Neonatal Hemorrhagic Stroke Research Articles

EEG alpha band functional brain network correlates of cognitive performance in children after perinatal stroke

Mechanisms underlying cognitive impairment after perinatal stroke could be explained through brain network alterations. With aim to explore this connection, we conducted a matched test-control study to find a correlation between functional brain network properties and cognitive functions in children after perinatal stroke. First, we analyzed resting-state functional connectomes in the alpha frequency band from a 64-channel resting state EEG in 24 children with a history of perinatal stroke (12 with neonatal arterial ischemic stroke and 12 with neonatal hemorrhagic stroke) and compared them to the functional connectomes of 24 healthy controls. Next, all participants underwent cognitive evaluation. We analyzed the differences in functional brain network properties and cognitive abilities between groups and studied the correlation between network characteristics and specific cognitive functions. Functional brain networks after perinatal stroke had lower modularity, higher clustering coefficient, higher interhemispheric strength, higher characteristic path length and higher small world index. Modularity correlated positively with the IQ and processing speed, while clustering coefficient correlated negatively with IQ. Graph metrics, reflecting network segregation (clustering coefficient and small world index) correlated positively with a tendency to impulsive decision making, which also correlated positively with graph metrics, reflecting stronger functional connectivity (characteristic path length and interhemispheric strength). Our study suggests that specific cognitive functions correlate with different brain network properties and that functional network characteristics after perinatal stroke reflect poorer cognitive functioning.

Risk factors of neonatal stroke from different origins: a systematic review and meta-analysis.

This study provides a succinct overview and comparative analysis of maternal, perinatal, and additional risk factors associated with neonatal cerebral artery ischemic stroke and neonatal hemorrhagic stroke, furnishing critical insights for healthcare practitioners involved in the diagnosis and prevention of neonatal stroke. This research also broadens the conceptual framework for future investigations. • Research indicates that prenatal, perinatal, and neonatal risk factors can elevate the risk of neonatal arterial ischemic stroke (NAIS). However, the risk factors for neonatal cerebral arterial ischemic stroke remain contentious, and those for neonatal hemorrhagic stroke (NHS) and neonatal cerebral venous sinus thrombosis (CVST) are still not well-defined. • This study is the inaugural comprehensive review and meta-analysis encompassing 19 studies that explore maternal, perinatal, and various risk factors linked to neonatal stroke of differing etiologies. Notably, our analysis elucidates eight risk factors associated with NAIS: gestational diabetes mellitus, a history of infertility, placenta previa, postdates, preterm birth, premature rupture of membranes, a prolonged second stage of labor, and chorioamnionitis. Furthermore, we identify six risk factors correlated with NHS: postdates, preterm birth, an abnormal CTG, the method of delivery, male gender, and vaginal delivery. Additionally, our systematic review delineates risk factors associated with CVST.

Prevalence & Risk Factors for Perinatal Stroke: A Population-Based Study.

The study objective was to calculate the birth prevalence of perinatal stroke and examine risk factors in term infants. Some risk factors are present in healthy infants, making it difficult to determine at-risk infants. Prospective population-based perinatal stroke data were compared to the Australian general population data using chi-squared and Fisher's exact tests and multivariable logistic regression analysis. Sixty perinatal stroke cases were reported between 2017 and 2019. Estimated stroke prevalence was 9.6/100,000 live births/year including 5.8 for neonatal arterial ischemic stroke and 2.9 for neonatal hemorrhagic stroke. Eighty seven percent had multiple risk factors. Significant risk factors were cesarean section (p = 0.04), 5-min Apgar score <7 (p < 0.01), neonatal resuscitation (p < 0.01) and nulliparity (p < 0.01). Statistically significant independent risk factors do not fully explain the cause of perinatal stroke, because they are not a direct causal pathway to stroke. These data now require validation in a case-control study.

Abstract WP175: A National, Population Based Study Of Neonatal Hemorrhagic And Ischemic Stroke

Background: Neonatal stroke occurs in an estimated 1 in 3000 live births and is the most common cause of hemiplegic cerebral palsy in term infants. Most population based studies on neonatal stroke in the past have been single center or regional, focused only on ischemic stroke, and with less than 100 cases. Large administrative datasets can provide information on comorbid perinatal conditions in neonatal stroke. Methods: Data for patients aged 0-28 days with a diagnosis of either ischemic or hemorrhagic stroke (either subarachnoid or intracerebral hemorrhage) were extracted from the Cerner Health Facts EMR database from 2000-2018. Incidence of birth demographics, perinatal complications, anti-epileptic use, and aspirin use was assessed. Odds ratios were calculated against a cohort of neonates without stroke. Results: Among 1,591,104 neonates in the Cerner EMR database, 452 (59%) neonates were identified with ischemic stroke and 311 (41%) with hemorrhagic stroke. The most common comorbidities for ischemic stroke were neonatal sepsis (16%, OR=13.1), head and scalp birth injury (13%, OR=7.1) and hypoxic injury (12%, OR=38.7). The most common comorbidities for hemorrhagic stroke were head and scalp birth injury (30%, OR=19.5), prematurity (26%, OR=4.2) and neonatal sepsis (23%, OR=13.1). Procedure codes for intubation, neonatal resuscitation, and epinephrine use were prominent in both hemorrhagic (15.1%, OR=35) and ischemic stroke (8.9%, OR=19.1). The proportion of hemorrhagic and ischemic stroke patients receiving antiepileptics was 23% and 27%, respectively. The proportion of ischemic stroke patients who received aspirin was 16.4%. Conclusion: This population based study of neonatal stroke, the largest of its kind, demonstrated a wide variety of comorbid conditions with ischemic and hemorrhagic stroke. Antiepileptic use is common in neonatal ischemic stroke, though in our population-based study of both academic and non-academic centers the prevalence is less than prior estimates. Sepsis, head and scalp injuries, prematurity, and hypoxic injury are associated with neonatal hemorrhagic and ischemic stroke, though prevalence varies between types. More study is needed on specific risk factors and pathogenesis in neonatal stroke.

B.3 The incidence of perinatal stroke is 1:1200 births in Southern Alberta: Population-based incidence of disease-specific perinatal stroke

Background: Perinatal stroke encompasses six cerebrovascular syndromes which occur between the 20th week of gestation and the 28th post-natal day. Subtypes are neonatal arterial ischemic stroke (NAIS), neonatal cerebral sinovenous thrombosis (CSVT), neonatal hemorrhagic stroke (NHS), arterial presumed perinatal ischemic stroke (APPIS), periventricular venous infarction (PVI), and presumed perinatal hemorrhagic stroke (PPHS). Inconsistent terminology and lack of population-based case series has limited accurate measurement of disease-specific perinatal stroke incidence. Our objective was to define the incidence of the subtypes of perinatal stroke using a population-based cohort. Methods: The Alberta Perinatal Stroke Project is a research cohort established in 2008 in Southern Alberta. Case acquisition included retrospective hospital and ICD code searches (1990-2008) and prospective enrollment from all NICU and neurology/stroke clinics (2008-2017). Results: The overall incidence of perinatal stroke in Southern Alberta was 9.0 cases per 10,000 births, or 1:1200 births. Per 10,000 births, the incidence of each subtype was: NAIS = 3.2 (~1:3000), APPIS =1.2 (~1:8500), PVI = 1.5 (~1:6500), CSVT = 1.0 (~1:9900), NHS = 1.4 (~1/7300), PPHS = 0.1 (1/82,000). Conclusions: The overall incidence of perinatal stroke in Southern Alberta is 1:1200 live births. Population-based sampling of disease-specific states may explain why this rate is much higher than previous estimates

Abstract P581: Neonatal Stroke is Not Associated With Birth Trauma

Acute neonatal stroke causes cerebral palsy, lifelong morbidity and mortality. Neonatal arterial ischemic stroke (NAIS) and hemorrhagic stroke (NHS) are most common. Pathophysiology is poorly understood and causation is often attributed to observed obstetrical factors such as instrumentation (forceps or vacuum) or operative delivery despite no empiric evidence supporting an association. We explored the relationship between birth trauma and neonatal stroke via population-based, prospectively collected registries in Southern Alberta, Canada. Consecutive cases of NAIS (n=59), NHS (n=20), and neonatal hypoxic-ischemic encephalopathy HIE with MRI-confirmed injury (HIE+, n=78)) were compared to neonates without injury (HIE-n=77). Cranial soft tissue swelling was objectively quantified as a trauma score from T1-weighted images using a semi-automatic segmentation method performed by two blinded investigators. Maternal, obstetrical, perinatal, and outcome variables were obtained from medical records. Multinomial regression modeling evaluated the relationship between diagnosis and birth trauma as measured by total soft tissue swelling score and diagnosis (HIE- as controls). Across the 234 infants studied, mean age at MRI (4.1+/-1.3 days) and sex (54% male) were comparable. Measurable scalp trauma was present in 93(40%), the proportion of which did not differ across groups. On univariate analysis, mean trauma scores did not differ between groups, were not associated with NHS or HIE+, and were lower for the NAIS group compared to HIE- (controls). Multinomial modeling revealed no relationship between scalp trauma and outcome. We conclude that the leading forms of acquired neonatal brain injury are not associated with objectively measured birth trauma. The term “birth trauma” should be removed from the perinatal stroke vernacular to help counsel traumatized parents and advance studies of genuine pathophysiology.

Population Based Birth Prevalence of Disease-Specific Perinatal Stroke.

Perinatal stroke encompasses multiple disease-specific cerebrovascular syndromes that cause lifelong neurodevelopmental morbidity for millions worldwide. Acute presentations include neonatal arterial ischemic stroke (NAIS), neonatal cerebral sinovenous thrombosis, and neonatal hemorrhagic stroke (NHS). Delayed presentations include arterial presumed perinatal ischemic stroke, periventricular venous infarction, and presumed perinatal hemorrhagic stroke. Our objective was to define the birth prevalence of all subtypes of perinatal stroke by using a population-based cohort. The Alberta Perinatal Stroke Project is a research cohort established in 2008 in southern Alberta, Canada, with prospective (2008-2017) and retrospective (1990-2008) enrollment leveraging universal health care at a single tertiary care pediatric center. The primary outcome was the estimated birth prevalence of each perinatal stroke syndrome, secondary outcomes were birth prevalence over time, sex ratios, and change in age at diagnosis. Analysis included Poisson regression, Wilcoxon rank test, and Fisher exact test. The overall estimated birth prevalence of term-born perinatal stroke was 1:1100. The estimated birth prevalence was 1:3000 for NAIS, 1:7900 for arterial presumed perinatal ischemic stroke, 1:6000 for periventricular venous infarction, 1:9100 for cerebral sinovenous thrombosis, 1:6800 for NHS, and 1:65000 for presumed perinatal hemorrhagic stroke. The apparent birth prevalence of NAIS and NHS increased over time. There were more males affected than females. The age at diagnosis decreased for late-presenting stroke types. The estimated birth prevalence of term perinatal stroke is higher than previous estimates, which may be explained by population-based sampling of disease-specific states. This emphasizes the need for further studies to better understand the disease-specific pathophysiology to improve treatment and prevention strategies.

Deep medullary vein engorgement and superficial medullary vein engorgement: two patterns of perinatal venous stroke.

Perinatal venous stroke has classically been attributed to cerebral sinovenous thrombosis with resultant congestion or thrombosis of the small veins draining the cerebrum. Advances in brain MRI, in particular susceptibility-weighted imaging, have enabled the visualization of the engorged small intracerebral veins, and the spectrum of perinatal venous stroke has expanded to include isolated congestion or thrombosis of the deep medullary veins and the superficial intracerebral veins. Congestion or thrombosis of the deep medullary veins or the superficial intracerebral veins can result in vasogenic edema, cytotoxic edema or hemorrhage in the territory of disrupted venous flow. Deep medullary vein engorgement and superficial medullary vein engorgement have characteristic findings on MRI and should be differentiated from neonatal hemorrhagic stroke.

Abstract 51: The Incidence of Perinatal Stroke is 1:1200 Live Births: A Population-Based Study in Alberta Canada

Introduction: Perinatal stroke encompasses six cerebrovascular syndromes which occur between the 20 th week of gestation and the 28 th post-natal day. Morbidity is significant including motor, language, behavioral, and cognitive challenges, as well as epilepsy. Acute presentations include neonatal arterial ischemic stroke (NAIS), neonatal cerebral sinovenous thrombosis (CSVT), and neonatal hemorrhagic stroke (NHS). Delayed presentations include arterial presumed perinatal ischemic stroke (APPIS), periventricular venous infarction (PVI), and presumed perinatal hemorrhagic stroke (PPHS). Inconsistent terminology and lack of population-based cohorts has limited accurate measurement of disease-specific perinatal stroke incidence. Our objective was to define the incidence of the subtypes of perinatal stroke using a population-based cohort. Methods: The Alberta Perinatal Stroke Project is a research cohort established in 2008 in Southern Alberta, Canada (population ~2.1 million). Leveraging universal health care at a single tertiary care pediatric center facilitated true population-based epidemiology. Patients included had neuroimaging-confirmed perinatal stroke. Case acquisition included exhaustive retrospective hospital and ICD code searches (1990-2008) and prospective enrollment from all NICU and neurology/stroke clinics (2008-2018). Live birth rate denominators were determined from the provincial census. Results: The overall incidence of perinatal stroke in Southern Alberta from 2008-2018 was 81 cases per 100,000 live births, or 1 case per approximately 1200 live births. The incidence of NAIS was 31 per 100,000 (~1/3000), APPIS was 11 per 100,000 (~1/9000), PVI was 18 per 100,000 (~1/5500), and CSVT was 10 per 100,000 (~1/9800). The incidence of NAIS increased after implementing prospective case identification, from 8.5 (95% CI 5.3-11.6) per 100,000 to 31 per 100,000 (95% CI 24.4-38.2), p&lt;0.00001, the remainder of stroke subtypes were stable over time. Conclusions: The overall incidence of perinatal stroke in Southern Alberta is 1:1200 live births. Population-based sampling of disease-specific states may explain why this rate is much higher than previous estimates.

Perinatal Stroke

Perinatal strokes are a diverse but specific group of focal cerebrovascular injuries that occur early in brain development and affect an estimated 5 million people worldwide. The objective of this review is to describe the epidemiology, clinical presentations, pathophysiology, outcomes, and management for the 6 subtypes of perinatal stroke. Some perinatal strokes are symptomatic in the first days of life, typically with seizures, including neonatal arterial ischemic stroke, neonatal hemorrhagic stroke, and cerebral sinovenous thrombosis. The remaining subtypes present in the first year of life or later, usually with motor asymmetry and include arterial presumed perinatal ischemic stroke, presumed perinatal hemorrhagic stroke, and in utero periventricular venous infarction. The consequences of these injuries include cerebral palsy, epilepsy, and cognitive and behavioral challenges, in addition to the psychosocial impact on families. While there have been significant advances in understanding mechanisms of both injury and recovery, there is still a great deal to learn regarding causation and the optimization of outcomes.

Epidemiology of neonatal stroke: A population-based study.

The goal of this study was to obtain population-based data on the incidence, clinical presentation, management, imaging features, and long-term outcomes of patients with all types of neonatal stroke (NS). Full-term neonates with NS born between January 2007 and December 2013 were identified through the Nova Scotia Provincial Perinatal Follow-up Program Database. Perinatal data and neonatal course were reviewed. Neurodevelopmental outcomes were assessed at 18 and 36 months of age using standardized testing. Twenty-nine neonates with NS were identified during the study period, giving an incidence of 47 per 100,000 live births in Nova Scotia. Arterial ischemic stroke was the most common stroke type (76%), followed by neonatal hemorrhagic stroke (17%), then cerebral sinovenous thrombosis (7%). The majority of neonates presented with seizures (86%) on the first day of life (76%). At 36 months of age, 23 (79%) of the children had a normal outcome, while 3 (10%) were diagnosed with cerebral palsy (2 with neonatal arterial stroke and one with neonatal hemorrhagic stroke) and 3 (10%) had recurrent seizures (1 patient from each stroke subtype group). The incidence of NS in Nova Scotia is higher than what has been reported internationally in the literature. However, the neurodevelopmental outcomes at 3 years of age are better. Further studies are required to better understand the reasons for these findings.

Epilepsy after perinatal stroke with different vascular subtypes.

SummaryObjectiveWith an incidence up to 63 per 100,000 live births, perinatal stroke is an important cause of childhood epilepsy. The aim of the study was to find the prevalence of and predictive factors for epilepsy, and to describe the course of epilepsy in children with perinatal stroke with different vascular subtypes.MethodsPatients were retrieved from the Estonian Paediatric Stroke Database with follow‐up time at least 24 months. Patients were divided into 5 perinatal stroke syndromes: neonatal arterial ischemic stroke (AIS), neonatal hemorrhagic stroke, neonatal cerebral sinovenous thrombosis, presumed AIS, and presumed periventricular venous infarction.ResultsThe final study group included 73 children with perinatal stroke (39 boys). With a median follow‐up time of 8.6 years, epilepsy was diagnosed in 21/73 (29%) children, most of whom had AIS (17/21, 81%). The 18‐year cumulative poststroke epilepsy risk according to the Kaplan‐Meier estimator was 40.8% (95% confidence interval [CI] 20.7–55.9%). The median age at epilepsy diagnosis was 50 months (range 1 month to 18.4 years). Children with neonatal AIS had the highest risk of epilepsy, but children with presumed AIS more often had severe epilepsy syndromes. Cortical lesions (odds ratio [OR] 19.7, 95% CI 2.9–133), and involvement of thalamus (OR 9.8, 95% CI 1.8–53.5) and temporal lobe (OR 8.3, 95% CI 1.8–39.6) were independently associated with poststroke epilepsy.SignificanceThe risk for poststroke epilepsy after perinatal stroke depends on the vascular subtype. Patients with perinatal AIS need close follow‐up to detect epilepsy and start with antiepileptic treatment on time.

Duplex Sonographic Diagnosis of Perinatal Hemorrhagic Stroke.

Children are particularly at risk for stroke in the neonatal period. Neonatal hemorrhagic stroke is rarer than ischemic stroke. The incidence is 40.7/100 000 live births. Hemorrhagic stroke is caused by a disruption in venous drainage usually due to local thrombosis. As a result of the nonspecific clinical symptoms in this age group, diagnosis is usually made too late. The only relatively specific symptom is a cerebral seizure during the first week of life. Therefore, stroke should be ruled out by diagnostic imaging in the case of any seizure in the first days of life. The diagnostic method of choice is MRI, but it is not always available. Most neonatal strokes can be detected with high-resolution duplex ultrasound. Hemorrhagic stroke appears as a focal increase in echogenicity in a venous drainage area on ultrasound. The corresponding venous drainage can be visualized with duplex ultrasound and measured with spectral Doppler. Hemorrhagic stroke of the internal veins appears as hemorrhage in the basal ganglia. Venous thrombosis must be ruled out in every cerebral hemorrhage of unclear origin in an otherwise healthy term newborn. In the case of hemorrhagic infarction of the basal ganglia, both internal cerebral veins, the great vein of Galen, and the straight sinus must be examined with Doppler ultrasound. Doppler ultrasound should be used to differentiate between complete occlusion and severe stenosis. The recanalization of vessels and the morphological consequences of hemorrhagic stroke can be visualized in the further course.

Thalamic Hemorrhagic Stroke in the Term Newborn: A Specific Neonatal Syndrome With Non-uniform Outcome.

Neonatal thalamic hemorrhagic stroke is related to cerebral sinus venous thrombosis and associated with neurological sequelae. Predicting factors are however lacking. Clinical and radiological findings at onset and on follow-up of 5 neonates with thalamic hemorrhage stroke are described. All neonates presented with abrupt lethargy, ophistotonos, irritability and/or seizures. The thalamic hemorrhagic stroke was most often unilateral (4/5), involving the posterior/entire thalamus in 3 cases and the anterior thalamus in 2. Cerebral venous thrombosis was identified in a single patient. At follow-up, children with unilateral anterior thalamic hemorrhagic stroke demonstrated thalamic atrophy without neurological symptoms, whereas children whose thalamus lesion was extensive exhibit a porencephalic cavity and presented with late-onset epilepsy. Although deep cerebral venous thrombosis is probably the cause of neonatal thalamic hemorrhagic stroke, its radiological evidence is challenging. Outcome seems dependent of the size and location of thalamic hemorrhagic stroke. Epilepsy is a frequent morbidity after thalamic hemorrhagic stroke.

Clinical Characteristics, Risk Factors, and Outcomes Associated With Neonatal Hemorrhagic Stroke

Hemorrhage into the brain of term newborns often results in major injury and lifelong disability. The clinical epidemiology of neonatal hemorrhagic stroke (NHS) remains undefined, hindering the development of strategies to improve outcomes. To characterize the incidence, types, presentations, associated factors, and outcomes of neonatal hemorrhagic stroke. Population-based, nested case-control study. The Alberta Perinatal Stroke Project, a provincial registry, ascertained NHS cases using exhaustive diagnostic code searching (1992-2010, >2500 medical record reviews). Prospective cases were captured through the Calgary Pediatric Stroke Program (2007-2014). Participants included term neonates with magnetic resonance imaging-confirmed NHS including primary and secondary intracerebral hemorrhage, hemorrhagic transformation of ischemic injury, and presumed perinatal hemorrhagic stroke. Control infants with common data were recruited from a population-based study (4 to 1 ratio). Infants with NHS underwent structured medical record review using data-capture forms and blinded scoring of neuroimaging. Clinical risk factor common data elements were explored using logistic regression. Provincial live births were obtained from Statistics Canada. Outcomes were extrapolated to the Pediatric Stroke Outcome Measure. We identified 86 cases: 51 infants (59%) with NHS, of which 32 (67%) were idiopathic, 30 (35%) were hemorrhagic transformation of primary ischemic injuries (14 with neonatal cerebral sinovenous thrombosis, 11 with hypoxic ischemic encephalopathy, and 5 with neonatal arterial ischemic stroke), and 5 were presumed perinatal hemorrhagic stroke. Sixty-two percent were male. Incidence of pure NHS was 1 in 9500 live births and 1 in 6300 for all forms. Most presented in the first week of life with seizures and encephalopathy. Acute neurosurgical intervention was rare (3 of 86 total cases; 3.5%). Temporal lobe was the most common NHS location (16 of 51 pure NHS cases; 31%). A primary cause was evident in 19 of the 51 cases of non-hemorrhagic transformation NHS (37%). Idiopathic NHS was independently associated with lower maternal age (odds ratio [OR], 0.87; 95% CI, 0.78-0.94), primiparity (OR, 2.98; 95% CI, 1.18-7.50), prior spontaneous abortion (OR, 0.11; 95% CI, 0.02-0.53), difficult fetal transition (bradycardia [OR, 15.0; 95% CI, 2.19-101.9] and low Apgar [OR, 14.3; 95% CI, 2.77-73.5]), and small for gestational age (OR, 14.3; 95% CI, 1.62-126.1). Follow-up of 50 cases at a median of 37 months demonstrated poor neurological outcomes in 21 patients (44%). Neonatal hemorrhagic stroke is more common than previously reported, occurring in at least 1 in 6300 live births. Etiologies are approximately equally distributed between idiopathic, secondary, and hemorrhagic transformation. Clinical associations do not suggest a common mechanism or predictability of NHS. Recurrence is rare. Outcomes are often poor, mandating attention to prevention and rehabilitation.

Optical monitoring of stress-related changes in the brain tissues and vessels associated with hemorrhagic stroke in newborn rats.

Stress is a major factor for a risk of cerebrovascular catastrophes. Studying of mechanisms underlying stress-related brain-injures in neonates is crucial for development of strategy to prevent of neonatal stroke. Here, using a model of sound-stress-induced intracranial hemorrhages in newborn rats and optical methods, we found that cerebral veins are more sensitive to the deleterious effect of stress than arteries and microvessels. The development of venous insufficiency with decreased blood outflow from the brain accompanied by hypoxia, reduction of complexity of venous blood flow and high production of beta-arrestin-1 are possible mechanisms responsible for a risk of neonatal hemorrhagic stroke.

Neonatal hemorrhagic stroke: population-based epidemology

Background: Stroke is a leading cause of perinatal brain injury and cerebral palsy. Term neonatal hemorrhagic stroke (NHS) is a common syndrome with poorly defined epidemiology. We aimed to determine incidence and mechanisms within a large population-based NHS sample. Methods: The Alberta Perinatal Stroke Project (APSP), a provincial registry ascertained NHS cases using exhaustive ICD-9/10 code searching (1992-2012, &gt;2400 chart reviews). Prospective cases were captured through the Calgary Pediatric Stroke Program from 2007-2014 (n=387). All NHS cases underwent structured chart review using a data capture form and blinded review of neuroimaging. Provincial live births were obtained from statistics Canada. Outcomes were extrapolated to the Pediatric Stroke Outcome Measure (PSOM). Results: We identified 74 cases: 49 NHS (26 retrospective, 27 prospective), 4 presumed perinatal HS (PPHS), and 21 hemorrhagic transformation (HT) of ischemic injury. Incidence of NHS was 1:8800 live births (1:5820 for all forms). HT was common (28.4%) including global, arterial venous ischemic lesions. Presumed perinatal hemorrhagic stroke presented with epilepsy. No risk factor was identified in 68% of cases. Outcomes were abnormal (PSOM 1 or more) in 30% and better in the HT group. Conclusion: NHS occurs in 1:8800 live births. Imaging classification is essential to define mechanisms.

Life After Perinatal Stroke

Perinatal strokes are a well-defined group of cerebrovascular diseases that damage the brain early in life and account for most cases of hemiparetic cerebral palsy. The motor deficits are now sufficiently researched to inform early prognostication, the construction of developmental plasticity models, and new clinical trials. Nonmotor outcomes are more complex and are challenging to measure given their emergence with time during developmental maturation. Several fundamental gaps in the understanding of perinatal stroke outcomes are of essential clinical relevance. How can 2 children with virtually identical brain lesions acquired at the same time have extremely different outcomes? How does a child develop new skills that his or her brain has never possessed during stroke recovery? How do we measure outcome as the child continues to grow into deficits with maturation? What are the modulators of developmental plasticity that might be targeted to achieve better functional outcomes? We review the current state of knowledge on perinatal stroke outcomes and attempt to highlight elements that might provide insight into these pressing questions. The most focused lifetime risk for stroke is the week surrounding birth.1 A term newborn carries a risk of ischemic stroke of ≥1:3500, triple the weekly stroke risk of a smoking adult with diabetes mellitus and hypertension.1,2 Adding in populations of neonatal hemorrhagic stroke, sinovenous thrombosis, and late presenting presumed perinatal strokes likely more than doubles the incidence of perinatal stroke.3,4 Outcomes are generally poor with disability often lasting an entire lifetime, resulting in a large global burden of disease. Perinatal stroke is the most common cause of hemiparetic cerebral palsy, and many survivors have additional neurological sequelae including intellectual disabilities, developmental and behavioral disorders, and epilepsy. Identification of a causative factor for perinatal stroke remains elusive in most cases1 with no …

Rare neonatal diabetes insipidus and associated late risks: Case report

BackgroundMost cases of neonatal central diabetes insipidus are caused by an injury, which often results in other handicaps in the patient. The infant’s prognosis will be determined by his or her own early age and disability as well as by the physician’s skill. However, the rarity of this condition prevents the acquisition of personal experience dealing with it.Case Presentation A neonatal hemorrhagic stroke, caused by an aortic coarctation, caused right lower limb paresis, swallowing disability, and central diabetes insipidus in a term infant. The scant oral intake, as a consequence of his disability, caused progressive undernutrition which closed a vicious circle, delaying his development and his ability to overcome the swallowing handicap. On the other hand, nasal desmopressin absorption was blocked by several common colds, resulting in brain bleeding because of severe dehydration. This even greater brain damage hampered the improvement of swallowing, closing a second harmful circle. Moreover, a devastating central myelinolysis with quadriplegia, caused by an uncontrolled intravenous infusion, consummated a pernicious sequence, possibly unreported.ConclusionsThe child’s overall development advanced rapidly when his nutrition was improved by gastrostomy: This was a key effect of nutrition on his highly sensitive neurodevelopment. Besides, this case shows potential risks related to intranasal desmopressin treatment in young children.