Idiopathic Posterior Reversible Encephalopathy Syndrome (PRES) in a 4-Month-Old Infant: A Case Report

Idiopathic Posterior Reversible Encephalopathy Syndrome (PRES) in a 4-Month-Old Infant: A Case Report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Idiopathic Posterior Reversible Encephalopathy Syndrome (PRES) in a 4-Month-Old Infant: A Case Report Mehdi Oudrhiri Safiani, Hamza Zarouali, Saad El Harrak, Laarbi Ed Dafali, and 4 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8731584/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 16 You are reading this latest preprint version Abstract Posterior Reversible Encephalopathy Syndrome (PRES) is a clinico–radiological syndrome characterized by acute neurological manifestations related to reversible vasogenic cerebral edema. Although increasingly recognized in pediatric populations, it remains exceptionally rare in infants younger than six months, in whom the diagnosis may be particularly challenging. We report the case of a 4-month-old infant with no significant medical history admitted for recurrent generalized tonic-clonic seizures in an afebrile context. Initial clinical, biological, and cranial computed tomography assessments were unremarkable. Brain MRI revealed imaging features consistent with PRES. An extensive etiological workup, including metabolic, infectious, autoimmune, and toxicological investigations, was negative, supporting the diagnosis of idiopathic PRES. The patient responded favorably to antiepileptic therapy, with no recurrence of seizures. This case underscores the importance of considering PRES in the differential diagnosis of seizures in early infancy, even in the absence of identifiable risk factors. Posterior Reversible Encephalopathy Syndrome (PRES) 4 months Seizure Idiopathic Case Report. Figures Figure 1 Figure 2 Introduction Posterior Reversible Encephalopathy Syndrome (PRES) is a rare but potentially serious neurological condition ( 1 ). It typically presents with acute neurological manifestations—including headache, visual disturbances, seizures, and altered consciousness—and is characterized by radiological abnormalities that predominantly involve the parieto-occipital regions ( 2 ). Although several studies have investigated PRES in pediatric populations ( 3 , 4 , 5 ), it remains infrequent in children and exceptionally rare in infancy. To our knowledge, no cases have been reported in infants younger than six months. We herein describe an idiopathic case of PRES in a 4-month-old infant admitted for recurrent seizures. Case Report We present the case of a 4-month-old male infant with no significant medical history. Pregnancy was full-term and medically monitored, with no reported exposure to medications, toxins, or infectious diseases. Delivery was vaginal and uncomplicated, with immediate neonatal crying. No neonatal infections were reported. Apgar scores were 10 at 1, 3, 5, and 10 minutes. Psychomotor development was appropriate for age, including adequate head control. He was the youngest of four siblings, all in good health. The mother (G5P4) reported no consanguinity or notable familial medical conditions. Symptoms began on the day of admission, with recurrent spontaneous generalized tonic-clonic seizures in an afebrile context. Between episodes, the infant had postictal recovery and preserved consciousness. This presentation prompted an emergency department consultation. On arrival, neurological examination showed a conscious, interactive infant without sensory or motor deficits. Pupillary responses were normal, and no seizure activity was observed during the assessment. There were no signs of raised intracranial pressure, including bulging fontanelle or projectile vomiting. Respiratory examination revealed eupnea with an oxygen saturation of 97% on room air and clear auscultation. Hemodynamic status was stable (blood pressure 100/70 mmHg; heart rate 120 bpm; warm extremities). The infant was afebrile (36.5°C), and capillary blood glucose was 1.9 g/L. Muscle tone, including the lower limbs, was normal. The infant was admitted to the pediatric neurology unit for further evaluation. Initial cranial computed tomography (CT) was normal. Additional seizure episodes occurred, resolving spontaneously or after midazolam administration (0.15 mg/kg), with complete recovery between episodes. Phenobarbital (20 mg/kg) was initiated, and a nasogastric tube was placed for airway protection during convulsions. Given concern for impending status epilepticus, the patient was transferred to the pediatric intensive care unit (PICU) for close monitoring and management. Upon PICU admission, the patient was actively seizing, with perioral cyanosis and oral frothing. Heart rate increased to 200 beats per minute, and blood pressure transiently rose to 120/70 mmHg, with warm extremities. The infant remained afebrile (36.5°C), and capillary blood glucose was 1.7 g/L. A bolus of midazolam (0.15 mg/kg) resulted in rapid seizure cessation, normalization of heart rate to 140 bpm, and full recovery of consciousness. Continuous non-invasive monitoring was instituted and peripheral venous access was secured. Phenobarbital was continued, and sodium valproate was introduced as second-line antiepileptic therapy, with strict hepatic monitoring given the patient’s age. No further seizures occurred after initiation of dual therapy. A repeat cranial CT scan remained normal (Fig. 1 ). Lumbar puncture showed normal cerebrospinal fluid findings. Given persistent diagnostic uncertainty, brain magnetic resonance imaging (MRI) was performed and revealed features characteristic of Posterior Reversible Encephalopathy Syndrome (Fig. 2 ). The lesion showed hyperintensity on FLAIR (A) and diffusion-weighted (B) sequences, with corresponding hypointensity on the ADC map (C), consistent with recent cerebral hypoperfusion. MRI demonstrated bilateral, closely symmetrical cortico-subcortical signal abnormalities in the occipital lobes, with hyperintensity on T2-weighted and FLAIR sequences, no true diffusion restriction on DWI, and preserved ADC values—findings consistent with vasogenic edema. A comprehensive etiological assessment for PRES was undertaken, including metabolic, hepatic, and renal panels, as well as a complete blood count to exclude leukemia. All investigations were normal. There was no evidence of nephrotic syndrome or an infectious etiology. Blood pressure monitoring did not reveal sustained arterial hypertension outside seizure episodes. HIV, HBV, and HCV serologies were negative, as were autoimmune markers including p-ANCA, ANA, and others. Toxicology screening was negative for exogenous substances. Interictal electroencephalography performed 48 hours after stabilization showed no epileptiform discharges. This does not exclude an acute epileptic process, as interictal recordings may be normal outside ictal and immediate postictal periods, particularly in acute symptomatic seizures. We concluded that the recurrent seizures were secondary to idiopathic PRES in this 4-month-old infant. The clinical course was favorable under treatment, with no recurrence of seizures. The patient was transferred back to the pediatric neurology unit for continued care. Short-term follow-up at one month showed persistent clinical stability. Table 1 Timeline of clinical events Time point Events Day 0 – Morning Sudden onset of recurrent spontaneous generalized tonic–clonic seizures in an afebrile context, with preserved consciousness and postictal recovery between episodes. Day 0 – ED admission Neurological examination: conscious, interactive infant, no focal deficits. Normal pupils. No signs of raised intracranial pressure. Stable respiratory and hemodynamic status (BP 100/70 mmHg, HR 120 bpm, SpO₂ 97% on room air). Afebrile (36.5°C). Capillary blood glucose 1.9 g/L. Day 0 – Neurology unit Admission for evaluation. Initial cranial CT scan normal. Recurrent seizures occurred, resolving spontaneously or after midazolam (0.15 mg/kg). Phenobarbital loading dose (20 mg/kg) initiated. Day 0 – PICU admission Transfer due to concern for impending status epilepticus. Active seizure with perioral cyanosis and frothing. Transient tachycardia (HR 200 bpm) and blood pressure elevation (120/70 mmHg). Midazolam bolus (0.15 mg/kg) led to rapid seizure cessation and full recovery. Continuous monitoring established. Day 0–1 Phenobarbital continued. Sodium valproate introduced as second-line antiepileptic therapy with close hepatic monitoring. No further seizures observed. Day 1 Repeat cranial CT scan normal. Lumbar puncture revealed normal cerebrospinal fluid findings. Day 2 Brain MRI performed due to diagnostic uncertainty: bilateral symmetrical cortico-subcortical occipital hyperintensities on T2 and FLAIR sequences, no diffusion restriction on DWI, preserved ADC values—consistent with PRES. Day 2–3 Extensive etiological workup: metabolic, hepatic, renal, hematological, infectious, autoimmune, and toxicological investigations all normal. No sustained hypertension outside seizure episodes. Day 3 Interictal EEG (48 h after stabilization) showed no epileptiform discharges. Discussion PRES is a clinico-radiological syndrome presenting with non-specific neurological symptoms—such as headache, visual disturbances, focal deficits, seizures, and altered consciousness—accompanied by characteristic imaging findings ( 1 , 2 ). While well described in adults and older children, it remains exceptionally rare in early infancy ( 6 ). The pathophysiology of PRES remains incompletely understood, and two principal mechanisms are classically proposed ( 7 ): The hyperperfusion theory postulates failure of cerebral autoregulation in the setting of acute blood pressure elevation, leading to blood–brain barrier disruption and vasogenic edema ( 8 ), particularly in the posterior circulation where sympathetic innervation is less developed ( 9 ). The endothelial dysfunction theory suggests a primary injury of the cerebral endothelium due to circulating toxins (endogenous or exogenous), inflammatory mediators, sepsis, autoimmune processes, or cytotoxic drugs, resulting in increased vascular permeability and secondary hypertension ( 10 ). Current evidence indicates that these mechanisms may coexist ( 7 ), with relative contributions varying across etiologies and patient populations. In pediatric patients, PRES is most commonly associated with renal disease, severe hypertension, immunosuppressive or chemotherapeutic agents, autoimmune disorders, and severe infections ( 11 ). However, normotensive PRES has been increasingly reported in children, suggesting that endothelial dysfunction alone may be sufficient to induce vasogenic edema even in the absence of sustained hypertension ( 12 ). In the present case, the documented blood pressure elevation occurred exclusively during active seizures, suggesting a seizure-related sympathetic surge rather than sustained arterial hypertension. Whether seizures were the primary trigger of PRES through acute hemodynamic fluctuations, or an early manifestation of evolving vasogenic edema, cannot be formally determined and likely reflects a bidirectional interaction. In early infancy, immaturity of cerebrovascular autoregulation and reduced sympathetic innervation of the posterior circulation may facilitate blood–brain barrier disruption even during short-lasting hemodynamic fluctuations ( 12 ). According to published pediatric PRES causality frameworks, our patient fulfills criteria for idiopathic PRES after exclusion of hypertensive, renal, infectious, toxic, metabolic, and autoimmune etiologies. Seizures are the most frequent presenting manifestation of pediatric PRES ( 3 , 4 , 5 ). Visual symptoms and encephalopathy may be difficult to assess in very young infants, potentially delaying diagnosis. MRI remains the gold standard for diagnosis, typically revealing bilateral, symmetric parieto-occipital FLAIR hyperintensities reflecting vasogenic edema ( 13 ). Diffusion restriction, hemorrhage, and necrosis are considered atypical and are associated with more severe disease and possibly incomplete reversibility. Although follow-up MRI was not available in our patient, the typical radiological pattern combined with complete clinical recovery strongly supports a reversible vasogenic process consistent with PRES. Despite its name, PRES is not invariably reversible; neurological sequelae and death have been reported ( 14 ). The term “potentially reversible encephalopathy syndrome” has been proposed to reflect this variability ( 15 ). In our case, outcome was favorable, without neurological sequelae. Treatment involves both symptomatic control and targeted management of the underlying cause: Hemodynamic stabilization: For hypertension, aim to reduce blood pressure by 20–25% within two hours. Rapid reductions should be avoided. Neurological complications: Airway protection and rapid sequence intubation may be necessary during refractory status epilepticus or reduced consciousness. Etiological correction: Essential for long-term prognosis. Conclusion Posterior Reversible Encephalopathy Syndrome (PRES) is a rare and complex disorder with distinctive clinical and radiological features. This case illustrates an exceptionally early presentation of PRES in infancy—a scenario scarcely documented in the literature. Greater awareness among healthcare professionals, together with further research, is needed to clarify age-specific pathophysiological mechanisms and improve diagnostic and management strategies in pediatric PRES. Abbreviations ADC Apparent diffusion coefficient ANA Antinuclear antibodies ANCA Antineutrophil cytoplasmic antibodies CT Computed tomography DWI Diffusion-weighted imaging FLAIR Fluid-attenuated inversion recovery HBV Hepatitis B virus HCV Hepatitis C virus HIV Human immunodeficiency virus MRI Magnetic resonance imaging PICU Pediatric intensive care unit PRES Posterior reversible encephalopathy syndrome Declarations Ethics approval and consent to participate Ethical approval was not required for this case report in accordance with local institutional policies. Consent for publication Written informed consent was obtained from the the patient’s parent for publication of this case report and any accompanying images. Availability of data and materials Not applicable. Competing interests The authors declare that they have no competing interests. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Authors’ contributions MOS drafted and wrote the manuscript. HZ contributed to manuscript writing. SEH critically revised the manuscript. LED, HZi, and ME supervised the preparation of the manuscript. AB and SECEK approved the final version of the manuscript. All authors read and approved the final manuscript. Acknowledgements Not applicable. Authors’ information MOS is a resident in Anesthesiology and Critical Care Medicine at University Mohamed V of Rabat. His academic interests include neurocritical care, clinical research methodology, and case-based medical education. He also serves as a regular peer reviewer for BMC Neurology . References Chaudhuri J, et al. Posterior Reversible Leucoencephalopathy Syndrome: Case Series, Comments, and Diagnostic Dilemma. Curr Neurol Neurosci Rep vol. 2023;23(8):433–49. Liman TG, Bohner G, Heuschmann PU, Endres M, Siebert E. The clinical and radiological spectrum of posterior reversible encephalopathy syndrome: the retrospective Berlin PRES study. J Neurol. 2012;259(1):155–64. Cordelli D, Maria, et al. Posterior reversible encephalopathy syndrome in infants and young children. Eur J Pediatr Neurol. 2021;30:128–33. Habetz K, et al. Posterior reversible encephalopathy syndrome: a comparative study of pediatric versus adult patients. Pediatr Neurol. 2016;65:45–51. Chen T-H. Childhood posterior reversible encephalopathy syndrome: clinicoradiological characteristics, managements, and outcome. Front Pead. 2020;8:585. Cordelli DM, Marra C, Ciampoli L, et al. Posterior Reversible Encephalopathy Syndrome in infants and young children. Eur J Paediatr Neurol. 2021;30:128–33. 10.1016/j.ejpn.2020.10.009 . Bartynski WS. Posterior reversible encephalopathy syndrome, part 2: controversies surrounding pathophysiology of vasogenic edema. AJNR Am J Neuroradiol. 2008;29(6):1043–9. MacKenzie ET, Strandgaard S, Graham DI, Jones JV, Harper AM, Farrar JK. Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier. Circ Res. 1976;39(1):33–41. Ando Y, et al. Posterior Reversible Encephalopathy Syndrome: A Review of the Literature. Intern Med (Tokyo Japan) vol. 2022;61(2):135–41. Marra A, Vargas M, Striano P, Del Guercio L, Buonanno P, Servillo G. Posterior reversible encephalopathy syndrome: the endothelial hypotheses. Med Hypotheses. 2014;82(5):619–22. Ghali MGZ, Davanzo J, Leo M, Rizk E. Posterior reversible encephalopathy syndrome in pediatric patients: pathophysiology, diagnosis, and management. Leuk Lymphoma. 2019;60(10):2365–72. 10.1080/10428194.2019.1594210 . Ekinci F, Yildizdas D, Horoz OO, et al. Pediatric posterior reversible encephalopathy syndrome: Age related clinico-radiological profile and neurologic outcomes. Pediatr Int. 2023;65(1):e15562. 10.1111/ped.15562 . Bartynski WS, Boardman JF. Distinct Imaging Patterns and Lesion Distribution in Posterior Reversible Encephalopathy Syndrome. Am J Neuroradiol 1 août. 2007;28(7):1320–7. Burnett MM, Hess CP, Roberts JP, et al. Presentation of reversible posterior leukoencephalopathy syndrome in patients on calcineurin inhibitors. Clin Neurol Neurosurg. 2010;112:886–91. Narbone MC, Musolino R, Granata F, et al. PRES: posterior or potentially reversible encephalopathy syndrome? Neurol Sci. 2006;27:187–9. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Revision requested 13 Mar, 2026 Reviews received at journal 13 Mar, 2026 Reviews received at journal 12 Mar, 2026 Reviewers agreed at journal 12 Mar, 2026 Reviewers agreed at journal 11 Mar, 2026 Reviewers agreed at journal 08 Mar, 2026 Reviewers agreed at journal 07 Mar, 2026 Reviews received at journal 03 Mar, 2026 Reviewers agreed at journal 03 Mar, 2026 Reviews received at journal 03 Mar, 2026 Reviewers agreed at journal 25 Feb, 2026 Reviewers invited by journal 24 Feb, 2026 Editor invited by journal 30 Jan, 2026 Editor assigned by journal 30 Jan, 2026 Submission checks completed at journal 30 Jan, 2026 First submitted to journal 29 Jan, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8731584","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":596639870,"identity":"ca8147d4-d3f3-4fcd-afa0-ed264f15cc4f","order_by":0,"name":"Mehdi Oudrhiri Safiani","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABMUlEQVRIie3PsUrDQBjA8e+4weUk6xXUPIFwUgjZfBCXlIBTgoUsGWrIlCwtXQNKfQVFCI4JgXQ5dI0IWik46SAuERS8tB2KaQ1uIvcf7o7jftwdgEz2N2MYGBAANEkAqNggQA1XzBj7DQSzJcIrgn4gszBbbAiCgmqxmijUjN+63fstNcxQ8n6lw244SIvH0fGBEgpSuvF30ooOnZOIOYRxE9IBp6Dxa1PvxGM7ypCP+vyu9qrCamPCDMLgKEk2A0EKS6OdOLd9QTAK1hN1OIX0syIPz4Kc5vZZE4HChGx+CxHE79nna0ir/+TMH1ZMIdsOKNG41daNPLEvBElX/EXZMC8x+TD21aGJX18Cb0cb873bsufZo5ssnZRujdQiizmbjUnj+aW83xyWyWSy/90X1eVyNz7oFPIAAAAASUVORK5CYII=","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":true,"prefix":"","firstName":"Mehdi","middleName":"Oudrhiri","lastName":"Safiani","suffix":""},{"id":596639871,"identity":"1385825a-40b2-43cb-9ca5-ac76384c25f6","order_by":1,"name":"Hamza Zarouali","email":"","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":false,"prefix":"","firstName":"Hamza","middleName":"","lastName":"Zarouali","suffix":""},{"id":596639872,"identity":"ef13d7c3-8c35-4e05-b768-1b09d9b0e01f","order_by":2,"name":"Saad El Harrak","email":"","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":false,"prefix":"","firstName":"Saad","middleName":"El","lastName":"Harrak","suffix":""},{"id":596639873,"identity":"dc42ccf1-27ec-47c7-b572-54f33afa1b90","order_by":3,"name":"Laarbi Ed Dafali","email":"","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":false,"prefix":"","firstName":"Laarbi","middleName":"Ed","lastName":"Dafali","suffix":""},{"id":596639874,"identity":"9fab0b3b-b32a-4375-b38d-40c9b286f96a","order_by":4,"name":"Hicham Ziani","email":"","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":false,"prefix":"","firstName":"Hicham","middleName":"","lastName":"Ziani","suffix":""},{"id":596639875,"identity":"c9ccc5ac-08f7-4efe-9242-d5aa0d7888ab","order_by":5,"name":"Meryem Ennafiri","email":"","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":false,"prefix":"","firstName":"Meryem","middleName":"","lastName":"Ennafiri","suffix":""},{"id":596639876,"identity":"ba3cd53f-dcfe-4558-a55c-16976c0d5105","order_by":6,"name":"Aziza Bentalha","email":"","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":false,"prefix":"","firstName":"Aziza","middleName":"","lastName":"Bentalha","suffix":""},{"id":596639877,"identity":"49747dcb-d7a2-4d04-8c26-bb4a63eacdc4","order_by":7,"name":"Salma Ech Cherif El Kettani","email":"","orcid":"","institution":"Pediatric Intensive Care and Anestesiology Department CHU Ibn Sina, Rabat, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University of Rabat, Rabat, Morocco.","correspondingAuthor":false,"prefix":"","firstName":"Salma","middleName":"Ech Cherif El","lastName":"Kettani","suffix":""}],"badges":[],"createdAt":"2026-01-29 12:38:18","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8731584/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8731584/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":103582997,"identity":"1a2689ae-e56a-4d7d-bd04-4606f15697e3","added_by":"auto","created_at":"2026-02-27 10:37:13","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":272703,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eAxial brain CT scan revealing no parenchymal lesions or extra-axial collections.\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"floatimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8731584/v1/d5a4d3d24ff31d3cf29039f4.jpeg"},{"id":103582996,"identity":"d2ae67d0-7b2e-49ee-906a-41179ce94b93","added_by":"auto","created_at":"2026-02-27 10:37:13","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":221670,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eMRI identified a cortico-subcortical signal abnormality in the occipital lobes (thin arrows), bilaterally distributed with close symmetry.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eThe lesion showed hyperintensity on FLAIR (A) and diffusion-weighted (B) sequences, with corresponding hypointensity on the ADC map (C), consistent with recent cerebral hypoperfusion.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-8731584/v1/9817eeaeee00c87f7b71a964.png"},{"id":104399410,"identity":"ffc7fc9f-0161-4fd6-ad04-58a52be58647","added_by":"auto","created_at":"2026-03-11 12:05:59","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1016931,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8731584/v1/5be56818-6042-4785-99f9-4edeff59f32d.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Idiopathic Posterior Reversible Encephalopathy Syndrome (PRES) in a 4-Month-Old Infant: A Case Report","fulltext":[{"header":"Introduction","content":"\u003cp\u003ePosterior Reversible Encephalopathy Syndrome (PRES) is a rare but potentially serious neurological condition (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). It typically presents with acute neurological manifestations\u0026mdash;including headache, visual disturbances, seizures, and altered consciousness\u0026mdash;and is characterized by radiological abnormalities that predominantly involve the parieto-occipital regions (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eAlthough several studies have investigated PRES in pediatric populations (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e), it remains infrequent in children and exceptionally rare in infancy. To our knowledge, no cases have been reported in infants younger than six months. We herein describe an idiopathic case of PRES in a 4-month-old infant admitted for recurrent seizures.\u003c/p\u003e"},{"header":"Case Report","content":"\u003cp\u003eWe present the case of a 4-month-old male infant with no significant medical history. Pregnancy was full-term and medically monitored, with no reported exposure to medications, toxins, or infectious diseases. Delivery was vaginal and uncomplicated, with immediate neonatal crying. No neonatal infections were reported. Apgar scores were 10 at 1, 3, 5, and 10 minutes. Psychomotor development was appropriate for age, including adequate head control. He was the youngest of four siblings, all in good health. The mother (G5P4) reported no consanguinity or notable familial medical conditions.\u003c/p\u003e \u003cp\u003eSymptoms began on the day of admission, with recurrent spontaneous generalized tonic-clonic seizures in an afebrile context. Between episodes, the infant had postictal recovery and preserved consciousness. This presentation prompted an emergency department consultation. On arrival, neurological examination showed a conscious, interactive infant without sensory or motor deficits. Pupillary responses were normal, and no seizure activity was observed during the assessment. There were no signs of raised intracranial pressure, including bulging fontanelle or projectile vomiting. Respiratory examination revealed eupnea with an oxygen saturation of 97% on room air and clear auscultation. Hemodynamic status was stable (blood pressure 100/70 mmHg; heart rate 120 bpm; warm extremities). The infant was afebrile (36.5\u0026deg;C), and capillary blood glucose was 1.9 g/L. Muscle tone, including the lower limbs, was normal.\u003c/p\u003e \u003cp\u003eThe infant was admitted to the pediatric neurology unit for further evaluation. Initial cranial computed tomography (CT) was normal. Additional seizure episodes occurred, resolving spontaneously or after midazolam administration (0.15 mg/kg), with complete recovery between episodes. Phenobarbital (20 mg/kg) was initiated, and a nasogastric tube was placed for airway protection during convulsions. Given concern for impending status epilepticus, the patient was transferred to the pediatric intensive care unit (PICU) for close monitoring and management.\u003c/p\u003e \u003cp\u003eUpon PICU admission, the patient was actively seizing, with perioral cyanosis and oral frothing. Heart rate increased to 200 beats per minute, and blood pressure transiently rose to 120/70 mmHg, with warm extremities. The infant remained afebrile (36.5\u0026deg;C), and capillary blood glucose was 1.7 g/L. A bolus of midazolam (0.15 mg/kg) resulted in rapid seizure cessation, normalization of heart rate to 140 bpm, and full recovery of consciousness. Continuous non-invasive monitoring was instituted and peripheral venous access was secured. Phenobarbital was continued, and sodium valproate was introduced as second-line antiepileptic therapy, with strict hepatic monitoring given the patient\u0026rsquo;s age. No further seizures occurred after initiation of dual therapy.\u003c/p\u003e \u003cp\u003eA repeat cranial CT scan remained normal (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eLumbar puncture showed normal cerebrospinal fluid findings. Given persistent diagnostic uncertainty, brain magnetic resonance imaging (MRI) was performed and revealed features characteristic of Posterior Reversible Encephalopathy Syndrome (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003cem\u003eThe lesion showed hyperintensity on FLAIR (A) and diffusion-weighted (B) sequences, with corresponding hypointensity on the ADC map (C), consistent with recent cerebral hypoperfusion.\u003c/em\u003e \u003c/p\u003e \u003cp\u003eMRI demonstrated bilateral, closely symmetrical cortico-subcortical signal abnormalities in the occipital lobes, with hyperintensity on T2-weighted and FLAIR sequences, no true diffusion restriction on DWI, and preserved ADC values\u0026mdash;findings consistent with vasogenic edema.\u003c/p\u003e \u003cp\u003eA comprehensive etiological assessment for PRES was undertaken, including metabolic, hepatic, and renal panels, as well as a complete blood count to exclude leukemia. All investigations were normal. There was no evidence of nephrotic syndrome or an infectious etiology. Blood pressure monitoring did not reveal sustained arterial hypertension outside seizure episodes. HIV, HBV, and HCV serologies were negative, as were autoimmune markers including p-ANCA, ANA, and others. Toxicology screening was negative for exogenous substances.\u003c/p\u003e \u003cp\u003eInterictal electroencephalography performed 48 hours after stabilization showed no epileptiform discharges. This does not exclude an acute epileptic process, as interictal recordings may be normal outside ictal and immediate postictal periods, particularly in acute symptomatic seizures.\u003c/p\u003e \u003cp\u003eWe concluded that the recurrent seizures were secondary to idiopathic PRES in this 4-month-old infant. The clinical course was favorable under treatment, with no recurrence of seizures. The patient was transferred back to the pediatric neurology unit for continued care. Short-term follow-up at one month showed persistent clinical stability.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTimeline of clinical events\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"2\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTime point\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eEvents\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 0 \u0026ndash; Morning\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSudden onset of recurrent spontaneous generalized tonic\u0026ndash;clonic seizures in an afebrile context, with preserved consciousness and postictal recovery between episodes.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 0 \u0026ndash; ED admission\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNeurological examination: conscious, interactive infant, no focal deficits. Normal pupils. No signs of raised intracranial pressure. Stable respiratory and hemodynamic status (BP 100/70 mmHg, HR 120 bpm, SpO₂ 97% on room air). Afebrile (36.5\u0026deg;C). Capillary blood glucose 1.9 g/L.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 0 \u0026ndash; Neurology unit\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAdmission for evaluation. Initial cranial CT scan normal. Recurrent seizures occurred, resolving spontaneously or after midazolam (0.15 mg/kg). Phenobarbital loading dose (20 mg/kg) initiated.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 0 \u0026ndash; PICU admission\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eTransfer due to concern for impending status epilepticus. Active seizure with perioral cyanosis and frothing. Transient tachycardia (HR 200 bpm) and blood pressure elevation (120/70 mmHg). Midazolam bolus (0.15 mg/kg) led to rapid seizure cessation and full recovery. Continuous monitoring established.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 0\u0026ndash;1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePhenobarbital continued. Sodium valproate introduced as second-line antiepileptic therapy with close hepatic monitoring. No further seizures observed.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eRepeat cranial CT scan normal. Lumbar puncture revealed normal cerebrospinal fluid findings.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eBrain MRI performed due to diagnostic uncertainty: bilateral symmetrical cortico-subcortical occipital hyperintensities on T2 and FLAIR sequences, no diffusion restriction on DWI, preserved ADC values\u0026mdash;consistent with PRES.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 2\u0026ndash;3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eExtensive etiological workup: metabolic, hepatic, renal, hematological, infectious, autoimmune, and toxicological investigations all normal. No sustained hypertension outside seizure episodes.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eInterictal EEG (48 h after stabilization) showed no epileptiform discharges.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003ePRES is a clinico-radiological syndrome presenting with non-specific neurological symptoms\u0026mdash;such as headache, visual disturbances, focal deficits, seizures, and altered consciousness\u0026mdash;accompanied by characteristic imaging findings (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). While well described in adults and older children, it remains exceptionally rare in early infancy (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe pathophysiology of PRES remains incompletely understood, and two principal mechanisms are classically proposed (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e):\u003c/p\u003e \u003cp\u003eThe hyperperfusion theory postulates failure of cerebral autoregulation in the setting of acute blood pressure elevation, leading to blood\u0026ndash;brain barrier disruption and vasogenic edema (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e), particularly in the posterior circulation where sympathetic innervation is less developed (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe endothelial dysfunction theory suggests a primary injury of the cerebral endothelium due to circulating toxins (endogenous or exogenous), inflammatory mediators, sepsis, autoimmune processes, or cytotoxic drugs, resulting in increased vascular permeability and secondary hypertension (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eCurrent evidence indicates that these mechanisms may coexist (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e), with relative contributions varying across etiologies and patient populations.\u003c/p\u003e \u003cp\u003eIn pediatric patients, PRES is most commonly associated with renal disease, severe hypertension, immunosuppressive or chemotherapeutic agents, autoimmune disorders, and severe infections (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). However, normotensive PRES has been increasingly reported in children, suggesting that endothelial dysfunction alone may be sufficient to induce vasogenic edema even in the absence of sustained hypertension (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn the present case, the documented blood pressure elevation occurred exclusively during active seizures, suggesting a seizure-related sympathetic surge rather than sustained arterial hypertension. Whether seizures were the primary trigger of PRES through acute hemodynamic fluctuations, or an early manifestation of evolving vasogenic edema, cannot be formally determined and likely reflects a bidirectional interaction. In early infancy, immaturity of cerebrovascular autoregulation and reduced sympathetic innervation of the posterior circulation may facilitate blood\u0026ndash;brain barrier disruption even during short-lasting hemodynamic fluctuations (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eAccording to published pediatric PRES causality frameworks, our patient fulfills criteria for idiopathic PRES after exclusion of hypertensive, renal, infectious, toxic, metabolic, and autoimmune etiologies. Seizures are the most frequent presenting manifestation of pediatric PRES (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). Visual symptoms and encephalopathy may be difficult to assess in very young infants, potentially delaying diagnosis.\u003c/p\u003e \u003cp\u003eMRI remains the gold standard for diagnosis, typically revealing bilateral, symmetric parieto-occipital FLAIR hyperintensities reflecting vasogenic edema (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Diffusion restriction, hemorrhage, and necrosis are considered atypical and are associated with more severe disease and possibly incomplete reversibility. Although follow-up MRI was not available in our patient, the typical radiological pattern combined with complete clinical recovery strongly supports a reversible vasogenic process consistent with PRES.\u003c/p\u003e \u003cp\u003eDespite its name, PRES is not invariably reversible; neurological sequelae and death have been reported (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). The term \u0026ldquo;potentially reversible encephalopathy syndrome\u0026rdquo; has been proposed to reflect this variability (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). In our case, outcome was favorable, without neurological sequelae.\u003c/p\u003e \u003cp\u003eTreatment involves both symptomatic control and targeted management of the underlying cause:\u003c/p\u003e \u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003eHemodynamic stabilization: For hypertension, aim to reduce blood pressure by 20\u0026ndash;25% within two hours. Rapid reductions should be avoided.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eNeurological complications: Airway protection and rapid sequence intubation may be necessary during refractory status epilepticus or reduced consciousness.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eEtiological correction: Essential for long-term prognosis.\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003ePosterior Reversible Encephalopathy Syndrome (PRES) is a rare and complex disorder with distinctive clinical and radiological features. This case illustrates an exceptionally early presentation of PRES in infancy\u0026mdash;a scenario scarcely documented in the literature. Greater awareness among healthcare professionals, together with further research, is needed to clarify age-specific pathophysiological mechanisms and improve diagnostic and management strategies in pediatric PRES.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eADC\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eApparent diffusion coefficient\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eANA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAntinuclear antibodies\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eANCA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAntineutrophil cytoplasmic antibodies\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eCT\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eComputed tomography\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eDWI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eDiffusion-weighted imaging\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eFLAIR\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eFluid-attenuated inversion recovery\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHBV\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHepatitis B virus\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHCV\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHepatitis C virus\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHIV\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHuman immunodeficiency virus\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eMRI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eMagnetic resonance imaging\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ePICU\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003ePediatric intensive care unit\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ePRES\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003ePosterior reversible encephalopathy syndrome\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eEthical approval was not required for this case report in accordance with local institutional policies.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the the patient\u0026rsquo;s parent for publication of this case report and any accompanying images.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026rsquo; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eMOS drafted and wrote the manuscript. HZ contributed to manuscript writing. SEH critically revised the manuscript. LED, HZi, and ME supervised the preparation of the manuscript. AB and SECEK approved the final version of the manuscript. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026rsquo; information\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eMOS is a resident in Anesthesiology and Critical Care Medicine at University Mohamed V of Rabat. His academic interests include neurocritical care, clinical research methodology, and case-based medical education. He also serves as a regular peer reviewer for \u003cem\u003eBMC Neurology\u003c/em\u003e.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eChaudhuri J, et al. Posterior Reversible Leucoencephalopathy Syndrome: Case Series, Comments, and Diagnostic Dilemma. Curr Neurol Neurosci Rep vol. 2023;23(8):433\u0026ndash;49.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiman TG, Bohner G, Heuschmann PU, Endres M, Siebert E. The clinical and radiological spectrum of posterior reversible encephalopathy syndrome: the retrospective Berlin PRES study. J Neurol. 2012;259(1):155\u0026ndash;64.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCordelli D, Maria, et al. Posterior reversible encephalopathy syndrome in infants and young children. Eur J Pediatr Neurol. 2021;30:128\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHabetz K, et al. Posterior reversible encephalopathy syndrome: a comparative study of pediatric versus adult patients. Pediatr Neurol. 2016;65:45\u0026ndash;51.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChen T-H. Childhood posterior reversible encephalopathy syndrome: clinicoradiological characteristics, managements, and outcome. Front Pead. 2020;8:585.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCordelli DM, Marra C, Ciampoli L, et al. Posterior Reversible Encephalopathy Syndrome in infants and young children. Eur J Paediatr Neurol. 2021;30:128\u0026ndash;33. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.ejpn.2020.10.009\u003c/span\u003e\u003cspan address=\"10.1016/j.ejpn.2020.10.009\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBartynski WS. Posterior reversible encephalopathy syndrome, part 2: controversies surrounding pathophysiology of vasogenic edema. AJNR Am J Neuroradiol. 2008;29(6):1043\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMacKenzie ET, Strandgaard S, Graham DI, Jones JV, Harper AM, Farrar JK. Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier. Circ Res. 1976;39(1):33\u0026ndash;41.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAndo Y, et al. Posterior Reversible Encephalopathy Syndrome: A Review of the Literature. Intern Med (Tokyo Japan) vol. 2022;61(2):135\u0026ndash;41.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMarra A, Vargas M, Striano P, Del Guercio L, Buonanno P, Servillo G. Posterior reversible encephalopathy syndrome: the endothelial hypotheses. Med Hypotheses. 2014;82(5):619\u0026ndash;22.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGhali MGZ, Davanzo J, Leo M, Rizk E. Posterior reversible encephalopathy syndrome in pediatric patients: pathophysiology, diagnosis, and management. Leuk Lymphoma. 2019;60(10):2365\u0026ndash;72. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1080/10428194.2019.1594210\u003c/span\u003e\u003cspan address=\"10.1080/10428194.2019.1594210\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEkinci F, Yildizdas D, Horoz OO, et al. Pediatric posterior reversible encephalopathy syndrome: Age related clinico-radiological profile and neurologic outcomes. Pediatr Int. 2023;65(1):e15562. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1111/ped.15562\u003c/span\u003e\u003cspan address=\"10.1111/ped.15562\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBartynski WS, Boardman JF. Distinct Imaging Patterns and Lesion Distribution in Posterior Reversible Encephalopathy Syndrome. Am J Neuroradiol 1 ao\u0026ucirc;t. 2007;28(7):1320\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBurnett MM, Hess CP, Roberts JP, et al. Presentation of reversible posterior leukoencephalopathy syndrome in patients on calcineurin inhibitors. Clin Neurol Neurosurg. 2010;112:886\u0026ndash;91.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNarbone MC, Musolino R, Granata F, et al. PRES: posterior or potentially reversible encephalopathy syndrome? Neurol Sci. 2006;27:187\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Posterior Reversible Encephalopathy Syndrome (PRES), 4 months, Seizure, Idiopathic, Case Report.","lastPublishedDoi":"10.21203/rs.3.rs-8731584/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8731584/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003ePosterior Reversible Encephalopathy Syndrome (PRES) is a clinico\u0026ndash;radiological syndrome characterized by acute neurological manifestations related to reversible vasogenic cerebral edema. Although increasingly recognized in pediatric populations, it remains exceptionally rare in infants younger than six months, in whom the diagnosis may be particularly challenging.\u003c/p\u003e \u003cp\u003eWe report the case of a 4-month-old infant with no significant medical history admitted for recurrent generalized tonic-clonic seizures in an afebrile context. Initial clinical, biological, and cranial computed tomography assessments were unremarkable. Brain MRI revealed imaging features consistent with PRES. An extensive etiological workup, including metabolic, infectious, autoimmune, and toxicological investigations, was negative, supporting the diagnosis of idiopathic PRES. The patient responded favorably to antiepileptic therapy, with no recurrence of seizures.\u003c/p\u003e \u003cp\u003eThis case underscores the importance of considering PRES in the differential diagnosis of seizures in early infancy, even in the absence of identifiable risk factors.\u003c/p\u003e","manuscriptTitle":"Idiopathic Posterior Reversible Encephalopathy Syndrome (PRES) in a 4-Month-Old Infant: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-27 10:37:07","doi":"10.21203/rs.3.rs-8731584/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-13T13:01:16+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-13T06:17:11+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-12T13:47:31+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"273217266485484059882590774001518905969","date":"2026-03-12T09:52:10+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"147907919326941867581005753341836738159","date":"2026-03-12T02:59:05+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"329279896944528270343049129403363894645","date":"2026-03-09T00:21:51+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"80446540144358250777340167883241520365","date":"2026-03-08T01:54:45+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-03T14:42:06+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"6093255330802534926455986100567452833","date":"2026-03-03T14:23:09+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-03T06:38:47+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"326263017333597682992234009616672833915","date":"2026-02-26T03:56:46+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-02-24T07:05:27+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-01-30T12:50:16+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-30T07:56:34+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-30T07:54:59+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Neurology","date":"2026-01-29T11:55:26+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"ac5a16aa-998f-4387-aa47-93105bff1db0","owner":[],"postedDate":"February 27th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-05-18T22:38:16+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-27 10:37:07","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8731584","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8731584","identity":"rs-8731584","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}