They are all diagnosed by the criteria laid down by the international classification of headache disorders (ICHD 3 beta). Central neuropathic are diagnosed by criteria laid down by group of expert from the neurologic and pain community. The mechanism behind reduction of
headache after developing neuropathic pain is not known. Migraine and neuropathic pain management both are necessary for best outcome.
Recent Publications :
1. Moskowitz M A (1984) Th e neurobiology of vascular head pain. Ann Neurol 16(2):157-168.
2. Weiller C, May A, Limmrolu V, et al. (1995) Brain stem activation in spontaneous human migraine attacks. Nature Medicine 1(7):658-660.
3. Headache Classifi cation Committee of the International Headache Society (IHS) (2013) International Classifi cation of Headache Disorders 3rd edition beta version. Cephalalgia 33(9):629-808.
4. R D Treede, Troels Staehelin Jensen, J N Campbell, G Cruccu, J O Dostrovsky and J W Griffi n (2008) Neuropathic pain: Redefi nition and a grading system for clinical and research purposes. Neurology 70(18):1630-1635.


Umur Kayabasi

Bahcesehir University, Turkey

Title: Tau Protein in the retina

Time : 12:40-13:10


Umur Kayabasi is a graduate of Istanbul Medical Faculty. After working as an Assistant in Ophthalmology, he completed his Clinical Fellowship Program of Neuroophthalmology and Electrophysiology at Michigan StateUniversity in 1995. After working as a Consultant Neuro-ophthalmologist in Istanbul, he worked at Wills Eye Hospital for three months as an Observer. He has been working at World Eye Hospital since 2000. He has chapters in different neuro-ophthalmology books, arranged international symposiums, attended TV programs to advertise the neuro-ophthalmology subspecialty. He has also given lectures at local and international meetings, plus published papers in neuro ophthalmology. He became an Assistant Professor at Uskudar University-Istanbul in 2015.


Background: Recent research suggests that tau is the culprit lesion along with neuroinflammation in the etiology of Alzheimer' s Disease (AD). Retina is the extention of the brain and is the most easily approachable part of the central nervous system. Detection of the pathological protein accumulations may be possible by using spectral domain optical coherescent tomography (SD-OCT) and fundus autofluorescein (FAF). There is evidence showing that retinal plaques start accumulating even earlier than the ones in the brain. Most recent tau protein images in the brain consist of normal or reverse C-shaped paired hellical filaments.
Methods: Twenty patients with PET proven AD were examined by SD-OCT and FAF. Mean age was 72. Hypo or hyperfl uorescent retinal lesions were scanned by SD-OCT and C shaped paired hellical fi laments were investigated in a masked fashion. The researchers agreed on the shape of the lesions. Both C-shaped (normal or reverse) filaments and thinner fibrillary structures were taken into consideration.
Results: In all the patients, paired hellical filaments that exactly corresponded with the histopathologic and cryo-EM images of tau in terms of shape and dimension were detected along with thin fibrils and lesions similar to amyloid beta. The number of the retinal filaments and other abnormal proteins was in concordance with the severity of the disease process. Th e advanced retinal filaments had normal or reverse paired C shapes and thin fibrils had the shape of histopathologic images seen in early developmental stages of the disease.
Conclusions: Retinal images of tau were disclosed for the first time in live AD patients. Retinal neuroimaging is a trustable biomarker and tool for monitoring the disease.

Break: Lunch Break 13:10-14:10 @ Nature Restaurant
  • Special Session
Location: Madrid, Spain

Session Introduction

Max Leone

Licensed NLP Trainer, Italy

Title: How to use your brain to motivate yourself

Time : 14:10-15:10


Max Leone is a professional speaker, coach and author who has been involved in the personal growth field for more than ten years. He studied with some of the greatest masters in the field, such as Wayne Dyer, Deepak Chopra, Neale Walsh, Anthony Robbins, Eckhart Tolle. Max studied NLP with the founder Richard Bandler, with whom he became a Certified Trainer of Neuro-Linguistic-Programming. He qualified and studied extensively a variety of disciplines such as Translation Analysis, ACT (Acceptance and Commitment Therapy), The Sylva Method, Hypnosis, DHE (Designing human Engineering) and other techniques he uses with individuals and groups. He has been interviewed on radio stations, such as New York Coaching Common Radio, 103.2, Radio Dublin, and his work has been featured in magazines and newspapers, among which are Positive Life, The Irish Times, New Thoughts Magazines, to mention some. Max is the author of "Daily Tips for Success & Fulfilment”.


Problem Statement: In my career as a life and business coach I see a significant number of people who know what they want to create in life, and yet they find it hard to be motivated to go through the action steps required to succeed. I also see people who feel drawn towards something that they know is not beneficial to them, and yet they keep pursuing it just because they feel “compelled” to do so. Th e common issue for these people is that their choices and their motivation are out of alignment, and the typical reaction is to use self-discipline “to get things done,” which causes a sort of inner battle that quickly depletes our energy, making it hard to perform at the level of excellence. Because of that, they start to experience a sense of frustration, guilt, and sometimes helplessness that results in a strong decrease in personal productivity.
Discoveries: What has been discovered is that lack of motivation is simply caused by the weakness of a desire, rather than being a deficiency of the individual, and that by changing the way we represent our goals, we can stimulate a strong drive to move away or towards something in everyone. Therefore, motivation is something that each and all of us have as humans, and all we need to do to fill the gap between what we want (provided that it is congruent with our values) and the willingness to act at the best of our ability is to change the inner representation of the object of our desire.
Conclusion & Significance: To do so there are principles that can be applied successfully to everyone indistinctly, and specific ones that are unique to each individual that allow them to tap into even greater levels of motivation. By doing so we will go from being a passive witness of the rising and falling of motivation to a conscious creator who is able address it in the pursuit of worthwhile goals.