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PERSISTENT HEADACHE AFTER CEREBELLUM HEMORRHAGE STROKE Nata Sanjaya; Shahdevi Nandar Kurniawan
Journal of Pain, Headache and Vertigo Vol. 3 No. 2 (2022): September
Publisher : Journal of Pain, Headache and Vertigo

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jphv.2022.003.02.4

Abstract

Cerebrovascular disease is the number one cause of epilepsy in the elderly population. Headaches are relatively common in patients with cerebrovascular disorders. The frequency of stroke-related headaches ranges from 7% to 65% with different types of headaches. The prevalence of persistent post-stroke headaches from 7-23%, with follow-up times ranging from 3 months to 3 years after stroke. Persistent headache in the population was associated with high depression and fatigue scores and significantly impacted returning to work. Most headaches at stroke onset will resolve, persistent headaches are a real entity even years after the stroke. The mechanism that might explain the relationship between headache and hemorrhagic stroke is still unclear, including changes in blood vessel walls supported by endothelial dysfunction in migraine sufferers as well as comorbid vascular risk factors such as arterial hypertension or platelet dysfunction. Headache after stroke intracerebral hemorrhage is believed to be the result of vasoconstriction that causes ischemia of the vessel wall.
Neuropathy in Vitamin Deficiency Shahdevi NK
Journal of Global Pharma Technology Volume 12 Issue 06 (2020) June 2020
Publisher : Journal of Global Pharma Technology

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Abstract

Neuropathy is a disorder of the motor nerves, sensory disorders and also autonomic and tendon reflexes. The Neuropathy that occurs can be caused by systemic diseases (diabetes, hypothyroidism), drugs, infections and also vitamin deficiencies. Vitamins are organic components with a high level of potential. Vitamins themselves are classified into 2 which are air soluble and fat-soluble, for fat-soluble vitamins, there are vitamins A, D, E, K and for vitamin B complex including vitamins that are soluble in air. Vitamin B plays an important role as a co-factor or co-enzyme in various metabolic processes in the body. A continuous lack of vitamins will cause damage to the peripheral nervous system so that symptoms of neuropathy appear. Deficiency of vitamin E and vitamin B can cause damage to the nervous system and neuropathy occurs. Vitamin B which has several kinds, such as B1 (thiamine), B2 (riboflavin), B3 (niacin), B5 (pantonetate), B6 (pyridoxine), B7 (biotin), B9 (folate) and B12 (cobalamin) where this B vitamin has a neurotrophic function. Vitamin B cannot be produced by mammals, so we can get this vitamin through food and supplementation. Vitamins themselves function to maintain the body's physiological functions and also maintain optimal health. Keyword: Neuropathy, Vitamin, Thiamine, Cobalamin, Pyridoxine.
The Effect of Nimodipine to Reactive Oxygent Species (ROS) in SHSY-5Y Cell-Line Culture Expressed by Chronic Hyperglycemia Shahdevi NK
Journal of Global Pharma Technology Volume 12 Issue 01
Publisher : Journal of Global Pharma Technology

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Abstract

Background: Diabetes mellitus is a metabolic disease with a chronic hyperglycemia condition. Diabetic peripheral neuropathy is a condition that arises from long-term damage due to chronic and hyperglycemia combination of various factors and pathways. One of them is the occurrence of oxidative stress caused by an increase in ROS intracellular. The accumulation of ROS can activate other pathways and result in an ion imbalance Ca2+. Nimodipine is a type L calcium channel blocker which has neuroprotective properties. Therefore, nimodipine is expected to reduce the expression of ROS in neurons that occur due to chronic hyperglycemia conditions. Objective: To determine the effect of nimodipine on ROS in culture of SH-SY5Y-induced cell-line neurons chronic hyperglycemia. Methods: Experimental research with in vitro methods using the exposed SH-SY5Y neuronal cell line chronic hyperglycemia. The study sample was divided into 9 groups, the control normoglycemic group, hyperglycemia control 25 mM and 50 mM, normoglycemia with nimodipine 10 nM and 100 nM, hyperglycemia 25 mM with nimodipine 10 nM and 100 nM, and 50 mM hyperglycemia group with nimodipine 10 nM and 100 nM. Nimodipine is given for 30 minutes on Sh-Sy5Y cells that have previously been exposed to hyperglycemia conditions chronic for 6 days. The intensity of intracellular ROS was observed by immunohistochemical methods on the sixth day. Results: In comparison of normoglycemic conditions (5 mM) and hyperglycemia 25 mM, normoglycemic conditions 5 mM resulting in a significantly higher ROS intensity (p <0.05). Whereas in comparison normoglycemia (5 mM) and hyperglycemia 50 mM had a significant increase in ROS intensity (p <0.05). Expose glucose 5 mM can increase ROS expression due to a series of processes due to hypoglycemic conditions. Exposure to high doses of glucose (50 mM) can increase ROS formation. Giving nimodipine to cells able to reduce the intensity of ROS on glucose exposure 5 mM, 25 mM and 50 mM significantly (p <0.05). Conclusion: Chronic hyperglycemia conditions can increase the formation of ROS in SH-SY5Y and cell cultures nimodipine can significantly reduce ROS levels.Keywords: Nimodipine, SH-SY5Y, ROS, Hyperglycemia, Neuropathy. 
POST HERPETIC NEURALGIA Irsyah Dwi Rohmayanti; Shahdevi Nandar Kurniawan
Journal of Pain, Headache and Vertigo Vol. 4 No. 1 (2023): March
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jphv.2023.004.01.1

Abstract

Postherpetic neuralgia (PHN) is a chronic neuropathic pain condition that lasts 3 months or more after an outbreak of shingles. Herpes zoster, especially acute herpes zoster, is associated with the reactivation of the inactivated varicella zoster virus in individuals who have had chickenpox. PHN is associated with persistent and often refractory neuropathic pain. Patients may experience several types of pain, including deep pain, intolerable pain, burning, paroxysmal pain, stabbing pain, hyperalgesia, and allodynia. Pharmacological treatment of PHN may include a variety of drugs, including alpha-2 delta ligands (gabapentin and pregabalin), other anticonvulsants (carbamazepine), tricyclic antidepressants (amitriptyline, nortriptyline, doxepin), topical analgesics (5% lidocaine patch, capsaicin) tramadol, or other opioids. The sizeable side effect profile of commonly used oral drugs often limits their practical use, and a combination of topical and systemic agents may be required for optimal results. Doctors and other care providers must adapt treatment based on individual patient responses.
LEPROSY NEUROPATHY Fahrani Yossa Prachika; Shahdevi Nandar Kurniawan
Journal of Pain, Headache and Vertigo Vol. 4 No. 1 (2023): March
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jphv.2023.004.01.3

Abstract

Leprosy is a major cause of peripheral neuropathy in developing countries, affecting sensory, motor, and autonomic nerve function. Neuropathy complications can include sensory loss and muscle weakness. Impaired sensory nerve function is often the first symptom encountered in leprosy neuropathy. Early detection and treatment of neuropathy in leprosy are important to prevent disability.
HNP LUMBALIS Mega Yulia Rusmayanti; Shahdevi Nandar Kurniawan
Journal of Pain, Headache and Vertigo Vol. 4 No. 1 (2023): March
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jphv.2023.004.01.2

Abstract

Lumbar herniated nucleus pulposus (HNP) is a disorder characterized by local displacement of the disc beyond the anatomical boundaries of the intervertebral space causing pain, weakness or numbness, and/or tingling in myotomal or dermatomal distribution. HNP is the most common cause of low back pain. Lumbar HNP itself has several underlying etiologies, such as old age, excessive axial load, connective tissue disorders, and congenital abnormalities. Management of HNP can be carried out non-operatively or operatively, depending on the severity, the symptoms that arise, and the response to non-operative treatment.
MYASTHENIA GRAVIS Dewi Permata Sari; Shahdevi Nandar Kurniawan
Journal of Pain, Headache and Vertigo Vol. 4 No. 1 (2023): March
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jphv.2022.004.01.4

Abstract

Myasthenia gravis is an autoimmune disease of the postsynaptic membrane, especially acetylcholine receptors in the neuromuscular link of skeletal muscle. Patients with myasthenia gravis have a high number globally. The disease occurs due to a disorder that impairs the impulse connection between chemicals traveling from nerve endings and receptors. Clinical symptoms include weakness of the eye muscles (ptosis and diplopia), difficulty swallowing, and difficulty speaking. The diagnosis of myasthenia gravis is based on the patient's complaints obtained in the history, physical and neurological examination, and supporting examinations. The management that can be given is intravenous immunoglobulin (IVIg) therapy, plasma exchange (PE), corticosteroids given together with IVIg and PE, or acetylcholinesterase inhibitors. These treatments can determine the patient's prognosis. If the patient with myasthenia gravis is left to involve the respiratory muscles, then the patient's prognosis becomes worse. In addition, myasthenic crisis and cholinergic crisis may occur, which is a medical emergency.
PATHOPHYSIOLOGY IN CLUSTER HEADACHE: AN UPDATE Wa Ode Intan Nur Octina; Shahdevi Nandar Kurniawan
Journal of Pain, Headache and Vertigo Vol. 4 No. 1 (2023): March
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jphv.2022.004.01.5

Abstract

Cluster headache (CH) is a rare and very painful primary headache syndrome, with an estimated population prevalence of 0.12%. This condition can be episodic (ECH), lasting from 7 days to a year. A consensus statement from the European Headache Federation defines refractory CCH as a CCH with at least three severe attacks per week, even though at least three consecutive trials of adequate preventive care have been tested and managed with both acute and preventive treatment. Inhaled oxygen and subcutaneous sumatriptan are the two most effective acute treatment options for people with CH. Several preventive medications are also available, and the most effective is verapamil. However, most of these agents are not supported by strong clinical evidence. In some patients, this option may be ineffective, particularly in those with chronic CH. Surgical procedures for chronic refractory forms of disorder should then be considered.
NEUROPROTECTANT OF 7,8-DIHYDROXYFLAVONE IN ISCHEMIC STROKE THROUGH MODULATION GLUTATHIONE S-TRANSFERASE AND TYROSINE RECEPTOR KINASE C: A BIOINFORMATICS STUDY Aldita Husna Violita; Safira Dita Arviana; Rislan Faiz Muhammad; Basyar Adnani; Titin Andri Wihastuti; Husnul Khotimah; Shahdevi Nandar Kurniawan; Yuyun Yueniwati
MNJ (Malang Neurology Journal) Vol. 9 No. 2 (2023): July
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.mnj.2023.009.02.8

Abstract

Background: Times New Roman 9, single space, contains the brief description of the research. Stroke is the greatest cause of disability and mortality worldwide. Several biological mechanisms underlying this disease such as failure of glutamate reuptake and ATP synthesis, resulting in high levels of reactive oxygen species (ROS), neuroinflammatory responses, and apoptosis, resulted in cell death and brain tissue damage. Neurotherapeutics agents are given to affect the pathophysiological pathways and prevent expanding infarct area. Objective: This study aims to analyze the modulation of Gluthatione S-Transferase (GST) and Tyrosine kinase receptor C (TrkC) by 7,8-DHF as neuroprotective agent in ischemic in silico. Methods: This study used in silico simulation to predict 7,8-dihydroxyflavone (DHF) as neuroprotective agent by using PubChem, RCSB, Biovia Discovery Studio, PyRx, and PyMol. This study analyzes the pharmacodynamics, pharmacokinetics, and molecular interactions between 7,8-DHF as a ligand with GST (13GS) and TrkC (6KZC) as protein target, compared to their native ligand. Results: 7,8-DHF may increase intracellular endogenous antioxidants mainly GST and stimulate TrkC to activate further neuron survival signaling. 7,8 DHF has a much lower bond energy (-8.1 Kcal/mol) when it binds to GST compared to the native ligand (-5.9 Kcal/mol). Besides, binding affinity between 7,8-DHF-TrkC was -9 Kcal/mol, while native ligand-TrkC was -10.6 Kcal/mol. This study showed that there were the same amino acid residues between 7,8-DHF-GST and 7,8-DHF-TrkC, compared to their native ligand. Conclusion: As an adaptive response to hypoxia caused by ischemic stroke, these findings are likely to induce protective mechanism through indirectly TrkC activation which regulates neurogenesis and increasing intracellular endogenous antioxidants.
BIOINFORMATICS STUDY OF 7,8-DIHYDROXYFLAVONE AS A NEUROPROTECTIVE AGENT IN ISCHEMIC STROKE VIA TRKB REGULATION AND GLUTAMINASE INHIBITION Rislan Faiz Muhammad; Basya Adnani; Safira Dita Arviana; Aldita Husna Violita; Husnul Khotimah; Shahdevi Nandar Kurniawan; Mokhamad Fahmi Rizki Syaban; Yuyun Yueniwati Prabowowati Wadjib; Masruroh Rahayu
MNJ (Malang Neurology Journal) Vol. 9 No. 2 (2023): July
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.mnj.2023.009.02.12

Abstract

Background: Stroke, particularly ischemic stroke, is one of the leading causes of death worldwide. Ischemic stroke causes a failure of oxidative phosphorylation and ATP synthesis, resulting in high levels of reactive oxygen species (ROS), neuroinflammatory responses, and apoptosis, all of which result in cell death. Neuroprotective agents are given to prevent the infarct area from expanding. Objective: This study aims to predict an in silico interaction by 7,8-dihydroxyflavone as neuprotective agent through TrkB signaling and inhibiting Glutaminase activity. Methods: In silico simulation with 7,8-dihydroxyflavone (DHF) as neuroprotective agent using PubChem, RCSB, Biovia Discovery Studio, PyRx, and PyMol software. This study analyzes the pharmacokinetics, pharmacodynamics, and protein-ligand interactions between 7,8-DHF as a ligand with TrkB (4AT5) and Glutaminase (5JYO) as protein target, compared to their native ligand. Results: 7,8 DHF binds to 4AT5 and 5JYO with lower bond energy (-9.4 Kcal/mol and -6.3 Kcal/mol, respectively) than the native ligand (-5 Kcal/mol and -5.9 Kcal/mol, respectively). It means that 7,8-DHF may increase protective mechanism. Conclusion: These findings tend to increase downstream signaling pathways, leading to increased TrkB expression, which induces protective mechanisms, and decreased glutamate expression, which reduces glutamate toxicity.
Co-Authors Abdul Gofur Afiyfah Kaysa Waafi Al-Rasyid, Harun Aldita Husna Violita Aldita Husna Violita Andaru Cahya S Anggraini, Vivi Laras Anggraini, Vivid Prety Anisa Syahfitri Hanum Annisatul Hakimah Asmiragani, Syaifullah Auliya Nur Muthmainnina Badrul Munir Badrul Munir, Badrul Basya Adnani Basyar Adnani Chomsin Sulistya Widodo Chozin, Iin Noor Dalhar, Mochamad Damayanti, Ria DAMAYANTI, ZUHRIA PUSPITA Dessika Rahmawati Devi Annisa Devita Anggraeni Soeroso Dewi Permata Sari Dheka Sapti Iskandar Dhelya Widasmara Didi Candradikusuma Dini Jatiya Anggraini, Dini Jatiya Dwi, Pratiwi Suryanti Dyah Kusuma Wardhani Edi Widjajanto Eko Arisetijono Ekowati Retnaningtyas F, Fahimma Fahrani Yossa Prachika Farida Widyastuti Fitria Nikmahtustsani, Mulika Ade Gerry Gunawan, Gerry Gonius, Andry Gyang Hanandita Gusti Putri Hanestya Oky Hermawan, Hanestya Oky Hani Susianti Harbiyanti, Novita Titis Hardi Adiyatma Harun Al Rasyid Helena Era Millennie Heri, Sutanto Herwinda Brahmanti Husnul Khotimah Husnul Khotimah I Ketut Suada Irawan Satriotomo Irsyah Dwi Rohmayanti Izza Ayudia Hakim Janet, Karensa Abby Jatmiko, Sarazata Indi Rozaany Kadek Putri Paramita Abyuda Kartika Agustina Kinesya, Billi Lestari, Dwi Indriani Machlusil Husna Machlusil Husna, Machlusil Made Ayu Hariningsih Sunaga Masruroh Rahayu Masruroh Rahayu Masruroh Rahayu Masruroh Rahayu Masruroh Rahayu Masruroh Rahayu, Masruroh Masykur, Umar Jundullah Maziya, Yulianda Mega Yulia Rusmayanti Michelle Anisa Misnasari, Putri Priela Mochammad Istiadjid Eddy Santoso Mokhamad Fahmi Rizki Syaban Mondiani, Yeni Quinta Muhammad Welly Dafif Nadia Artha Dewi Nadiya Elfira Bilqis, Nadiya Elfira Nasution, Ali Napiah Nata Sanjaya Nectarine Natasya Regitta Yasmin Nidia Suriani Nurvia Andriani Petrarizky, Alfred Julius Pramesti, Fathia Annis Pratiwi, Made Dinda Pringga, Gutama Arya Pudji, Rosalyna Purbasari, Bethasiwi Putri, Dwi Sandhi Aulia Pramesti Putri, Laily Ardhianti Putri, Mutiara Kristiani R, Rahmad Rahma, Annisa Rahmasari, Herisa Rahmawati, Dessika Raisa, Neila Reza Rachmantoko Rislan Faiz Muhammad Rislan Faiz Muhammad Ristiawan Muji Laksono Rizki Rahamatullah Noer Rodhiyan Rakhmatiar Rulli Rosandi Safira Dita Arviana Sari, Atika Windra Sari, Diane Tantia Sari, Diane Tantia Sela Pricilia Siti Nurlaela Sri Budhi Rianawati Sri Budhi Rianawati, Sri Budhi Sri Budi Rianawati Suratmono, Mia Fajarningtyas Syafiatul Azizah Titin Andri Wihastuti Tri Wahju Astuti, Tri Wahju Vely Eva Meria Wa Ode Intan Nur Octina Wahyuni Ramadhani Suaib Widiatmoko, Arif Widodo Mardi Santoso Widodo Mardi Santoso, Widodo Mardi Wirathmawati, Andina Yudiansyah, Anggi Gilang Yuyun Yueniwati Zahra, Farah Shabri Alifia Zamroni Afif