FETAL INTRACRANIAL ANOMALIES (CATEGORY AVERSION)

INTRODUCTION

Fetal central nervous system (CNS) abnormalities are some of the most common congenitalabnormalities, with an incidence of 14 per 10,000 births. Neural tube defects are the most frequent CNSmalformations, occurring in approximately one to two cases per 1000 births. During pregnancy,assessment of the fetal intracranial anatomy is typically performed at the time of the mid-trimesterultrasound at approximately 18-22 weeks’ gestation. As described in the International Society ofUltrasound in Obstetrics and Gynecology (ISUOG) updated guidelines on the performance of thescreening examination of the fetal CNS, scanning is usually performed in the axial plane, withincorporation of three views. These include the transventricular, transthalamic and transcerebellar asshown in Figure 1. The transventricular view includes assessment of the anterior and posterior horns ofthe lateral ventricles, choroid plexus, cavum septum pellucidum (CSP), the midline falx, cerebral cortexand the calvarium. The CSP is an important marker of fetal CNS midline integrity that should always bediscernable between 18 and 37 weeks.

Figure 1. Fetal CNS Three Axial Planes

VENTRICULOMEGALY

The measurement of the lateral ventricle should be performed at the level of the atrium, which is thepart at which the body, posterior horn, and temporal horn converge. The far-field ventricle is typicallyassessed as the skull ossification can create artifact such that visualization of the near-field ventricle maybe difficult, although attempts to assess both ventricles should be undertaken.Fetal cerebral ventriculomegaly is defined as an atrial diameter of greater than or equal to 10 mm and isoften associated with numerous CNS anomalies. It is usually defined as mild, moderate or severedepending upon the measurement of the atrial diameter. As per recommendations by the Society ofMaternal-Fetal Medicine (SMFM), ventriculomegaly is classified as mild if the atrial diameter is 10-12 mm,moderate if 13-15 mm and severe if > 15 mm. These measurements influence patient counseling, as therisk of an adverse outcome and possibility of other abnormalities increase as the ventriculomegalyincreases. The most common cause of severe ventriculomegaly is aqueductal stenosis (discussed below).Examples of mild ventriculomegaly and severe ventriculomegaly are shown in Figures 2 and 3,respectively. Normally, the choroid plexus should fill at least 60% of the width of the ventricle. In thecase of more severe ventriculomegaly (hydrocephalus), the choroid plexus takes up less than one-half ofthe cerebrospinal fluid (CSF) space, giving it a “dangling” appearance, hence the term “dangling choroid”sign.The term hydrocephalus often refers to an atrial diameter > 15 mm, and there is some underlying

process (often obstructive) that has occurred. However, keep in mind that both the termsventriculomegaly and hydrocephalus are descriptive findings and not diagnoses. Hydrocephalus caneither be due to an obstructive process, with the blockage of flow of CSF within the ventricular system(referred to as noncommunicating), or failure of CSF resorption, also known as communicatinghydrocephalus.When ventriculomegaly is suspected, SMFM guidelines recommend offering screening for an infectiousetiology (cytomegalovirus and toxoplasmosis) which is identified in approximately 5% of cases of mild tomoderate ventriculomegaly. Diagnostic testing for chromosomal abnormalities with amniocentesis shouldalso be considered as 5% of cases of isolated mild to moderate ventriculomegaly will have an abnormalkaryotype, with trisomy 21 (Down syndrome) the most commonly encountered aneuploidy. Non-invasiveprenatal screening, also known as cell-free DNA (cfDNA) screening can be offered if the patient declinesinvasive testing with amniocentesis, however cfDNA is limited in that it only screens for a limited numberof conditions. SMFM also recommends consideration of fetal magnetic resonance imaging (MRI) in casesof mild or moderate fetal ventriculomegaly of the findings. In terms of counseling, if mildventriculomegaly is identified in isolation, survival is reported to be very high, with reported rates of93-98%, and there is > 90% chance of a normal neurodevelopmental outcome. Whenever ventriculomegaly is noted, it is essential for the sonographer to perform a comprehensive fetalCNS examination, including assessment of the third and fourth ventricle. In fetuses with mild or moderateventriculomegaly, the incidence of additional anomalies (both CNS and non-CNS) has a broad range, butthe data suggest it is less than 50%. Atrial measurements at the upper limits of normal (close to or at 10mm) usually represent a normal variant. In greater than 90% of cases in fetuses in which mildventriculomegaly is detected prenatally, the postnatal evaluation is normal.

Figure 2. Mild Ventriculomegaly

Figure 3. Severe Ventriculomegaly

ANENCEPHALY/EXENCEPHALY

Both of these conditions represent the most severe form of a neural tube defect (NTD).With a prevalenceof approximately 3 per 10,000 births, anencephaly, which is also referred to as acrania is the mostcommon NTD. It is more commonly seen in the Caucasian and Hispanic population and less so in those ofAfrican descent.Closure of the neural tube begins in the cervical region and proceeds in both a cranial and caudaldirection. Neural tube defects result from failure of closure of the neural tube between 25 and 27 daysafter conception. It is failure of closure of the rostral (most cranial) neuropore around postovulatory day25 that results in anencephaly/exencephaly. The skull is usually completely formed by 10 weeks’ gestation, thus these defects can be reliably diagnosed in the first-trimester. Anencephaly is suspected when no calvarium or brain tissue can be identified about the orbits.Exencephaly precedes anencephaly where brain tissue is still present. However, due to the toxic effectsof amniotic fluid on brain tissue, disintegration occurs which evolves into anencephaly. Ultrasoundfindings are often described as “froglike facies” (Figure 4). Maternal serum aneuploidy screening willreveal an increased maternal serum alpha-fetoprotein in 90% of anencephaly cases. Often, whendetected in the first-trimester, the crown-rump length is less than expected. Facial features associatedwith anencephaly include hypertelorism (eyes too widely spaced), proptosis (protrusion of the eyeball)and cleft lip and palate. Other neural tube defects such as a lumbar myelomeningocele may be present.Due to impaired fetal swallowing, polyhydramnios is often noted in the second and third trimester, andthe amniotic fluid may appear echogenic due to dissolved neural tissue. Anencephaly is universally

lethal.

Figure 4. Anencephaly

HOLOPROSENCEPHALY

Holoprosencephaly (HPE) results from failure of the embryonic forebrain, known as the prosencephalon,to separate in a normal fashion. The result is failure of division into separate lobes. This maldevelopmentoccurs between the third and fourth gestational week. In liveborn neonates, the reported prevalence is 1in 10,000. HPE is the most common forebrain abnormality. There are three types of HPE. From least to most severe, these are noted as lobar, semilobar and alobar.Approximately two-thirds of those with HPE have the alobar type. A finding in all three types is absenceof the CSP which helps in diagnosing the milder forms of HPE. The ultrasound findings of alobar HPEinclude a single ventricular cavity (monoventricle), absence of midline structures including the CSP, falxcerebri, third ventricle and corpus callosum. The thalami are fused (non-cleaved) and a dorsal cyst isoften identified. Figure 5 is an example of alobar HPE. Of note, the posterior fossa is usually normal.There are several facial anomalies that may be identified in the setting of HPE. This is consistent with theclassic ultrasound principle that “the face predicts the brain”. Cyclopia (fused single eye with a singleorbit), central proboscis with absence of a normal nose, hypotelorism (orbits too close together) and cleftlip/palate.

Chromosome abnormalities are seen in 25-75% of cases, with trisomy 13 the most common. Syndromiccauses are also possible, and these include Smith-Lemli-Opitz, Aicardi, Fryns and Meckel-Gruber. Variousgenetic mutations have also been identified in cases of HPE. Pregestational diabetes, alcohol and retinoicacid have a reported association with HPE.

Figure 5. Alobar HPE

AGENESIS OF THE CORPUS CALLOSUM

This entity refers to absence of the nerve fiber tracts that connect the cerebral hemispheres. In agenesisof the corpus callosum (ACC) can be complete or partial. In partial agenesis, the posterior segments ofthe corpus callosum are usually missing. Complete agenesis may not be fully apparent until after 22weeks’ gestation. Other abnormalities of the corpus callosum include an abnormal shape (dysgenesis)and decreased thickness (hypoplasia). The etiology of ACC can be chromosomal, syndromic or part of asingle-gene disorder. In terms of ultrasound findings, one of the first clues to making the diagnosis of ACC is an absent CSP.Embryologically, a CSP cannot be present if the corpus callosum failed to develop. Disproportionatedilation of the posterior portion of the lateral ventricle as compared to the anterior portion will result in ateardrop shaped lateral ventricle, referred to as colpocephaly (figure 6). Still, prior to 24 weeks’gestation, the atrial width is usually within the normal range (< 10 mm). Once a CSP is found to be absent, ACC is one of several diagnoses that are possible. Thus, to helpconfirming a diagnosis of ACC, ideally sagittal and coronal planes should be assessed, and if the fetus is

in a cephalic presentation, transvaginal ultrasound may be employed to better visualize the intracranialanatomy. The third ventricle is often described as “high-riding”, which is best assessed in the coronalplane. Also in the coronal plane, one can appreciate lateral ventricles that are wildly spaced and parallel,creating a “steer horn” appearance of the frontal horns. The sagittal plane allows for interrogation of thepericallosal artery. The pericallosal artery is normally located just above the corpus callosum and itscourse appears to outline the shape of the corpus callosum. In ACC, the pericallosal artery appearsdisorganized, not following its typical course outlining the corpus callosum. In approximately 50% of cases, other fetal CNS anomalies may be seen when ACC is suspected. Thisincludes midline facial anomalies, Dandy-Walker malformation (discussed below), vermian dysgenesis,Chiari 2 malformation, encephaloceles and neuronal migration disorders. ACC may be seen as part of asyndrome, as more than 200 genetic syndromes have been linked to the presence of ACC, andchromosomal anomalies have also been identified in 17% of cases of ACC. In approximately 60% ofcases, non-CNS anomalies may be seen, including both cardiac and genitourinary abnormalities as wellas congenital diaphragmatic hernia.

Figure 6. ACC Teardrop

AQUEDUCTAL STENOSIS

As noted above, aqueductal stenosis is the most common cause of severe ventriculomegaly. Theaqueduct of Sylvius is the narrowest part of the ventricular system that connects the third and fourthventricle. In aqueductal stenosis, there is a narrowing of the aqueduct of Sylvius that results in an

obstructive hydrocephalus. In some cases, the hydrocephalus doesn’t develop until late in pregnancy orthe neonatal period. Although most cases are sporadic, aqueductal stenosis can be X-linked when seen ina male fetus, and in half of cases, deformity of the thumbs is also noted. The cause of aqueductalstenosis is not completely understood. The narrowing may be due to infectious, inflammatory ordevelopmental causes. Tumors and hemorrhage may also be a cause. Ultrasound findings consistent with aqueductal stenosis include a dilated third ventricle, often assuminga funnel shape, and a normal appearing fourth ventricle. As the ventriculomegaly is often severe, a“dangling choroid” sign can be seen. As ventricular pressure builds up due to the obstruction, theadjacent brain parenchyma can be compressed resulting in thinning of the cortical mantle and thinningof the corpus callosum. Often the CSF may be absent. The head is often large (macrocephaly).Importantly, the posterior fossa is normal. Figure 7 is an example of some of these ultrasound findings.Of note, the more proximal the stenosis, the more severe the hydrocephalus.

Figure 7. Aqueductal Stenosis

DANDY-WALKER MALFORMATION

Dandy-Walker malformation (DWM) is an abnormality of the cerebellum and posterior fossa. Most casesare sporadic, although there may be an increased risk in first-degree relatives. The estimated incidenceis 1:25,000-35,000 live births. The three primary ultrasound findings that constitute DWM includecomplete or partial agenesis of cerebellar vermis, cystic dilation of fourth ventricle and an enlargedposterior fossa due to elevation of cerebellar tentorium and torcular of Herophili. The latter marks theposition of the confluence of venous sinuses (transverse, straight and superior sagittal). The cerebellar

vermis is not fully formed prior to 20 weeks’ gestation, thus a conclusive diagnosis of DWM cannot bemade before this. In the axial plane, the transcerebellar view will show an enlarged cisterna magna (> 10mm) and cerebellar hemispheres that are splayed apart. Figure 8 illustrates the absence of the vermiswith communication between the fourth ventricle and cisterna maga. When assessing the cerebellum inthe axial plane, if the angulation is too steep, it could lead to a false diagnosis by suggesting a cleft in thevermis which is an artifact. Both the falx and cerebral cortex usually are normal appearing.Ultrasound assessment of the sagittal plane is extremely helpful to confirm the diagnosis of DWM. Thisview provides the ability to distinguish DWM from other posterior fossa abnormalities, including Blake’spouch cyst, mega cisterna magna and vermian hypoplasia. Vermian hypoplasia has also been referred toDandy-Walker variant, where there is a cleft seen in the inferior portion of the vermis but the remainderof the vermis is intact. If the fetus is in a cephalic presentation, transvaginal ultrasound can be useful inassessing the posterior fossa in the sagittal plane. Associated anomalies, both intracranial and extracranial are seen in 70-90% of DWM cases. Of theintracranial findings, ventriculomegaly is the most common. Other CNS anomalies include ACC,holoprosencephaly and encephalocele. Non-CNS anomalies include congenital heart defects, polycystickidneys and facial clefts. Other less frequent anomalies include limb and abdominal wall abnormalities,diaphragmatic hernia, ambiguous genitalia and fetal growth restriction. DWM may also be associatedwith chromosomal abnormalities in approximately 50% of cases. These include trisomies 9, 13, 18, and21 and triploidy. Walker-Warburg, Meckel-Gruber and Joubert are syndromes associated with DWM.Environmental exposures such as alcohol and maternal diabetes, and infections such as rubella andcytomegalovirus have been linked to DWM.The prognosis of DWM is dependent upon the presence of additional abnormalities, the degree ofhydrocephalus and whether a chromosomal abnormality or genetic syndrome is diagnosed. Up to one-third of survivors with DWM will demonstrate normal neurodevelopment. However, a mortality rate of upto 40% in infancy and early childhood has been reported.

Figure 8. DWM

CHIARI II MALFORMATION

This lesion is seen in conjunction with an open NTD. The pathophysiology is thought to be due to a CSFleak due to the open NTD that results in obliteration of the cisterna magna and an inferiorly andposteriorly displaced cerebellum, fourth ventricle and medulla. Ventriculomegaly is commonly identified,seen in 70% of fetuses at 20-24 weeks and 85% of fetuses at 30-32 weeks. It is due to obstruction of CSFflow through the fourth ventricle and posterior fossa and is often progressive as the pregnancyprogresses. The most specific ultrasound sign of the Chiari II malformation is the banana sign in whichthe cerebellum loses its bilobed shape and is compressed, wrapping around the midbrain and obliteratingthe cisterna magna. The amount of hindbrain compression is variable. A cisterna magna < 3 mm isconsidered small. A frontal bone concavity known as the lemon sign may also be seen, although in and ofitself, it is not diagnostic of a Chiari 2 malformation. It is identified in 1% of all fetuses at midtrimesterand is a transient finding whether or not an open NTD is present. The head size is usually normal orsmall, even if severe ventriculomegaly is identified. Figure 9 demonstrates the banana and lemon sign.Other anomalies are noted in approximately 40% of Chiari 2 cases. These include CNS anomalies such asACC, an interhemispheric cyst or heterotopia (nodular appearance to the walls of the lateral ventricle dueto an abnormal location of nerve cells. Clubfoot, scoliosis, kyphosis and a tethered spinal cord are alsooften identified.

Figure 9. Chiari 2

HYDRANENCEPHALY

This lesion represents an extreme destructive process that results in liquefaction of the cerebralhemispheres. It is rare, seen in 1-2 per 10,000 live births and usually occurs in a sporadic fashion. Theetiology of this severe condition is unclear. Occlusion of the internal carotid arteries, infections, hypoxiaand thromboembolism have all been considered as etiologies. This lesion is usually lethal.On ultrasound, the classic appearance is complete absence of a cortical mantle. Unlike alobarholoprosencephaly where a falx is absent, in hydranencephaly, a falx is present because it receives itsblood supply from the external carotid artery which is unaffected. Other structures including the thalami,choroid, posterior fossa and brainstem are preserved. Severe hydrocephalus with a very thin corticalmantle due to compression by the CSF pressure can mimic hydranencephaly, however it is important tomake this distinction and these two entities carry a different prognosis. The fluid in the brain may appearsomewhat echogenic due to residual tissue. The head size is typically normal, however macrocephalymay occur if CSF production continues without resorption. In some cases, transvaginal ultrasound can behelpful if the fetus is in a cephalic presentation to assess for the presence of cortical mantle. Figure 10 isan example of hydranencephaly.

Figure 10. Hydranence

ARACHNOID CYST

This entity represents an extraaxial cyst that contains CSF with a thin and smooth wall. Extraaxial meansthe cyst is not within the brain parenchyma itself (intraaxial) but rather can have a mass like effect anddisplace brain parenchyma. These cysts are rare and represent only about 1% of space occupying lesionsof the CNS. Approximately two-thirds or arachnoid cysts are supratentorial, and the remaining third areinfratentorial in the area of the posterior fossa. There is usually one singular cyst that displaces thenormal brain parenchyma. In The majority of these cysts are identified after 20 weeks’ gestation. Theremaining part of the brain is usually normal. Color Doppler will demonstrate this cyst is non-vascular.Figure 11 demonstrates the appearance of an arachnoid cyst. When identified in isolation, the outcome is usually favorable from a developmental standpoint. Isolatedfetal arachnoid cysts are usually associated with a favorable developmental outcome. However, the sizeof the cyst may be variable, and in some cases, these cysts may rapidly increase in size and result inobstructive hydrocephalus. Large cysts can result in a significant mass effect. Thus, if an arachnoid cystis identified, follow-up with serial ultrasounds is indicated to monitor growth of the cyst.Neurodevelopment can be impaired with large cysts or if other structural anomalies are present. Usually,the most commonly associated anomalies are with the CNS. These include ACC (partial or complete) andventriculomegaly. Anomalies outside of the CNS that are may be associated with arachnoid cysts includecleft lip/palate, omphalocele, short long bones and cardiac defects, including tetralogy of Fallot andventricular septal defect.Most of arachnoid cysts occur sporadically, although they may be syndromic in nature, seen in suchsyndromes as Aicardi, neurofibromatosis type 1, and trisomies 8, 13, 18 and 20.

Figure 11. Arachnoid Cyst

BRAIN TUMORS

These represent rare fetal CNS lesions, with a reported incidence of 0.31 per million live births. Itcomprises approximately 10% of all fetal neoplasms, which contrasts with the pediatric population wherebrain tumors are the most common solid tumors. Evidence of a solid intracranial mass with color flow is ahelpful diagnostic clue. These tumors usually present in the third trimester with evidence of a mass,macrocephaly and hydrocephalus. Approximately 70% of fetal brain tumors are supratentorial, again incontrast to the pediatric population where pediatric tumors are more commonly infratentorial. Commonlocations for fetal tumors include the pineal gland and cerebral hemispheres although often the originallocation cannot be determined.These tumors may exhibit rapid growth which can distort cerebral architecture, and as noted above, mayresult in hydrocephalus (that may continue to worsen) and macrocephaly. Thus extremely closeultrasound surveillance is warranted. Sometimes hemorrhage can occur within the tumor anddifferentiating this type of hemorrhage due to a neoplasm vs. a spontaneous intracranial hemorrhage isimportant. Color Doppler can be helpful, as the tumor is often extremely vascular, whereas aspontaneous intracranial hemorrhage has no blood flow. An arachnoid cyst is also distinct from a braintumor as it is purely cystic without a solid component is not intraparenchymal (extraaxial as notedabove). If the hypothalamus is involved, this may impair fetal swallowing which can lead topolyhydramnios. Hydrops (fluid in two or more extravascular compartments) may also develop.The most common intracranial neoplasm is a teratoma, which comprises approximately 50% of cases. Itis complex in nature, with both solid and cystic components. It is typically midline in location, andcalcifications within the mass may be seen. Other examples of fetal brain tumors include astrocytomas,which usually are noted in the cerebrum, craniopharyngiomas which can be difficult to differentiate fromteratomas, meningiomas which often result in skull deformity, and ependymomas which originate fromthe lateral and fourth ventricles. Prognosis in the setting of these lesions tends to be dismal, with areported 97% mortality if diagnosed prior to 30 weeks’ gestation. Large tumors, even if benign are aslethal as malignant ones.

VEIN OF GALEN ANEURYSM

This lesion is an abnormality of the CNS venous system, with an estimated incidence of 1 in 10,000 to 1in 25,000 births. It is not associated with any chromosomal abnormalities or syndromes. Its name issomewhat of a misnomer in that it represents an arteriovenous fistula that develops in the first-trimester.It is the most common vascular anomaly of the CNS in the fetus, typically identified in the late second orthird trimester. On ultrasound, typically a midline anechoic mass is identified that is superior to the thirdventricle and thalamus. It may mimic the appearance of an arachnoid cyst, however color Doppler isnecessary to differentiate between these entities, as an arachnoid cyst is avascular. Color flow in a veinof Galen malformation will be turbulent. Figure 12 is an example of this vascular lesion.A vein of Galen malformation can result in high-cardiac output failure, which can result in cardiomegalyand fetal hydrops. If there is a mass effect causing obstruction of the aqueduct of Sylvius, hydrocephalus

may develop. If hydrops develops, the mortality rate is extremely high.

Figure 12. Vein of Gale

SCHIZENCEPHALY

Cell migration is a component of cerebral cortex development that occurs between the 3rd and 5thmonths of gestation. Schizencephaly is a disorder of neural migration, although it may the result of adestructive process that is mediated by vascular injury. It has a reported prevalence of 1.5 per 100,000live births.It is characterized by CSF containing clefts that extend from the inner table of the skull to the lateralventricle. These clefts area lined with gray matter. Figure 13 is an example of open-lip schizencephaly.There is both open-lip and closed-lip schizencephaly, with the latter often difficult to diagnose prenatally.In open-lip schizencephaly, the walls of the cleft are separate from each other, and the lateral ventriclemay be distorted. In addition, the CSP is absent in greater than 50% of cases due to either damage ormalformation. Schizencephaly is often identified in the parietal or frontal lobes and may be eitherunilateral or bilateral. In is rarely seen in the occipital lobe. The CSP is almost always absent whenschizencephaly is bilateral. The size can vary, and in some cases can be very large (giant open-lipvariety). Both acquired (infections, teratogens) and genetic etiologies of been described forschizencephaly. Associated CNS abnormalities are demonstrated in approximately two-thirds of schizencephaly cases.This includes cortical dysplasia, heterotopia (abnormal location of neurons between the cerebral cortexand lateral ventricles), callosal dysgenesis/agenesis and septo-optic malformations. Ventriculomegaly

may also be seen in approximately 60% of cases. The face and profile are typically normal inschizencephaly which distinguishes it from holoprosencephaly.The majority of schizencephaly cases are identified after birth. The majority of infants have neurologicimpairments. Motor and cognitive dysfunction are common and are both strongly associated withbilateral clefts. Microcephaly is seen in approximately 40%, and epilepsy is seen in over 70% of cases. The differential diagnosis when schizencephaly is suspected includes an arachnoid cyst, porencephaliccyst, holoprosencephaly and hydranencephaly. We have discussed most of the entities above. Anarachnoid cyst is extraaxial, does not communicate with the lateral ventricle and will often have a masseffect on the adjacent brain tissue. A porencephalic cyst is not lined with gray matter and is a destructivelesion that is often secondary to an intracranial hemorrhage. Hydrancephaly, unlike schizencephaly willreveal complete destruction of the cerebral hemispheres with preservation of the infratentorial structures(cerebellum and brainstem). Small amounts of residual brain tissue could technically cause confusionwith bilateral giant open-lip schizencephaly.

Figure 13. Example of open-lip schizencephaly showing a large cleft(yellow arrow)

REFERENCES

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