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Deciphering Developmental Epileptic Encephalopathies (DEE): Unravelling the Key Signs Suryawijaya, Evlyne Erlyana; Lokito, Shania
Medicinus Vol 13, No 3 (2024): June
Publisher : Fakultas Kedokteran Universitas Pelita Harapan

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19166/med.v13i3.8882

Background: Epilepsy, a chronic neurological disorder affecting over 50 million people worldwide, is marked by recurrent seizures and loss of consciousness. It is categorized based on EEG features, etiologies, and comorbidities. Developmental Encephalopathy (DE) involves developmental delays and early-onset seizures without causing developmental regression. In contrast, Epileptic Encephalopathy (EE) features severe epilepsy syndromes where frequent seizures result in developmental delays or regression.Methods: This review explores the clinical definitions, epidemiology, and diagnostic criteria for DE, EE, and DEEs. It covers their etiologies, clinical features, diagnostic methods, and treatment strategies, including genetic, structural, metabolic, and immune-related factors.Results: DE features developmental impairment with epilepsy, while EE involves severe epilepsy causing cognitive and behavioral dysfunction. DEEs are marked by early-onset severe epilepsy and EEG abnormalities that worsen developmental impairments. Essential diagnostic tools include EEG, neuroimaging, and genetic testing. Effective management requires personalized interventions to control seizures and address cognitive deficits.Conclusion: DEEs are a complex epilepsy subset with major developmental and cognitive challenges. Early diagnosis and targeted treatments are crucial for improving outcomes. Ongoing research into DEEs' genetic and pathophysiological mechanisms is key to enhancing understanding and management.

Deciphering Developmental Epileptic Encephalopathies (DEE): Unravelling the Key Signs Suryawijaya, Evlyne Erlyana; Lokito, Shania
Medicinus Vol. 13 No. 3 (2024): June
Publisher : Fakultas Kedokteran Universitas Pelita Harapan

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19166/med.v13i3.8882

Background: Epilepsy, a chronic neurological disorder affecting over 50 million people worldwide, is marked by recurrent seizures and loss of consciousness. It is categorized based on EEG features, etiologies, and comorbidities. Developmental Encephalopathy (DE) involves developmental delays and early-onset seizures without causing developmental regression. In contrast, Epileptic Encephalopathy (EE) features severe epilepsy syndromes where frequent seizures result in developmental delays or regression.Methods: This review explores the clinical definitions, epidemiology, and diagnostic criteria for DE, EE, and DEEs. It covers their etiologies, clinical features, diagnostic methods, and treatment strategies, including genetic, structural, metabolic, and immune-related factors.Results: DE features developmental impairment with epilepsy, while EE involves severe epilepsy causing cognitive and behavioral dysfunction. DEEs are marked by early-onset severe epilepsy and EEG abnormalities that worsen developmental impairments. Essential diagnostic tools include EEG, neuroimaging, and genetic testing. Effective management requires personalized interventions to control seizures and address cognitive deficits.Conclusion: DEEs are a complex epilepsy subset with major developmental and cognitive challenges. Early diagnosis and targeted treatments are crucial for improving outcomes. Ongoing research into DEEs' genetic and pathophysiological mechanisms is key to enhancing understanding and management.

Tuberculoma With Visual and Vestibular Symptoms in A β-Thalassemia Patient: A Case Report Suryawijaya, Evlyne Erlyana; Ariarini, Ni Nengah Rida; Diafiri, Dinda; Dewati, Eva; Sitorus, Freddy
Medicinus Vol. 14 No. 3 (2025): June
Publisher : Fakultas Kedokteran Universitas Pelita Harapan

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19166/med.v14i3.10163

Background: Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis, which can affect the lungs (pulmonary TB) as well as other organs (extrapulmonary TB), including the central nervous system (CNS). The number of TB cases in Indonesia remains high, with 969,000 cases reported in 2021. Tuberculoma is a manifestation of TB in the CNS, presenting as an intracranial mass due to the spread of TB from other organs. It is a rare and serious form of CNS TB infection. The presence of congenital β-thalassemia adds complexity to the pathogenesis, diagnosis, and treatment of tuberculoma. Case Description: A 25-year-old female with a history of β-thalassemia HbE intermedia with a major phenotype presented with the main complaint of blurred vision in the lower right visual field. The patient also experienced vertigo, headache, and a history of seizures. Examination revealed inferior right quadrantanopia, anemia, leukopenia, and thrombocytopenia. Imaging and CSF analysis supported a diagnosis of intracranial tuberculoma. The patient was treated with anti-TB medication and intravenous dexamethasone. Discussion: Patients with thalassemia may have an increased risk of TB infection, including CNS TB. Tuberculoma involves granuloma formation in the brain, often in the meninges and cerebrum. Its manifestations vary and can include headaches and seizures. Diagnosis is based on clinical history, radiological findings, and laboratory results. The patient’s symptoms and imaging findings supported a diagnosis of tuberculoma, for which anti-TB and neurorestorative therapy was administered. Conclusions: Tuberculoma, as a manifestation of CNS TB, presents with variable and non-specific symptoms. Visual field disturbances can be one of the presenting symptoms that aid in diagnosis. Clinical, radiological, and laboratory evaluations are necessary for prompt and accurate diagnosis. Treatment involves anti-TB therapy and dexamethasone. This case highlights the importance of early diagnosis and comprehensive management of complex extrapulmonary TB infections.

EFFECT OF LOW-DOSE BOTULINUM TOXIN ON HEMIFACIAL SPASM SEVERITY Wirawan, Clarissa; Siahaan, Yusak Mangara Tua; Suryawijaya, Evlyne Erlyana; Ketaren, Retno Jayantri
MNJ (Malang Neurology Journal) Vol. 12 No. 1 (2026): 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.2025.012.01.02

Background: Hemifacial spasm is a condition in which there are unilateral contractions of facial muscles. One of the most effective forms of treatment is botulinum toxin injections. However, this therapy only temporarily relieves symptoms, so repeated injections are necessary. This may place a significant economic strain on patients. Due to this, this study aims to see if low-dose botulinum toxin reduces the severity of hemifacial spasm. Objective: To find out whether there is an effect of low-dose botulinum toxin on the severity of hemifacial spasm. Methods: This study is a paired comparison test with a retrospective cohort design. Primary (HFS Score) and secondary (medical record) data was collected from hemifacial spasm patients at Siloam Hospitals Lippo Village Building B. Results: Data was collected from the 36 patients that fulfilled the inclusion and exclusion criteria. All patients were treated with 10 U or less of botulinum toxin. Results show that for HFS Clinical there was a decrease from a mean of 13,03 ± 2,077 to 6,44 ± 2,311 (p < 0,001), whereas HFS Subjective decreased from a mean of 401,53 ± 229,748 to 95,42 ± 151,607 (p < 0,001). Both components have a p-value < 0,001, making it statistically significant. Conclusion: Low-dose botulinum toxin affects the severity of hemifacial spasm in patients at Siloam Hospitals Lippo Village Building B.

Fluctuating Neurological Deficits in Severe Proximal Basilar Artery Stenosis: Conservative Management or Endovascular Angioplasty? Yong, Yee Wen; Puspitasari, Vivien; Suryawijaya, Evlyne Erlyana; Goenawan, Vonny Fibrianty
Acta Neurologica Indonesia Vol. 4 No. 3 (2026): Acta Neurologica Indonesia
Publisher : Departemen Neurologi Fakultas Kedokteran Universitas Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.69868/ani.v4i3.142

Introduction : Symptomatic basilar artery (BA) stenosis is a high-risk cause of posterior circulation ischemia with potential for recurrent events despite optimal medical therapy. The decision between conservative treatment and endovascular angioplasty remains challenging, particularly in patients with fluctuating symptoms. Case Report : A 62-year-old man with hypertension, poorly controlled type 2 diabetes mellitus, and prior ischemic stroke presented with a two-month history of oscillopsia, intermittent headache, and transient left-sided weakness. Symptoms progressed to persistent imbalance, diplopia, and gait instability. Brain imaging demonstrated acute infarctions in the left thalamus and right anterior pons, multiple chronic posterior circulation infarcts, occlusion of the right vertebral artery, and severe proximal BA stenosis. Digital subtraction angiography (DSA) confirmed approximately 90% symptomatic proximal BA stenosis with reduced flow to the right anterior inferior cerebellar artery. Despite risk factor control, the patient continued to experience symptoms that significantly interfered with daily activities. Given the high procedural risk, conservative management was chosen with close monitoring. A three-month observation period with repeat DSA was planned to reassess the need for angioplasty. Discussion : This case highlights the unstable course of severe BA stenosis despite medical therapy. Although angioplasty may improve perfusion, BA interventions carry substantial risk due to brainstem perforators, with perforator infarction from “snow-plow” effect during angioplasty being a major concern, particularly in proximal lesions. Conclusion : Severe symptomatic BA stenosis presents a challenging therapeutic dilemma. Short-term observation with planned reassessment may be appropriate, but progressive symptoms require close follow-up and early consideration of endovascular treatment.

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