AbstractHydrocephalus is a frequent presentation topediatrics, radiology, and clinical neuroradiol-ogy with surgical intervention often required todivert CSF. The role of the neuroradiologist iscritical in understanding the difference betweencongenital and acquired etiologies and advisingon subsequent management. A robust neurora-diological imaging strategy is required to obtainall of the relevant information and allow identi-fication of any associated findings, particularlyin hydrocephalus secondary to congenitalmalformations. Recognizing potential geneticcauses can help clinicians counsel families.
TFE) in the sagittal plane to assess the cerebralaqueduct.
• Non-flow compensated T2 weighted spin echoimaging in the sagittal plane to identify CSF flowthrough the aqueduct (or third ventriculostomy ifattempting to characterize patency).
• Phase-contrast CSF flow studies (ideally withcardiac-gating) are a useful addition and withexperience can provide quantitative data tobetter understand CSF dynamics.
Routine follow-Up:
• Axial T2 (Blade or HASTE sequences toassess ventricular volume)
• 3D steady-state gradient echo (CISS, FIESTA,TFE) in the sagittal plane to assess the cerebralaqueduct.
• +/� Non-flow compensated T2 weighted spinecho imaging in the sagittal plane
As in adults, hydrocephalus in children can bedivided into obstructive or communicating hydro-cephalus depending on the underlying mechanism.
Obstructive Hydrocephalus
A physical barrier such as a membrane or tumorprevents CSF flow through the normal anatomicalchannels.
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Communicating Hydrocephalus
There is no physical obstruction to CSF flow butan imbalance between CSF production andabsorption. In the vast majority of cases, thisinvolves impaired absorption.
In children, it is also important to try and dif-ferentiate between congenital and acquired hydro-cephalus. Congenital hydrocephalus implies thecondition is present at birth, although it is impor-tant to understand that the developing fetus maysuffer from similar acquired pathologies in uteroas the neonate (infection, intraventricular hemor-rhage, tumor, etc). Therefore, the strict definitionof congenital hydrocephalus should ideally beused exclusively for in-built genetic errors orhydrocephalus secondary to congenitalmalformations.
Congenital Hydrocephalus
Hydrocephalus and ventriculomegaly are well-recognized manifestations of numerous congeni-tal malformation syndromes. The most recog-nized malformations affect the posterior fossaand although they are discussed in more detail inthe paediatric neuroradiology chapter, they war-rant brief discussion here.
The Chiari II Malformation
The Chiari II malformation is a combination ofhind-brain herniation and a lumbarmyelomeningocele (see Fig. 1). The incidence is3.4/10,000 births with a mortality rate of 10% andlong-term disability in surviving children includ-ing developmental delay, bladder and bowel dys-function and paralysis.
Several theories exist to why hydrocephalusand the hindbrain malformation develop. Funda-mentally the difference in opinion lies betweenthose who believe the hydrocephalus is a primaryfinding causing hindbrain herniation and thosethat believe that it is secondary to the hindbrainherniation (Shoja et al. 2017). Even in 1891,Arnold and Chiari disagreed on whether hydro-cephalus was primary or secondary. Theoriesfavoring a primary etiology include reduced CSFabsorption (due to increased venous pressuresleading to decreased venous outflow), CSFobstruction (due to aqueductal stenosis or atresiaof the fourth ventricular outflow tracts) and evenincreased CSF production from overactive cho-roid plexus. The most common theories favoringsecondary hydrocephalus either suggest hindbrainherniation is due to caudal traction (due to themyelomeningocele) or to a differential in pres-sures between the relatively high intracranial
Fig. 1 Treated hydrocephalus in the Chiari II malforma-tion. (a) Axial T2W image at 6 days of age shows markedventricular dilatation with compression of the cerebralmantle. (b) Axial T2W image at 26 months shows a rightparietal VP shunt with drainage of the ventricles andimproved hemispheric volume. (c) Sagittal T2W image
shows persisting descent of the hindbrain through theforamen magnum and an upper cervical syrinx. (d) SagittalT2W image of the lumbar spine shows a complex lumbarmyelomeningocele with L3/4 segmentation abnormalityand a diastematomyelia (not shown)
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compartment and the spine (due to chronic CSFleakage through the myelocele into the amnioticcavity).
Whatever the underlying cause, the MOMStrial showed a significant advantage in repairingthe myelomeningocele in utero (Adzick et al.2011). This emphasizes the critical role of fetalMRI in characterizing these malformations to helpguide surgical intervention.
Dandy Walker Malformation
Hydrocephalus occurs in approximately 80% ofpatients with the Dandy Walker malformation(DWM) although the exact etiology remainsunclear (See Fig. 2). Venous hypertension (dueto upwards elevation of the torcula and elongatedtransverse sinuses), CSF obstruction (due to fail-ure of formation of the fourth ventricular outflowtracts) and aqueductal stenosis (secondary toupwards displacement of the tectal plate fromthe posterior fossa cyst) have all been suggested(Spennato et al. 2011). Phase contrast CSF flowstudies are recommended to guide potential CSFdiversion.
Blake’s Pouch
Around the fourth month of embryological devel-opment, the foramen of Magendie is formed byperforation in the median aperture of the posteriormembranous area. Failure to rupture can result inevagination of the persisting membrane, coined asBlake’s pouch. If this obstruction to CSF flowcannot be compensated for by other outflowtracts, hydrocephalus can develop.
Arachnoid Cysts
The vast majority of posterior fossa arachnoidcysts are found incidentally and do not cause anyclinical problems. However, if eloquently located,often near the foramen magnum, they can causedistal fourth ventricular outflow obstruction and
subsequent hydrocephalus. On T2 weightedimages, the CSF within the arachnoid cyst shouldbe “clean” with a lack of flow void compared tothe intraventricular CSF (see Fig. 2). The sagittalCISS sequence can be useful to delineate mem-branes and guide surgical intervention.
Brainstem Malformations
Hydrocephalus is seen in several genetic syn-dromes secondary to the characteristic brainstemmalformations (see Fig. 3). Examples include thedystroglycanopathies (commonly due to mutationin POMGnT1) and Walker-Warburg Syndrome(due to a mutation in one of the POMT genes).
X-Linked Hydrocephalus
There are a number of genetic causes of hydro-cephalus beyond the remit of this chapter (Zhanget al. 2006). The most common form of congenitalhydrocephalus is due to mutations in the L1-CAMgene inherited in an X-linked pattern with anincidence estimated of approximately 1 in30,000 births. Hydrocephalus is most commonlydue to aqueductal stenosis.
Acquired Hydrocephalus
Children most frequently acquire hydrocephalussecondary to intracranial hemorrhage, infection,or tumors. Traumatic head injury, stroke, andinflammatory conditions are less common causesof hydrocephalus in this age group but should beconsidered if patients have a concerning history ordelayed presentation and the radiologist shouldhave a short threshold for repeat imaging.Although commonly secondary to the aforemen-tioned pathologies, aqueductal stenosis merits dis-cussion as a separate entity. Other concepts suchas the encysted fourth ventricle, arrested hydro-cephalus, and external hydrocephalus also war-rant discussion in this section.
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Fig. 2 Hydrocephalus secondary to posterior fossa abnor-malities of the posterior fossa. (a) Dandy Walker Malfor-mation with vermian dysgenesis, an enlarged posteriorfossa with elevated torcular and dilatation of the fourthventricle. The cerebral aqueduct appears patent. (b)Blake’s pouch. The median aperture of the fourth ventriclefails to perforate with a persiting membrane evident on the
sagittal CISS sequence. This can evaginate causing a largecyst which communicates with the fourth ventricle. (c) Amidline arachnoid cyst obstructs the foramen of Magendieof the fourth ventricle with subsequent supratentorialhydrocephalus. A prominent flow void is seen throughthe aqueduct but the CSF within the cyst remains “clean”
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Posthemorrhagic Hydrocephalus
Germinal matrix and intraventricular hemorrhageare relatively common complications of prematu-rity and the most common cause of acquiredhydrocephalus in the neonate. It is estimated thatup to one half of neonates with a Grade III orGrade IV IVH will develop posthemorrhagichydrocephalus (PHH) (Robinson 2012). Thismost commonly presents as obstructive hydro-cephalus due to aqueductal stenosis or an encystedfourth ventricle but can also present with
communicating hydrocephalus due to alterationin CSF dynamics.
It is important to try and differentiate PHHfrom more benign post-haemorrhagic ventriculardilatation. Hydrocephalus should have the fea-tures of raised CSF pressure such as progressivemacrocephaly and bradycardia. Chronic raisedintracranial pressure can cause delayedmyelination which is reversed with early surgicalintervention (Dorner et al. 2018).
Although cranial USS can be used to screen forIVH and assess for progressive ventricular
Fig. 3 Hydrocephalus in dystroglycanopathies. (a) and(b) Muscle-eye-brain disease in a 2-year-old boy second-ary to mutation in the POMgnT1 gene. Axial T2 showsdilated temporal horns with associated leukoence-phalopathy and aqueductal stenosis on the T1 sagittalimage. Posterior convexity to the pons with a ventral cleft
and cerebellar cysts. (c) and (d)WalkerWarburg Syndromein a 3-month-old boy secondary to mutation in the POMT1gene. Axial T2 sequence shows cobblestone lissencephalyand dilated ventricles. Sagittal CISS sequence showsaqueductal stenosis secondary to a kink in the brainstem
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dilatation, MRI is important as it is more sensitivein characterizing the primary hemorrhage (and thepresence of any associated parenchymal injurysuch as periventricular venous infarction) andproviding evidence of obstruction to CSF flow.This may also include the presence of post-hemorrhagic septations in the prepontine cistern,a feature which may contraindicate thirdventriculostomy (although this is rarely consid-ered to be the primary CSF diversion in neonates).For this reason, the use of susceptibility weightedimaging, standard T2 sagittal spin echo (withoutflow compensation) and sagittal steady-state gra-dient echo sequence (e.g, CISS or FIESTA-C) isadvocated in the protocol (see Fig. 4).
Infection
Intracranial infection, particularly meningitis andventriculitis frequently causes hydrocephaluseither due to ependymal damage or frank obstruc-tion to CSF flow. This can either occur acutely atthe time of active infection or as a secondaryphenomenon, most commonly due to debris ormembranes causing aqueductal stenosis (Fig. 5).
Tumors
Tumors arising in the ventricular system or caus-ing obstruction of the ventricular system by direct
Fig. 4 MRI brain of a neonate born at 33 weeks gestationpresenting with 3 week history of increasing head circum-ference. Cranial USS showed intraventricularhaemorrhage. (a) Ax T2FSE shows ventricular dilatationand a Grade III/IV left sided IVH. (b) SWI showsependymal ghosting confirming IVH (c) Sag T2FSE (with-out flow compensation) shows a prominent flow void
through the cerebral aqueduct. Anterior bowing of thelamina terminalis and prominence of the pineal recessconfirms raised third ventricular pressure. (d) SagittalCISS confirms patency of the aqueduct but fourth ventric-ular outflow obstruction secondary to membranes at theinferior border of the foramen of Magendie. There are alsoseptae in the pre-pontine cistern
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mass effect can result in hydrocephalus. The com-mon posterior fossa tumours are not considered inthis chapter but frequently present due to thesymptoms of hydrocephalus. Aqueductal tumorsshould be considered as a separate entity as can beoverlooked in patients with hydrocephalus, par-ticularly if limited imaging protocols areperformed (See Fig. 6).
Aqueductal Stenosis
The cerebral aqueduct is particularly prone tostenosis as it is the narrowest tract in the CSF
pathway measuring 0.5 mm2 in children. In mostcases of non-tumoral narrowing, the cause isunknown but can be due to genetic factors (e.g.,L1-CAM in X-linked hydrocephalus) or acquiredpathology (e.g., infection or hemorrhage). Speci-men analysis found that the lumen of the aqueductcan be narrowed by atresia, by forking of thelumen, by membrane/septal formation, or bygliosis of the tectal glial cells; the latter two arerecognizable on high resolution MRI. Septal for-mation from previous intraventricular hemor-rhage or infection can occur anywhere along theaqueduct but idiopathic septae occur most fre-quently in the distal aqueduct at the level of the
Fig. 5 MRI of an 18-month-old boy presented in septicshock and decreased GCS. MRI performed at Day 2 con-firmed basal meningitis and ventriculitis. (a) Axial T2showing dilatation of the lateral and third ventricles. (b)B1000 image from DWI shows cytotoxic edema in thebasal ganglia and debris with restricted diffusion layering
in the lateral ventricles. (c) Sagittal T1 imaging showsrelative collapse of the fourth ventricle. (d) Axial T1 +Gad-olinium shows enhancement of the basal meninges andvessel-wall enhancement of theM1 segments of the middlecerebral arteries
Fig. 6 Tectal astrocytoma in a 12-year-old presentingwith progressive headaches. (a) Axial T2W image showsearly dilatation of the temporal horns, anterior third ven-tricle and apparent aqueductal widening. (b) Sagittal T2W
image shows apparent dilatation of the aqueduct and nor-mal calibre fourth ventricle. (c) Axial FLAIR image con-firms a mass in the right tectal plate. (d) Sagittal CISSimage shows tumoral aqueductal stenosis
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inferior colliculus. This results in a characteristicdilatation of the proximal aqueduct and posteriortilting of the tectum (see Fig. 7). Nodular hyper-plasia or glial proliferation can occur in certaingenetic conditions such as neurofibromatosis andis also thought to occur due to a generalizedependymitis, often secondary to exposure tohaemorrhage, infection, or toxins (see Fig. 7). Itis this nodular hyperplasia which requires distinc-tion from tectal astrocytomas, the latter oftenreturning different signal to the normal tectalplate parenchyma.
The degree of stenosis does not necessarilyremain stable with chronically raised flow pres-sures thought to cause stress to the ependymalwall and increase cell proliferation. Further insults(e.g., shunt infection or traumatic head injury) can
shift the balance away from a CSF system that iscompensating for the stenosis. Hydrocephalus candevelop acutely in aqueductal stenosis but is morecommonly insidious, presenting characteristicallywith worsening headache particularly on coughingand straining. Drop attacks have been reported and15% have epilepsy (Little et al. 1975).
Sagittal CISS images are particularly importantin characterizing the aqueduct (see Fig. 7), andphase-contrast CSF studies help assess whether astenosis is complete.
Arrested Hydrocephalus
Hydrocephalus may not present immediately fol-lowing haemorrhage or infection. Patients can
Fig. 7 The use of sagittal 3D steady-state GE sequences incharacterizing aqueductal stenosis. (a) Membranous steno-sis at the level of the inferior colliculus with posteriorpivoting of the tectal plate. This can occur secondary tohaemorrhage or infection but can also be idiopathic (b)Nodular stenosis at the distal aperture in a patient with prior
haemorrhagic hydrocephlaus. (c) Nodular stenosis at theproximal aperture in a patient with prior meningitis (d)Tumoral stenosis secondary to a tectal plate low gradeastrocytoma (e) Stenosis secondary to an intraluminaltumor (subependymoma)
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compensate for incomplete obstruction of CSFflow (e.g., partial aqueductal stenosis) reachingan equilibrium between CSF production andabsorption (see Fig. 8). This may result in a degreeof nonsymptomatic stable ventriculomegalywhich can often be found incidentally. However,decompensation can occur with presenting symp-toms including headache, seizure, or cognitivedecline. This can occur at any age, acutely orover a longer period of time with more subtleneurological dysfunction.
Encysted Fourth Ventricle
The encysted (entrapped or isolated) fourth ven-tricle occurs when there is caudal and rostralobstruction to CSF flow resulting in gradualenlargement of the ventricle which eventuallycompresses the cerebellum and brainstem (seeFig. 9). It occurs most commonly as a late com-plication in patients treated for hydrocephaluswith lateral ventricle shunt diversion (see Fig. 9).However, it can also occur in conditions that
Fig. 8 MRI surveillance in 18-month-old boy with aprevious history of neonatal meningitis. MRI showsarrested/compensated hydrocephalus but no acuteventriculitis. (a) Axial T2 shows chronic ventricular dila-tation with perforation of the septum pellucidum. (b) Sag-ittal CISS sequence shows stenosis of the cerebral
aqueduct at the level of the third ventricular aperture. Thethird ventricle is not acutely enlarged with normal config-uration of the floor, the lamina terminalis, and pinealrecess. (c) Magnitude image and (d) phase image from acardiac-gated CSF sequence confirms aqueductal stenosis
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predispose to membrane formation (in particularPHH and infection). Surgical intervention isrequired to divert CSF, usually via peritonealshunt insertion.
Benign Enlargementof the Subarachnoid Spaces
Benign enlargement of the subarachnoid spaces(BESS) is a condition that presents in infancy withmacrocephaly associated with enlarged
subarachnoid spaces. The head circumference isoften large at birth but increases and is often wellover the 95th centile at presentation. The sub-arachnoid spaces are particularly enlarged overthe frontal lobes but also within theinterhemispheric and Sylvian fissures. The lateralventricles are often prominent but there should beno signs of raised intraventricular pressure. Thereis usually enlargement of the suprasellar cistern(see Fig. 10). Although the clinical history is oftenstrongly suggestive, it is important to differentiateradiologically between fluid in the subarachnoid
Fig. 9 MRI of two patients with encysted or entrappedfourth ventricles. A to D shows images from a 12-month-old previously treated by CSF shunt diversion for hydro-cephalus secondary to meningitis. E and F shows imagesfrom a 4-year-old boy previously treated for post-haemorrhagic hydrocephalus (a) Axial T2 weightedimage shows the presence of an appropriately sited rightparietal VP shunt and bilateral subdural effusions as acomplication of over-shunting. (b) Axial T2 weightedimage shows disproportionate dilatation of the fourth
ventricle with edema in the surrounding parenchyma. (c)Sagittal CISS sequence shows an entrapped fourth ventri-cle with cranial occlusion of the cerebral aqueduct andcaudal obstruction of the foramen of Magendie. (d) Sagit-tal non-compensated T2 weighted image shows no flowvoid in the fourth ventricle. (e) Axial T2 weighted imageshows collapsed lateral ventricles with irregular bordersconsistent with prior white matter volume loss secondaryto hemorrhagic infarction. (f) Sagittal CISS sequenceshows cranial and caudal obstruction to the fourth ventricle
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spaces and in the subdural space. The fluid shouldreturn the same signal as CSF on all sequences,and the presence of vessels traversing the fluidcollections confirms they are in the subarachnoidcompartment. Once this has been established, it isalso important to exclude other causes of enlargedsubarachnoid spaces including malnutrition,dehydration, and treatment with steroids.
The exact cause of BESS is poorly understood.It has been hypothesized that there is a delay inmaturity in the arachnoid granulations withimpaired resorption of CSF in the subarachnoidspaces. The increase in head circumference tendsto curtail at 18-months and imaging often returnsto normal without intervention at 2 years. Anextremely rare but well-recognised complicationof external hydrocephalus is spontaneous sub-dural effusions. This is an important considerationwhen interpreting such studies as referring clini-cians may raise abusive head trauma as a potentialdifferential. This can often be excluded by takinga thorough clinical history. Subdural collectionsassociated with BESS are never associated withthe other manifestations of abusive head trauma
such as retinal hemorrhages, hypoxic ischemicinjury, or spinal subdural hemorrhages.
Treatment
Treatment depends on the underlying cause forthe hydrocephalus (see Fig. 11). For instance,arrested hydrocephalus can often undergo aperiod of monitoring (using a protocol discussedabove) followed by clinical follow-up. Once thefontanelles and sutures have closed, the ventricu-lar dimensions often remain static although therecan be a sudden decompensation.
In obstructive hydrocephalus, secondary toaqueductal stenosis, increasing ventricular sizecan be treated with CSF diversion. This can eitherbe achieved via VP shunt or via thirdventriculostomy. Follow-up imaging is thenoften used to either assess ventricular size orpatency of the ventriculostomy. In more complexcases of hydrocephalus (such as the encystedfourth ventricle), other procedures can beperformed to divert CSF either into the peritonealor rarely the pleural cavity.
Fig. 10 MRI of a 5-month-old boy presenting with anenlarging head circumference (>99 centile). Axial T2weighted images show enlarged external subarachnoidspaces (a) with modest ventriculomegaly. This extendsalong the interhemispheric fissure. (b). The signal intensityshould mirror that of CSF on all sequences and the
presence of bridging vessels across the subarachnoidspaces can be useful to differentiate fluid in the subarach-noid space from subdural collections. Sagittal CISSsequence (c) shows a patent cerebral aqueduct and onlyminor dilatation of the third ventricle. There is enlargementof the suprasellar cistern
There is dilatation of the lateral, third and fourthventricles with relative effacement of the cerebralsulci and Sylvian fissures. Anterior bowing of thelamina terminalis on the sagittal images suggestsraised intraventricular pressure. The cerebralaqueduct is patent with a prominent flow-voidon the non-flow compensated T2 images. Thereare multiple septations seen inferior to the fourthventricle suggesting outflow obstruction. Further
Fig. 11 Examples of surgical CSF diversion in hydro-cephalus. (a) Shows a patient with inferior aqueductalstenosis secondary to a membrane which was treated by athird ventriculostomy. This was shown to be patent with aprominent flow void on the non-flow compensated T2sagittal image (left) and a defect in the tuber cinereum onthe CISS image (right). (b) Shows a patient with compen-sated aqueductal stenosis (note the normal third ventricle)
and entrapment of the fourth ventricle (left). The patientpresented 4 days later with acute hydrocephalus (middleimage) and more definitive treatment was performed withinsertion of a trans-aqueductal catheter. The patient alsohad a VP catheter (not shown) effectively diverting CSFfrom the entrapped fourth to the peritoneal cavity
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septae are seen within the pre-pontine cistern. Thegradient echo sequence shows signal susceptibil-ity in the wall of the left lateral ventricle withfurther ependymal haemosiderin staining consis-tent with prior intraventricular hemorrhage.
Summary/Conclusion
Posthemorrhagic obstructive hydrocephalus isdue to fourth ventricular outflow obstruction. Athird ventriculostomy is relatively contraindicateddue to further septa in the pre-pontine cistern.
Checklist for Reporting
Are the ventricles enlarged?
• Lateral• Third• Fourth
Are the ventricles enlarged compared to previ-ous imaging (if available)?
• Is the aqueduct patent?• If not is there a mass? Give contrast?• Is there a benign membrane?
Are there signs of raised intraventricularpressure?
• Anterior bowing of the lamina terminalis(in sagittal plane)
• Periventricular edema• Rounded temporal horns• Rounded anterior third ventricle (in axial
plane)
Is there evidence of previous hemorrhage orinfection?
Is there evidence of a congenital malformation?
References
Adzick NS, Thom EA, Spong CY, Brock JWI, BurrowsPK, Johnson MP, et al. A randomized trial of prenatalversus postnatal repair of myelomeningocele. MassMed Soc. 2011;364(11):1–12. https://doi.org/10.1056/NEJMoa1014379.
Dorner RA, Burton VJ, Allen MC, Robinson S, SoaresBP. Preterm neuroimaging and neurodevelopmentaloutcome: a focus on intraventricular hemorrhage,post-hemorrhagic hydrocephalus, and associated braininjury. J Perinatol. 2018;38:1431–1443. Springer US
Little JR, Houser OW, MacCarty CS. Clinical manifesta-tions of aqueductal stenosis in adults. J Neurosurg. 2nded. 1975;43(5):546–52.
Robinson S. Neonatal posthemorrhagic hydrocephalusfrom prematurity: pathophysiology and current treat-ment concepts. J Neurosurgery Pediatr. 5 ed. 2012;9(3):242–58.
ShojaMM, Johal J, OakesWJ, Tubbs RS. Embryology andpathophysiology of the Chiari I and II malformations: acomprehensive review. Clin Anat. 2nd ed. 2017;31(2):202–15.
Spennato P, Mirone G, Nastro A, Buonocore MC,Ruggiero C, Trischitta V, et al. Hydrocephalus inDandy–Walker malformation. Childs Nerv Syst.2011;27(10):1665–81.
Zhang J, Williams MA, Rigamonti D. Genetics of humanhydrocephalus. J Neurol. 2006;253(10):1255–66.Steinkopff-Verlag
Further Reading
Barkovich J, Raybaud C. Hydrocephalus. Chapter 8. In:Pediatric neuroimaging. 6th ed. Lippincott, Williams &Wilkins, Philadelphia; 2019.
Cinalli G, Spennato P, Nastro A, Aliberti F, Trischitta V,Ruggiero C, Mirone G, Cianciull E. Hydrocephalus inaqueductal stenosis. Childs Nerv Syst.2011;27:1621–42.
Raybaud C. MR assessment of pediatric hydrocephalus: aroad map. Childs Nerv Syst. 2016;32:19–41.
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