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The Successfulness of A Multidisciplinary Approach For Obstructive Sleep Apnea Susianti, Noor Alia; Nathania, Caroline Evanthe; Prodjohardjono, Astuti; Vidyanti, Amelia Nur; Gofir, Abdul; Setyaningsih, Indarwati; Setyaningrum, Cempaka Thursina Srie; Sutarni, Sri
Academic Hospital Journal Vol 7, No 1 (2025)
Publisher : Rumah Sakit Akademik Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22146/ahj.v7i1.103305

Abstract

Background: Obstructive Sleep Apnea (OSA) is a global problem that has an impact on health and quality of life (QOL). There are a lot of risk factors for OSA, i.e. anatomical abnormality and comorbidity. A multidisciplinary approach can improve the symptoms and the impact of OSA and QOL too.Materials and methods: This case report is structured according to The CARE (Case Report) guideline.Case: A male, 37 years old, came with the chief complaint of snoring for 6 years. The patient felt unfit and dissatisfied with his sleep (Sleep Condition Indicator: 2.5). This impacted the daily activities and caused excessive daytime sleepiness. He could fall asleep while doing activities (Epsworth Sleepiness Scale: 24). The condition was worsening and he was often found apnea during sleep. The patient’s body mass index was 38.3kg/m2 (type I obesity) and the neck diameter was 43 cm. The polysomnography showed sleep architectural abnormality and the patients suffered from moderate OSA (Apnea-Hipopnea Index: 23.7). The patient was hospitalized for 7 days and got a Continuous Positive Airway Pressure Device (CPAP). Anatomical abnormality was investigated but none needed surgical intervention. Metabolic syndrome intervention includes therapy for hypertension, dyslipidemia, and diabetes. Collaboration with a clinical nutritionist for nutritional intervention. After 7 days, the sleep quality, the symptoms, and the SCI score were improved (7.1). Conclusion: OSA risk factors are varied and needed to be identified. In addition to definitive therapy, management of comorbidities, such as metabolic syndrome, should be addressed. A multidisciplinary approach can thereby improve OSA, patient’s health, and QOL.
NYERI KEPALA PASCATRAUMA: TELAAH EPIDEMIOLOGI DAN PATOFISIOLOGI Setyaningsih, Indarwati; Kurniandari, Nindriya; Habibi, Muhammad Najmi; Sejahtera, Desin Pambudi
Majalah Kedokteran Neurosains Perhimpunan Dokter Spesialis Saraf Indonesia Vol 41 No 5: Edisi Suplemen Neurona Bekerjasama dengan JogjaCLAN 2025
Publisher : PERDOSNI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52386/neurona.v41i5.867

Abstract

Post-traumatic headache (PTH) is one of the most common complications following mild traumatic brain injury (TBI). Its clinical presentation often resembles primary headache disorders, such as migraine or tension-type headache; however, it possesses a more complex and multifactorial pathophysiological basis. This article aims to review the epidemiological aspects and pathophysiological mechanisms of PTH based on recent literature. Globally, more than 69 million individuals experience TBI each year, and up to two-thirds of patients with mild TBI are reported to develop PTH. While most cases are transient, approximately 15–25% progress to persistent PTH. The pathogenesis of PTH involves interactions among structural damage, neurometabolic dysfunction, and neuroinflammatory processes that trigger activation of the trigeminovascular system and both peripheral and central sensitization. Cervical factors, hyperadrenergic mechanisms, and disturbances in the descending pain modulatory system further exacerbate symptoms. Advanced neuroimaging studies such as diffusion tensor imaging (DTI), Voxel-based morphometry (VBM), and magnetic resonance spectroscopy (MRS) provide supporting evidence of axonal injury, cortical thinning, and neuronal metabolic abnormalities associated with symptom persistence. A deeper understanding of the interaction among structural, metabolic, and inflammatory dysfunctions may serve as the foundation for developing more effective diagnostic and therapeutic strategies to improve patient’s clinical outcome. Keywords: post-traumatic headache, traumatic brain injury, neuroinflammation, central sensitization, peripheral sensitization
Dementia Mimicking Presentation in Normopressure Hydrocephalus: A Case Report Susianti, Noor Alia; Nathania, Caroline Evanthe; Prodjohardjono, Astuti; Gofir, Abdul; Setyaningsih, Indarwati; Setyaningrum, Cempaka Thursina Srie; Sutarni, Sri; Putri, Vega Pratiwi
AKSONA Vol. 6 No. 1 (2026): JANUARY 2026
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/aksona.v6i1.70306

Abstract

Highlight: Normal pressure hydrocephalus (NPH) is characterized by gait apraxia, urinary incontinence, ventriculomegaly, and cognitive impairment that mimics dementia, potentially leading to misdiagnosis. Comprehensive assessment, including clinical examination, brain imaging, and CSF testing, is critical for distinguishing NPH from dementia. Early and prompt diagnosis and treatment of NPH are crucial for improving long-term outcomes.   ABSTRACT Introduction: Normal Pressure Hydrocephalus (NPH) can occur following Traumatic Brain Injury (TBI). It is characterized by ventricular enlargement and presents with a classic triad: gait apraxia, urinary incontinence, and cognitive impairment. Cognitive impairment in NPH often overlaps with other neurocognitive disorders, such as dementia, which frequently leads to misdiagnosis. Case: A 59-year-old man presented with progressive memory decline, bladder incontinence, and gait apraxia following a head trauma. A CT scan performed after the head trauma revealed an intracerebral hemorrhage in the right thalamus. One year later, the patient complained of gait disturbance, as well as urinary and fecal incontinence. His general examination was normal, but the neurological examination showed the presence of a primitive reflex, specifically, the glabellar sign—and the patient exhibited a gait apraxia, poor spontaneity, and slowed speech. Neurobehavioral assessment showed attention and orientation disturbances, sensory cortical aphasia, and dementia syndrome. A follow-up CT scan revealed cerebral atrophy with ventriculomegaly ex vacuo with cerebrospinal fluid leakage. The patient subsequently underwent ventriculoperitoneal shunt therapy, and the cognitive assessment score showed improvement after the procedure. Conclusion: Diagnosing an NPH remains challenging due to the overlap of its cognitive impairment symptoms with other neurocognitive disorders. Furthermore, the treatment response varies widely, posing a further obstacle for clinicians to effectively manage NPH patients. Although early and prompt diagnosis is crucial for successful therapy, it continues to pose a significant challenge for clinicians.