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Table of Contents    
ORIGINAL ARTICLE
Year : 2021  |  Volume : 69  |  Issue : 1  |  Page : 62-65

Clinico-Epidemiological Profile, Etiology, and Imaging in Neonatal Stroke: An Observational Study from Eastern India


1 Department of Pediatric Medicine, Institute of Child Health, Kolkata, West Bengal, India
2 Department of Radiology, Institute of Child Health, Kolkata, West Bengal, India

Date of Submission13-Jan-2018
Date of Decision13-Jan-2018
Date of Acceptance16-Mar-2018
Date of Web Publication24-Feb-2021

Correspondence Address:
Devdeep Mukherjee
Department of Pediatric Medicine, Institute of Child Health, Kolkata - 700019, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.310081

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 » Abstract 


Aim: The aim of this study was to assess the clinico-epidemiological profile, etiology, and imaging findings in neonatal stroke (NS).
Materials and Methods: This was a retrospective, observational study on neonates presenting with stroke between August 2014 and July 2016 to a tertiary care hospital in eastern India.
Results: In all, 43 neonates were analyzed, with a male-to-female ratio of 2.3:1. About 88% babies were born at term and the rest were preterm. In 37%, the etiology of stroke was related to hypoxic injury, 21% had sepsis, and 35% had idiopathic causes. Seizures were the most common mode of presentation (62%) followed by poor feeding, abnormal tone, recurrent apnea, encephalopathy, and hemiparesis. There was an almost equal prevalence of ischemic stroke (53%) and hemorrhagic stroke (HS). Middle cerebral artery territory was the primary site of involvement in arterial ischemic stroke, and intra ventricular hemorrhage was the most common presentation of HS.
Conclusion: NS is an acute emergency with high morbidity and mortality. Magnetic resonance imaging helps in diagnosis and prognostication in the absence or paucity of focal neurological signs in neonates.


Keywords: Arterial ischemic stroke (AIS), encephalopathy, hemorrhagic stroke (HS), magnetic resonance imaging (MRI), neonatal stroke (NS), seizures
Key Message: Neonatal stroke is n acute emergency. Hypoxic injury and sepsis are the commonest etiology in the neonates. Magnetic resonance imaging helps in diagnosis and prognosticatication.


How to cite this article:
Mukherjee D, Kalita D, Das D, Kumar T, Kundu R. Clinico-Epidemiological Profile, Etiology, and Imaging in Neonatal Stroke: An Observational Study from Eastern India. Neurol India 2021;69:62-5

How to cite this URL:
Mukherjee D, Kalita D, Das D, Kumar T, Kundu R. Clinico-Epidemiological Profile, Etiology, and Imaging in Neonatal Stroke: An Observational Study from Eastern India. Neurol India [serial online] 2021 [cited 2021 Aug 4];69:62-5. Available from: https://www.neurologyindia.com/text.asp?2021/69/1/62/310081




Stroke in pediatrics can be classified as perinatal or childhood stroke. Perinatal stroke (PS) can be further subclassified into presumed perinatal and neonatal stroke (NS). PS can occur as a result of vascular insult to the developing fetal brain between 20th week of gestation and 28 days of life. The incidence of PS is 1 in 2300–5000 live births. The onset of stroke between birth and 28 days of life is called as NS.[1],[2],[3],[4] Based on anatomical involvement, NS can be further classified into arterial ischemic stroke (AIS), hemorrhagic stroke (HS), cerebral sinovenous thrombosis (CST), and peri-ventricular venous infarction.[3]This can be differentiated by imaging. NS is a medical emergency and is associated with multiple risk factors. It is associated with long-term morbidity such as hemiplegic cerebral palsy, seizures, and neurodevelopmental delay.[4] Mortality rates are between 1% and 25%.[2] Till date, there are no studies available from India which have looked into the profile of stroke in neonates. This study retrospectively evaluates the clinico-epidemiological profile and imaging findings of neonates admitted with stroke to a tertiary care hospital in eastern India.

Objectives

  1. Clinico-epidemiological profile and risk factors of neonates admitted with stroke
  2. Imaging findings on magnetic resonance imaging (MRI)



 » Materials and Methods Top


Study setting

This study was carried out in a neonatal intensive care unit (NICU) of a tertiary care hospital in eastern India.

Study period

All neonates diagnosed to have a stroke and admitted to NICU between August 2014 and July 2016 were included.

Study design

This was a retrospective, observational, descriptive study.

Study population

A total of 43 neonates diagnosed to have NS by 28 days of life were included. Neonates with trauma to the head were excluded. Patients were classified under AIS or HS. A registry was maintained to document the clinico-epidemiological profile, clinical symptoms, and signs at presentation. “Hypoxic injury” was considered when there was evidence of fetal distress characterized by absent/reduced fetal movements or inadequate/absence of resuscitation measures following delivery and before referral to a tertiary care unit. “Neonatal encephalopathy” was defined as an abnormal level of consciousness with diminished tone and reflex, with/without seizures.[5] Patients were evaluated for infection (blood, cerebro-spinal fluid study), hypoglycemia, electrolytes, or clotting abnormalities. Electroencephalogram (EEG) was done when there was clinical evidence of seizures. Electrocardiogram (ECG) was performed in all babies admitted with stroke to detect evidence of arrhythmia if any. Echocardiography was done if there was clinical evidence of murmur, difference in pre-ductal and post-ductal saturations, or if femoral pulses were absent. MRI was performed on all babies in our hospital. Ethical clearance was obtained from the hospital ethics committee.


 » Results Top


A total of 43 neonates admitted with NS to our NICU were analyzed for this study. Antenatal history of maternal sepsis was present in five neonates (12%). About 88% (n = 38) were born at term (37–40 weeks) and the remaining (n = 5) were pre-term (≥34 to < 37 weeks). Around 70% (n = 30) were male infants with the male-to-female ratio being 2.3:1. There was a male preponderance in both the pre-term and the term populations. APGAR scores were not documented for all patients and hence were not considered for analysis. The median age of presentation in pre-terms was four days. However, term babies presented late and had a median age of presentation of 11 days.

In pre-terms, poor feeding (n = 4), abnormal tone (n = 3), and recurrent apnea (n = 3) were the most common presentation followed by seizures (n = 2) [Table 1]. About 60% (n = 3) had hypoxic injury and 40% (n = 2) had sepsis, of which one baby had Escherichia coli isolated from blood and the other had necrotizing enterocolitis.
Table 1: Clinicoepidemiological profile and etiology for neonatal stroke in preterm infants

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In term babies, seizures were documented in 67% (n = 25) and was the most common presentation followed by poor feeding in 32% (n = 12) and abnormal tone in 26% (n = 10) [Table 2]. The remaining presented with recurrent apnea, encephalopathy, hemiparesis, and abnormal tone. A total of 39% (n = 15) remained undiagnosed as financial constraints prevented us from performing thrombophilia or metabolic screen in these babies. Hypoxic injury remained the most commonly diagnosed etiology in 38% (n = 13) babies followed by sepsis in 18%. One baby had hypoglycemia, one had fatty acid oxidation defect, and another had complex cardiac disease [total anomalous pulmonary venous drainage (TAPVD)].
Table 2: Clinicoepidemiological profile and etiology for neonatal stroke in term infants

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MRI brain revealed 53% (n = 23) to be having AIS and 47% with HS [Table 3]. There was an increase in male preponderance in both the groups with median presentation being seven days in both AIS and HS. Around 70% (n = 16) had involvement of the middle cerebral artery (MCA) which was the most common area of distribution in AIS [Table 4]; [Figure 1]. Among 20 babies with HS, 11 had intra ventricular hemorrhage (IVH), 4 had intra parenchymal hemorrhage (IPH), and the remaining five had both IPH and IVH. There was one baby with sepsis and extensive hemorrhage involving the brain stem who died.
Table 3: Demographics in AIS and HS

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Figure 1: Varying presentation of MRI brain in neonates presenting with stroke

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Table 4: MRI findings in neonatal stroke

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 » Discussion Top


The etiology of NS is still not well-explained in literature. In about 25%–50% of cases, the etiology may remain unexplained.[6],[7] The acute presentation is usually as neonatal encephalopathy. Neurodevelopmental delay, sensori-motor deficits, poor cognition, epilepsy, and behavioural problems have been noted in infants having an early insult to the developing brain.[8],[9] However, studies have shown a more favorable outcome in neonates compared with other population group due to the increased plasticity of the developing brain. Imaging techniques especially MRI remains the investigation of choice as focal neurological signs are often difficult to elicit in neonates.[10]

NS especially HS is quite common in less than 32 weeks of gestation, mainly due to germinal matrix hemorrhage. However, they have been documented in late pre-term and term infants as we found in our study.[2] NS was more common in males in our study, although no such prevalence has been noted in previous studies.

NS has been associated with sepsis/meningitis, fetal hypoxia, embolism, trauma, arteriopathy, vascular malformations, prothrombotic conditions, and idiopathic reasons.[3],[11],[12],[13] In our population, we found an increasing association with hypoxia (37%) and sepsis (21%). About 35% remained undiagnosed similar to previous studies.[3] The significant large number of patients with hypoxia is possible because of limited resuscitation facilities and inadequate airway support during transport. National neonatal perinatal database has documented perinatal asphyxia contributing to 20% of neonatal deaths and a third of still births in 2000.[14]We were also not able to perform thrombophilia screen because of financial constraints. Several studies have documented prothrombotic conditions to be the etiology behind 30% of NS.[12] Hence, a considerable number of neonates remained undiagnosed.

Seizures were the most common symptom in our study similar to other studies and usually were noted within the first 24 h. Apnea, altered tone, hemiparesis, encephalopathy, poor feeding, and irritability were also noted.[15] Apnea along with bradycardia or change in tone was considered as a manifestation of seizure.

Although AIS remains the most common subtype of NS, we found an almost equal distribution of AIS and HS.[3],[4] This might be because of the small population size of our study. MCA territory was the most common site of involvement in AIS similar to other studies.[1],[16] IVH was the most common form of involvement in HS. Subdural and subarachnoid hemorrhage was also noted along with IPH.[2] MRI is the most sensitive tool for diagnosis and prognostication of outcome in NS.[17] Diffusion-weighted imaging along with T1- and T2-weighted sequence help in early delineation of AIS within the first week of life.

Congenital heart disease has been documented to cause HS in several studies.[2],[18] Because our hospital is not a cardiac referral center, we had only one baby with TAPVD with HS. Babies should undergo ECG and echocardiography whenever there is suspicion of cardiac involvement.

Limitations of the study

We did a retrospective collection of data on a small population referred to our hospital for diagnosis and management. Antenatal risk factors for stroke were therefore difficult to document for all the patients. Placental biopsy and thrombophilia screen were also not possible due to various constraints. Thrombophilia remains one of the common causes of NS.[12]Metabolic panel was done in only four babies due to financial constraints.


 » Conclusion Top


NS remains an acute emergency with high morbidity and mortality. Seizures remain the most common presenting symptom. MRI helps in delineating and prognostication of infants with NS. Improvement in resuscitation facilities and better antenatal monitoring will help in improving the outcome in neonates and reduce the incidence of NS in India.

Source of support

None.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Ghotra SK, Johnson JA, Qiu W, Newton A, Rasmussen C, Yager JY. Age at stroke onset influences the clinical outcome and health-related quality of life in pediatric ischemic stroke survivors. Dev Med Child Neurol 2015;57:1027-34.  Back to cited text no. 1
    
2.
Bruno CJ, Beslow LA, Witmer CM, Vossough A, Jordan LC, Zelonis S. Haemorrhagic stroke in term and late preterm neonates. Arch Dis Child Fetal Neonatal Ed 2014;99:F48-53.  Back to cited text no. 2
    
3.
Govaert P, Ramenghi L, Taal R, Dudink J, Lequin M. Diagnosis of perinatal stroke II: Mechanisms and clinical phenotypes. Acta Paediatr 2009;98:1720.  Back to cited text no. 3
    
4.
Lehman LL, Rivkin MJ. Perinatal arterial ischemic stroke: Presentation, risk factors, evaluation, and outcome. Pediatr Neurol 2014;51:760.  Back to cited text no. 4
    
5.
Mcintyre S, Badawi N, Blair E, Nelson KB. Does aetiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy influence the outcome of treatment? Dev Med Child Neurol 2015;57(Suppl 3):2-7.  Back to cited text no. 5
    
6.
Adén U. Neonatal stroke is not a harmless condition. Stroke 2009;40:1948-9.  Back to cited text no. 6
    
7.
Govaert P, Matthys E, Zecic A, Roelens F, Oostra A, Vanzieleghem B. Perinatal cortical infarction within middle cerebral artery trunks. Arch Dis Child Fetal Neonatal Ed 2000;82:F59-63.  Back to cited text no. 7
    
8.
Lynch JK, Hirtz DG, DeVeber G, Nelson KB. Report of the National Institute of Neurological Disorders and Stroke workshop on perinatal and childhood stroke. Pediatrics 2002;109:116-23.  Back to cited text no. 8
    
9.
Raju TN, Nelson KB, Ferriero D, Lynch JK, Participants N-NPSW. Ischemic perinatal stroke: Summary of a workshop sponsored by the National Institute of Child Health and Human Development and the National Institute of Neurological Disorders and Stroke. Pediatrics 2007;120:609-16.  Back to cited text no. 9
    
10.
Venkataraman A, Kingsley PB, Kalina P, Pavlakis SG, Buckwald S, Spinazzola R, et al. Newborn brain infarction: Clinical aspects and magnetic resonance imaging. CNS Spectr 2004;9:436-44.  Back to cited text no. 10
    
11.
Armstrong-Wells J, Johnston SC, Wu YW, Sidney S, Fullerton HJ. Prevalence and predictors of perinatal hemorrhagic stroke: Results from the kaiser pediatric stroke study. Pediatrics 2009;123:823.  Back to cited text no. 11
    
12.
Günther G, Junker R, Sträter R, Schobess R, Kurnik K, Heller C, et al. Symptomatic ischemic stroke in full-term neonates: Role of acquired and genetic prothrombotic risk factors. Stroke 2000;31:2437.  Back to cited text no. 12
    
13.
Simchen MJ, Goldstein G, Lubetsky A, Strauss T, Schiff E, Kenet G, et al. Factor v Leiden and antiphospholipid antibodies in either mothers or infants increase the risk for perinatal arterial ischemic stroke. Stroke 2009;40:65.  Back to cited text no. 13
    
14.
Report of the National Neonatal Perinatal Database (National Neonatology Forum, India); 2000.  Back to cited text no. 14
    
15.
Lehman LL, Rivkin MJ. Perinatal arterial ischemic stroke: Presentation, risk factors, evaluation, and outcome. Pediatr Neurol 2014;51:760.  Back to cited text no. 15
    
16.
Ecury-Goossen GM, Raets MM, Lequin M, Feijen-Roon M, Govaert P, Dudink J, et al. Risk factors, clinical presentation, and neuroimaging findings of neonatal perforator stroke. Stroke 2013;44:2115.  Back to cited text no. 16
    
17.
Varghese B, Xavier R, Manoj VC, Aneesh MK, Priya PS, Kumar A. Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury. Indian J Radiol Imaging 2016;26:316-27.  Back to cited text no. 17
[PUBMED]  [Full text]  
18.
Renjen PN, Chaudhari D, Meman M. An unusual combination of patent foramen ovale with pulmonary arteriovenous malformation in a young patient with stroke. Neurol India 2017;65:891-2.  Back to cited text no. 18
[PUBMED]  [Full text]  


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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