Neonatal imaging of the brain is often performed on infants who are premature or critically ill. The infant is examined in the incubator, and care should be taken to maintain body temperature with warm gel, avoidance of unnecessary exposure, and minimization of scanning time. To reduce stress on the infant, a quiet, dark atmosphere is maintained; care should be taken to avoid disruption of that environment. Many infants are immunosuppressed, so proper transducer disinfection and hand washing between infants is imperative for preventing the spread of infection.

Imaging technique should include the selection of the highest frequency transducer possible without sacrifice of adequate penetration. Transducers of 7.5 to 10 MHz are typically selected for premature infants, and 5-MHz transducers are usually adequate for infants with larger heads. A small footprint transducer is needed for imaging through the small fontanelles. Linear array transducers are useful in evaluating superficial structures. Routine neonatal brain imaging is performed through the anterior fontanelle in the coronal, sagittal, and parasagittal planes. Parasagittal views are lateral to the midline (true sagittal) plane but are referred to as sagittal images in this chapter. The posterior and mastoid fontanelles provide additional acoustic windows for further evaluation of the posterior fossa (Fig. 32-2).¹

For coronal imaging, the transducer is placed transversely in the anterior fontanelle with the right side of the brain displayed on the left side of the image. Sweeping anterior to posterior, six standard coronal views are recorded, as follows:

C1: Frontal lobes of the brain, anterior to the frontal horns of the lateral ventricle (Fig. 32-3, A).

C2: Frontal horns of lateral ventricles. Anatomy visualized includes falx, corpus callosum, cavum septi pellucidi (CSP), lateral ventricles, caudate nucleus, putamen, and temporal lobe (Fig. 32-3, B).

C3: Lateral ventricles at the level of the third ventricle and foramen of Monro. Structures visualized include corpus callosum, CSP, frontal horns, foramen of Monro, third ventricle, thalami, sylvian fissure, and brainstem (Fig. 32-3, C).

C4: Bodies of the lateral ventricles. Anatomy includes corpus callosum, CSP, choroid plexus in the body of the lateral ventricle, thalami, choroidal fissure, temporal horn, tentorium, cerebellum, and cisterna magna (Fig. 32-3, D).

C5: Atria of the lateral ventricles. Anatomic structures include the parietal lobe, glomus of the choroid plexus, and cerebellum (Fig. 32-3, E).

C6: Occipital lobe of the brain (Fig. 32-3, F).

For sagittal imaging, the transducer is placed longitudinally in the anterior fontanelle so that the anterior aspect of the brain is displayed on the left side of the image. Images are recorded midline and with transducer angulation to the right and left hemispheres, as follows:

Sag ML: Midline image of the brain visualizing the cingulate sulcus, corpus callosum, CSP, third and fourth ventricles, cerebellar vermis, and cisterna magna (Fig. 32-4, A).

Sag Left or Right 1: Lateral ventricle demonstrating the caudothalamic notch. Anatomy visualized includes the caudate nucleus, thalamus, and caudothalamic notch (Fig. 32-4, B).

Sag Left or Right 2: Entire lateral ventricle showing the frontal, temporal, and occipital horns; glomus of the choroid plexus; caudate nucleus; and thalami (Fig. 32-4, C).

Sag Left or Right 3: Periventricular white matter (Fig. 32-4, D).

Sag Left or Right 4: Sylvian fissure containing the middle cerebral artery (Fig. 32-4, E).

In addition, longitudinal placement of the transducer in the posterior fontanelle, with left and right angulation, allows assessment of the occipital horn for intraventricular hemorrhage. Placement of the transducer in the mastoid fontanelle, with superior to inferior angulation, aids in evaluating the cerebellum and cisterna magna (Fig. 32-5).

Intracranial Hemorrhage

Intracranial hemorrhage may be seen in premature and full-term infants and may be the sequela of an ischemic or hypoxic event, trauma, infarction, vascular malformation, or bleeding disorder. Germinal matrix–intraventricular hemorrhage is the most commonly diagnosed brain lesion in premature newborns.² Complications of posthemorrhagic ventricular dilation and parenchymal injury may result in devastating neurologic effects. Cranial sonography is a reliable method for the screening of low-birth-weight (<1500g) or premature (<30 weeks’ gestational age) infants at increased risk for development of an intracranial hemorrhage. Approximately 80% of hemorrhages occur within the first 3 days of life, and screening for hemorrhage is usually performed at 1 week of age.³

The most common location for the origin of intracranial hemorrhage in a premature infant is in the germinal matrix, located between head of the caudate nucleus and the thalamus. This embryonic structure contains a fragile network of vessels that are prone to rupture with changes in blood pressure. The germinal matrix is greatest in size between 24 and 32 weeks’ gestation and progressively decreases in size with only a small amount present at term, which explains why the risk for hemorrhage is greatest in preterm infants.

The severity of intracranial hemorrhage may be classified by the extent and location of the hemorrhage and the presence of ventricular enlargement. A grade I hemorrhage, also known as a germinal matrix or subependymal hemorrhage, is confined to the subependymal region at the caudothalamic notch. A grade II hemorrhage is defined by extension of the hemorrhage into the ventricle, without ventriculomegaly. A grade III hemorrhage is an intraventricular hemorrhage with ventriculomegaly. A grade IV hemorrhage is defined as parenchymal involvement with or without associated ventriculomegaly.

The prognosis of intracranial hemorrhage is variable depending on the extent of the bleed and includes an increase in morbidity and mortality. Grade I and grade II hemorrhages may spontaneously regress without evidence of long-term effects. Infants with grade III and IV hemorrhages are more likely to have neurologic effects, which range from developmental delays and behavioral problems to spastic motor deficits that may be accompanied by intellectual deficits.

Treatment for intracranial hemorrhage primarily focuses on controlling hydrocephalus to decrease neurologic deficits. Medical management may be used to decrease production of cerebrospinal fluid (CSF). Lumbar and percutaneous ventricular puncture can be used to drain excess CSF. Long-term treatment usually involves the placement of a ventricular shunt for drainage of CSF into the peritoneal cavity. Although this treatment is considered effective, it is not without complications, such as increased infections and shunt blockage.

Sonographic Findings

Sonographic imaging for hemorrhage should identify the absence or presence of hemorrhage, ventricular enlargement, and parenchymal extension. Acute grade I hemorrhage is identified as a homogeneous, echogenic mass at the caudothalamic groove (Fig. 32-6, A and B). Subependymal hemorrhages are similar in echogenicity to the choroid plexus. Aging of a grade I hemorrhage may result in the formation of a subependymal cyst (Fig. 32-6, C). Grade II intraventricular hemorrhage can be diagnosed by evidence of echogenic material that partially or completely fills the ventricular cavity (Fig. 32-7). Development of ventriculomegaly related to the hemorrhage is classified as a grade III hemorrhage (Fig. 32-8). Grade IV or parenchymal hemorrhage is initially identified as an echogenic, homogeneous mass extending from the ventricle into the adjacent white matter (Fig. 32-9). Over time, the echogenicity of blood decreases, resulting in a cystic cavity extending from the ventricle to the parenchyma. This is known as a porencephalic cyst.

Periventricular Leukomalacia

Periventricular leukomalacia (PVL) is defined as infarction and necrosis of the periventricular white matter. In a premature infant, the periventricular white matter, or watershed area, is poorly supplied because it lies between the distribution of arterial border zones. The lack of vascular maturation in this area makes it especially susceptible to changes in blood pressure. The white matter most affected is adjacent to the trigone of the lateral ventricle and near the foramen of Monro. In addition to prematurity, maternal chorioamnionitis has been identified as a risk factor contributing to the development of PVL. The outcome for infants with PVL is variable, depending on the severity and extent of white matter necrosis. Cerebral palsy is a prevalent sequela in infants with PVL. Infants usually have major long-term neurologic deficits, including spastic diplegia, quadriplegia, seizure disorder, visual impairment, and mental retardation.

Sonographic Findings

Sonographic findings of PVL in the acute stage show bilateral areas of increased echogenicity in the white matter superior and lateral to the ventricular margins of the brain (Fig. 32-10, A). This finding may resolve or progress to cystic PVL. Cystic PVL typically develops 2 to 3 weeks after the insult and manifests as numerous, small cystic lesions paralleling the lateral ventricle of the brain (Fig. 32-10, B). These findings resolve within a few months, with resultant brain atrophy and subsequent ventriculomegaly.

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related posts:

Renal Mass: Cystic versus Solid Hematuria Uncertain Last Menstrual Period Elevated Prostate Specific Antigen Right Upper Quadrant Pain Abnormal Uterine Bleeding

Stay updated, free articles. Join our Telegram channel

Join