Perinatal stroke in term infants with neonatal encephalopathy
Frances MCowan, Imperial College, London, Dept. of Paediatrics, Hammersmith Hospital, DuCane Rd, London W12 OHS, UK[email protected]
Eugenio Mercuri, Mary A Rutherford
Submitted August 31, 2004
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
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