Perinatal Stroke in Two Neonates: Divergent Clinical Presentations From Early Seizures to Incidental Neuroimaging Detection

Perinatal Stroke in Two Neonates: Divergent Clinical Presentations From Early Seizures to Incidental Neuroimaging Detection | 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 Article Perinatal Stroke in Two Neonates: Divergent Clinical Presentations From Early Seizures to Incidental Neuroimaging Detection Yunis Mohamed, Hani Hassan Hassan, Naziha Elreih, Mohammad N.Almohammal Almohammal, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9315390/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Perinatal stroke is an important cause of neonatal neurological morbidity and may present with diverse clinical manifestations ranging from seizures to completely asymptomatic cases. Early recognition is challenging because many neonates demonstrate nonspecific or delayed symptoms. We report two neonates diagnosed with perinatal stroke during the first week of life. The first case presented on the third day of life with focal clonic seizures and was found to have a large infarction in the left middle cerebral artery territory with hemorrhagic transformation. The second neonate was admitted with respiratory distress and was later found to have cerebral infarction incidentally during routine cranial ultrasonography. These cases illustrate the variable clinical presentation of perinatal stroke and emphasize the importance of early neuroimaging and multidisciplinary management for accurate diagnosis and long-term neurological follow-up Health sciences/Diseases/Neurological disorders/Brain injuries Health sciences/Diseases Figures Figure 1 Figure 2 Figure 3 Figure 4 Introduction Perinatal stroke is defined as a cerebrovascular event occurring between 20 weeks of Fetal life and 28 days after birth. It represents one of the most important causes of neonatal neurological injury and long-term neurodevelopmental disability, including cerebral palsy, epilepsy, and cognitive impairment. The estimated incidence of perinatal stroke ranges from approximately 1 in 1000 to 1 in 5000 live births depending on the diagnostic criteria and subtype. Perinatal stroke encompasses several clinical entities including neonatal arterial ischemic stroke (NAIS), neonatal hemorrhagic stroke (NHS), neonatal cerebral sinovenous thrombosis (CSVT), arterial presumed perinatal ischemic stroke (APPIS), periventricular venous infarction (PVI), and presumed perinatal hemorrhagic stroke (PPHS).The clinical presentation may vary widely. Some neonates present with early focal seizures or encephalopathy during the first days of life, whereas others remain asymptomatic and are diagnosed later during infancy after the development of neurological deficits. Here we report two neonatal cases of perinatal stroke with different clinical presentations managed in neonatal intensive care units in Saudi Arabia. CASE ONE Clinical Background A full-term female neonate was delivered at 41 weeks of gestation to a gravida 5 para 3+1 mother with no significant medical history. Delivery was performed via emergency caesarean section due to non-reactive cardiotocography. The infant was born vigorous with grade II meconium-stained amniotic fluid and Apgar scores of 9 and 9 at one and five minutes, respectively. The neonate remained with the mother for routine postnatal care and breastfeeding. On the third day of life, the neonate developed sudden focal clonic seizures involving both lower limbs lasting approximately five seconds and resolving spontaneously. Initial bedside glucose testing was normal. Laboratory investigations revealed significant hypocalcemia, which was corrected with intravenous calcium gluconate. A brain computed tomography (CT) scan demonstrated a large hypodense infarction involving the left parietal, temporal, and occipital lobes with mild midline shift, consistent with an acute infarction in the territory of the left middle cerebral artery. The neonate was transferred to the neonatal intensive care unit and monitored using a cerebral function monitor (CFM). Phenobarbital was administered as a loading dose followed by maintenance therapy. Sepsis evaluation was performed and empirical antibiotics were initiated but discontinued after 72 hours due to negative cultures. Magnetic resonance imaging (MRI) confirmed a large cortical infarction with hemorrhagic transformation in the left middle cerebral artery territory. The infant remained clinically stable, tolerated oral feeding, and was discharged on day 7 of life with scheduled follow-up in the high-risk neonatal clinic and pediatric neurology service. Course and progression Vital signs upon admission; • Heart rate: 140 beats per minute • Blood pressure: 69/40 mmHg • Respiratory rate: 49 per minute • Temperatures: 35.1 C • Oxygen saturation: 95% on room air Physical examination · Birth weight : 4300grams, birth length : 51, birth head circumference: 34.5 cm. · General appearance: Pink ,not dysmorphic , not distress. · Head: Well-formed skull shape , flat and soft anterior fontanelles ,sutures are intact. · Eyes :Normal conjunctiva , normal red reflex , no discharge. · Nose: Normal examination and both nostrils are patent · Neck: No findings of note · Mouth: Intact plate, normal tongue, no oral lesions, moist mucosa. · Neurologic: Alert, calm, normal sucking, rooting, grasp, and Moro reflexes, normotonic. · Lungs: Clear, equal breath rounds no retractions, no tachypnoea present. · Cardiovascular: heart sounds are audible ,intact femoral pulses . Less than 2 second capillary refill. · Abdomen: Nontender and non-distended, positive bowel sounds, liver edge just palpable below costal margin. · Genitourinary: Normal female genitalia ,both testicles in scrotum, patent anus · Skeletal : extended knees , bilateral hyper lax hips , normal upper limbs . · Skin: no skin stigmata Laboratory Work Up , Imaging and monitoring Full blood count : Hb, WBC ,platelets ,all within normal range Renal profile : Within normal limit Liver profile : Normal Coagulation profile: Normal Blood culture : No growth C-reactive protein : Negative Thrombophilia workup: Negative Metabolic screening : Negative Thrombophilia workup: negative Echocardiography: Normal study Cranial ultrasound : Unremarkable CT-scan (figure1) A- axial , B- Sagittal ,C, Coronal sections showed large left cortical tempo-occipital parietal hypodense area with cortical hyper- density ,displaying effacement of cortical sulci and compressing of ipsilateral ventricle feature of acute haemorrhagic infraction territory of left middle cerebral artery. Brain MRI (figure2) (A),T1: shows left cortical hypointense area with peripheral hyperintensity (B), T2: shows left cortical hyperintense area with hypointense area (C), FLAIR : shows left cortical hypointense area with peripheral hyperintense (D),DWI : shows cortical restricted diffusion Brain MRV/MRI-Venogram: Normal signal form all dural venous sinuses(figer2) Brain MRA /MRI-Arteriogram: Left collateral vessels (figure2) CFM: Burst suppression for 24 hours with three episodes of seizures ,then discontinuous low voltage and normalised. CASE TWO Clinical Vignette A male neonate was born at 37 weeks of gestation through spontaneous vaginal delivery to a 28-year-old gravida 4 para 3 mother with no significant antenatal complications. The infant had Apgar scores of 7 and 9 at one and five minutes respectively. Shortly after birth, the neonate developed respiratory distress requiring admission to the neonatal intensive care unit. Initially the infant was supported with continuous positive airway pressure (CPAP). Due to worsening respiratory distress, endotracheal intubation was performed and a single dose of surfactant was administered. The infant improved clinically and was extubated after 24 hours to high-flow nasal cannula oxygen and later to room air. On the third day of life, routine cranial ultrasonography revealed a suspicious hemorrhagic lesion outside the ventricular zone. A CT scan demonstrated a cortical hypodense lesion in the left temporal region suggestive of subacute infarction. Subsequent MRI confirmed infarction involving the left occipital and parietal cortex with restricted diffusion on diffusion-weighted imaging. Magnetic resonance venography demonstrated reduced flow in the superior sagittal sinus suggestive of cerebral venous thrombosis. The neonate remained neurologically stable without seizures and was discharged home on day 5 with outpatient neurological follow-up.. Course and progression Vital signs upon admission; • Heart rate: 129 beats per minute • Blood pressure: 60/38 mmHg-MAP(45mmHg) • Respiratory rate: 68-80 per minute • Temperatures: 37 C • Oxygen saturation: 98% Physical screening · Birth weight : 3000grams, birth length : 48.5cm, birth head circumference: 34.7 cm. · General appearance: Distressed, not dysmorphic · Head: Well-formed skull shape , flat and soft anterior fontanelles ,sutures are intact. · Eyes :Normal conjunctiva , normal red reflex , no discharge. · Nose: Both nostrils are patent · Neck: No findings of note · Mouth: Intact plate, normal tongue, no oral lesions, moist mucosa. · Neurologic: Alert, calm, normal sucking, rooting, grasp, and Moro reflexes, normotonic , no abnormal movement at the time · Back and spine : normal examination · Lungs: Air entry equal in both lungs with retractions and tachypnoea present. · Cardiovascular: heart sounds are audible over all auscultatory areas ,intact femoral pulses , normal perfusion · Abdomen: Nontender ,soft, non-distended, positive bowel sounds, liver edge just palpable below costal margin. · Genitalia : Normal male genitalia , testicles settle in scrotum, with moderate hydrocele , patent anus. · Skeletal : Bilateral hip laxity , no malformations . · Skin: no skin stigmata Laboratory Work Up , Imaging and monitoring Test Description Results Serum Albumin 36.5 g/L -32.4 g/L Serum Calcium 2.63 ,1.92mmol/L Serum Chloride 106 mmol/L Serum Sodium 138 ,135mmol/L 2 Serum Potassium 4.8 ,5.1mmol/L Serum Magnesium 0.82,070 mmol/L Serum Phosphate 2.55 ,1.70mmol/L Serum Creatinine 81 μmol/L Urea 2.94 mmol/L Total serum Bilirubin 15.30,16.41, 12.57μmol/L Serum Alanine Amino transferase 9 U/L Serum Aspartate amino transferase 65 U/L C-reactive protein 5.21 mg/L White blood cell count 11.66 , 8.59.10*3/uL Hemoglobin 9.9, 11.5g/dl Platelets 464 -291*10*3/uL APTT 32.8 Second PT 14.8 Second INR 1.09 10*3/uL Blood cultures No growth Newborn Metabolic screening Negative Thrombophilia workup Negative CT scan (figure3): A-axial , B- coronal sections ,showed cortical left temporal hypodense area displaying effacement of cortical sulci and mild compression of ipsilateral ventricle ,feature of acute infraction MRI/MRA/MRV (figure4): (A),T1: shows left occipital hypointense area with cortical hyperintense (B), T2: shows cortical and occipital hyperintense signal (C),DWI: shows restricted diffusion at left cortical and occipitoparietal area (D),Flair : shows left occipital area with hyperintense signal ( E), MRV, shows loss of signal flow at superior sagittal sinus (F), MRA, shows normal study DISCUSSION Perinatal stroke is a significant cause of neonatal neurological injury and long-term neurodevelopmental impairment. It is defined as a focal cerebrovascular event occurring between 20 weeks of gestation and 28 days after birth and represents one of the leading causes of hemiplegic cerebral palsy and epilepsy in children (Raju, Nelson, Ferriero, & Lynch, 2007; Nelson & Lynch, 2001). The reported incidence varies between 1 in 1,000 and 1 in 5,000 live births, depending on diagnostic criteria and the stroke subtype included in epidemiological studies (Nelson, 2007).In Saudi Arabia, perinatal stroke contributes significantly to the burden of pediatric neurological disease. Salih et al. (2006) reported that 23 of 104 children with stroke (22%) had evidence of perinatal onset, highlighting the importance of early neonatal recognition. More recently, Alfayez et al. (2025) identified 32 patients diagnosed with perinatal stroke over a 13-year period at King Saud University Medical City, most of whom were born following uncomplicated pregnancies, emphasizing the unpredictable nature of this condition. Perinatal stroke is a heterogeneous entity encompassing several distinct clinical and pathological subtypes. These include neonatal arterial ischemic stroke (NAIS), neonatal hemorrhagic stroke (NHS), neonatal cerebral sinovenous thrombosis (CSVT), arterial presumed perinatal ischemic stroke (APPIS), periventricular venous infarction (PVI), and presumed perinatal hemorrhagic stroke (PPHS) (Raju et al., 2007; Nelson & Lynch, 2001). Among these, NAIS is the most common subtype, accounting for approximately 70–80% of cases (Lee et al., 2005). The estimated incidence of NAIS ranges between 1 in 2,300 and 1 in 5,000 live births, with a slight predominance in male infants and term gestations (Li, Miao, Xu, et al., 2017). The pathophysiology of perinatal stroke is complex and multifactorial. Several maternal, placental, and neonatal risk factors have been identified, although causality remains difficult to establish in many cases. Reported maternal risk factors include primiparity, diabetes mellitus, preeclampsia, autoimmune disease, thrombophilia, infertility treatment, and placental abnormalities (Lee et al., 2005; Li et al., 2017). Neonatal and fetal risk factors include birth asphyxia, congenital heart disease, infection, polycythemia, thrombophilia, metabolic disorders, and birth trauma. Intrapartum factors such as Fetal heart rate abnormalities, meconium-stained amniotic fluid, prolonged rupture of membranes, and emergency caesarean delivery have also been associated with perinatal stroke (Li et al., 2017; Liu, Zhang, Yang, & Xia, 2025). In the first case presented in this report, the neonate developed focal seizures on the third day of life and was found to have a large infarction within the territory of the left middle cerebral artery with hemorrhagic transformation, consistent with NAIS. Seizures represent the most common presenting manifestation of NAIS, occurring in approximately 70–90% of affected neonates, typically within the first 12–72 hours of life (Nelson, 2007; Liu et al., 2025). Diffuse neurological symptoms such as abnormal tone, altered level of consciousness, respiratory abnormalities, and feeding difficulties are also frequently observed (Raju et al., 2007).The second case illustrates a different clinical scenario in which the neonate remained neurologically asymptomatic, and the diagnosis was made incidentally during routine neuroimaging. This finding aligns with previous reports suggesting that up to 40% of perinatal strokes may remain clinically silent during the neonatal period, with neurological deficits becoming apparent later in infancy or early childhood, often manifesting as hemiparesis, early hand preference, developmental delay, or epilepsy (Nelson & Lynch, 2001; Alfayez et al., 2025). Neonatal hemorrhagic stroke, defined as focal bleeding within the brain parenchyma resulting from primary intracerebral hemorrhage or hemorrhagic transformation of ischemic injury, is less common than NAIS, with an estimated incidence of 1 in 6,300 live births. Clinical manifestations frequently include seizures, altered consciousness, or signs of increased intracranial pressure depending on the size and location of the hemorrhage (Pai & Shroff, 2026). Neonatal CSVT, caused by thrombus formation within cerebral venous sinuses or veins, has an incidence ranging from 1 to 12 per 100,000 live births and a slight male predominance (Pabst, Lisa, et al,2024). Neonates are particularly vulnerable due to maternal hypercoagulability, neonatal hematologic immaturity, reduced fibrinolytic activity, and mechanical compression of venous sinuses during labor (Alshammari, Shamseldin, Essbaiheen, et al., 2024). Neuroimaging is crucial in the diagnosis and classification of perinatal stroke. Cranial ultrasonography is commonly used in neonatal intensive care units but has limited sensitivity for cortical infarctions. CT is useful for detecting intracranial hemorrhage, whereas MRI remains the gold standard for diagnosis, enabling accurate characterization of ischemic lesions, hemorrhage, and venous thrombosis. Diffusion-weighted imaging is particularly sensitive for early ischemic injury, while MR angiography and MR venography help evaluate arterial and venous circulation, respectively (Pai & Shroff, 2026; Neuroimaging & Neurological Outcomes, 2024). These cases highlight the heterogeneous clinical presentation of perinatal stroke, ranging from early symptomatic seizures to incidental detection on neuroimaging. Early recognition and multidisciplinary management involving neonatologists, neurologists, and radiologists are essential to optimize clinical outcomes and ensure appropriate long-term neurodevelopmental follow-up (Raju et al., 2007; Salih et al., 2006). Conclusion Perinatal stroke is an important yet often under-recognized cause of neonatal neurological injury and long-term neurodevelopmental impairment. The clinical presentation may vary widely, ranging from early symptomatic seizures to completely asymptomatic cases detected incidentally on neuroimaging. The two cases presented in this report illustrate the heterogeneity of clinical manifestations and emphasize the importance of maintaining a high index of suspicion when evaluating neonates with seizures or unexplained neurological findings. Early neuroimaging, particularly magnetic resonance imaging, plays a critical role in establishing the diagnosis and identifying the underlying subtype of perinatal stroke. Prompt multidisciplinary management and long-term neurological follow-up are essential to optimize neurodevelopmental outcomes and to identify potential complications such as cerebral palsy, epilepsy, and cognitive impairment Declarations The parents of the infants provided written informed consent for participation and for the publication of their clinical case details. All information included in the report has been anonymized to protect patient identity, and no identifiable personal data have been disclosed. Acknowledgment : The authors would like to thank the neonatal intensive care unit staff, nurses, and laboratory team for their support and collaboration in the management of these cases. References Raju TN, Nelson KB, Ferriero D, Lynch JK. Ischemic perinatal stroke: summary of a workshop sponsored by the National Institute of Child Health and Human Development. Pediatrics. 2007;120(3):609-616. Lynch JK, Nelson KB. Epidemiology of perinatal stroke. Curr Opin Pediatr. 2001;13(6):499-505. Nelson KB. Perinatal ischemic stroke. Stroke. 2007 Feb 1;38(2):742-5. Salih MA, Abdel-Gader AG, Al-Jarallah AA, Kentab AY, Al-Orainy IA. Perinatal stroke in Saudi children: clinical features and risk factors. Saudi Med J. 2006;27(9):1335-1340. Alfayez SS, Hamad MH, Kentab AY, et al. Risk factors, clinical characteristics, and outcomes of perinatal stroke in a tertiary university hospital in Saudi Arabia. Neurosciences (Riyadh). 2025;30(2):138–143 Lee J, Croen LA, Lindan C, et al. Predictors of outcome in perinatal arterial stroke: a population-based study. Ann Neurol. 2005;58(2):303-308. Li C, Miao JK, Xu Y, et al. Prenatal, perinatal, and neonatal risk factors for perinatal arterial ischemic stroke: systematic review and meta-analysis. Eur J Neurol. 2017;24(8):1006–1015 Liu C, Zhang Y, Yang R, Xia S. Clinical characteristics and risk factors for perinatal arterial ischemic and hemorrhagic stroke. Front Pediatr. 2025;13:1540173. Pai V, Shroff M. Neonatal arterial ischemic stroke: an imaging overview. Pediatric Radiology. 2026 Jan 31:1-21. Pabst L, Hoyt CR, Felling RJ, Smith AE, Harpster K, Pardo AC, Bridge JA, Jiang B, Gehred A, Lo W. Neuroimaging and neurological outcomes in perinatal arterial ischemic stroke: a systematic review and meta-analysis. Pediatric neurology. 2024 Aug 1;157:19-28. Alshammari MJ, Shamseldin HE, Essbaiheen F, Eltahir SH, Alruwaili AR, Abdulwahab F, Alkuraya FS. Genomic analysis of presumed perinatal stroke in Saudi Arabia reveals a strong monogenic contribution. Human Genetics. 2024 Jan;143(1):59-69. Additional Declarations There is NO conflict of interest to disclose. Cite Share Download PDF Status: Posted Version 1 posted 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. 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birth. It represents one of the most important causes of neonatal neurological injury and long-term neurodevelopmental disability, including cerebral palsy, epilepsy, and cognitive impairment. The estimated incidence of perinatal stroke ranges from approximately 1 in 1000 to 1 in 5000 live births depending on the diagnostic criteria and subtype. Perinatal stroke encompasses several clinical entities including neonatal arterial ischemic stroke (NAIS), neonatal hemorrhagic stroke (NHS), neonatal cerebral sinovenous thrombosis (CSVT), arterial presumed perinatal ischemic stroke (APPIS), periventricular venous infarction (PVI), and presumed perinatal hemorrhagic stroke (PPHS).The clinical presentation may vary widely. Some neonates present with early focal seizures or encephalopathy during the first days of life, whereas others remain asymptomatic and are diagnosed later during infancy after the development of neurological deficits. Here we report two neonatal cases of perinatal stroke with different clinical presentations managed in neonatal intensive care units in Saudi Arabia.\u003c/p\u003e"},{"header":"CASE ONE ","content":"\u003cp\u003e\u003cstrong\u003eClinical Background\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA full-term female neonate was delivered at 41 weeks of gestation to a gravida 5 para 3+1 mother with no significant medical history. Delivery was performed via emergency caesarean section due to non-reactive cardiotocography. The infant was born vigorous with grade II meconium-stained amniotic fluid and Apgar scores of 9 and 9 at one and five minutes, respectively. The neonate remained with the mother for routine postnatal care and breastfeeding. On the third day of life, the neonate developed sudden focal clonic seizures involving both lower limbs lasting approximately five seconds and resolving spontaneously. Initial bedside glucose testing was normal. Laboratory investigations revealed significant hypocalcemia, which was corrected with intravenous calcium gluconate. A brain computed tomography (CT) scan demonstrated a large hypodense infarction involving the left parietal, temporal, and occipital lobes with mild midline shift, consistent with an acute infarction in the territory of the left middle cerebral artery. The neonate was transferred to the neonatal intensive care unit and monitored using a cerebral function monitor (CFM). Phenobarbital was administered as a loading dose followed by maintenance therapy. Sepsis evaluation was performed and empirical antibiotics were initiated but discontinued after 72 hours due to negative cultures. Magnetic resonance imaging (MRI) confirmed a large cortical infarction with hemorrhagic transformation in the left middle cerebral artery territory.\u003c/p\u003e\n\u003cp\u003eThe infant remained clinically stable, tolerated oral feeding, and was discharged on day 7 of life with scheduled follow-up in the high-risk neonatal clinic and pediatric neurology service.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCourse and progression\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eVital signs upon admission;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u0026nbsp;• Heart rate: \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;140 beats per minute\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Blood pressure: 69/40 mmHg\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Respiratory rate: 49 per minute\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Temperatures: \u0026nbsp; \u0026nbsp;35.1 C\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Oxygen saturation: 95% on room air\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePhysical examination\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Birth weight : 4300grams, birth length : 51, birth head circumference: 34.5 cm.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;General appearance: Pink ,not dysmorphic , not distress.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Head: Well-formed skull shape , flat and soft anterior fontanelles ,sutures are intact.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Eyes :Normal conjunctiva , normal red reflex , no discharge.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Nose: Normal examination and both nostrils are patent\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Neck: No findings of note\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Mouth: Intact plate, normal tongue, no oral lesions, \u0026nbsp;moist mucosa.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Neurologic: Alert, calm, normal sucking, rooting, grasp, and Moro reflexes, normotonic.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Lungs: Clear, equal breath rounds no retractions, no tachypnoea present.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Cardiovascular: heart sounds are audible ,intact \u0026nbsp;femoral pulses . Less than 2 second capillary refill.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Abdomen: Nontender and non-distended, positive bowel sounds, liver edge just \u0026nbsp;palpable below costal margin.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Genitourinary: Normal female genitalia ,both testicles in scrotum, patent \u0026nbsp;anus\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Skeletal : extended knees , bilateral hyper lax hips , normal upper limbs .\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Skin: no skin stigmata\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLaboratory Work Up , Imaging and monitoring\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cul\u003e\n \u003cli\u003eFull blood count \u0026nbsp; \u0026nbsp;: Hb, WBC ,platelets ,all within normal range \u0026nbsp;\u003c/li\u003e\n \u003cli\u003eRenal profile \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; : Within normal limit\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eLiver profile \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;: Normal\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eCoagulation profile: Normal\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eBlood culture \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; : No growth\u003c/li\u003e\n \u003cli\u003eC-reactive protein \u0026nbsp; : Negative \u0026nbsp;\u003c/li\u003e\n \u003cli\u003eThrombophilia workup: Negative\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eMetabolic screening : Negative\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eThrombophilia workup: negative\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eEchocardiography: Normal study\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eCranial ultrasound : Unremarkable\u003c/li\u003e\n \u003cli\u003eCT-scan (figure1)\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003eA- axial , B- Sagittal ,C, Coronal sections showed large left\u003c/p\u003e\n\u003cp\u003ecortical tempo-occipital parietal hypodense area with cortical hyper-\u003c/p\u003e\n\u003cp\u003edensity ,displaying effacement of cortical sulci and compressing of\u003c/p\u003e\n\u003cp\u003eipsilateral ventricle feature of acute haemorrhagic infraction territory of left\u003c/p\u003e\n\u003cp\u003emiddle cerebral artery.\u003c/p\u003e\n\u003cul\u003e\n \u003cli\u003eBrain MRI (figure2)\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u0026nbsp; \u0026nbsp; \u0026nbsp; (A),T1: shows left cortical hypointense area with peripheral hyperintensity\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;(B), T2: shows left cortical hyperintense area with hypointense area\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;(C), FLAIR : shows left cortical hypointense area with peripheral hyperintense\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; (D),DWI : shows cortical restricted diffusion\u0026nbsp;\u003c/p\u003e\n\u003cul\u003e\n \u003cli\u003eBrain MRV/MRI-Venogram: Normal signal form all dural venous sinuses(figer2)\u003c/li\u003e\n \u003cli\u003eBrain MRA /MRI-Arteriogram: \u0026nbsp;Left collateral vessels (figure2)\u003c/li\u003e\n \u003cli\u003eCFM: Burst suppression for 24 hours with three episodes of seizures ,then discontinuous low voltage and normalised.\u003c/li\u003e\n\u003c/ul\u003e"},{"header":"CASE TWO","content":"\u003cp\u003e\u003cstrong\u003eClinical Vignette\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA male neonate was born at 37 weeks of gestation through spontaneous vaginal delivery to a 28-year-old gravida 4 para 3 mother with no significant antenatal complications. The infant had Apgar scores of 7 and 9 at one and five minutes respectively. Shortly after birth, the neonate developed respiratory distress requiring admission to the neonatal intensive care unit. Initially the infant was supported with continuous positive airway pressure (CPAP). Due to worsening respiratory distress, endotracheal intubation was performed and a single dose of surfactant was administered. The infant improved clinically and was extubated after 24 hours to high-flow nasal cannula oxygen and later to room air. On the third day of life, routine cranial ultrasonography revealed a suspicious hemorrhagic lesion outside the ventricular zone. A CT scan demonstrated a cortical hypodense lesion in the left temporal region suggestive of subacute infarction. Subsequent MRI confirmed infarction involving the left occipital and parietal cortex with restricted diffusion on diffusion-weighted imaging. Magnetic resonance venography demonstrated reduced flow in the superior sagittal sinus suggestive of cerebral venous thrombosis. The neonate remained neurologically stable without seizures and was discharged home on day 5 with outpatient neurological follow-up..\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCourse and progression\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eVital signs upon admission;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Heart rate: \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;129 beats per minute\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Blood pressure: 60/38 mmHg-MAP(45mmHg)\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Respiratory rate: 68-80 per minute\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Temperatures: \u0026nbsp; \u0026nbsp;37 C\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; • Oxygen saturation: 98%\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; \u003cstrong\u003ePhysical screening\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Birth weight : 3000grams, birth length : 48.5cm, birth head circumference: 34.7 cm.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;General appearance: \u0026nbsp;Distressed, not dysmorphic\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Head: Well-formed skull shape , flat and soft anterior fontanelles ,sutures are intact.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Eyes :Normal conjunctiva , normal red reflex , no discharge.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Nose: Both nostrils are patent\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Neck: No findings of note\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Mouth: Intact plate, normal tongue, no oral lesions, \u0026nbsp;moist mucosa.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Neurologic: Alert, calm, normal sucking, rooting, grasp, and Moro reflexes, normotonic , no abnormal movement at the time\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Back and spine : normal examination\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Lungs: Air entry equal in both lungs \u0026nbsp; with \u0026nbsp;retractions and \u0026nbsp;tachypnoea present.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Cardiovascular: heart sounds are audible over all auscultatory areas \u0026nbsp;,intact \u0026nbsp; femoral pulses , normal perfusion \u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Abdomen: Nontender ,soft, non-distended, positive bowel sounds, liver edge just \u0026nbsp;palpable below costal margin.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;Genitalia : Normal male genitalia , testicles settle in scrotum, with moderate hydrocele , \u0026nbsp;patent \u0026nbsp;anus.\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Skeletal : Bilateral hip laxity , no malformations .\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e·\u0026nbsp;\u0026nbsp;Skin: no skin stigmata\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLaboratory Work Up , Imaging and monitoring\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eTest Description\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003eResults\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Albumin\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e36.5 g/L -32.4 g/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Calcium\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.63 ,1.92mmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Chloride\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e106 mmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Sodium\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e138 ,135mmol/L 2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Potassium\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.8 ,5.1mmol/L\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Magnesium\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.82,070 mmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Phosphate\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.55 ,1.70mmol/L\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Creatinine\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e81 μmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eUrea\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.94 mmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eTotal serum Bilirubin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e15.30,16.41, 12.57μmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Alanine Amino transferase\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e9 U/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSerum Aspartate amino transferase\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e65 U/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eC-reactive protein\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.21 mg/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eWhite blood cell count\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e11.66 , 8.59.10*3/uL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eHemoglobin\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e9.9, 11.5g/dl\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003ePlatelets\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e464 -291*10*3/uL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eAPTT\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e32.8 Second\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003ePT\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e14.8 Second\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eINR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.09 10*3/uL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eBlood cultures\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003eNo growth\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eNewborn Metabolic screening\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003eNegative\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eThrombophilia workup\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003eNegative\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003e\u003cu\u003eCT scan\u003c/u\u003e\u003c/em\u003e (figure3): A-axial , B- coronal sections ,showed cortical left temporal hypodense area displaying effacement of cortical sulci and mild compression of ipsilateral ventricle ,feature of acute infraction\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cu\u003eMRI/MRA/MRV\u003c/u\u003e\u003c/em\u003e (figure4):\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e(A),T1: shows left occipital hypointense area with cortical hyperintense\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e(B), T2: shows cortical and occipital \u0026nbsp;hyperintense signal\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e(C),DWI: shows restricted diffusion at left cortical and occipitoparietal area\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e(D),Flair : shows left occipital area with hyperintense signal\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003csub\u003e\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; (\u003c/sub\u003eE), MRV, shows loss of signal flow at superior sagittal sinus\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; (F), MRA, shows normal study\u0026nbsp;\u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003ePerinatal stroke is a significant cause of neonatal neurological injury and long-term neurodevelopmental impairment. It is defined as a focal cerebrovascular event occurring between 20 weeks of gestation and 28 days after birth and represents one of the leading causes of hemiplegic cerebral palsy and epilepsy in children (Raju, Nelson, Ferriero, \u0026amp; Lynch, 2007; Nelson \u0026amp; Lynch, 2001). The reported incidence varies between 1 in 1,000 and 1 in 5,000 live births, depending on diagnostic criteria and the stroke subtype included in epidemiological studies (Nelson, 2007).In Saudi Arabia, perinatal stroke contributes significantly to the burden of pediatric neurological disease. Salih et al. (2006) reported that 23 of 104 children with stroke (22%) had evidence of perinatal onset, highlighting the importance of early neonatal recognition. More recently, Alfayez et al. (2025) identified 32 patients diagnosed with perinatal stroke over a 13-year period at King Saud University Medical City, most of whom were born following uncomplicated pregnancies, emphasizing the unpredictable nature of this condition.\u003c/p\u003e\n\u003cp\u003ePerinatal stroke is a heterogeneous entity encompassing several distinct clinical and pathological subtypes. These include neonatal arterial ischemic stroke (NAIS), neonatal hemorrhagic stroke (NHS), neonatal cerebral sinovenous thrombosis (CSVT), arterial presumed perinatal ischemic stroke (APPIS), periventricular venous infarction (PVI), and presumed perinatal hemorrhagic stroke (PPHS) (Raju et al., 2007; Nelson \u0026amp; Lynch, 2001). Among these, NAIS is the most common subtype, accounting for approximately 70–80% of cases (Lee et al., 2005). The estimated incidence of NAIS ranges between 1 in 2,300 and 1 in 5,000 live births, with a slight predominance in male infants and term gestations (Li, Miao, Xu, et al., 2017).\u003c/p\u003e\n\u003cp\u003eThe pathophysiology of perinatal stroke is complex and multifactorial. Several maternal, placental, and neonatal risk factors have been identified, although causality remains difficult to establish in many cases. Reported maternal risk factors include primiparity, diabetes mellitus, preeclampsia, autoimmune disease, thrombophilia, infertility treatment, and placental abnormalities (Lee et al., 2005; Li et al., 2017). Neonatal and fetal risk factors include birth asphyxia, congenital heart disease, infection, polycythemia, thrombophilia, metabolic disorders, and birth trauma. Intrapartum factors such as Fetal heart rate abnormalities, meconium-stained amniotic fluid, prolonged rupture of membranes, and emergency caesarean delivery have also been associated with perinatal stroke (Li et al., 2017; Liu, Zhang, Yang, \u0026amp; Xia, 2025).\u003c/p\u003e\n\u003cp\u003eIn the first case presented in this report, the neonate developed focal seizures on the third day of life and was found to have a large infarction within the territory of the left middle cerebral artery with hemorrhagic transformation, consistent with NAIS. Seizures represent the most common presenting manifestation of NAIS, occurring in approximately 70–90% of affected neonates, typically within the first 12–72 hours of life (Nelson, 2007; Liu et al., 2025). Diffuse neurological symptoms such as abnormal tone, altered level of consciousness, respiratory abnormalities, and feeding difficulties are also frequently observed (Raju et al., 2007).The second case illustrates a different clinical scenario in which the neonate remained neurologically asymptomatic, and the diagnosis was made incidentally during routine neuroimaging. This finding aligns with previous reports suggesting that up to 40% of perinatal strokes may remain clinically silent during the neonatal period, with neurological deficits becoming apparent later in infancy or early childhood, often manifesting as hemiparesis, early hand preference, developmental delay, or epilepsy (Nelson \u0026amp; Lynch, 2001; Alfayez et al., 2025).\u003c/p\u003e\n\u003cp\u003eNeonatal hemorrhagic stroke, defined as focal bleeding within the brain parenchyma resulting from primary intracerebral hemorrhage or hemorrhagic transformation of ischemic injury, is less common than NAIS, with an estimated incidence of 1 in 6,300 live births. Clinical manifestations frequently include seizures, altered consciousness, or signs of increased intracranial pressure depending on the size and location of the hemorrhage (Pai \u0026amp; Shroff, 2026). Neonatal CSVT, caused by thrombus formation within cerebral venous sinuses or veins, has an incidence ranging from 1 to 12 per 100,000 live births and a slight male predominance (Pabst, Lisa, et al,2024). Neonates are particularly vulnerable due to maternal hypercoagulability, neonatal hematologic immaturity, reduced fibrinolytic activity, and mechanical compression of venous sinuses during labor (Alshammari, Shamseldin, Essbaiheen, et al., 2024).\u003c/p\u003e\n\u003cp\u003eNeuroimaging is crucial in the diagnosis and classification of perinatal stroke. Cranial ultrasonography is commonly used in neonatal intensive care units but has limited sensitivity for cortical infarctions. CT is useful for detecting intracranial hemorrhage, whereas MRI remains the gold standard for diagnosis, enabling accurate characterization of ischemic lesions, hemorrhage, and venous thrombosis. Diffusion-weighted imaging is particularly sensitive for early ischemic injury, while MR angiography and MR venography help evaluate arterial and venous circulation, respectively (Pai \u0026amp; Shroff, 2026; Neuroimaging \u0026amp; Neurological Outcomes, 2024).\u003c/p\u003e\n\u003cp\u003eThese cases highlight the heterogeneous clinical presentation of perinatal stroke, ranging from early symptomatic seizures to incidental detection on neuroimaging. Early recognition and multidisciplinary management involving neonatologists, neurologists, and radiologists are essential to optimize clinical outcomes and ensure appropriate long-term neurodevelopmental follow-up (Raju et al., 2007; Salih et al., 2006).\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003ePerinatal stroke is an important yet often under-recognized cause of neonatal neurological injury and long-term neurodevelopmental impairment. The clinical presentation may vary widely, ranging from early symptomatic seizures to completely asymptomatic cases detected incidentally on neuroimaging. The two cases presented in this report illustrate the heterogeneity of clinical manifestations and emphasize the importance of maintaining a high index of suspicion when evaluating neonates with seizures or unexplained neurological findings. Early neuroimaging, particularly magnetic resonance imaging, plays a critical role in establishing the diagnosis and identifying the underlying subtype of perinatal stroke. Prompt multidisciplinary management and long-term neurological follow-up are essential to optimize neurodevelopmental outcomes and to identify potential complications such as cerebral palsy, epilepsy, and cognitive impairment\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eThe parents of the infants provided written informed consent for participation and for the publication of their clinical case details. All information included in the report has been anonymized to protect patient identity, and no identifiable personal data have been disclosed.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eAcknowledgment :\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors would like to thank the neonatal intensive care unit staff, nurses, and laboratory team for their support and collaboration in the management of these cases.\u003c/p\u003e"},{"header":"References","content":"\u003col start=\"1\" type=\"1\"\u003e\n \u003cli\u003eRaju TN, Nelson KB, Ferriero D, Lynch JK. Ischemic perinatal stroke: summary of a workshop sponsored by the National Institute of Child Health and Human Development.\u0026nbsp;\u003cem\u003ePediatrics.\u003c/em\u003e 2007;120(3):609-616.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eLynch JK, Nelson KB. Epidemiology of perinatal stroke.\u0026nbsp;\u003cem\u003eCurr Opin Pediatr.\u003c/em\u003e 2001;13(6):499-505.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eNelson KB. Perinatal ischemic stroke. Stroke. 2007 Feb 1;38(2):742-5.\u003c/li\u003e\n \u003cli\u003eSalih MA, Abdel-Gader AG, Al-Jarallah AA, Kentab AY, Al-Orainy IA. Perinatal stroke in Saudi children: clinical features and risk factors.\u0026nbsp;\u003cem\u003eSaudi Med J.\u003c/em\u003e 2006;27(9):1335-1340.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eAlfayez SS, Hamad MH, Kentab AY, et al. Risk factors, clinical characteristics, and outcomes of perinatal stroke in a tertiary university hospital in Saudi Arabia.\u0026nbsp;\u003cem\u003eNeurosciences (Riyadh).\u003c/em\u003e 2025;30(2):138–143\u003c/li\u003e\n \u003cli\u003eLee J, Croen LA, Lindan C, et al. Predictors of outcome in perinatal arterial stroke: a population-based study.\u0026nbsp;\u003cem\u003eAnn Neurol.\u003c/em\u003e 2005;58(2):303-308.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eLi C, Miao JK, Xu Y, et al. Prenatal, perinatal, and neonatal risk factors for perinatal arterial ischemic stroke: systematic review and meta-analysis.\u0026nbsp;\u003cem\u003eEur J Neurol.\u003c/em\u003e 2017;24(8):1006–1015\u003c/li\u003e\n \u003cli\u003eLiu C, Zhang Y, Yang R, Xia S. Clinical characteristics and risk factors for perinatal arterial ischemic and hemorrhagic stroke.\u0026nbsp;\u003cem\u003eFront Pediatr.\u003c/em\u003e 2025;13:1540173.\u003c/li\u003e\n \u003cli\u003ePai V, Shroff M. Neonatal arterial ischemic stroke: an imaging overview. Pediatric Radiology. 2026 Jan 31:1-21.\u003c/li\u003e\n \u003cli\u003ePabst L, Hoyt CR, Felling RJ, Smith AE, Harpster K, Pardo AC, Bridge JA, Jiang B, Gehred A, Lo W. Neuroimaging and neurological outcomes in perinatal arterial ischemic stroke: a systematic review and meta-analysis. Pediatric neurology. 2024 Aug 1;157:19-28.\u003c/li\u003e\n \u003cli\u003eAlshammari MJ, Shamseldin HE, Essbaiheen F, Eltahir SH, Alruwaili AR, Abdulwahab F, Alkuraya FS. Genomic analysis of presumed perinatal stroke in Saudi Arabia reveals a strong monogenic contribution. Human Genetics. 2024 Jan;143(1):59-69.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"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":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"","lastPublishedDoi":"10.21203/rs.3.rs-9315390/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9315390/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"Perinatal stroke is an important cause of neonatal neurological morbidity and may present with diverse clinical manifestations ranging from seizures to completely asymptomatic cases. Early recognition is challenging because many neonates demonstrate nonspecific or delayed symptoms. We report two neonates diagnosed with perinatal stroke during the first week of life. The first case presented on the third day of life with focal clonic seizures and was found to have a large infarction in the left middle cerebral artery territory with hemorrhagic transformation. The second neonate was admitted with respiratory distress and was later found to have cerebral infarction incidentally during routine cranial ultrasonography. These cases illustrate the variable clinical presentation of perinatal stroke and emphasize the importance of early neuroimaging and multidisciplinary management for accurate diagnosis and long-term neurological follow-up","manuscriptTitle":"Perinatal Stroke in Two Neonates: Divergent Clinical Presentations From Early Seizures to Incidental Neuroimaging Detection","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-09 16:02:36","doi":"10.21203/rs.3.rs-9315390/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"ef4086c5-be65-4122-8ced-79eaf1060a80","owner":[],"postedDate":"April 9th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":65994030,"name":"Health sciences/Diseases/Neurological disorders/Brain injuries"},{"id":65994031,"name":"Health sciences/Diseases"}],"tags":[],"updatedAt":"2026-04-14T19:15:26+00:00","versionOfRecord":[],"versionCreatedAt":"2026-04-09 16:02:36","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9315390","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9315390","identity":"rs-9315390","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}