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All Journal Berkala Ilmiah Kedokteran Duta Wacana Magna Neurologica
irfan pranowo
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Biochemistry, Genetics & Molecular Biology Health Professions Immunology & microbiology Medicine & Pharmacology Neuroscience Public Health

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CENTRAL VERTIGO SYNDROME AS A CLINICAL MANIFESTATION IN ALCOHOL INTOXICATION irfan pranowo
Berkala Ilmiah Kedokteran Duta Wacana Vol 3, No 2 (2018): BERKALA ILMIAH KEDOKTERAN DUTA WACANA
Publisher : Faculty of Medicine Universitas Kristen Duta Wacana

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (861.37 KB) | DOI: 10.21460/bikdw.v3i2.87

Abstract

ABSTRACT Background : Vertigo syndrome is one of the clinical features in patients with alcohol intoxication. Cerebellar dysfunction (ie, ataxia, sluured speech, and nystagmus) generally occurs in a state of toxicity with greater alcohol concentration, a condition caused by involvement in the brainstem. Among the neurological complications of alcoholism, brainstem lesions are often present in Wernicke-Korsakoff syndrome, cerebellar degeneration, and central pontine myelinolysis.3 Objective: To Describe a central vertigo case in alcohol intoxication patient Case Description: A 21-year-old male, with a neck complaint that feels left and right pulled, since 1 day before admission. felt appeared 8 times. followed with dizzines, mild-moderate intensity, with symptoms of heartburn and nausea. Patients is an alcohol drinkers since 8 years ago, and active smokers who can spend a day a pack of cigarettes. On examination was found sufficient nutritional status, blood pressure 117/73 mmHg, pulse 80x / minute, respiration 22x / minute, temperature 36,8o C, and scale VVS 2. From physical examination obtained vertical and bidirectional horizontal nystagmus. The results of routine blood laboratory examination found blood leukocyte level 12.12 x103 / uL, others in normal limit Therapy: injection omeprazole 1 amp / 12 hours, flunarizin 5 mg / 12 hours, alprazolam 0.5 mg / 24 hours. After 3 days treatment, he was discharged with clinical improvement. Conclusions: An Alcohol intoxication patients in the presence of central vertigo syndrome in this case showed clinical improvement after treatment, then patients were advised to routine control.
Haemorrhagic Transformation in Ischemic Stroke Induced by Polycythemia Vera: A Case Report Zalafi Kartika Azka; Irfan Pranowo
Magna Neurologica Vol. 4 No. 1 (2026): January
Publisher : Department of Neurology Faculty of Medicine Universitas Sebelas Maret

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20961/magnaneurologica.v4i1.2195

Abstract

Background: Polycythemia vera (PV) is a myeloproliferative neoplasm characterized by the overproduction of red blood cells. This can lead to hyperviscosity, which significantly increases the risk of thrombosis, which in turn increases the risk of ischemic stroke. There is currently no reported case of haemorrhagic transformation of PV-induced acute ischemic stroke in Indonesia. Case: A 62-year-old female was admitted to the emergency department after a sudden onset of left-sided weakness one hour before admission. She has a history of polycythemia vera, with prior hemoglobin levels reaching 22 g/dL, and had a previous ischemic stroke one year prior. On physical examination, the patient was alert, with a GCS of 15, blood pressure of 168/94 mmHg, left-sided hemiparesis, dysarthria, and facial drooping. Laboratory tests revealed elevated hemoglobin 16.8 g/dL, hematocrit 56%, platelets 466,000/µL, and leukocytes 20.4 x 10³/µL. A non-contrast head CT showed a hypodense lesion in the right temporoparietal lobe with a hyperdense spot, consistent with hemorrhagic transformation of a thromboembolic infarction in the right middle cerebral artery (MCA) region, an infarct in the left thalamus, and cerebral atrophy. Discussion: PV-induced ischemic strokes involve a confluence of hyperviscosity, endothelial activation, and platelet aggregation. The thickened blood compromises microcirculatory flow, particularly in the cerebral vascular, increasing embolic risks. HT occurs due to the reperfusion of ischemic tissues following the breakdown of the blood-brain barrier (BBB). Conclusion: Hemorrhagic transformation can develop in PV-induced acute ischemic stroke. Effective management requires a multidisciplinary approach, integrating acute stroke care, rigorous hematologic control, antihypertensive therapy, lifestyle modifications, and antiplatelet treatment.
Co-Authors Zalafi Kartika Azka