Rattanawong, Wanakorn
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Preferred name
Rattanawong, Wanakorn
Alternative Name
Rattanawong, W.
Main Affiliation
Email
wanakorn.ra@kmitl.ac.th
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Item type:Publication, A case of successive development of possible acute necrotizing encephalopathy after COVID-19 pneumonia(2022-03-01) ;Hemachudha, Pasin ;Pongpitakmetha, Thanakit; ;Thanapornsungsuth, PoosanuJoyjinda, YutthanaCOVID-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. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Neurofilament light is associated with clinical outcome and hemorrhagic transformation in moderate to severe ischemic stroke(2023-01-01); ;Ongphichetmetha, Tatchaporn ;Hemachudha, ThiravatThanapornsangsuth, PoosanuBackground: Ischemic stroke is a leading cause of morbidity and mortality worldwide. One possible predictor is the use of biomarkers especially neurofilament light chain (NFL). Objectives: To explore whether NFL could predict clinical outcome and hemorrhagic transformation in moderate to severe stroke. Design: Single center prospective cohort study. Methods: Fifty-one moderate to severe ischemic stroke patients were recruited. Blood NFL was obtained from patients at admission (First sample) and 24-96 hours later (Second sample). NFL was analyzed with the ultrasensitive single molecule array (Simoa). Later, we calculated incremental rate NFL (IRN) by changes in NFL per day from baseline. We evaluated National Institute of Health stroke scale (NIHSS), modified Rankins score (mRs), and the presence of hemorrhagic transformation (HT). Results: IRN was found to be higher in patients with unfavorable outcome (7.12 vs 24.07, P =.04) as well as Second sample (49.06 vs 71.41, P =.011), while NFL First sample was not significant. IRN had a great correlation with mRS (r =.552, P <.001). Univariate logistic regression model showed OR of IRN and Second sample to be 1.081 (95% CI 1.016-1.149, P =.013) and 1.019 (1.002-1.037, P =.03), respectively. Multiple logistic regression model has shown to be significant. In receiver operating analysis, IRN, Second sample, combined IRN with NIHSS and combined Second sample with NIHSS showed AUC (.744, P =.004; 0.713, P =.01; 0.805, P <.001; 0.803, P <.001, respectively). For HT, First sample and Second sample had significant difference with HT (Z = 2.13, P =.033; Z = 2.487, P =.013, respectively). Conclusion: NFL was found to correlate and predict clinical outcome. In addition, it was found to correlate with HT. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Understanding the genetics and neurology: an overview of adult neurogenetics(2025-08-01) ;Hemachudha, Pasin ;Anukoolwittaya, Prakit ;Pongpitakmetha, Thanakit ;Joyjinda, YutthanaRuchisrisarod, ChanidaNeurogenetics 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. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Neurofilament light chain for classifying the aetiology of alteration of consciousness(2023-01-01) ;Ongphichetmetha, Tatchaporn ;Thanapornsangsuth, Poosanu ;Luechaipanit, Watayuth ;Loymunkong, NattawanNeurofilament light chain has become a promising biomarker for neuroaxonal injury; however, its diagnostic utility is limited to chronic disorders or specific contexts. Alteration of consciousness is a common clinical problem with diverse aetiologies, many of which require timely diagnoses. We evaluated the value of neurofilament light chain alone, as well as creating diagnostic models, in distinguishing causes of alteration of consciousness. Patients presenting with alteration of consciousness were enrolled. Initial clinical data of each participant were evaluated by a neurologist to give a provisional diagnosis. Each participant subsequently received advanced investigations and follow-up to conclude the final diagnosis. All diagnoses were classified into a structural or non-structural cause of alteration of consciousness. Plasma and cerebrospinal fluid levels of neurofilament light chain were measured. Cerebrospinal fluid neurofilament light chain and other clinical parameters were used to develop logistic regression models. The performance of cerebrospinal fluid neurofilament light chain, the neurologist's provisional diagnosis, and the model to predict the final diagnosis were compared. For the results, among 71 participants enrolled, 67.6% and 32.4% of their final diagnoses were classified as structural and non-structural, respectively. Cerebrospinal fluid neurofilament light chain demonstrated an area under the curve of 0.75 (95% confidence interval 0.63-0.88) which was not significantly different from a neurologist's provisional diagnosis 0.85 (95% confidence interval 0.75-0.94) (P = 0.14). The multivariable regression model using cerebrospinal fluid neurofilament light chain and other basic clinical data achieved an area under the curve of 0.90 (95% confidence interval 0.83-0.98). In conclusion, neurofilament light chain classified causes of alteration of consciousness with moderate accuracy. Nevertheless, including other basic clinical data to construct a model improved the performance to a level that was comparable to clinical neurologists. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, 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 ;Hemachudha, Pasin; ;Thanapornsangsuth, PoosanuViswanathan, AnandBackground: 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.
