Cerebral infarction in the
full-term infant

Eugenio Mercuri, Lilly Dubowitz and Mary A Rutherford

Chapter Contents

Introduction
Arterial infarction
Borderzone infarcts
Neurodevelopmental outcome in arterial
Case histories
Summary
References

Introduction

Neonatal cerebral infarction or stroke may be defined as ‘a severe disorganization of gray and/or white matter architecture caused by embolic, thrombotic or ischemic events’. The increase in neonatal imaging in infants with abnormal neurological signs has highlighted the wide spectrum of these lesions^{2,
4,
6,
8,
9,
11,
13,
16,
19,
23,
26,
29}. Infarcts may be divided into two main types: those occurring within the territory of a major artery and those occurring in the borderzone or watershed areas.

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Arterial infarction

AETIOLOGY

The most commonly reported type of neonatal cerebral infarction in the full-term infant are ischemic lesions in the territory of a major cerebral artery. The middle cerebral artery is most commonly affected and, as found in adult stroke, the left middle cerebral artery is three to four times more frequently involved than the right¹⁵. Infants with involvement of the anterior or posterior cerebral artery may be asymptomatic and therefore underdiagnosed. In addition, lesions in these regions can be difficult to detect with cranial ultrasound^{19, 23}.

Before the advent of neuroimaging, infarction was thought to be a rare condition, recognized only at postmortem examination in infants with congenital heart disease or other life-threatening conditions such as disseminated intravascular coagulation or sepsis.

Following the introduction of neonatal cranial ultrasound and CT scanning in the late 1970s, cerebral infarcts were also identified in infants who survived, most of them being associated with severe perinatal asphyxia². Large infarcts were also observed in young children who had no obvious perinatal problems and it was thought that in these cases the infarcts must have occurred antenatally. More recently, early and serial imaging in the newborn has allowed us to recognize that infarcts are more frequent than assumed, and has also provided information about the spectrum of these lesions and their possible etiology^{4,
6,
8,
9,
11,
13,
16,
19,
23,
26,
29}.

The etiology of most arterial infarcts remains unclear as only a minority are associated with the clinical conditions reported in earlier studies. Severe adverse antenatal and perinatal factors are relatively rare, and whilst many of these infants have some signs of fetal distress, their Apgar scores are usually normal at 5min¹⁹. The onset of convulsions in the first days of life is usually the first clinical sign leading to diagnostic investigation. In recent years, the etiological role of hematological factors in cerebral infarction has been studied, with some reports of an increased incidence of heterozygosity for factor V Leiden. In our own cohort of 24 infants with arterial infarction, five infants were heterozygous for factor V Leiden all of whom developed a hemiplegia, compared to only one of the 19 infants without factor V Leiden²⁴.

CLINICAL FINDINGS

Infants with focal infarction do not usually have an encephalopathy; they are alert and responsive to visual and auditory stimuli. Convulsions are often the first and only clinical sign, which will draw attention to the presence of the lesion in the first days of life. The convulsions are usually unilateral at the onset but may become generalized during the seizure. Some infants may show abnormal tone in the limbs usually contralateral but occasionally ipsilateral to the lesion⁷. These abnormal neonatal signs, if present, are often transient and do not predict later outcome²³. In some cases abnormal clinical signs during the neonatal period are either absent or so subtle that they escape detection (Fig. 7.2). The neurodevelopmental outcome in infants with perinatal infarction is variable, ranging from normality to the presence of a hemiplegia. Early continuous EEG may demonstrate seizure activity but assessment of the background activity is most important for predicting motor outcome^{23, 32}. Infants with or without a later hemiplegia may be at risk for non-motor impairments that become obvious in early childhood (see case histories).

Fig. 7.1 (a) Inversion recovery sequence (IR 3800/30/950). Infant aged 3 weeks. There is a small infarct involving the head of the caudate nucleus and the lentiform on the left (arrow). (b) Inversion recovery sequence (IR 3800/30/800). Infant aged 12 months. There is extensive infarction and atrophy of the left hemisphere. There is reduced high signal intensity from myelination on the left. The ventricles are dilated. (c) T1 weighted spin echo sequence (SE 860/20). Infant aged 7 days. There is abnormal signal intensity within the caudate head and lentiform on the left (long arrow). There is additional highlighting of the Sylvian cortex and low signal within the adjacent subcortical white matter (short arrow). (d) Inversion recovery sequence (IR 3800/30/950). Infant aged 9 days. There is an infarct involving the left parieto/temporal/occipital region. The involvement of the medial aspect of the occipital lobe (arrow) indicates posterior cerebral artery territory. This lesion may represent an asymmetrical watershed lesion. Careful examination of all levels of imaging to identify involvement of other watershed areas is indicated.

Fig. 7.2 (a),(b),(c) Fast spin echo sequence (FSE 3000/208). Infant aged 3 days. This infant was enrolled as a control patient for an imaging study. He had no presenting signs. The infarct in the territory of the MCA was picked up incidentally. There is loss of gray/white matter differentiation with abnormal high signal intensity (arrows) involving the parietal (a), occipital (b) and temporal (c) lobes. The signal intensity changes are consistent with a perinatal insult.

MRI FINDINGS

The spectrum of lesions is wide, ranging from small abnormalities in the basal ganglia (Fig. 7.1a) to very extensive ones, which involve most of the hemisphere (Fig. 7.1b). There may also be combinations of lesions within the same infant (Fig. 7.1c). The exact site of an infarct may be difficult to define. Infarcts in the posterior territory of the middle cerebral artery may be confused with infarcts arising from the posterior cerebral artery or from asymmetrical watershed lesions (see below) (Fig. 7.1d). Confusion may arise because of individual variation in the arterial distribution to the brain. In addition, as the brain grows and the infarct evolves, the site of abnormality on MRI may appear to shift, further complicating the issue (case 7.3).

The following classification for middle cerebral artery infarcts according to the branch involved has been suggested by de Vries et al.⁶:

main branch
cortical branch
lenticulostriate branches.

Although all these lesions can occur in both preterm and full-term infants, the involvement of the main branch or of one of the cortical branches is more frequently observed in the full-term infant and lesions in the lenticulostriate branch in the preterm infant (see Chapter 8).

Fig. 7.3 Inversion recovery sequence (IR 3800/30/950). Infant aged 14 days. There is a large infarct involving the left hemisphere. There are additional abnormal high and low signal intensities within the basal ganglia and thalamus and the internal capsule on the left. The normal signal from myelin in the posterior limb of the internal capsule is only seen on the right (arrow).

Fig. 7.4 Inversion recovery sequence (IR 3800/30/950). Infant aged 6 days. There is a small area of infarction in the temporal pole on the left (arrowhead). The infarct was more extensive on superior slices. There is a small hemorrhagic lesion in the right mesencephalon (long arrow). There is subdural hemorrhage around the surface of the brain (short arrow).

Main branch/cortical branch

In the neonate these lesions are mainly ischemic without a hemorrhagic component, unlike the infarcts which occur in older children and in adults. The initial lesion is seen as a loss of gray/white matter differentiation with mainly low signal intensity on T1 and high signal intensity on T2 weighted images (Fig. 7.2)

Infarcts associated with occlusion of the main branch of the middle cerebral artery (MCA) may involve the white matter and cortex within the frontal, parietal, temporal and occipital lobes (Fig. 7.2) There may be additional involvement of the ipsilateral internal capsule and the basal ganglia/thalamus (Fig. 7.3). An infarct in the territory of a cerebral artery may also occur in association with other ischemic or hemorrhagic lesions in the ipsilateral or contralateral hemisphere (Fig. 7.4). The main infarction can be associated with a contralateral infarction (case 7.7), with more discrete ischemic lesions (Fig. 7.5) or punctate hemorrhagic lesions (Fig. 7.6) in the white matter. Infants with bilateral MCA territory lesions may develop the perisylvian syndrome (case 7.7).

The site and extent of the changes relating to occlusion of a cortical branch is quite variable. In our recent series of 20 infants with cortical branch infarcts, only four infants had additional lesions within the basal ganglia/thalamus and the internal capsule²³.

Using serial imaging it is possible to observe the evolution of infarcted areas over the first few weeks and months of life.

Fig. 7.5 Inversion recovery sequence (IR 3800/30/ 950). (a, b) Infant aged 6 days. There is abnormal high signal intensity within the cortex of the right Sylvian fissure. (a) (arrow) There is an asymmetry of the signal intensity from myelin in the posterior limb of the internal capsule with decreased signal intensity on the right (long arrow). There is an additional abnormal low signal intensity within the right thalamus and lentiform nucleus. There is an additional area of abnormal high signal intensity within the left occipital lobe (b) (arrow). T2 weighted sequence (SE 3000/120). Same infant aged 6 days. (c) The abnormalities within the cortex are seen as low signal intensity and are more obvious. The abnormalities within the lentiform and thalamus are seen as high signal intensity. The posterior limb of the internal capsule has abnormally high signal intensity throughout (arrow). Inversion recovery sequence (IR 3400/30/800) (d) at 20 months of age. There are two discrete areas of infarction (arrows) and mild dilation of the ventricles.

Fig. 7.6 T1 weighted spin echo sequence (SE860/20). (a), (b) Infant aged 7 days (as in Fig. 7.1c). There are small high signal intensity hemorrhagic lesions in the white matter and basal ganglia (arrows).

Evolution first week

Changes during the first few days of life may be difficult to identify with conventional imaging alone (Fig. 7.7). Conventional imaging during the first week will show a loss of gray/white matter differentiation with a generally low signal intensity in the region of the infarct on T1 weighted images. On T2 weighted images there is a loss of differentiation and generally increased signal intensity (Fig. 7.8). Changes are usually easier to identify on T2 weighted scans (Fig. 7.8). Diffusion weighted imaging during the first week ‘highlights’ infarcted areas and this then aids detection on the conventional images (Fig. 7.7 and Fig. 7.8). The abnormalities on diffusion weighted imaging become less obvious by the end of the first week by which time the abnormalities are more obvious on the conventional T1 and T2 weighted images (Fig. 7.8). Animal studies have reported that changes on diffusion are more evident a few hours after an acute ischemic insult and tend to be less evident a few days after, thus the sequence of findings in infants with infarcts suggest that the acute event occurred around the perinatal period⁵.

Fig. 7.7 Left-sided MCA infarct. Infant aged 4 days. T1 weighted spin echo (SE 860/20) (a), T2 weighted spin echo sequence (b), and diffusion weighted image (c) anterio-posterior sensitization. The abnormalities on conventional imaging are subtle. The diffusion changes consistent with restriction of water.

Fig. 7.8 (a) T1 weighted sequence (SE 860/20). (b) T2 weighted sequence (SE 2700/120). Left-sided infarct, probably in the territory of the posterior cerebral artery (arrows). (c) Diffusion weighted imaging. Infant aged 4 days. The abnormalities are more striking on the diffusion weighted images. (d) T1 weighted sequence (SE 860/20). (e) T2 weighted sequence (SE 2700/120). (f) Diffusion weighted imaging. Same infant aged 9 days. The abnormalities are more obvious on the conventional spin echo sequence images. The diffusion abnormalities are no longer evident.

Fig. 7.9 T1 weighted volume acquisition images taken at 4 weeks (a) and 3 months (b). There is a region of infarction in the left posterior parietal lobe, which has decreased in size. After registering (a) and (b) there is high signal intensity consistent with new brain growth (arrow) within the original infarcted area (c).

Fig. 7.10 Inversion recovery sequence (IR 3800/30/950). Infant aged 12 months. Left MCA infarction with involvement of the anterior temporal lobe (arrowhead). There is asymmetry of the mesencephalon with atrophy consistent with Wallerian degeneration on the left (arrow).

Fig. 7.11 Inversion recovery sequence (IR 3800/30/950). Infant aged 2 weeks. There is obvious asymmetry of the brain stem, with atrophy of the left in this infant who presented with seizures on day 2. The infarct seen in the left anterior lobe (arrow) looks about 1–2 weeks old. The brain stem asymmetry may originate from a previous lesion that is no longer identifiable.

Fig. 7.12 Inversion recovery sequence (IR 3800/30/950). Infant aged 6 days. There is a hemorrhagic infarct in the left caudate head (arrow).

Fig. 7.13 Inversion recovery sequence (IR 3800/30/950). Term infant presenting with seizures following delivery on to the floor at home. Imaged at 5 days. There is bilateral loss of gray/white matter differentiation in the posterior parietal and temporal lobes. The basal ganglia are normal and the internal capsule is appropriately myelinated. This infant became microcephalic, has mild developmental delay but a normal motor outcome.

Evolution second to sixth week

During the second week following an infarction there may be an exaggeration of gray/white matter differentiation with areas of cortex becoming highlighted and white matter becoming even lower signal intensity using T1 weighted imaging (Fig. 7.8). From 2 weeks onwards there may be breakdown of infarcted tissue. The extracerebral space may widen. A porencephalic cyst may form although there is usually some tissue visible within it, especially if windowed appropriately prior to image processing (case 7.1). On T1 weighted sequences high signal areas may appear around the penumbra of the infarct. The histological correlation for this lesion is not clear but it may represent capillary proliferation or possibly the presence of lipid-laden macrophages.

Evolution 6 weeks to 1 year

Over the next few months as the brain grows the infarct may appear to decrease in size and in some infants the original lesion may be difficult to identify (case 7.3). The affected hemisphere, however, usually looks smaller than the non-affected one and shows a generalized decrease in myelination most obvious around the site of the infarct. This clearly relates to the original size of the lesion and its evolution. Using a specifically designed computer program we have been able to accurately match and subtract serially acquired volume acquisition images in infants with focal infarcts²⁷. Using this technique we have been able to identify the early changes in signal intensity and tissue breakdown. Matching and then subtracting the serially acquired images has then shown us that there may be excessive growth in and around the infarct over the next few months (Fig. 7.9). These changes are not detectable on visual analysis of the conventional images. This excessive growth may lead to the virtual disappearance of smaller infarcts. Regions of unexpected excessive growth may correspond to previously unrecognized regions of white matter damage (Fig. 7.15). Conventional imaging shows that regions of excessive growth appear to have normal imaging characteristics and that in general infants with focal infarction have relatively small amounts of glial tissue on later imaging. The period of excess growth seems to start around 6 weeks and end by approximately 1 year of age.

Wallerian degeneration

In the acute stages of MCA infarction there may be abnormal signal intensity within the brain stem, presumably resulting from the phenomenon of diaschisis (case 7.7). Diaschisis is the term applied to acute metabolic changes that occur in connected but distant areas of the brain in response to a focal injury. This has been traditionally used to describe changes in the cerebellum following infarction of the forebrain.

In both perinatal main and cortical branch infarction changes in the size of brain stem due to secondary atrophy, Wallerian degeneration, become evident after 6–8 weeks and may become progressively more obvious (Fig. 7.10). Infants that show earlier asymmetry may have had an antenatal insult in addition to their perinatal infarct (Fig. 7.11). Early serial imaging may help to distinguish separate insults (case 7.1). Secondary degeneration may also give rise to atrophy of the ipsilateral thalamus, in the absence of initial involvement. Both ipsilateral and contralateral cerebellar atrophy have been demonstrated following focal infarction. This is thought to arise from the phenomenon of diaschisis. However, in a series of 10 term infants with perinatal focal infarction we have shown that cerebellar hemisphere growth was symmetrical and comparable to controls over the first year of life¹⁴.

Lenticulostriate branch

These lesions are more frequently observed in preterm infants6 but can occasionally be seen in full-term infants (see Chapter 8). Unlike infarcts in the territory of cortical branches, they often have a hemorrhagic component. The lesions generally involve the lentiform and, sometimes, the caudate and/or the thalamus and the internal capsule (Fig. 7.12). Infants may also show a combination of cortical branch and basal ganglia lesions (Fig. 7.3). Small cystic lesions within the basal ganglia found incidentally on imaging are likely to represent small old infarcts (case 7.1).

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Borderzone infarcts

ETIOLOGY

Perinatally acquired infarcts may also occur not in the distribution of one main artery but in the borderzone or watershed regions between arterial territories, so-called parasagittal lesions³¹. These lesions which, so far, have only been described in full-term infants, are thought to be due to an acute decrease in cerebral blood flow³¹. The affected areas will therefore be those that are most susceptible to hypotension and a fall in perfusion, such as the regions in the posterior lobes which represent the end fields among all the three main cerebral arteries.

Adverse antenatal factors are not frequent but in our experience these lesions, unlike the arterial infarcts, are usually associated with perinatal distress and/or mild signs of hypoxic–ischemic encephalopathy. These infants may show CTG abnormalities, meconium-staining liquor and instrumental deliveries are frequent. They may require some respiratory assistance such as facial O₂ or bagging but not intubation. The Apgar scores are often low at 1min but recover quickly within 5 or 10min (case 7.5). This pattern of injury may also be seen in infants with hypoglycemia¹.

CLINICAL FINDINGS

Infants with parasagittal lesions may develop seizures in the first 48h although this may not be the first presenting sign. On neurological examination these infants are hypotonic; this is partly due to the fact that they are often assessed after the onset of seizures and the administration of anticonvulsants. The neonatal EEG may be normal, show epileptic discharges but a normal background or, in some cases, show a discontinuous background activity²³.

MRI FINDINGS

Fig. 7.14 Asymmetrical borderzone infarction. Diffusion weighted image, infant aged 6 days, showing abnormal restriction giving high signal intensity in the left frontal, parietal, temporal and occipital lobes. There is no obvious involvement of the right hemisphere at this level.

The lesions are generally bilateral, involving the posterior convexity (Fig. 7.13, case 7.5)and, in some cases, the anterior lobes. These lesions are quite symmetrical but in some, the lesion can be more predominant on one side, involving the anterior and posterior lobes and giving only a minimal involvement of the contralateral hemisphere (Fig. 7.14). The lesions are ischemic and seen as low signal intensity on T1 and high signal intensity on T2, but may have hemorrhagic components. The evolution of these lesions is similar to that observed in more focal cerebral infarcts with similar changes of excessive growth demonstrable on serial registration (Fig. 7.15). Occasionally, areas of infarction are seen adjacent to subdural hemorrhage (case 7.6). The exact association between these two lesions is unclear. It is possible that the subdural hemorrhage interferes with venous drainage resulting in venous infarction of the adjacent parenchyma. It has also been suggested that the infarction results from arterial spasm.

Fig. 7.15 Registration and subtraction of images. T1 weighted volume acquisition. (a) Aged 2 months, note the highlighting around the edge of the infarcted tissue on the left (arrowhead). There is an additional small area of infarction on the right (arrow). (b) Aged 6 months. There is atrophy and decreased myelin throughout the left hemisphere. (c) Subtraction image. There is high signal intensity around the atrophied left hemisphere consistent with new brain growth (arrow). There is high signal intensity along the medial aspect of the right occipital lobe with a resultant decreased width of the interhemispheric fissure. This may represent an area of previously unrecognized white matter injury.

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Neurodevelopmental outcome in arterial and borderzone infarcts: prognostic factors

MOTOR OUTCOME

Until a few years ago most of the studies on neonatal infarcts, with a few exceptions, reported a very high incidence of abnormal motor outcome, mainly hemiplegia^{3, 10, 12, 13, 16–18, 25, 28, 30, 33}Because of these early studies, parents of infants with cerebral infarction have been counselled about the high risk of their children developing cerebral palsy. With the increase in the detection of infarcts in infants without birth asphyxia, however, it has become evident that the incidence of abnormal motor outcome is lower than assumed^{8, 23}.

We have reviewed a series of 24 children all of whom had early neonatal MRI²³. The infants were followed longitudinally for at least 2 years in order to establish the best prognostic indicators in the neonatal period. Hemiplegia was present in only 20% of the children investigated. The presence of adverse antenatal and perinatal factors was not significantly associated with abnormal outcome.

We were unable to find any significant association between the neonatal neurological examination and outcome as abnormal signs in the neonatal period were found in infants with and without a normal outcome.

Neonatal MRI findings were better predictors of outcome. The presence of hemiplegia, however, did not seem to relate to the type of infarction, as the incidence was similar in both arterial and borderzone infarcts. In contrast, the extent of the lesion, and in particular the concomitant involvement of hemisphere, basal ganglia and internal capsule, was significantly associated with outcome. While infants who had involvement of one or two of these three components tended to have a normal motor outcome, infants with involvement of all three sites, developed an abnormal motor outcome (cases 7.4 and 7.7).

We have also shown that neonatal EEG can be equally predictive of late outcome. While all the infants who had normal background activity had a normal motor outcome²³, irrespective of the presence or absence of epileptic discharges, all the infants with abnormal background activity, unilateral or bilateral, developed hemiplegia.

Our recent studies24 on the association between perinatal infarction and thrombotic disorders have shown a strong association between factor V Leiden and the development of hemiplegia. Further studies are warranted to look at this relationship in more detail and to investigate the potential role of other prothrombotic factors such as the G20210A mutation in the prothrombin gene and the C677T mutation in the methylenetetrahydrofolate reductase gene.

VISUAL OUTCOME

The association between cerebral infarction and visual abnormalities has been well documented in children and adults suffering from stroke^{20, 34}. In these cases there appears to be a good correlation between the severity of MRI abnormalities and the severity of visual impairment. Lesions affecting the striate occipital cortex and the optic radiations are generally associated with contralateral hemianopia and lesions affecting the parietal lobe with abnormal visual attention and, in the most severe cases, with contralateral visual neglect.

Using a battery of tests, which were specifically designed to evaluate visual function in the first year of life, we have been able to demonstrate that infants with infarction have normal acuity and ocular movements but may show narrower visual fields and abnormal visual attention, as tested by fixation shift^{21, 22}. It is of interest, however, that in contrast to adults, not all the children who had involvement of the structures of the visual pathway on MRI developed abnormal visual function. Only 50% of the infants with involvement of the optic radiation had abnormal fields and only 50% of the infants with parietal lobe lesions had an abnormal fixation shift in the first year of life. These findings suggest that the immature brain can to some extent compensate for early lesions affecting the visual pathway.

NEUROCOGNITIVE OUTCOME

The plasticity of the neonatal brain may allow normal motor function in the presence of large areas of infarction; however, this may cause a ‘crowding out’ effect and occur at the expense of neurocognitive functions that develop later in childhood (see case histories). Long-term prospective follow-up studies to assess language, behaviour and neurocognitive functions in infants with and without a motor impairment will further define the extent and quality of compensation following perinatal infarction.

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Case histories

CASE 7.1

This male infant was born at 39 weeks’ gestation (birth weight 3.132 kg).

Antenatal

His mother was a caucasian primigravida with known endometriosis. She was admitted to hospital at 34 weeks with abdominal pain, which settled spontaneously. Fetal movement and heart rate monitoring were satisfactory.

Labor and delivery

The onset of labor was spontaneous at 39.6 weeks. Five hours before delivery there were variable decelerations to 70 beats/min on the cardiotocogram (CTG) for which she was given facial oxygen. Three hours before delivery, grade 1 meconium was noted, a fetal blood sample at that time showed a pH of 7.3². The variable decelerations continued and a cesarian section was performed for failure to progress and fetal distress. The cord pH was 7.1⁵. Apgar scores were 9 at 1min and 10 at 5min but thick meconium was present. Suction revealed that this was all above the cords.

• Neurodevelopmental outcome is not always predictable.

Maternal pathology

At the time of the cesarian section lesions were noted in both ovaries with adhesions to the parametrium. On microscopy, these were shown to contain hemorrhagic decidua with thrombotic vessels. Coagulation and thrombophilic screening were normal.

Postnatal course

The infant was transferred to the postnatal ward but became jittery at 24h, which was more marked on the left. Episodes of desaturations were noted at 36h and an EEG confirmed neonatal convulsions. The EEG on day 3 showed continuous background activity with seizure activity mainly on the right.

Neurological evaluation

Neonatal neurological examination on day 3 showed asymmetrical limb tone fisting and nystagmus. On day 9 the asymmetrical limb tone persisted; his head control and visual alertness were poor. At 1 month he still had poor head control and asymmetrical arm tone. At 3 months there was no asymmetry of tone but he tended to first with both hands more so on the right. At 9 months he had a tight right popliteal angle but no other asymmetries were present. At 4 years he had mild general hypotonia with very mildly increased tone in the lower limb on the right the ipsilateral side of the main infarct. He had a strong preference for his left hand and although he had a pincer grasp on the right, this was cruder than on the left. On Griffiths developmental scales he scored at a 4-year level on all subscales except for performance where he performed at a 3-year 8-month level. He has had no further convulsions. Visual function is normal.

Thrombotic screen

Coagulation and thrombophilic screening was normal.

Comment

This infant had a substantial infarct on the right, yet developed a right-sided hemiplegia, presumably related to the very small lesion seen in the left hemisphere and associated with abnormalities in the left internal capsule.

Fig. 7.16A Early imaging, Cranial ultrasound showed a right-sided echo density and a small left-sided hemorrhagic lesion on day 5. Inversion recovery sequence (IR 3800/30/950) (a) at 5 days of age shows a large area with loss of gray/white matter differentiation on the right (arrowhead) and a small cyst on the lateral edge of the right lentiform nucleus (arrow). The areas of abnormality are well shown on the diffusion weighted imaging in the coronal plane. There is some additional increased signal intensity on the left. (b). Early angiography (day 5) shows poor filling in the MCA on the right (arrow) (c). This has improved 1 week later (day 11) (arrow) (d).

Fig. 7.16B Late imaging. Inversion recovery sequence (IR 3400/30/800). (e) Aged 1 year. There is a large infarct on the right. The separate cystic lesion is seen on the lateral border of the lentiform nucleus (long arrow). There is abnormal signal intensity within the internal capsule on left (short arrow) FLAIR (IR 6500/160/600) sequence. (f) Abnormal signal intensity within the internal capsule is seen as high signal intensity (long arrow). This may be related to the left-sided lesion seen on early diffusion images. Strands of tissue within the infarct are more easily visible (short arrow).