{"title":"LEVELS’ INFLUENCE OF IFN-γ AND IL-10 IN CHILDREN WITH EPILEPTICUS STATUS","authors":"I. Salim, M. Muid, H. Sujuti","doi":"10.21776/ub.mnj.2018.004.01.4","DOIUrl":"https://doi.org/10.21776/ub.mnj.2018.004.01.4","url":null,"abstract":"Background. Seizures are a common clinical manifestation in the emergency room. Nearly 5% of children aged under 16 years. Seizures are important as a sign of neurological disorders. Members of interferon are widely studied with seizures and epileptogenesis is interferon-γ. In a study by Choi in 2011, a study of seizures in humans showed that the condition of status epilepticus increased levels of interferon-γ which is quite high compared to patients not status epilepticus seizures. In response to the aftermath of the seizure, Interferon-γ system induces the formation of IL-10 acts as an anti-inflammatory agent that aims to put an end to the action of Interferon-γ. Objective. To know role of Interferon-γ and IL-10 in children with status epilepticus. Methods. This research using cross sectional design with recruiting 30 study sample consisted of 15 children in the seizure group SE and 15 children in the group without SE seizures. Measured levels of IFN-γ and interleukin-10 by ELISA. Results were analyzed with the Mann-Whitney and corelation Spearman to see the relationship levels of IFN-γ and IL-10 in children with status epilepticus with SPSS-23. Results. The results showed significant differences between groups SE and convulsive seizures non SE ;IL10 (p = 0.000) and IFN-γ (p= 000). Conclusion. There are significant correlation between the levels of IFN-γ and IL-10 with status epilepticus.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"4 1","pages":"19-24"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68324791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"AMPLITUDO SENSORY NEURON ACTION POTENTIAL USING AS INSTALLATION OF POLYNEUROPATHY DIAGNOSIS","authors":"Billi Kinesya, M. Husna, S. Kurniawan, M. Ridwan","doi":"10.21776/UB.MNJ.2018.004.01.2","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2018.004.01.2","url":null,"abstract":"Background. Polyneuropathy is the pathologic changes and functional disturbances in the peripheral nervous system. These changes manifest as sign and symptoms such as numbness, burning, allodynia, atrophy, and lose of stimulation responses. Diagnosing polyneuropathy can use electrodiagnostic method like electroneuromyography (ENMG). One of the most sensitive ENMG parameters for polyneuropathy is SNAP amplitude which can be measured at Sural Nerve. Objective. The goal of this study is to know whether SNAP amplitude can be used to diagnose polyneuropathy. Methods. The study design is diagnostic test in cross-sectional method. Results. Samples were taken from 108 ENMG medical records of Neurology Department Saiful Anwar General Hospital during the whole 2014. Two variables which are compared are polyneuropathy diagnosis and SNAP amplitude. Fisher test shows significant differences between the two with p = 0.04. Diagnostic test shows sensitivity 68.3%, spesifisity 80%, positive predictive value 97.1%, and negative predictive value 20.5%. Conclusion. There is a significant relationship between SNAP amplitude reduction with the diagnosis of polyneuropathy.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"4 1","pages":"7-11"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68324684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"BIOMOLECULAR MECHANISM OF ANTI EPILEPTIC DRUGS","authors":"M. Husna, S. Kurniawan","doi":"10.21776/UB.MNJ.2018.004.01.7","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2018.004.01.7","url":null,"abstract":"Epilepsy therapy is almost always chronic and often used more than one drug. Currently, antiepileptic drugs are still the mainstay of therapy for epilepsy. An understanding of the pharmacodynamics and pharmacokinetics of these drugs would be very helpful in choosing the right medication and develop a study to determine the drug's mechanism further. Mechanism of action of AED (anti epileptic drug) can be categorized into four main groups: (1) modulation of voltage-gated ion channels, including sodium, calcium, and potassium; (2) increase in GABA inhibition through an effect on GABA-A receptors, the GAT-1 GABA transporter, or GABA transaminase; (3) direct modulation of the synaptic release of such SV2A and α2δ; and (4) inhibition of excitatory synapses through ionotropik glutamate receptors including AMPA receptors. AED work to balance the process of inhibition and excitation in the brain, so it can be used both for epilepsy and other diseases with similarities with the pathophysiology of epilepsy.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"4 1","pages":"38-45"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68325164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"THE EFFECT OF HSP65 MYCOBACTERIUM TUBERCULOSIS ON THE VACCINATION TOWARDS AORTIC THICKNESS OF MICE THAT HAVE BEEN INDUCED ATHEROSCLEROSIS","authors":"D. A. Sari","doi":"10.21776/ub.mnj.2017.003.02.1","DOIUrl":"https://doi.org/10.21776/ub.mnj.2017.003.02.1","url":null,"abstract":"Background. Atherosclerosis is an inflammatory process of the blood vessels accompanied by immune activity which is signed by the enhancement of histopathologic. One of the protective proteins in the human artery wall expressed when there is endothelial stress is HSP60. HSP65 is an HSP60 homologous protein found in bacteria, such as Mycobacterium tuberculosis. Objective . To determine the effect of HSP65 through aorta thickness of mice. Methods. This research applied experimental study using post-test control group design in which subjects were divided into 5 groups. Each group consisted of 5 mice. Group I mice fed a diet normokolesterolemia (negative control), group II mice given atherogenic diet without vaccine (positive control), group III mice given atherogenic diet and 0,5μg accination, group IV mice were given atherogenic diet and 0,75μg vaccination, group V mice were given atherogenic diet and 1μg vaccination. Results. There was a difference between the atherogenic diet and vaccination group (p <0.05). There was a significant decrease in aortic thickness of atherosclerosis mice with HSP65 vaccination dose 0,75µg (r= -0,449, p= 0,024). Conclusion. HSP65 Mycobacterium tuberculosis vaccination can reduce the thickness of the aorta in mice induced atherosclerosis and the effective dose is 0.75 mg dose.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"3 1","pages":"47-54"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45190307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"THE EFFECTS OF EARTHWORMS’ (PHERETIMA ASPERGILLUM) ETHANOL EXTRACT TOWARD THE IMPROVEMENT OF NERVE FIBERS DENSITY IN DIABETIC ULCERS CARE DEGREE II OF RATS WISTAR","authors":"H. Kristianto, Ni Putu Jeny Mardiati","doi":"10.21776/UB.MNJ.2017.003.02.3","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2017.003.02.3","url":null,"abstract":"Background. Diabetic ulcer is a chronic complication of diabetes mellitus which lead to infection and lower extremity amputation. Earthworm (Pheretima aspergillum) has bioactive substance of IGF-1 (insulin like growth factor 1) to promote Schwann cell proliferation, survival, and migration into the distal end in the injured nerve area to support axonal re-growth. Objective. To investigate the effect of earthworm extract (Pheretima aspergillum) on the enhancement of nervous fibers density in rats induced diabetic ulcer stage II. Methods. This study applied a true-experimental posttest only controlled group design. Samples were divided into five groups: Normal Saline as a negative control group, Hydrogel as a positive control group, and the three treatment groups received earthworm extract via topical, oral, and topical-oral. The patterns of nervous fibers connecting to hair follicles were identified using silver impregnation stain. Results. The result shows the groups receiving earthworm extract have significantly higher nervous fibers density compared to the control groups (p=0.000). The administered of earthworm extract via topical has an optimal effect on improving nervous fibers density. Conclusion. Earthworm extract promote regeneration of peripheral nerve in rats model of diabetic.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"3 1","pages":"61-72"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49441281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"PATHOPHYSIOLOGY AND MANAGEMENT OF CEREBRAL EDEMA","authors":"U. Husna, M. Dalhar","doi":"10.21776/UB.MNJ.2017.003.02.7","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2017.003.02.7","url":null,"abstract":"Cerebral edema comprehensively defined as a pathological increase of water in the whole brain that leads to an increased of brain volume. Cerebral edema can be classified into focal or global topography. According to the etiology, it can be categorized as cytotoxic, vasogenic, interstitial, or a combination. The symptoms of cerebral edema are not specific and are associated with secondary effects of mass, vascular compression and herniation. Clinical and radiological changes are usually reversible in the early stages during the underlying cause is corrected. Cerebral edema need to be discussed more specifically in the pathophysiology and management. By understanding the pathophysiology and management quickly and accurately will be able to improve the prognosis of patients with cerebral edema.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"3 1","pages":"94-107"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48841556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CLINICAL AND RADIOLOGICAL APPROACH OF POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME ON ECLAMPSIA","authors":"Fakhrurrazy Fakhrurrazy, Herly Maulida Surdhawati","doi":"10.21776/UB.MNJ.2017.003.02.6","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2017.003.02.6","url":null,"abstract":"Posterior reversible encephalopathy syndrome (PRES) is rare clinico-neuroradiologic condition and not commonly reported in the literature, a recently recognized syndrome characterized clinically by headache, confusion, seizure and visual loss associated, with imaging findings of bilateral cortical and subcortical oedema, predominantly posterior cerebral lesions (mainly occipito-parietal). Posterior reversible encephalopathy syndrome is an uncommon complication of severe preeclampsia/ eclampsia. The objective of this study is to report PRES case on eclampsia with clinical and radiological approach. We report a case of woman, 34 years old woman, with chief complaint tonic clonic general seizure and sudden headache previously. This patient had pregnancy 8 gestational month and had pregnancy termination with cesarean section recently. Patient had loss of consciousness, vision disturbance, and weakness of right extremities, all this symptom become well during treatment. The result of laboratory examination was HELLP syndrome (haemolysis, elevated liver enzymes and low-platelets). Head CT scan showed hypodense lesion in left parietooccipital region and MRI on T2W and T2FLAIR ADC MAPS found hyperintens lesion in right and left parietooccipital. Then it can be concluded that it have been reported cases of eclampsia with PRES with symptom of headache, seizure, mental status disturbance, visual disturbances. The pathological association between PRES and HELLP syndrome in a patient with eclampsia is poorly described.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"3 1","pages":"88-93"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46930334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
O. Paundralingga, Darmawan Darkim, B. Munir, B. H. Daeng
{"title":"EFFECTS OF ACUTE STRESS DURATION ON THE RAT BRAIN MAST CELL ACTIVATION","authors":"O. Paundralingga, Darmawan Darkim, B. Munir, B. H. Daeng","doi":"10.21776/UB.MNJ.2017.003.02.4","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2017.003.02.4","url":null,"abstract":"Background. Stress of varying duration and types are known to affect the number and activation level of cerebral mast cells (MCs) via plasma CRH. Although MC number is known not to be increased in acute stress, elevated plasma CRH might still activate brain MCs. Objective. To investigate the effect of acute stress of incremental duration to the activation level of thalamic and hippocampal mast cells using elevated platform test to elicit stress in male Wistar rats. Methods. This research used randomized post-test only control group design with 4 control group of 30, 60, and 90 minute stress exposure. Mast cell activation of the regiotalamus and hippocampus is assessed by histomorphometrics. Results. In the hippocampus, we found a significant difference of MC activation between control and experimental groups (p=0.014; p<0.05) but not among the incremental duration of acute stress. However, MC activation was not different between control and experimental groups in the thalamus . Conclusion. Acute stress exposure increases MC activation without recruiting further MCs in specific cerebral region but the duration of acute stress itself does not affect the activation level.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"3 1","pages":"73-77"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42265483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"MYCOBACTERIUM TUBERCULOSIS STRAIN H37RV INFECTION TOWARDS MATRIX METALLOPROTEINASE (MMP)-2 IN BRAIN","authors":"K. Hartono, Prasetyo Adi, D. Hidayati","doi":"10.21776/UB.MNJ.2017.003.02.2","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2017.003.02.2","url":null,"abstract":"Background. Tuberculous infection in brain can cause microglia to secrete inflammatory factors like Tumor Necrosis Factor alpha (TNF-α) and Interleukin 1 beta (IL-1β) which will be shown as body immune respons. Those inflammatory factors eventually can trigger microglia to secrete Matrix Metalloproteinase- 2 (MMP-2) which will regenerate necrotic or apoptosis cells because of inflammation process. MMP-2 has been proven to have important role in brain tuberculous infection. Objective. To ascertain MMP-2 expression in mus musculus brain tissue with no infection, infection for 8 weeks, and infection for 16 weeks. Methods. This research used semiquantitative method to compare MMP-2 expression in 3 samples group. Observation of MMP-2 expression in mus musculus brain tissue were made by using immunohistochemistry colouration method which then would be observed in microscope with 400x magnification. Brain cell which express MMP-2 will become brown in cell nucleus, cytoplasm, and wall. Results. The result which had be obtained was overtime reduction of MMP-2 expression. Conclusion. MMP-2 expression didn’t decrease after 8 weeks time of infection.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"3 1","pages":"55-60"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48226916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"DESIGN OF EXPERT SYSTEM AS A SUPPORT TOOL FOR EARLY DIAGNOSIS OF PRIMARY HEADACHE","authors":"Zahwa Arsy Azzahra, E. Purwanti, H. Hidayati","doi":"10.21776/UB.MNJ.2017.003.02.5","DOIUrl":"https://doi.org/10.21776/UB.MNJ.2017.003.02.5","url":null,"abstract":"Background. Headache is the top ranked with 42% percentage of all complaints neurology’s patients. Focused and systematic approach is needed in making a diagnosis of primary headache type because management of headache is different for each type. Objective. Enabling users to identify the type of headache. Methods. The experiment was conducted using Naive Bayes classifier method which is the principle is multiplying the percentage likelihood of each variable for each parameter for each class. Results. The percentage value of each parameter obtained from the data of headache patients at neurology polyclinic poly of Dr. Soetomo Hospital within 1 year from the year 2014 to 2015. The percentage value of each class likelihood sought highest value which is the output or decision-diagnosis program. Analysis of each of the input parameters, gender, age, location of head pain, headache characteristics, appeared least autonomous signs, and scale of headache may indicate that each of the options selected by the user influence the decision of the diagnosis program. Conclusion. The design of early detection of primary headaches with the input parameters as mentioned before derived from the raw data as electronic medical records to be analyzed based on methods Naive Bayes classifier resulted in the decision diagnosis of migraine, cluster and TTH have accuracy values by 92 %.","PeriodicalId":31552,"journal":{"name":"Malang Neurology Journal","volume":"3 1","pages":"78-87"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44252843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}