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All Journal MNJ (Malang Neurology Journal) Journal of Multidisciplinary Applied Natural Science
Bal’afif, Farhad
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Agriculture, Biological Sciences & Forestry Biochemistry, Genetics & Molecular Biology Chemical Engineering, Chemistry & Bioengineering Chemistry Energy Environmental Science Immunology & microbiology Materials Science & Nanotechnology Mathematics Neuroscience Physics

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CLINICAL ASPECT OF NORMAL PRESSURE HYDROCEPHALUS: WHAT TO DO? A LITERATURE REVIEW Nazwar, Tommy; Bal’afif, Farhad; Wardhana, Donny; Riskiyana, Riskiyana; Agustina, Kartika; Panjaitan, Christin
MNJ (Malang Neurology Journal) Vol. 11 No. 1 (2025): January
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.2025.011.01.14

Abstract

Normal pressure hydrocephalus (NPH) is a medical condition characterized by the enlargement of brain ventricles and associated clinical manifestations, including gait disturbance, cognitive impairment, and urinary incontinence. In many cases, NPH is often misdiagnosed or diagnosed late due to its symptoms closely resembling those seen in other neurological conditions. Therefore, a comprehensive understanding of the clinical characteristics of NPH is crucial. This article aims to present an in-depth literature review on the clinical aspects of NPH and offer valuable insights to clinicians regarding the appropriate approach to diagnosing and managing patients with NPH. Gait apraxia is usually the first symptom, followed by incontinence and cognitive impairment, particularly in attention and memory. The diagnosis of NPH follows specific criteria, classifying patients as "possible" or "probable." Imaging examinations, such as computed tomography (CT) scans and magnetic resonance imaging (MRI), are essential to assess ventricular size and identify radiological findings such as ventriculomegaly, disproportionately enlarged subarachnoid space hydrocephalus (DESH), callosal angle, temporal cornu enlargement, and white matter changes. NPH can be managed through conservative care, ventriculoperitoneal (VP) shunt surgery, and, in select cases, endoscopic third ventriculostomy (ETV). VP shunt surgery is the main surgical option, offering different valve choices such as fixed-pressure, programmable-pressure, and overdrainage prevention mechanisms. VP shunts have been shown to effectively relieve NPH symptoms, with lumbo-peritoneal (LP) shunts considered less favorable due to higher complications. ETV is a possibility for specific patients.
Furosemide Increases GABAA Receptor Activity via Antagonism to Sodium-Potassium-Chloride Cotransporter 1 In Silico and In Vivo Siregar, Marsintauli Hasudungan; Nurdiana, Nurdiana; Bal’afif, Farhad; Djajalaksana, Susanthy; Setiawansyah, Arif
Journal of Multidisciplinary Applied Natural Science Articles in Press
Publisher : Pandawa Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.47352/jmans.2774-3047.365

Abstract

GABAA receptor dysfunction and altered chloride homeostasis significantly contribute to seizure pathophysiology, with the sodium-potassium-chloride cotransporter 1 (NKCC1) playing a crucial role in regulating neuronal excitability. This study investigated furosemide's capacity to enhance GABAA receptor activity through NKCC1 antagonism and evaluated its therapeutic profile in combination with diazepam for seizure management. Comprehensive molecular docking analyses were conducted to assess binding affinities of furosemide and diazepam to NKCC1, followed by in vivo experiments using pentylenetetrazol-induced seizure models to evaluate GABAA receptor expression, seizure duration, and multiple pathophysiological biomarkers. Molecular analysis revealed that furosemide demonstrated measurable NKCC1 binding capacity (binding energy: -7.09 kcal/mol; Ki: 6.34 µM), though significantly lower affinity compared to diazepam (binding energy: -7.83 kcal/mol; Ki: 1.81 µM). The furosemide-diazepam combination exhibited complex competitive binding interactions, with furosemide substantially reducing diazepam's NKCC1 binding affinity. NKCC1 antagonism by furosemide effectively enhanced GABAA receptor expression by 29.8 ± 1.60% when used alone and 37.60 ± 2.0% in combination with diazepam. However, combination therapies resulted in significantly longer seizure durations (80 ± 3.0 s) compared to diazepam monotherapy (42.5 ± 2.10 s), suggesting antagonistic interactions on acute seizure suppression that may reflect altered chloride gradients or competitive pharmacokinetic effects. Despite reduced efficacy in seizure termination, combination therapy demonstrated selective advantages in other pathophysiological domains, including superior blood-brain barrier protection (reduced albumin level to 90.90 ± 2.70 µg/mL) and reduced excitotoxic damage. These findings indicate that furosemide-diazepam combination therapy presents a complex therapeutic profile characterized by trade-offs between acute seizure control and neuroprotective mechanisms. The data suggest potential utility in maintenance therapy or prevention of seizure-related complications rather than acute seizure termination, warranting further investigation into temporal optimization strategies and dose modifications.
Co-Authors Arif Setiawansyah Djajalaksana, Susanthy Kartika Agustina, Kartika Nazwar, Tommy Nurdiana Nurdiana Panjaitan, Christin Riskiyana, Riskiyana Siregar, Marsintauli Hasudungan Wardhana, Donny