Diagnostic ultrasound ( PDFDrive )

CHAPTER 45 Neonatal and Infant Brain Imaging 1551
Focal
(macroscopic)
A
Diffuse
IVH
GMH
GM
B
Cystic PVL
P
P
GP
GMH-IVH
GP
GM
T
T
Noncystic PVL
Focal
(microscopic)
Diffuse
PVI
IVH
GMH
FIG. 45.48 Cystic and Noncystic Periventricular Leukomalacia
(PVL) and Germinal Matrix Hemorrhage–Intraventricular Hemorrhage
(GMH-IVH) and Periventricular Hemorrhagic Infarction (PVI). Diagram
illustrates coronal sections from the brain of a 28-week-old premature
infant. The dorsal cerebral subventricular zone, the ventral germinative
epithelium of the germinal matrix (GM), thalamus (T), and putamen (P)
and globus pallidus (GP) are shown. (A) The focal necrotic lesions in
cystic PVL are macroscopic in size and evolve to cysts. The focal necrotic
lesions in noncystic PVL are microscopic in size and evolve to glial scars.
The diffuse component of both cystic and noncystic PVL (pink) is characterized
by the cellular changes. (B) Hemorrhage (red) into the GM results
in GMH, which could burst through the ependyma to cause an IVH (left).
When the GHM-IVH is large, PHI might result (right). (Adapted from
Volpe JJ. Brain injury in premature infants: a complex amalgam of
destructive and developmental disturbances. Lancet Neurol.
2009;8[1]:110-124. 46 )
T
T
GP
GP
P
GMH-IVH With PHI
P
In the cystic pattern of PVL, the white matter most afected
is in the arterial border zones at the level of the optic radiations
adjacent to the trigones of the lateral ventricles and the frontal
cerebral white matter near the foramina of Monro. his cystic
pattern can involve the white matter difusely as well. he
prevalence of PVL has been noted to increase with the duration
of survival in premature infants, raising the possibility of cumulative
postnatal insults, including circulatory compromise, patent
ductus arteriosus, apneic spells, and sepsis. 101,138,139
In the noncystic pattern of WMIP/PVL, there may be difuse
cerebral cortex white matter damage, microscopic focal white
matter damage, and basal ganglia, thalamic, 140 and cerebellar
damage that evolves to glial scars. Typically, the white matter is
thinned with irregular ventricular walls. here may also be corpus
callosum injury. Epelman and colleagues 141 have shown that
careful ultrasound evaluation may show increased callosal
echogenicity, which relects corpus callosum damage and can
be used as a speciic marker for this injury early when MRI is
less oten used. Near-term ultrasound and MRI at term-equivalent
age have been shown to predict neurodevelopmental outcomes
in extremely premature infants. 142
Maternal chorioamnionitis has been associated with WMIP/
PVL, possibly the result of vasoactive proteins being released
into the fetal circulation, causing luctuations in cerebral blood
low. Inlammatory responses to infection in the fetus or the
neonate that activate astrocytes and microglia may cause PVL, 143,144
or these may represent a pathologic response to repair the tissue
injury in PVL. 145 Proinlammatory cytokines found ater chorioamnionitis
correlate with PVL development. 146 Prevention of
PVL may depend on treatment with maternal antibiotics (in the
case of chorioamnionitis before delivery) or anticytokine agents
and therapy with free-radical scavengers.
Cystic PVL can been anticipated to follow a severe hemodynamic
event in 56% of premature infants with PVL. Unexpected
PVL (without a speciic clinical neonatal event) has been reported
in as many as 44% of cases. 147 his series of PVL patients had
been treated for preterm delivery and oten had maternal chorioamnionitis.
It is proposed that the maternal infection predisposes
to preterm delivery and PVL. Antenatal steroids have been
shown to decrease the incidence of PVL and the incidence of
IPH from GMH. 148-151
Later neurologic problems from cystic PVL/WMIP include
developmental delay and spastic diplegia involving both legs,
oten noticeable by 6 months of age. Spastic diplegia occurs
because the pyramidal tracts from the motor cortex that innervate
the legs pass through the internal capsule and travel close to the
lateral ventricular wall. Severe cases of PVL will also afect the
arms, resulting in spastic quadriplegia, and also cause vision and
intellectual deicits. 152-155 he prevalence of cerebral palsy was
evaluated in the French EPIPAGE cohort study of 2364 children
born at 22 to 32 weeks’ gestation; 1954 (83%) were studied at 2
years of age. Twenty percent had cerebral palsy if born at 24 to
26 weeks’ gestation, whereas only 4% had cerebral palsy if born
at 32 weeks. For those with neonatal head ultrasound and
follow-up, 17% of children with neonatal IVH (grade III) and
25% with neonatal white matter damage had cerebral palsy,
compared with 4% with normal ultrasound scans. 156