Rattanawong, Wanakorn

Preferred name

Alternative Name

Rattanawong, W.

Main Affiliation

Faculty of Medicine

wanakorn.ra@kmitl.ac.th

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Unusual thalamic mass and subsequent gelatinous pseudocysts in an immunocompetent host: A case report
(2022-01-01)
Watanabe, Apapatra Akiko
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Hemachudha, Pasin
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Rattanawong, Wanakorn
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Pongpitakmetha, Thanakit
Cryptococcal meningoencephalitis often occurs in an immunocompromised host with several known neurological manifestations including space-occupying lesions, meningitis or meningoencephalitis. Here, we describe a 38-year-old previously healthy durian farm owner with cryptococcoma and subsequent development of cryptococcus gelatinous pseudocyst after receiving high doses of intravenous dexamethasone to treat mass lesion presumed to be a malignant process. An MRI scan of the head demonstrated a 2-cm heterogeneous solitary enhancing cystic lesion at the right thalamus. Progression of neurological deficit and another repeat imaging showing typical appearance of gelatinous pseudocyst. Lumbar puncture found markedly elevated pressure and cryptococcal antigen strongly positive confirming the diagnosis. He was immediately started on amphotericin B and flucytosine for cryptococcus meningoencephalitis with partial improvement in his vision. This report highlights consideration of cryptococcal infection in an immunocompetent host to avoid delays in diagnosis and treatment.
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A case of successive development of possible acute necrotizing encephalopathy after COVID-19 pneumonia
(2022-03-01)
Hemachudha, Pasin
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Pongpitakmetha, Thanakit
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Rattanawong, Wanakorn
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Thanapornsungsuth, Poosanu
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Joyjinda, Yutthana
COVID-19 infection often results in an excessive inflammatory response with a spectrum of neurological manifestations. Here, we describe an 81-year-old female with severe COVID-19 pneumonia and subsequent alteration of consciousness after high-dose intravenous dexamethasone and remdesivir. A non-contrast head computed tomography (CT) demonstrated bilateral hypodensities involving bilateral cerebellar hemispheres, thalami, cerebral peduncles and medial parieto-occipital areas. There was no improvement and repeat CT showed progression with findings suggestive of acute necrotizing encephalopathy. Interleukin-6 levels were initially normal; however, subsequent levels were found to be markedly elevated. Acute necrotizing encephalopathy associated with COVID-19 may occur in the setting of severe pneumonia and may represent an immune-mediated process involving inflammatory cytokines such as interleukin-6.
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Fluorouracil-induced leukoencephalopathy mimicking neuroleptic malignant syndrome: a case report
(2023-12-01)
Hemachudha, Pasin
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Rattanawong, Wanakorn
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Pongpitakmetha, Thanakit
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Phuenpathom, Warongporn
Background: Fluorouracil-induced leukoencephalopathy is a rare complication and has been reported to present as confusion, oculomotor abnormality, ataxia, and parkinsonism; however, there is no previous report of a presentation mimicking neuroleptic malignant syndrome. Acute cerebellar syndrome may occur, which can be explained by the extremely high accumulation of the drug in the cerebellum. However, presentation mimicking neuroleptic malignant syndrome similar to our case has never been reported. Case presentation: Here, we describe a 68-year-old Thai male presenting with advanced-stage cecal adenocarcinoma, as well as symptoms and signs indicative of neuroleptic malignant syndrome. He received two doses of intravenous metoclopramide 10 mg 6 hours before his symptoms occurred. Magnetic resonance imaging scan revealed signal hyperintensity within the bilateral white matter. Further evaluation showed that his thiamine level was extremely low. Thus, he was diagnosed with fluorouracil-induced leukoencephalopathy mimicking neuroleptic malignant syndrome. The concomitant fluorouracil-induced thiamine deficiency eventually leads to rapid depletion of thiamine and was considered a risk factor for fluorouracil-induced leukoencephalopathy. Conclusion: Fluorouracil-induced leukoencephalopathy is believed to be caused by insult causing mitochondrial dysfunction. However, the exact mechanism remains unknown, but our finding suggests that thiamine deficiency plays a crucial role in fluorouracil-induced leukoencephalopathy. Diagnosis is usually delayed due to a lack of clinical suspicion and results in significant morbidity requiring unnecessary investigations.
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Cerebral Gnathostomiasis: An Unusual Course of Recurrent Hemorrhagic Stroke
(2022-07-01)
Rattanawong, Wanakorn
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Hemachudha, Pasin
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Anukoolwittaya, Prakit
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Pongpitakmetha, Thanakit
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Teaching NeuroImage: Branching Dura Mater in Primary CNS ALK-Positive Anaplastic Large Cell Lymphoma
(2023-10-24)
Rattanawong, Wanakorn
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Tekarnjnavanit, Arnant
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Marukatat, Chayoot
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Hemachudha, Pasin
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Pongpitakmetha, Thanakit
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Teaching NeuroImage: An Unusual Cause of Deep Cerebral Venous Sinus Thrombosis
(2026-08-11)
Yolsiriwat, Chayanis
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Phuenpathom, Warongporn
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Hemachudha, Pasin
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Roongaraya, Pitchapa
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Songsiriritthigul, Weekit
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Understanding the genetics and neurology: an overview of adult neurogenetics
(2025-08-01)
Hemachudha, Pasin
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Anukoolwittaya, Prakit
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Pongpitakmetha, Thanakit
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Joyjinda, Yutthana
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Ruchisrisarod, Chanida
Neurogenetics investigates the genetic basis of neurological disorders. It encompasses conditions ranging from neurodegenerative diseases with predominantly polygenic risk genes, such as Alzheimer's and Parkinson's, to monogenic diseases and repeated expansion disorders within movement and neuromuscular disorders, such as Friedreich ataxia and muscular dystrophies. Significant advances in recent years that have revolutionized our understanding of disease mechanisms and paved the way for personalized medicine approaches are due to the field of neurogenetics, with its intricate relationship both with clinical and genetic research. Therefore, all neurologists, even in resource-limited settings, are aware of the critical genetic basis; standard molecular diagnostic techniques such as next-generation sequencing, whole exome, and whole genome sequencing; and possible therapeutic modalities of their field. This review will also touch on elements of the neurogenetic clinic in tertiary care, ethical considerations, and insight into ongoing research that would help improve patient care and enhance clinical outcomes.
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The case of a 26-year-old male with subacute progressive visual loss
(2024-01-01)
Pongpitakmetha, Thanakit
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Hemachudha, Pasin
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Rattanawong, Wanakorn
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Mystery of CNS Invasion in HaNDL Syndrome: A First Case Report with Positive PCR EBV in CSF
(2023-12-01)
Anukoolwittaya, Prakit
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Hemachudha, Pasin
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Pongpitakmetha, Thanakit
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Rattanawong, Wanakorn
Headache with neurological deficits and cerebrospinal fluid lymphocytosis (HaNDL) syndrome is a rare and ambivalent condition that mimics certain diseases like stroke, primary cerebral vasculitis, meningoencephalitis, and migraine with aura. The cause is believed to be viral invasion. However, none has demonstrated such a hypothesis. Here, we present the first case of this syndrome with a presentation of ataxia along with a clear evidence of the Epstein-Bar virus in the CSF. A 28-year-old female presented with a right-sided headache followed by a transient episode of ataxia for 2 weeks. Five days later, she developed right-sided ataxia with a severe headache that did not subside despite paracetamol intake. At the hospital, she developed right-sided hemianesthesia involving both the body and face. An emergency brain magnetic resonance imaging was done. However, it did not reveal any vascular or parenchymal lesion. She was diagnosed with stroke in the young and was admitted. Lumbar puncture was performed for further evaluation showing 200 white cells per μL, normal glucose and protein level. Polymerase chain reaction of the viral panel was done showing positive for Epstein-Barr virus. Serum workups were within normal range. The EEG revealed the presence of occasional intermittent bursts of polymorphic slow predominantly over the left cerebral hemisphere. Therefore, the diagnosis of the syndrome of transient headache and HaNDL was made. Gabapentin was given with significant improvement. In this study, we presented the first case of HaNDL with evidence of CNS invasion. We found that EBV might be a trigger factor to the development of cortical spreading depression which is responsible for the focal neurological deficit seen in the patient. This finding is significant since no other report has proven the existence of the virus in the CNS and had led to a further understanding of the pathophysiology of HaNDL.
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COVID-19 related acute necrotizing encephalopathy with extremely high interleukin-6 and RANBP2 mutation in a patient with recently immunized inactivated virus vaccine and no pulmonary involvement
(2022-12-01)
Pongpitakmetha, Thanakit
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Hemachudha, Pasin
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Rattanawong, Wanakorn
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Thanapornsangsuth, Poosanu
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Viswanathan, Anand
Background: We report the first case of COVID-19 associated acute necrotizing encephalopathy (ANE) without pulmonary disease in a patient with an extremely high interleukin-6 (IL-6) level and Ran Binding Protein 2 (RANBP2) mutation. Case presentation: A 29-year-old woman recently immunized with inactivated viral vaccine—BBIBP32-CorV (Sinopharm) presented with alteration of consciousness. Her body temperature was 37° Celsius, blood pressure 42/31 mmHg, heart rate 130 bpm, respiratory rate 20 per minute, and oxygen saturation 98%. Respiratory examination was unremarkable. Neurological examination revealed stupor but preserved brainstem reflexes. Non-contrast computerized tomography of the brain showed symmetrical hypodense lesions involving bilateral thalami and cerebellar hemispheres characteristic of ANE. No pulmonary infiltration was found on chest radiograph. SARS-CoV-2 was detected by PCR; whole genome sequencing later confirmed the Delta variant. RANBP2 gene analysis revealed heterozygous Thr585Met mutation. Serum IL-6 was 7390 pg/mL. Urine examination showed pyelonephritis. Her clinical course was complicated by seizure, septic shock, acute kidney injury, and acute hepatic failure. She later developed coma and passed away in 6 days. Conclusions: ANE is caused by cytokine storm leading to necrosis and hemorrhage of the brain. IL-6 was deemed as a prognostic factor and a potential treatment target of ANE in previous studies. RANBP2 missense mutation strongly predisposes this condition by affecting mitochondrial function, viral entry, cytokine signaling, immune response, and blood–brain barrier maintenance. Also, inactivated vaccine has been reported to precipitate massive production of cytokines by antibody dependent enhancement (ADE). The true incidence of COVID-19 associated ANE is not known as were the predictors of its development. We proposed these potential two factors (RANBP2 mutation and ADE) that could participate in the pathogenesis of ANE in COVID-19 apart from SARS-CoV2 infection by itself. Further study is needed to confirm this hypothesis, specifically in the post-vaccination period. Role of RANBP2 mutation and its application in COVID-19 and ANE should be further elaborated.

Rattanawong, Wanakorn

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