Biography:

Dr. Kalliopi Megari is an experienced psychologist working in the hospital & health care industry. She is a lecturer at University of Western Macedonia in Greece. Skilled in Clinical Neuropsychology, Clinical Research and Learning Disabilities. Graduated from Aristotle University of Thessaloniki and attended further education from University of Macedonia, in people with special needs and disabilities. She holds undergraduate degrees in Nursing and Psychology, as well as a Master’s and a PhD in Neuropsychology from Aristotle University of Thessaloniki. She has many years of experience working with chronic disease patients as well with people with disabilities. Her work has earned her many prestigious international awards. She has given lectures at Aristotle University of Thessaloniki and University of Warsaw. She is postdoctoral researcher and has published more than 10 research articles in journals. She is the Global Engagement Representative of International Neuropsychological Society, General Secretary of the board of directors and member of the Ethics Committee of Hellenic Neuropsychological Society.

Abstract:

The risk of epileptic seizures is increased to a great extend in patients with cancer and exposure to chemotherapy or radiotherapy, cancer-related metabolic disturbances, and stroke can provoke seizures. Post chemotherapy cognitive impairment (PCCI), (or cognitive dysfunction), is referred to a decrease in neuropsychological performance of neurocognitive measures after chemotherapy for the treatment of cancer. Chemotherapeutic drugs are cytotoxic affecting both normal and cancer cells, contribute to cognitive impairment observed in some individuals following chemotherapy treatment and may lead to dementia. We investigated the manifestation of cognitive impairment related to chemotherapy, before chemotherapy (T1), immediately after chemotherapy-1 day (T2) and 6 months later (T3), among 187 adult patients with different types of cancer (breast, colorectal, prostate and thyroid cancer). Cognitive functions were assessed, such as attention and working memory, visuospatial perception, executive functions, complex scanning and visual tracking, as well as short and long-term memory using a battery of neuropsychological tests. We had an assessment of emotions, such as anxiety, depression, positive and negative mood to investigate the emotional functioning of cancer patients.  Results revealed a statistical significance in performance, immediately and 6 months post-chemotherapy (T3), although no statistically significant differences were found between the groups in any of the neuropsychological test, before chemotherapy. Patients showed lower performance immediately post-chemotherapy (T2) that remained stable 6 months post-chemotherapy (T3), compared to T2 in all cognitive domains (p<0,001). Patients with breast cancer showed significantly lower performance on all cognitive domains compared to other patients. In addition, all patients had a lower performance at T2, which means low emotional functioning with no statistical significant changes. At T3 all patients, had an increased performance with increased emotional functional 6 months post-chemotherapy. Cognitive change that can be detected with repeated testing is essential for an accurate interpretation of neuropsychological performance in studies with cancer patients.

Biography:

Dr. Felix-Martin Werner studied human medicine at the university of Bonn. He has been working as a medical teacher in the formation of geriatric nurses, occupational therapists and assistents of the medical doctor at the Euro Academy in Pößneck since 1999. He has been doing scientific work at the Institute of Neurosciences of Castilla and León (INCYL) in Salamanca (Spain) since 2002. With Prof. Rafael Coveñas, he assisted at over 30 national and 12 international congresses of neurology and published over 60 reviews about neural networks in neurological and psychiatric diseases. Since 2014, Dr. Werner has belonged to the editorial board of the Journal of Cytology & Histology.

Abstract:

Introduction: Based on interaction between classical neurotransmitters and neuropeptides between each other, a neural network in the hippocampus, the thalamus and the cortex is developed, while results from the audiogenic animal model are taken into consideration.

Methods/Materials: In generalized epilepsy alterations of ion channels and neurotransmitter and neuropeptide concentrations can be induced genetically or exogenously.

An enlarged neuronal network is described in order to point out the epileptogenesis as a consequence of the interaction between the corresponding neurotransmitters and neuropeptides and of stimulus enhancing the neurotransmitter imbalance.

Results: The neural network reads as follows: Dopaminergic neurons in the hippocampus transmit a strong postsynaptic excitatory impulse via D₂ receptors to glutaminergic neurons which strongly inhibit serotonergic neurons via NMDA receptors. The glutaminergic neurons can enhance epileptogenesis via an excitotoxic, postsynaptic excitatory effect via NMDA, AMPA and kainate receptors. The serotonergic neurons with a low activity transmit a weak activating impulse via 5-HT_2C receptors to GABAergic neurons which weakly inhibit dopaminergic neurons via GABA_A receptors. A withdrawal of GABAergic presynaptic inhibition of dopaminergic neurons can cause an epileptic seizure. GABAergic neurons weakly inhibit glutaminergic neurons in the thalamus, which transmit a strong activating impulse via NMDA receptors to dopamineragic neurons in the cortex. The cortical glutaminergic can enhance the activity of the dopaminergic neurons in the hippocampus via D₂ receptors. Other serotonergic neurons transmit a weak activating impulse to serotonergic neurons via 5-HT₇ receptors. Neuropeptide Y containing neurons in the dentate gyrus weakly inhibit glutaminergic neurons via NPY₂ receptors and transmit a weak activating impulse to GABAergic neurons via NPY₁ receptors. The serotonergic neurons transmit a weak postsynaptic excitatory impulse via 5-HT_2C receptors to GABAergic neurons which weakly inhibit adenosine neurons via GABA_A receptors. The adenosine neurons with a high activity transmit a strong activiting impulse via A_2A receptors to glutaminergic neurons which strongly inhibit serotonergic neurons via the subtype 5 of the glutaminergic metabotropic receptors.

The mechanism of action of conventional and newer antiepileptic drugs, such as lamotrigine, levetiracetam and topiramate is pointed out according to the neural network.

According to the neural networks described the following possible pharmacological options could exert an antiepileptic effect:

• Combined GABA_A agonists and NMDA antagonists.
• KA or AMPA receptor antagonists, which would inhibit epileptic glutamate emptying.
• NPY₂ receptor agonists, which would inhibit glutamate emptying.
• A_2A receptor antagonists, which would enhance serotonin levels.
• m5GluR receptor antagonists, which would enhance serotonin levels
• 5-HT₇ receptor agonists, which would increase serotonin levels.
• nAch alpha7 agonists.

Conclusion: It is important to examine neuronal networks in generalized epilepsy in order to optimize a multimodal pharmacotherapy of the disease.

Biography:

Peter S Tatum is currently working as a Neurology Resident at Tufts Medical Center, USA. His research interest includes Epilepsy and Neurological disorders.

Abstract:

Two patients with no seizure history or risk factors presented with new onset seizures within hours of vaping. This report includes a literature review on the relationship between seizures and vaping as well as results of a single institution survey on the frequency of neurology provider inquiry of vaping as a seizure provoking factor during patient interviews for new onset seizure. Although reports of a potential link between vaping and seizures have increased since 2019, there is likely still a majority of medical providers who are not subjectively qualifying vaping as a potential provoking factor during interactions with patients being seen for new onset seizures. Qualifying this information may prove to be an important part of the initial investigation on the pathophysiology of vaping as a seizure provoking factor and utility of antiepileptic drug (AED) initiation in these patients.

Biography:

Raffaele Pilla, Pharm.D., Ph.D., Doctor Europaeus, received his Master’s degree in Pharmacy at G. d’Annunzio University in Chieti-Pescara, Italy in 2005, where he also served internships at the Cell Physiology Laboratory and Molecular Biology Laboratory. Prior, he was an Erasmus Student at Faculté de Pharmacie de Reims in Reims, France. He received his Doctor Europaeus in 2010 from Pitié-Salpétrière Institute in Paris, France. Also in 2010, he received his Ph.D. in Biochemistry, Physiology, and Pathology of Muscle at G. d’Annunzio University in ChietiPescara, Italy. He was hired as a Postdoctoral Scholar in the Department of Pharmacology and Physiology at the University of South Florida in Tampa, on two research grants funded by the Office of Naval Research (US Navy) and Divers’ Alert Network. He has written and lectured widely worldwide. He has been involved in ongoing research at the University of South Florida with the use of ketone esters

Abstract:

It has been recently shown that nutritional ketosis is effective against seizure disorders and various acute/ chronic neurological disorders. Physiologically, glucose is the primary metabolic fuel for cells. However, many neurodegenerative disorders have been associated with impaired glucose transport/metabolism and with mitochondrial dysfunction, such as Alzheimer’s/Parkinson’s disease, general seizure disorders, and traumatic brain injury. Ketone bodies and tricarboxylic acid cycle intermediates represent alternative fuels for the brain and can bypass the rate- limiting steps associated with impaired neuronal glucose metabolism. Therefore, therapeutic ketosis can be considered as a metabolic therapy by providing alternative energy substrates. It has been estimated that the brain derives over 60% of its total energy from ketones when glucose availability is limited. In fact, after prolonged periods of fasting or ketogenic diet (KD), the body utilizes energy obtained from free fatty acids (FFAs) released from adipose tissue. Because the brain is unable to derive significant energy from FFAs, hepatic ketogenesis converts FFAs into ketone bodies-hydroxybutyrate (BHB) and acetoacetate (AcAc)-while a percentage of AcAc spontaneously decarboxylates to acetone. Large quantities of ketone bodies accumulate in the blood through this mechanism. This represents a state of normal physiological ketosis and can be therapeutic. Ketone bodies are transported across the blood-brain barrier by monocarboxylic acid transporters to fuel brain function. Starvation or nutritional ketosis is an essential survival mechanism that ensures metabolic flexibility during prolonged fasting or lack of carbohydrate ingestion. Therapeutic ketosis leads to metabolic adaptations that may improve brain metabolism, restore mitochondrial ATP production, decrease reactive oxygen species production, reduce inflammation, and increase neurotrophic factors’ function. It has been shown that KD mimics the effects of fasting and the lack of glucose/insulin signaling, promoting a metabolic shift towards fatty acid utilization. In this work, the author reports a number of successful case reports treated through metabolic ketosis. 

Biography:

Felix-Martin Werner studied Human Medicine at the University of Bonn. He has been working as a Medical Teacher in the formation of geriatric nurses, occupational therapists and assistents of the medical doctor at the Euro Academy in Pößneck since 1999. He has been doing scientific work at the Institute of Neurosciences of Castilla and León (INCYL) in Salamanca (Spain) since 2002. With Prof. Rafael Coveñas, he assisted at over 30 national and 12 international congresses of Neurology and published over 60 reviews about neural networks in neurological and psychiatric diseases. Since 2014, Dr. Werner has belonged to the editorial board of the Journal of Cytology & Histology.

Abstract:

We reviewed the alterations of neurotransmitters and neuropeptides in the following brain areas involved in generalized epilepsy: hippocampus, hypothalamus, thalamus and cerebral cortex. In these brain areas, neural networks are also updated. The mechanisms of action of newer antiepileptic drugs, for example a GABAB agonist, an AMPA receptor antagonist and brivaracetam, used in the treatment of generalized epilepsy are also pointed out. Updating the neural networks, we suggest that in the hippocampus GABAergic neurons presynaptically inhibit, via GABAB receptors, epileptogenic neurons. GABAergic, glutamatergic, serotonergic and dopaminergic neurons form the principal neural network, while GABA and serotonin deficiency and dopamine and glutamate hyperactivity have a proconvulsant effect. In preclinical studies, the GABAB receptor agonist GS-39,783 exerted a good antiepileptic effect. Perampanel, an AMPA receptor antagonist, showed good anticonvulsant effects in the treatment of partial-onset seizures and primary generalized tonic-clonic seizures. In this treatment, perampanel can be combined with other antiepileptic drugs. Brivaracetam, the mechanism of action of which will be explained in detail, showed a good efficacy in the treatment of adult focal seizures and secondarily generalized tonic-clonic seizures.