The Skull Base: Intracranial Abnormalities

10.1055/b-0034-87896

The Skull Base: Intracranial Abnormalities

Imaging Methods

Ultrasonography

Brain US plays a central role in the detection and management of neonatal disease in the preterm and term infant. Although a morphological study, by using high-frequency transducers it remains the cornerstone of neonatal intracranial imaging. Pulsed and color Doppler scans provide additional information and improve the diagnostic and prognostic accuracy of US. The value of Doppler techniques may be found in, for example, the demonstration of flow within the aqueduct of Sylvius, visualization of patency of the terminal veins and venous sinus, demonstration of Doppler spectrum fluctuations, and recognition of low or abnormally high blood flow.

Particular features of normal brain US in the neonate should be recognized and reported using a systematic approach, as outlined here

Starting with a coronal approach, it is easy to pick up asymmetric abnormalities through the anterior fontanelle and, if patent, the posterior fontanelle. Subsequent parasagittal images should incorporate the midline to the outer border of the cortex. Additionally, one can look at the asterion for interpreting abnormalities at the brainstem and cerebellum. With this total imaging approach, one can rule out abnormalities at the midline and can assess if the abnormality is infra- or supratentorial in location. Is it bi- or unilateral? Are the central and peripheral CSF spaces normal? Are there abnormalities of the gyri and sulci? If there is a focal lesion, is it hemorrhagic? Also, repeating the US examinations can help to focus the differential diagnosis or give a better insight into the neurologic outcome.

In extreme prematurity, one may see some specific abnormalities that occur with a higher incidence, like cerebral hemorrhage and its different patterns (intraventricular hemorrhage and periventricular hemorrhagic infarction) and periventricular leukomalacia (PVL). Especially in these infants, repeated US examinations (until near term) are important to rule out the development of cystic PVL.

Computed Tomography Scan

CT has no prominent place in imaging of preterm and term infants, except for ruling out intracranial calcifications or (sub) acute bleeding due to (birth) trauma.

Magnetic Resonance Imaging

MRI improves the radiologist’s ability to assess brain development and to detect anomalies of brain formation. In contrast to US and CT, MRI allows the assessment of brain development by analysis of the effects of myelination of the pediatric brain in both T1 and T2 modes. A continuously evolving pattern will normally be seen up to the age of 2 years. During prematurity, MRI provides excellent detail of the immature brain with good delineation of the cortex, white matter, and central gray matter structures. The cortex is seen as high signal intensity on T1-weighted imaging and low signal on T2-weighted imaging, reflecting its high cellular density. At 24 weeks gestational age, the surface of the brain appears smooth apart from the parieto-occipital fissure, central sulci, cingulate sulci, calcarine sulci, and very wide sylvian fissures. Sulcation and gyration develop at different rates in different regions of the brain. At any given age prior to term, the folding of the central sulcus is the most advanced, followed by the medial occipital lobe. The parietal lobe is the next most advanced, followed by the frontal and posterior temporal lobes. The anterior temporal region is the least well developed structure. At term, the cortex has extensive folding with the formation of tertiary sulci. Familiarity with this evolution of signal changes allows an estimation of the approximate stage of brain development. Although high-resolution multiplanar MRI is not better than those images acquired with US, using high-frequency transducers, MRI provides good anatomic detail, with excellent distinction between gray and white matter. This technique allows improved detection of many abnormalities of brain formation, some of which were previously detectable only at autopsy. These malformations and their imaging characteristics are discussed subsequently.

**Table 4.13 Abnormalities in preterm infants**
Diagnosis	Findings
Intraventricular–periventricular hemorrhagic disease Fig. 4.31	Classification in four grades: Grade I: hemorrhage in subependymal space Grade II: subependymal hemorrhage with bleeding into normal or minimally dilated ventricles Grade III: subependymal hemorrhage with blood in dilated ventricles Grade IV: similar to grade III hemorrhage, with hemorrhage in the adjacent brain parenchyma. The hemorrhage may be entirely intraparenchymal without ventricular involvement. Extremely rare.
Periventricular hemorrhagic infarction Fig. 4.31	This entity used to be considered a sequela of Grade III. The subependymal hemorrhage at the caudal-thalamic groove blocks the terminal vein and its drainage area, resulting in a venous infarction. It is much more frequent than a Grade IV hemorrhage. Even a Grade I hemorrhage can cause a venous infarction. On MRI, the periventricular hemorrhage is shown as a fan-shaped structure due to obstructed medullary veins; it is of low signal intensity on T2-weighted imaging.
Posthemorrhagic ventricular dilatation Fig. 4.32a, b	This affects approximately 36% of preterm infants with intraventricular hemorrhage, but resolves in 65% of affected infants. US can demonstrate the onset of ventricular dilatation and determines its progression or resolution. The pulsed Doppler scan may give additional information by demonstrating an increased resistance index in the presence of increased ICP.
PVL Fig. 4.33a–d	The sonographic diagnosis of PVL depends on the detection of abnormal periventricular parenchyma and diagnosis is difficult. Equal or higher echogenecity than the choroid plexus is abnormal. In equivocal cases, recognition of the optic radiation may be helpful. If the optic radiation is not visible (due to surrounding hyper-echogenicity), there is another indication of PVL. MRI may be helpful, especially if there is a hemorrhagic component. As a special MRI sequence, DWI will link PVL to areas of high signal intensity, representing restricted diffusion, before cysts are shown on US. On US, the pattern may show a lateral extension with spiculated margins, high hyperechogenicity with sharp margins, organization in clusters, butterfly appearance on coronal images, and extensive density with scattered punctate regions. Repeat the US examination to rule out development of cysts. When macrocysts appear, with their progressive confluent extension, the diagnosis is easy, but this is rare. Most often, there are microcysts, which are more difficult to detect even if surrounded by hyperechoic white matter. They appear between day 8 and day 25 after any type of echodensity. Their recognition is important because they are correlated with a suboptimal clinical outcome.
Brain infarction Fig. 4.34a–d Fig. 4.35a, b, p. 326	Unilateral infarction is more common on the left side (61%) than on the right (32%), whereas in 7% bilateral arterial distribution infarcts can occur. The majority of strokes involve the middle cerebral artery. Brain infarction is not uncommon in preterm infants with a gestational age of 34 wk, with an incidence of 7/1000, compared to an incidence of 1/4000 in full-term infants. Lenticulostriate infarcts appear to be especially common in the preterm population and can be well visualized by US and MRI.
Cerebellar hemorrhage	Observed in 10%–25% of very-low-birth-weight preterm infants at postmortem examination and is associated with traumatic birth, injury from overly tightly applied ventilator masks, and supratentorial hemorrhage. On MRI cerebellar hemorrhage is more frequently seen than with US. Morbidity is high for infants with large supratentorial and cerebellar hemorrhages.
Hypoxic/anoxic insult Fig. 4.36a, b, p. 326	In the premature infant, the white matter is damaged and this encephalopathy is often accompanied by peri-intraventricular hemorrhage. Gray matter is predominantly involved in the term baby.
Porencephalic cyst Fig. 4.37a, b, p. 327	Hypoechoic area on US as a result of hypoxic, ischemic insult or bleeding. On MRI the area has, on all sequences, the signal intensity of CSF. A true porencephalic cyst has to communicate with the ventricle.
Meningitis/encephalitis Fig. 4.38a, b, p. 327 Fig. 4.39, p. 328 Fig. 4.40a–c, p. 328	On US, hyperechoic areas near the brain surface; the arachnoid may be thickened with increased echogenicity due to increased cell count and/or proteins. In encephalitis, the subcortical white matter is also involved. Cystic degeneration or destruction of the affected white matter may occur, even quite rapidly (within a couple of days). MRI is the best technique to show the extent of brain damage.
Abscess/ventriculitis Fig. 4.41a–c, p. 329	Ventriculitis is easily detected by US, especially if intraventricular septa are present. In most of the cases, the ependyma is thickened. Abscess formation may be a complication of meningitis. MRI may be helpful in differentiating between bleedings, infarction, or tumors. A dark rim on T2-weighted images is characteristic for abscess formation.

**Fig. 4.31 Obstructive hydrocephalus** in an 8-day-old boy, born at 32 weeks, due to germinal matrix bleeding Grade II on the right side and Grade III on the left side. Note also the hemorrhagic venous infarct in the left frontal lobe that is hypointense on the T1-weighted image due to hemosiderin.

**Fig. 4.32a, b Posthemorrhagic ventricular dilatation.** (a) Posthemorrhagic dilatation of the lateral third and fourth ventricle in a preterm infant demonstrated on US. Note thickening of the ependyma. (b) Note the hemorrhagic clots in the occipital horn.

**Fig. 4.33a–d Periventricular leukomalacia.** (a) Classic PVL in a premature 14-month-old infant with spastic tetraplegia. Note the irregular wall of the ventricles and the periventricular white matter loss visible on this T1-weighted image. (b) Thin corpus callosum is due to white matter loss. (c) Axial T2-weighted image: note again the irregular wall of the ventricles, periventricular white matter loss, and prominent CSF spaces. (d) Coronal fluid-attenuated inversion recovery (FLAIR) image shows periventricular gliosis.

**Fig. 4.34a–d Brain infarction.** A 5-day-old boy with seizures due to a parietal and frontal infarct in the left medial cerebral artery distribution. Note the loss of gray and white matter differentiation and swelling of the left temporal lobe on the T1-weighted image (a) and (b) the T2-weighted image. (c) The infarct in the left medial cerebral artery distribution area presents as a hypersignal intensity on this DWI. (d) Note the deep, double peak at 1.33 ppm, presenting lactate due to severe ischemia in this area.

**Fig. 4.35a, b Brain infarction.** (a) A 10-month-old boy with hypotensive period during craniotomy resulting in cerebellar infarcts on both sides, presenting as hyperintense zones on T2-weighted images. (b) Apparent diffusion coeffcient (ADC) map shows the infarcted areas as hypointense.

**Fig. 4.36a, b Hypoxic/anoxic insult.** (a) T1-weighted image shows cortical involvement with a hemorrhagic component in a term infant with a history of severe asphyxia. (b) DWI shows destruction of the whole cortex.

**Fig. 4.37a, b Porencephalic cyst.** (a) A 9-month-old boy with an old infarction of the head of the left caudate nucleus. (b) Coronal FLAIR image shows that the old infarction of the head of the left caudate nucleus has the signal intensity of CSF.

**Fig. 4.38a, b Meningitis/encephalitis.** (a) CT of a 7-year old girl with a history of a pneumococcal meningitis and ventriculomegaly due to parenchymal loss and calcification frontoparietal. (b) Note the calcifications.

**Fig. 4.39 Occipital encephalitis/infarction** (on the left side) due to herpes simplex CNS infection in 3-year-old girl.

**Fig. 4.40a–c Meningitis/encephalitis.** (a) A 14-month-old girl with failure to thrive and proven cytomegalovirus (CMV) infection resulting in periventricular leukodystrophy. (b) CMV infection resulting in periventricular cysts in the temporal lobes that are hypointense on this T1-weighted image. (c) CMV infection resulting in subcortical leukomalacia in the frontal and temporal lobes.

**Fig. 4.41a–c Abscess/ventriculitis.** (a) A 6-year-old girl diagnosed with a temporoparietal abscess on the right side, visible on this T1 image as an inhomogeneous, hypointense, well-circumscribed lesion with a thick wall. (b) The abscess wall has a low signal intensity on this T2-weighted image. Extensive peripheral edema is noted. (c) Coronal T1-weighted image after Gd shows a ring-enhanced lesion, diagnosed as a right temporoparietal abscess.

**Table 4.14 Abnormalities of brain formation**
Diagnosis	Findings	Comments
Callosal agenesis Fig. 4.42a–c Fig. 4.43a–c	On US, abnormalities of the corpus callosum can be diffcult to identify. Indirect signs of callosal anomalies on US include lack of visualization of the cavum septi pellucidi, enlarged atria and occipital horns resulting in a teardrop configuration of the lateral ventricles, a high-riding third ventricle, and radiating medial hemispheric sulci. On MRI, abnormalities of the corpus callosum are more easily detected.	More than three-quarters of patients with callosal agenesis have additional CNS anomalies, and two-thirds have additional extra-CNS anomalies. Associations with callosal agenesis include Chiari type II malformation, Dandy-Walker malformation, gray matter heterotopia, holoprosencephaly, schizencephaly, and encephaloceles.
Holoprosencephaly Fig. 4.44a, b, p. 332	MRI is the imaging modality of choice. Alobar: Absence of falx, interhemispheric fissure, septum pellucidum, and superior sagittal sinus. Thalami are fused. Single mono-ventricle. Approximately 90% have severe facial abnormalities, the most severe is cyclopia. Semilobar: Partial development of falx, interhemispheric fis-sure, and superior sagittal sinus. Septum pellucidum is absent. Thalami may be fused. Thirty percent have facial abnormalities. Lobar: Midline structures almost normal. Septum pellucidum is absent. Rostral brain may show some midline deficiencies; posterior aspect of the brain is normal. May have severe facial abnormalities.	Different types of holoprosencephaly exist, representing a continuous spectrum. The most severe type is alobar, followed (in decreasing severity) by semilobar, and the lobar type. Semilobar most common type. Alobar usually lethal.
Septo-optic dysplasia	Third ventricle and thalami are normal. Also corpus callosum is present. Thin optic chiasm.	Some consider septo-optic dysplasia as a variant of lobar holoprosencephaly.
Cephaloceles	CT is the modality to show the bone defect; MRI is the best technique to confirm presence of brain tissue in a cephalocele.	Can occur anywhere in the cranial vault, but most commonly in the midline at the occiput, skull base, or vertex. The most common basal cephalocele is the sphenopharyngeal type.
Chiari malformations Fig. 4.45	Chiari malformation is more a MRI diagnosis than a US one. Chiari type I: cerebellar tonsils below foramen magnum > 5 mm, small posterior fossa, 50% asymptomatic, 50% hydromyelia, no myelomeningocele (MMC). Chiari type II: Cerebellar tonsils and part of vermis below foramen magnum. Dorsal medulla descends behind cervical spinal cord, kinking medullocervical junction. Beaking of tectum, hydrocephalus, small posterior fossa, strawlike fourth ventricle, and 100% associated with MMC. Chiari type III: occipital cephalocoele involving cerebellar tissue with traction on brainstem. Chiari type IV: Chiari type II with vanishing cerebellum.	All Chiari types are the result of lack of expansion of fourth ventricle with consequent hypoplasia of the posterior fossa.
Dandy-Walker complex	Hypoplasia of the vermis, a pseudocystic fourth ventricle, upward displacement of the tentorium, and torcular and AP enlargement of the posterior fossa. A Blake pouch cyst has also been referred to as Dandy-Walker variant. Although US can easily identify severe Dandy-Walker malformations, it is generally more limited in distinguishing mild forms of vermian hypoplasia from a mega cisterna magna or an arachnoid cyst than MRI.	A cerebellar vermis with three groups of lobes and two main fissures, identified on sagittal MRI T2 images, not only has the greatest chance not to be associated with other malformations but also to have a favorable neurocognitive outcome. On the contrary, a deeply dysgenetic vermis with only two or one recognizable lobes is not only constantly associated with other brain malformation but also with poor prognosis.
Cerebellar anomalies Fig. 4.46 Fig. 4.47a–c, p. 334	Cerebellar, vermian hypoplasia: focal and generalized hypoplasia (Dandy-Walker continuum with enlarged fourth ventricle, pontocerebellar hypoplasia with normal fourth ventricle). Cerebellar dysplasia: Focal vermian dysplasia with molar tooth sign (Joubert and Joubert-like syndromes) Rhombencephalosynapsis Generalized dysplasia: (congenital muscular dystrophies, CMV, lissencephaly with reelin [RELN] gene mutation, lissencephaly with agenesis of corpus callosum and cerebellar dysplasia, associated with diffuse cerebral polymicrogyria and diffusely abnormal foliation).
Spectrum of neuronal migration anomalies	MRI is superior to US in identifying schizencephaly, lissencephaly, polymicrogyria, and gray matter heterotopia.	Epilepsy is often present in patients with cortical malformations and tends to be severe, although its incidence and type vary in different malformations.
Periventricular nodular heterotopia (PNH) Fig. 4.48	Appears as nodules that are isointense to the gray matter and are located along the ventricular walls.	PNH is a malformation of neuronal migration in which a subset of neurons fails to migrate into the developing cerebral cortex. X-linked PNH is mainly seen in females and is often associated with focal epilepsy. Filamin A mutations have been reported in all familial cases and in about 25% of sporadic patients. A rare recessive form of PNH due to ARGEF2 gene mutations has also been reported in children with microcephaly, severe delay, and early seizures.
Lissencephaly (also known as agyria, smooth brain) and subcortical band heterotopia Fig. 4.49, p. 336 Fig. 4.50, p. 336	Classic lissencephaly is associated with the shallow appearance of the sylvian fissures, reduced number or complete absence of additional sulci for the expected gestational age of the fetus, absence of normal multilayered appearance of the brain, and a large thick band of arrested neurons within the developing white matter. Autosomal recessive lissencephaly with cerebellar hypoplasia, accompanied by severe delay, hypotonia, and seizures, has been associated with mutations of the RELN gene. X-linked lissencephaly with corpus callosum agenesis and ambiguous genitalia.	Disorders of neuronal migration represent a malformative spectrum resulting from mutations of either LIS1 or DCX genes. LIS1 mutations cause a more severe malformation in the posterior brain regions. Most children have severe developmental delay and infantile spasms, but milder phenotypes are on record, including posterior SBH owing to mosaic mutations of LIS1. DCX mutations usually cause anteriorly predominant lissencephaly in males and SBH in female patients. Mutations of DCX found in male patients with anterior subcortical band heterotopia (SBH) and in female relatives with normal brain MRI in genotypic males are associated with mutations of the ARX gene. Affected boys are severely delayed and show seizures with suppression-burst electroencephalogram. Early death is frequent. Carrier female patients can have isolated corpus callosum agenesis.
Schizencephaly Fig. 4.51, p. 336	Schizencephaly appears as a gray matter–lined cleft extending from the ventricle to the subarachnoid space. Closed-lip schizencephaly is characterized by gray matter–lined lips that are in contact with each other (type I). Open-lip schizencephaly has separated lips and a cleft of CSF, extending to the underlying ventricle (type II).	The etiology is unclear, although a primary malformation secondary to a neuronal migrational anomaly is considered most likely. Familial cases of schizencephaly have been reported, suggesting a possible genetic origin within a group of neuronal migration disorders. Heterozygous mutations of the EMX2 have been reported in cases with schizencephaly. However, early prenatal injury, such as that associated with drug abuse or abdominal trauma, has also been reported to be associated with schizencephaly, possibly from a vascular insult or resulting from CMV infection. Therefore, the appearance of schizencephaly is likely to be secondary to multiple factors, leading to a final common manifestation of abnormal neuronal migration.
Polymicrogyria Fig. 4.52, p. 336 Fig. 4.53, p. 337	Polymicrogyria appears as localized and/or generalized absence of normal sulcation with multiple abnormal infoldings of the affected cortex.	Among several syndromes featuring polymicrogyria, bilateral perisylvian polymicrogyria shows genetic heterogeneity, including linkage to chromosome Xq28 in some pedigrees, AD or recessive inheritance in others, and an association with chromosome 22q11.2 deletion in some patients. About 65% of patients have a severe form of epilepsy. Recessive bilateral frontoparietal polymicrogyria has been associated with mutations of the GPR56 gene.

**Fig. 4.42a–c Callosal agenesis.** (a) Coronal US shows callosal agenesis on the medial side of the frontal horns (the Probst bundles). (b) Sagittal T1-weighted image shows that the sulci are reaching the roof of the third ventricle wall due to absence of the corpus callosum. (c) Note the colpocephaly due to the absence of the corpus callosum on the CT.

**Fig. 4.43a–c Macrocephaly** in a 7-day-old boy. T1 (a) and T2 images (**b, c**) show callosal agenesis and noncommunicating interhemispheric cysts.

**Fig. 4.44a, b Holoprosencephaly.** (a) An 18-month-old boy with semilobar holoprosencephaly. Axial T2-weighted image shows fusion of the frontal lobes. (b) Coronal FLAIR image shows fusion of the frontal lobes and partial fusion of thalami.

**Fig. 4.45 Chiari malformation.** Sagittal T1-weighted image shows an occipital cephalocele involving cerebellar tissue with traction on the brainstem consistent with a Chiari type III malformation.

**Fig. 4.46 Cerebellar anomaly.** A term infant with clonic seizures. Coronal T2-weighted image shows cerebellar hypoplasia.

**Fig. 4.47a–c Cerebellar anomaly.** (a) A 2.5-year-old boy with difficulty maintaining his balance as well as impaired motor function and a hypotonic neck. Note the fusion of both cerebellar hemispheres on this axial T2-weighted image, compatible with the diagnosis of rhombencephalosynapsis. (b) Coronal FLAIR image. (c) Coronal T1 gradient echo sequence.

**Fig. 4.48 Periventricular nodular heterotopia.** Coronal T1-weighted image shows periventricular noduli in a 2-year-old girl.

**Fig. 4.49 Miller-Dieker lissencephaly syndrome.** A 3-year-old boy with mental retardation. This axial T2-weighted image shows few sulci, a cell-sparse zone, and that the parietal-occipital is more affected than frontal, which is compatible with Miller-Dieker syndrome.

**Fig. 4.50 Lissencephaly.** Axial T1-weighted image shows a band of heterotopia in a 9-year-old girl.

**Fig. 4.51 Schizencephaly.** Axial T2-weighted image shows an open lip schizencephaly in an 8-month-old boy with motor delay and early hand preference.

**Fig. 4.52 Bilateral polymicrogyria** is visible on this axial T1-weighted image.

**Fig. 4.53 Bilateral perisylvian polymicrogyria.**

**Table 4.15 Intracranial hemorrhage**
Diagnosis	Findings	Comments
Grade I–IV intracranial hemorrhage	See Table 4.13 abnormalities in premature infants
Venous infarction	See Table 4.13 abnormalities in premature infants
Intraparenchymal hemorrhage, acute Fig. 4.54a–c, p. 338	Logistic CT is the best imaging method. In infants with patent fontanelle, US may also be used. MRI can be used, especially as the FLAIR sequence can pick up acute hemorrhages.
Intraparenchymal hemorrhage, subacute Fig. 4.55a–c, p. 339	MRI is the modality of choice because it will best show the time at which different bleedings occurred. May be of significance in child abuse and shaken baby syndrome.
EDH Fig. 4.56	EDHs are hemorrhagic collections located between the inner table of the skull and the dura. Because the dura is tightly adherent to the inner table at cranial suture sites, EDHs do not typically cross cranial suture lines (unlike subdural hematomas [SDHs], which can freely cross these sites) unless the dura is lacerated. Whereas the extension of SDHs is restricted by the falx cerebri and tentorium cerebelli, EDHs can freely extend across these sites.	On occasion, EDH cannot be detected on CT because of its small size and may be first seen on MRI. The changes in density on CT and of signal intensity of EDH on MRI follow the same temporal progression as that of SDH.
SDH Fig. 4.57a–c Fig. 4.54a–c, p. 338	Acute SDHs located over the cerebral convexity appear as a hyperin-tense crescent-shaped collection with a sharp margin between the collection and adjacent brain. Alternatively, SDHs can have a biconvex (lentiform) shape like that of a typical EDH. SDHs undergo a typical temporal evolution on both CT and MRI. On CT, acute SDHs are characteristically hyperdense, with a few exceptions. At first, in the setting of severe anemia, acute SDHs can be isodense with gray matter. SDHs that are only a few hours old can have a mixed appearance of both hyperdense and hypodense regions because of the presence of uncoagulated blood before clot formation. Also, in neonates it can be difficult to differentiate SDH from the more dense aspect of fetal hemoglobin especially at the transverse sinus level. On MRI in the first few days, while blood is in the stage of intracellular deoxyhemoglobin, the SDH is isointense to gray matter on T1-weighted images and hypointense on T2-weighted images. SDHs become hyperintense on T1-weighted images after a few days because of blood in the stage of intracellular methemoglobin. After approximately the first week, with lysis of red blood cells and production of extracellular methemoglobin, SDHs become hyperintense on both T1- and T2-weighted images, a finding that may persist for many months. Thereafter, the pattern will be iso- or hypointense on T1 and hypointense on T2 due to hemosiderin, especially on T2* sequence.	SDHs most commonly occur at one of three locations: along the cerebral convexities, the falx cerebri, and the tentorium cerebelli. Child abuse should be ruled out, especially in cases of SDH with different densities, due to different timing of SDH. There is an important differential diagnosis, especially metabolic disease like Menkes disease and Glutaric aciduria type 1 and D-2-hydroxyglutaric aciduria.
Acute SDH		Acute SDHs are often seen after trauma and are frequently associated with a skull fracture. The term acute subdural hematoma is generally meant to refer to an SDH that is a few days old, whereas subacute is generally meant to refer to SDHs that are more than a few days but less than a few weeks old.
Chronic SDH Fig. 4.57a–c	Chronic SDH typically appears homogeneously hypodense relative to gray matter as red blood cells lyse and a proteinaceous fluid remains. When fresh hemorrhage occurs into a chronic SDH, a bilayered appearance typically results, with a hypodense layer (because of chronic hemorrhage) in the less dependent position and a hyperdense component (because of acute hemorrhage) in the dependent position.	The term chronic subdural hematoma generally refers to an SDH that is more than a few weeks old.
Subarachnoid hemorrhage (SAH) Fig. 4.58a–c, p. 342	CT is generally considered more sensitive than MRI in the detection of SAH. However, a number of recent articles have suggested that SAH is also readily detected on proton-density, T2-weighted MRI, but is best seen on FLAIR images.	A small amount of SAH is often seen after head trauma. Common sites of SAH include basilar cisterns such as the prepontine, ambient, inter-peduncular, and perimesencephalic cisterns. It is rare in the pediatric population, but SAHs do occur due to rupture of aneurysms.

**Fig. 4.54a–c Intraparenchymal hemorrhage, acute.** A 9-year-old boy with an epidural hematoma (EDH) at the left frontal side and infarcts in the occipital lobes based on child battering. It shows high signal intensity on T1- (a) and T2-weighted (b) image due to extracellular methemoglobin. (c) EDH with high signal intensity on a FLAIR image in the same patient.

**Fig. 4.55a–c Intraparenchymal hemorrhage, subacute.** (a) A 4-day-old girl term neonate with postpartum bleeding from umbilical cord and pulmonary arrest/irregular breathing. This T2-weighted image shows parenchymal bleeding involving almost the entire right temporal lobe. (b) On the T1-weighted image, the bleeding is hyperintense at the periphery and isointense centrally, compatible with intra- and extracellular methemoglobin. (c) Sagittal T1-weighted image shows the extent of the bleeding in the right temporal lobe.

**Fig. 4.56 Epidural hemorrhage.** A 4-month-old boy who has fallen down the stairs. CT shows a right EDH with midline shift and fracture.

**Fig. 4.57a–c Subdural hematoma.** (a) Multiple sharply demarcated lines are suspicious for fractures in child abuse. (b) Sagittal T1-weighted image showing subdural effusion with higher signal than CSF due to old bleeding and occipital parenchymal loss due to old bleeding or infarct. (c) T2-weighted image shows subdural effusion and old bleeding in the left hemisphere.

**Fig. 4.58a–c Subarachnoid hemorrhage.** (a) A 12-year-old girl with an acute onset of headache. CT shows subarachnoid blood at the basal cisterns, with the maximum of blood at the the A1 and M1 level on the right. (b) CTA shows an aneurysm at the A1/A2 level on the left. (c) Coronal reconstruction of the CTA confirms an aneurysm at the A1/A2 level on the left.

**Table 4.16 Cystic structures**
Diagnosis	Findings	Comments
Choroid plexus cyst (CPC) Fig. 4.59a–c	Best seen on US as a rounded hypoechoic mass of varying size. On MRI, hypointense on T1- and hyperintense on T2-weighted images.	CPCs are more common in fetuses with chromosomal aneuploi-dies, particularly trisomy 18.
Subependymal pseudocyst (germinal matrix cyst)		Subependymal pseudocysts are found in 5% of all neonates. When isolated, they have a good prognosis and regress spontaneously within a few months. However, associated anomalies are frequent and in such cases the prognosis is poor. They can be of infectious, vascular, metabolic, or chromosomal origin.
Dilatation of the cavum septum pellucidum	Expanded cystlike cavum septum pellucidum, may extend dorsally, called “et vergae.”	Cavum septi pellucidi may serve as a significant marker of cerebral dysfunction manifested by neurodevelopmental abnormalities while the cavum et vergae alone does not identify individuals at risk for cognitive delays.