The Role of Over-Nutrition and Obesity in Multiple Sclerosis

In countries with high standard of living, lowered risk of infectious diseases is parallel to increased incidence of autoimmune diseases. One of the autoimmune disorders, multiple sclerosis, affects genetically susceptible individuals. Genetic susceptibility is supposed to interact with lifestyle and environmental factors in developing autoimmunity in MS. From this point of view, epigenetics provides the bridge between the external environment and the internal genetic system. In MS, environmental burden can modulate gene expression by epigenetic modification of chromatin components, microRNAs or by subtle changes in DNA methylation. Our paper focuses on describing the epigenetic mechanisms linking environmental factors with pathogenesis of multiple sclerosis. We summarise current knowledge about the role of over-nutrition and obesity as epigenetic factors in multiple sclerosis

Genetic and Biochemical Factors Related to the Risk and Disability Progression in Multiple Sclerosis

Sclerosis multiplex (multiple sclerosis, MS) is a chronic autoimmune inflammatory disease of the central nervous system. The immune regulatory defects lead to the process of inflammation and neurodegenerationthat results in the deterioration of neurological functions. It is still unclear as to why MS is so devastating and rapidly progressive in one patient and less so in another. It is known that the etiopathogenesis of MS is very complex, and many factors can be involved in the risk and character of the disease and its progression. In this chapter, we discuss the general molecular and cellular mechanisms of action of genetic and biochemical factors that are related to immune system regulation and thus can be connected to the individually varying risk and disability progression of MS. We found that gene variants of the gene polymorphism rs6897932 in interleukin 7 receptor α chain gene rs10735810 in vitamin D receptor gene and HLA-DR and HLA-DQ genes as well as the serum level of vitamin D are associated with MS risk or disability progression in Central European Slovak population

Testiranje na antineuronska protutijela u neuobičajenom slučaju ponovljene Bellove paralize

The term Bell\u27s palsy (BP) is nowadays reserved for peripheral facial nerve paralysis without well-defined etiology and pathogenesis. BP is not a life threatening condition but it has a potential cosmetic mutilatory effect, and there is also a possibility of serious ophthalmologic complications (corneal ulcers). Recurrent paralyses are noted in 7% - 8% of BP cases. Only two patients with four BP episodes out of 170 patients, and only one patient with more than four BP episodes out of 2414 BP cases have been reported in the literature. The highest number of BP recurrences found in the available literature is nine. A brief review of the epidemiology and etiopathogenesis of BP is presented, a case of unusual recurrent BP is reported, and the immune pathomechanisms are discussed.Pojam Bellove paralize (BP) danas označava perifernu paralizu ličnoga živca nejasne etiologije i patogeneze. BP nije stanje koje bi ugrozilo život bolesnika, ali može imati znatne estetske posljedice te izazvati ozbiljne oftalmološke komplikacije (ulceracije rožnice). Ponovljene paralize javljaju se u 7% - 8% slučajeva BP. U literaturi je opisano samo dvoje bolesnika s četiri epizode BP od ukupno 1700 bolesnika, te samo jedan bolesnik s više od četiri epizode BP od ukupno 2414 slučajeva BP. U dostupnoj literaturi, najveći broj ponovljenih BP je devet. U radu se daje kratak pregled epidemiologije i etiopatogeneze BP, uz prikaz neuobičajenog slučaja ponovljene BP, uključujući raspravu o imunološkim patomehanizmima

Produljen tijek Creutzfeldt -Jakobove bolesti uz opsežnu degeneraciju središnjega živčanog sustava

In Slovak genetic Creutzfeldt-Jakob disease patients with E200K mutation in the prion protein gene the mean duration of clinical stage is significantly shorter in methionine homozygous then in methionine / valine heterozygous patients (3.70±2.00 vs. 7.84±7.30 months). An atypical prolonged course (13 months) of Creutzfeldt-Jakob disease complicated by malignant neuroleptic syndrome in a 48-year-old methionine homozygous carrier of E200K mutation is reported. Progression was documented by computed tomography, magnetic resonance imaging, functional-biochemical magnetic resonance spectroscopy, and electroencephalography. Post mortem neurohistologic findings confirmed the definitive diagnosis of Creutzfeldt-Jakob disease and revealed severe reduction of cerebral and cerebellar cortex with almost complete depletion of neuronal cells. The possible explanation of unusual duration of the disease in genetic Creutzfeldt-Jakob disease is discussed. The importance of early diagnosis and timely therapeutic intervention (when effective treatment becomes available) sufficiently preceding the development of irreversible degenerative changes if the central nervous system is emphasized.Srednje trajanje kliničkog stadija u slovačkih bolesnika s genetskom Creutzfeldt-Jakobovom bolešću s mutacijom EZOOK u genu prionskog proteina (PRNP) značajno je kraće u bolesnika homozigotnih za metionin nego u onih heterozigotnih za metionin/valin (3,70±Z,OO prema 7,84±7,30 mjeseci). Opisuje se atipičan produljeni tijek (13 mjeseci) Creutzfeldt-jakobove bolesti komplicirane malignim neurolepticnim sindromom u 48-godišnjeg nositelja mutacije EZOOK homozigotnog za metionin. Progresija je dokumentirana kompjutoriziranom tomografijom, magnetskom rezonancom, funkcionalno biokemijskom spektroskopijom magnetskom rezonancom i elektroencefalografijom. Neurohistološki nalazi pri obdukciji potvrdili su definitivnu dijagnozu Creutzfeldt-Jakobove bolesti i otkrili teško smanjenje cerebralnog i cerebelarnog korteksa uz gotovo potpun nestanak neuronskih stanica. Raspravlja se o mogućem objašnjenju neuobičajenog trajanja bolesti u slučaju genetske Creutzfeldt-Jakobove bolesti. Naglašava se važnost rane dijagnoze i terapijske intervencije (kad učinkovita terapija bude dostupna), koje ce dostatno prethoditi razvoju zapaženih ireverzibilnih degenerativnih promjena središnjega živčanog sustava

Flow Changes after Endovascular Treatment of a Wide-Neck Anterior Communicating Artery Aneurysm by using X-configured Kissing Stents (Cross-Kissing Stents) Technique

Endovascular treatment for a wide-neck anterior communicating artery (AcomA) aneurysm remains technically challenging. Stent-assisted embolization has been proposed as an alternative of treatment of complex aneurysms. The X-configuration double-stent-assisted technique was used to achieve successful coiling of wide-neck AcomA aneurysm. Implanted stent can alter intra-arterial flow. Follow-up angiograms 4 months later showed flow changes due to used X-technique of stents implantation and filling of the anterior cerebral artery from the opposite internal carotid artery

Produljen tijek Creutzfeldt -Jakobove bolesti uz opsežnu degeneraciju središnjega živčanog sustava

In Slovak genetic Creutzfeldt-Jakob disease patients with E200K mutation in the prion protein gene the mean duration of clinical stage is significantly shorter in methionine homozygous then in methionine / valine heterozygous patients (3.70±2.00 vs. 7.84±7.30 months). An atypical prolonged course (13 months) of Creutzfeldt-Jakob disease complicated by malignant neuroleptic syndrome in a 48-year-old methionine homozygous carrier of E200K mutation is reported. Progression was documented by computed tomography, magnetic resonance imaging, functional-biochemical magnetic resonance spectroscopy, and electroencephalography. Post mortem neurohistologic findings confirmed the definitive diagnosis of Creutzfeldt-Jakob disease and revealed severe reduction of cerebral and cerebellar cortex with almost complete depletion of neuronal cells. The possible explanation of unusual duration of the disease in genetic Creutzfeldt-Jakob disease is discussed. The importance of early diagnosis and timely therapeutic intervention (when effective treatment becomes available) sufficiently preceding the development of irreversible degenerative changes if the central nervous system is emphasized.Srednje trajanje kliničkog stadija u slovačkih bolesnika s genetskom Creutzfeldt-Jakobovom bolešću s mutacijom EZOOK u genu prionskog proteina (PRNP) značajno je kraće u bolesnika homozigotnih za metionin nego u onih heterozigotnih za metionin/valin (3,70±Z,OO prema 7,84±7,30 mjeseci). Opisuje se atipičan produljeni tijek (13 mjeseci) Creutzfeldt-jakobove bolesti komplicirane malignim neurolepticnim sindromom u 48-godišnjeg nositelja mutacije EZOOK homozigotnog za metionin. Progresija je dokumentirana kompjutoriziranom tomografijom, magnetskom rezonancom, funkcionalno biokemijskom spektroskopijom magnetskom rezonancom i elektroencefalografijom. Neurohistološki nalazi pri obdukciji potvrdili su definitivnu dijagnozu Creutzfeldt-Jakobove bolesti i otkrili teško smanjenje cerebralnog i cerebelarnog korteksa uz gotovo potpun nestanak neuronskih stanica. Raspravlja se o mogućem objašnjenju neuobičajenog trajanja bolesti u slučaju genetske Creutzfeldt-Jakobove bolesti. Naglašava se važnost rane dijagnoze i terapijske intervencije (kad učinkovita terapija bude dostupna), koje ce dostatno prethoditi razvoju zapaženih ireverzibilnih degenerativnih promjena središnjega živčanog sustava

Embolization of Ruptured Infratentorial Pial AVM in Pregnancy

A primigravida 22-year-old woman, at a gestation of 23 weeks, experienced bleeding from a pial arteriovenous malformation (AVM) located in the right cerebellum. After interdisciplinary consensus and with the informed consent of the patient and her family, AVM embolization was performed. Complete occlusion of the AVM was achieved by embolization with PHIL (precipitating hydrophobic injectable liquid). The calculated dose in the uterus was less than 1 µSv, which represents a negligible risk of harmful effects on the fetus. She delivered a baby at 37 weeks of gestation by cesarean section without complications. No congenital disorders were diagnosed by standard screening methods until the age of the newborn was two years. The angiography protocol must be optimized to minimize the radiation dose. Adequate shielding protection of the uterus is important. Premature termination of pregnancy is not necessary. Multidisciplinary care of neurologists, neurosurgeons, interventional radiologists, anesthesiologists, neonatologists, and obstetricians is necessary

Current Methods of Magnetic Resonance for Noninvasive Assessment of Molecular Aspects of Pathoetiology in Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune disease with expanding axonal and neuronal degeneration in the central nervous system leading to motoric dysfunctions, psychical disability, and cognitive impairment during MS progression. The exact cascade of pathological processes (inflammation, demyelination, excitotoxicity, diffuse neuro-axonal degeneration, oxidative and metabolic stress, etc.) causing MS onset is still not fully understood, although several accompanying biomarkers are particularly suitable for the detection of early subclinical changes. Magnetic resonance (MR) methods are generally considered to be the most sensitive diagnostic tools. Their advantages include their noninvasive nature and their ability to image tissue in vivo. In particular, MR spectroscopy (proton 1H and phosphorus 31P MRS) is a powerful analytical tool for the detection and analysis of biomedically relevant metabolites, amino acids, and bioelements, and thus for providing information about neuro-axonal degradation, demyelination, reactive gliosis, mitochondrial and neurotransmitter failure, cellular energetic and membrane alternation, and the imbalance of magnesium homeostasis in specific tissues. Furthermore, the MR relaxometry-based detection of accumulated biogenic iron in the brain tissue is useful in disease evaluation. The early description and understanding of the developing pathological process might be critical for establishing clinically effective MS-modifying therapies

The Intricate Network of Adipokines and Stroke

Cerebrovascular disorders, particularly ischemic stroke, are one of the most common neurological disorders. High rates of overweight and obesity support an interest in the role of adipose tissue and adipose tissue releasing cytokines in inducing associated comorbidities. Adipokines can serve as a key messenger to central energy homeostasis and metabolic homeostasis. They can contribute to the crosstalk between adipose tissue and brain. However recent research has offered ambiguous data on the network of adipose tissue, adipokines, and vascular disorders. In our paper we provide a critical insight into the role of adipokines in evolution of ischemic stroke