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BRIEF COMMUNICATIONS: V. Ramaswamy, S. P. Miller, A. J. Barkovich, J. C. Partridge, and D. M. Ferriero Perinatal stroke in term infants with neonatal encephalopathy Neurology 2004; 62: 2088-2091 [Abstract] [Full text] [PDF]

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Perinatal stroke in term infants with neonatal encephalopathy

Frances M Cowan, Eugenio Mercuri, Mary A Rutherford   (31 August 2004)

Reply to Cowan et al

Donna M. Ferriero, Vijay Ramaswamy, Steven P. Miller, A. James Barkovich, J. Colin Partridge   (31 August 2004)

Perinatal stroke in term infants with neonatal encephalopathy 31 August 2004
Frances M Cowan, Imperial College, London Dept. of Paediatrics, Hammersmith Hospital, DuCane Rd, London W12 OHS, UK, Eugenio Mercuri, Mary A Rutherford Send Correspondence to journal: Re: Perinatal stroke in term infants with neonatal encephalopathy f.cowan{at}imperial.ac.uk Frances M Cowan, et al.	We read with interest the article by Ramaswamy et al [1] on stroke in term infants presenting with early neonatal encephalopathy. We agree this is an unusual presentation of neonatal arterial territory stroke. We found a similar proportion with stroke (8/197,4%) in encephalopathic term infants. [2] However, we found that the majority of these infants do not have evidence of infection, cardiac disease or prothrombotic disorders. [3] Our experience is that cognitive outcome is generally good following unilateral arterial territory stroke. Hemiplegia will develop if basal ganglia, internal capsule (PLIC) and hemispheric tissue are involved in the primary lesion. [4] Cognition is poorer if there are bilateral infarcts or other imaging abnormalities. We have observed a poor cognitive outcome in two infants with small MCA territory infarcts but no hemiplegia – both are mildly dysmorphic without specific diagnoses despite extensive investigation. The other children with poor cognitive outcomes are those few that later develop seizures. We think the poor cognitive outcome reported here is mainly due to bilateral tissue involvement; extensive white matter involvement is associated with cognitive deficit. [5] If stroke is associated with basal ganglia lesions, those will dominate the motor outcome. In case 3 (Fig 1) in addition to the right-sided middle/posterior MCA territory infarction, we believe that the image shows severe abnormality in the left basal ganglia and PLIC. It is possible that the left-sided lesions together with the watershed lesions account for the severe outcome rather than the MCA territory lesion alone. Several of the cited cases are also complicated. Case 1 is an infant of a diabetic mother, a high risk group, case 2 has a large infarction on the background of infection which may affect white matter and can be difficult to assess on early conventional images. Cases 5 and 6 had additional lesions not confined to one arterial territory. We feel the emphasis given to poor outcome with MCA territory infarction is misleading and that the important issue in terms of cognitive outcome is the extent of the additional watershed or bilateral lesions. Nonetheless we strongly support that clinicians need to be aware that neonatal stroke, when it occurs in an unusual context, is more likely to be associated with a poorer cognitive outcome and such infants deserve close neurodevelopmental follow up. References 1.Ramaswamy V, Miller SP, Barkovich AJ, Partridge JC, Ferriero DM. Perinatal stroke in term infants with neonatal encephalopathy. Neurology 2004;62:2088-91 2.Cowan F, Rutherford M, Groenendaal F, Eken P, Mercuri E, Bydder GM, Meiners LC, Dubowitz L, de Vries LS. Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet 2003; 361:736-42 3.Cheong JLY Dammann O, Bartels D, Simpson J, Rutherford MA, Dubowitz L , Mercuri E, Cowan Focal brain lesions in the term infant: antenatal and perinatal factors 2004 Early Hum Dev 2004;78:148-9 4.Mercuri E, Rutherford M, Cowan F, Pennock J, Counsell S, Papadimitriou M, Azzopardi D, Bydder G, Dubowitz L. Early prognostic indicators in infants with neonatal cerebral infarction: a clinical, EEG and MRI study. Pediatrics 1999;103:39-46 5.Cowan F Dubowitz L, Mercuri E Counsell S, Barnett A, Rutherford MA Cognitive deficits without major motor difficulties following perinatal asphyxia and early encephalopathy: a consequence of white matter injury 2003 Early Hum Dev 2003;73:113-4
Reply to Cowan et al 31 August 2004
Donna M. Ferriero, University of California San Francisco Department of Neurology, Box 0663, 521 Parnassus Avenue, C215, San Francisco, CA 94143-0663, Vijay Ramaswamy, Steven P. Miller, A. James Barkovich, J. Colin Partridge Send Correspondence to journal: Re: Reply to Cowan et al dmf{at}itsa.ucsf.edu Donna M. Ferriero, et al.	We thank Cowan et al for their comments. It appears that our data and theirs differ in that underlying etiologies were not as common in their series. [2] However, in the 8/197 newborns with evidence of acute injury and neonatal encephalopathy and stroke, we were unable to substantiate whether these affected babies had abnormalities such as prothrombotic disease, infection or cardiac disease, since the data are not provided. Cowan reported that many babies had congenital malformations, metabolic disease and infections; these are exclusion criteria for our cohort. [1] However, in the past, this group has reported that 8/11 newborns with cerebral infarction had poor neurologic outcome in association with prothrombotic risk factors, while only 1/13 with normal outcome had these associations. [6] These data appear to support the data in our cohort. In addition, in the largest series published to date, 127 out of 215 neonates with stroke had a prothrombotic state. [7] It seems that the majority of infants reported to date, including data from Cowan's group, do have evidence of some underlying risk factors for stroke. We would like to believe that cognitive outcome is “generally good” following unilateral arterial stroke in the newborn, but data from one of the largest neonatal stroke cohorts [8, 9] suggest that > 50% have abnormal cognitive and neuromotor outcome. Cowan et al hypothesize that poor cognitive outcome in their and our series is due to 1) bilateral tissue involvement or 2) extensive white matter disease. Cases 3, 5 and 6 did exhibit involvement of the watershed zones bilaterally, but areas of signal abnormality were minor. This bilateral involvement may portend a worse prognosis as suggested, but larger series will be needed to confirm this hypothesis. Case 2 did not have other brain regions involved (despite the history that might suggest vulnerability to white matter). The cases that we reported are complicated in regard to their neonatal course, but these complications only confirm that newborns with neonatal encephalopathy must be considered for neuroimaging evaluation, and that stroke should be in the differential. We never saw “extensive white matter involvement” that Cowan et al hypothesize might be associated with cognitive abnormalities later in life. [5] Our study does not confirm the hypothesis that poor cognitive outcome is due to bilateral hemispheric involvement or extensive white matter disease. Only larger cohorts of newborns with stroke followed for long periods of time will be able to answer this query. References 5. Cowan F, Dubowitz L, Mercuri E, Counsell S, Rutherford M, Barnett A. White matter injury can lead to cognitive deficits without major motor difficulties following perinatal asphyxia and early encephalopathy. In: Early Human Development; 2003. p. 113-114. 6. Mercuri E, Cowan F, Gupte G, Manning R, Laffan M, Rutherford M, et al. Prothrombotic disorders and abnormal neurodevelopmental outcome in infants with neonatal cerebral infarction. Pediatrics 2001;107(6):1400-1404. 7. Kurnik K, Kosch A, Strater R, Schobess R, Heller C, Nowak-Gottl U. Recurrent thromboembolism in infants and children suffering from symptomatic neonatal arterial stroke: a prospective follow-up study. Stroke 2003;34(12):2887-2892. 8. deVeber GA, MacGregor D, Curtis R, Mayank S. Neurologic outcome in survivors of childhood arterial ischemic stroke and sinovenous thrombosis. Journal of Child Neurology 2000;15(5):316-324. 9. deVeber GA, MacGregor D, Curtis R, Friefeld S, Anderson P, Chan A, et al. Neurological outcome in survivors of neonatal arterial ischemic stroke. Pediatric Research 2003;53(4 Part 2):537A.