Maria I. Argyropoulou, Andrea Rossi, Roxana S. Gunny, W.K. ‘Kling’ Chong Brain maturation is assessed by observing tissue characteristics related to myelination, as well as variations in morphology. Most of the changes associated with myelination occur in the first 2 years of life and gyral and sulcal development mainly occurs in utero or in the premature brain, while other morphological changes are observable later in life. Myelination is the process by which brain oligodendrocytes produce layers of myelin that wrap around the neuronal axons and act as a layer of insulation for the transmission of electric action potentials down the neuronal axon. Axonal transmission is facilitated at the junctions between these myelin sheaths or nodes of Ranvier by a process known as saltatory conduction. The extent of myelination of the infant brain can be assessed by magnetic resonance imaging (MRI) according to specific milestones which are analogous to the normal milestones of clinical development. During earliest brain development none of the brain is myelinated. By term, key structures such as the ventrolateral thalami, dorsolateral putamina, posterior limb of the internal capsule, inferior colliculi, medial longitudinal fasciculus and dorsal brainstem nuclei are already myelinated. As the brain matures, there is progressive T1 and T2 shortening of the white matter due to an increase in the lipid content and reduced water content of developing myelin and packing of myelinated white matter tracts.1 This follows a centrifugal posterior-to-anterior and caudal-to-cranial pattern and is virtually complete by the age of 2 years (Fig. 82-1). Advanced MRI techniques show progressive reduction in free water diffusion, increased fractional anisotropy (assessed by diffusion tensor imaging) and increased magnetisation transfer.2–4 Brain myelination is detected in grey matter earlier on T2-weighted fast spin-echo (FSE) and in the white matter tracts earlier on T1-weighted spin-echo (SE) or inversion recovery (STIR) sequences. Most myelination occurs post-term in the first 8 months of life, although the final parts of this process may extend into adulthood. The brain should appear virtually fully myelinated on T2-weighted sequences by 2 years, with almost an adult appearance on T1-weighted sequences by 10 months (Fig. 82-2). The newborn has limited motor function but a well-developed sensory system. Thus the myelination pattern seen at birth at full term is primarily in the sensory tracts. During the first 6 months of life the process of myelination is easiest to follow on T1-weighted images, where the myelinated areas appear bright. T2-weighted images are less sensitive and it takes much more myelin to produce a hypointense signal within the white matter. During this period T2-weighted images show only subtle myelination. At full term, T1-weighted images should show high signal in the dorsal medulla and brainstem, the cerebellar peduncles, a small part of the cerebral peduncles, about a third of the posterior limb of the internal capsule, the central corona radiata, and the deep white matter in the region of the pre- and post-central gyrus.5 Progression of myelination is seen in the optic radiations during the first months of life. The internal capsule will demonstrate T1 shortening within the anterior limb by 3 months, while on T2-weighted images the hypointensity due to myelin is not seen until about 8 months of age. The splenium of the corpus callosum on T2-weighted images becomes hypointense at 3 months of age. The hypointense signal extends anteriorly along the body and genu, and the complete corpus callosum is myelinated at 6 months.6 After 6 months the signal pattern on T1-weighted images becomes less precise, and after 10 months the brain is fully myelinated by T1 criteria. T2-weighted images are then used to assess the myelination from 6 months to 24 months of age, when the signal pattern generally is fully mature and has a completely adult pattern, though the milestones of myelination are much more imprecise than during the first 6 months of life. On T2-weighted images the first signs of mature subcortical white matter are found around the calcarine fissure at 4 months and in the pre- and post-central gyri at 8 months. By 10 months the occipital subcortical white matter appears isointense with the overlying grey matter and finally shows mature hypointense signal around 1 year of age. This process proceeds anteriorly and by 18 months has finally reached the most frontal parts and the frontal poles of the temporal lobes. Regions of persistent hyperintensity on T2-weighted sequences known as the ‘terminal myelination zones’7 may be seen within the peritrigonal areas well into adulthood. They can be distinguished from white matter disease by the presence of a rim of normal myelinated brain between these areas and the ventricular margin, and no evidence of white matter volume loss such as ventricular enlargement or irregularity of the ventricular margins. Other areas may also persist as regions of signal hyperintensity beyond 2 years, e.g. in the frontotemporal subcortical white matter and peritrigonal white matter, and should not be mistaken for disease (Fig. 82-3). Gyration is the process by which the individual gyri and sulci of the cerebral hemispheres form (Fig. 82-4). The MRI appearances lag behind the extent of gyral formation seen at the same age at post-mortem. The surface of the cerebral hemispheres is initially smooth, with the interhemispheric fissure and Sylvian fissures having already formed by 16 weeks’ gestation. Other primary sulci, such as the callosal sulcus and parieto-occipital fissure, are recognisable at 22 weeks’ gestation, followed by the cingular and calcarine sulci. The central sulcus is seen in most infants by 27 weeks. Gyration then continues into the post-term period in a standardised and consistent sequence, beginning with the sensorimotor regions and visual pathways, areas that are also myelinating at the same time. The slowest regions of gyration are also those with the slowest myelination, such as the frontal and temporal poles. By term the gyral pattern is nearly the same as the appearance in adults, with further deepening of the sulci occurring post-term. The Sylvian fissures are also wider and vertically oriented and these continue to mature post-term.8,9 Development of the corpus callosum begins with the posterior genu, body and splenium, and then the anterior genu and rostrum. All these components are present by 20 weeks’ gestation; however, it continues to grow in length and thickness through the rest of the fetal period and post-term. The adult appearance with full thickness of the corpus callosum is achieved by 8–10 months of age, and bulking up of the splenium as the visual pathways mature occurs by 4–6 months.10 In the adult there are several regions where there is relative T2 hypointensity, considered to be due to the normal deposition of iron; these are the basal ganglia, particularly the globus pallidus, substantia nigra, and red nucleus. In the infant the basal ganglia begin to appear relatively T2 hypointense to cortex by about 6 months of age due to myelination, but the putamen and globus pallidus are isointense to each other and the internal capsule. They then become relatively bright with respect to white matter as this begins to myelinate. By 9 or 10 years there is a second stage of T2 shortening in the globus pallidus, substantia nigra and red nucleus, which reduces further during the second decade.11 The dentate nuclei show similar though less marked changes by about age 15 years. This phase is due to iron deposition, which continues throughout adult life. In normal infants up to the age of 2 months the anterior pituitary gland has a convex upper border and is of relatively high T1-weighted signal.12 From 2 months the pituitary gland has a flat surface and is isointense with grey matter. It slowly grows during childhood and ranges from 2 to 6 mm in vertical diameter until puberty, when it enlarges again. The cerebellum may be small due to lack of formation or due to cerebellar atrophy. Cerebellar hypoplasia may be due to an acquired brain injury, such as infection (especially congenital cytomegalovirus (CMV)), infarction or preterm ischaemic insult, toxins or a paraneoplastic condition, or the hypoplasia may be due to a genetic, neurometabolic or neurodegenerative condition, or a malformation. In many children (up to 50% in our series), despite extensive testing the cause remains unknown. It has been suggested that the timing of onset is the key feature which determines whether the cerebellum is involved in isolation or whether the pons is also involved. This imaging finding may indicate an earlier disease onset with early neuronal injury to the cerebellum causing pontine hypoplasia by affecting the development of synaptic connections from the hypoplastic cerebellum or supratentorial white matter. The inherited neurometabolic or neurodegenerative conditions causing cerebellar hypoplasia comprise an extremely wide range of aetiologies. Most are autosomal recessive, but autososomal dominant (often seen in adults), X-linked or maternally inherited forms are recognised. Clinically the child may present with progressive or intermittent hypotonia or ataxia, although there is often no clear correlation between the severity of the imaging findings and the clinical presentation. Among common causes are Friedreich’s ataxia, oculomotor apraxia types 1 and 2, ataxia telangiectasia, infantile onset spinocerebellar ataxia, congenital disorders of gylycosylation and infantile neuroaxonal dystrophy (Fig. 82-5). The imaging findings in this large group of conditions are abnormal but are non-specific and include: symmetrical atrophy of the cerebellar folia with widened cerebellar fissures; progressive cerebellar atrophy on sequential images; and variable cerebellar signal changes (less common). The vermis is more frequently affected but the atrophy may be diffuse and bilateral. In most cases there are no additional imaging changes pointing to a specific imaging diagnosis. However, unilateral cerebellar atrophy is more likely to be due to an acquired insult, including in utero infection, stroke or germinal matrix haemorrhage. Many cases of genetic degenerative cerebellar hypoplasia are not associated with significant brainstem hypoplasia. Cerebellar white matter changes are seen in infantile Refsum’s disease, adrenomyeloneuropathy and cerebrotendinosis xanthomatosis. Cerebellar grey matter signal abnormality is uncommon but may suggest diagnoses such as infantile neuroaxonal dystrophy, late infantile neuronal ceroid lipofuscinosis, mitochondrial disorders or Marinesco Sjögren’s syndrome. There is also a specific group of conditions in which the pons is more severely affected along with the cerebellum. These are known as the pontocerebellar hypoplasias (PCH) and there are six types (PCH1–6). Some are associated with a typical clinical phenotype, and others with both a classical clinical and imaging phenotype. PCH1 is associated with muscle hypotonia, joint contractures, microcephaly and breathing difficulties from birth with loss of spinal cord motor neurons. Most affected children do not survive infancy. In children with PCH2 there is lack of voluntary movements, dysphagia and absent speech as well as clonus, muscle spasms and classically dystonia, though some children may present purely with spasticity. PCH4 has a similar phenotype but is more severe. PCH3 is associated with optic atrophy. PCH6 is characterised by hypotonia, poor feeding in infancy, progressive developmental delay and seizures; typically a rapidly progressive neonatal or early infancy epileptic encephalopathy with intractabale seizures is seen. The pontocerebellar hypoplasias may be associated with mutations in specific genes related to neuronal development and survival. Some cases of PCH1 have a specific genetic mutation, VRK1. PCH2 is associated with three related genetic mutations: TSEN54 (the commonest), TSEN2 and TSEN34. PCH4 is also associated with TSEN54 mutation. RARS2 may be seen in PCH6, while specific genetic mutations for PCH3 and PCH5 are not yet known. All have varying degrees of pontocerebellar hypoplasia on brain MRI. A ‘dragonfly’ appearances of the cerebellum is recognised typically in PCH2 commonly with TSEN54 mutations; there is marked cerebellar hemisphere atrophy with relative vermian sparing. Cerebral hemisphere cortical atrophy and cerebellar hemisphere cysts may also be seen (Fig. 82-6). In other mutations or unknown genetic mutations a more non-specific ‘butterfly’ appearance may be seen when there is equal involvement of the cerebellar hemispheres and vermis. Another group of conditions which can present with both cerebellar and pontine hypoplasia are the congenital disorders of glycosylation type IA. The cerebellum may also be involved in acute presentations of neurometabolic disease or with supratentorial abnormalities and will be discussed in the context of neurometabolic disease later in the chapter. This describes a spectrum of cystic posterior fossa malformations ranging from the complete Dandy–Walker malformation to a persistent Blake’s pouch and mega cisterna magna, all of which have in common a focal extra-axial cerebrospinal fluid (CSF) collection continuous with the fourth ventricle, and variable cerebellar hypoplasia.13 The classical Dandy–Walker malformation is the most severe posterior fossa malformation in this spectrum. It is characterised by cystic dilatation of the fourth ventricle, an enlarged posterior fossa, often with elevation of the venous confluence of the torcula above the lambdoid suture, which may be seen on plain radiography, computed tomography (CT) and MRI, and elevation of the tentorium. There is aplasia or hypoplasia of the cerebellar vermis, with vermian rotation (Fig. 82-7).14 The Dandy–Walker malformation is associated with hydrocephalus and other midline anomalies, and can be an indicator for underlying clinical syndromes and chromosomal abnormalities. Children with any of these developmental anomalies may present as incidental findings or with developmental delay, seizures and hydrocephalus. At the mildest end of the spectrum, the mega cisterna magna is seen as an incidental finding of no clinical significance and consists of an infracerebellar CSF collection (or normal cisternal space), with a normal cerebellum and fourth ventricle. The presence of crossing vessels and falx cerebelli favours the mega cisterna magna over a posterior fossa arachnoid cyst. Unlike the mega cisterna magna, posterior fossa arachnoid cysts are not in continuity with the fourth ventricle. They may be associated with mass effect on the adjacent cerebellum and enlargement of the posterior fossa. Mainly these are clinically incidental findings but, like suprasellar arachnoid cysts, may occasionally increase in size in the neonatal period or infancy and cause obstructive hydrocephalus requiring surgical intervention. Arachnoid cysts do not communicate with the fourth ventricle. These are a group of recessive congenital ataxia disorders in which typically there is neonatal hypotonia, tachypnoea, abnormal eye movements and mental retardation15 associated with a particular pattern of cerebellar dysgenesis with a molar tooth-type malformation and vermis hypoplasia. The typical imaging findings may be seen in children without the full triad of clinical features. Cilia are found as projections from the neuron and ependyma; to date three known causative genes have been identified in primary ciliary protein genes and JSRD is, therefore, considered to be a cilopathy. Several syndromes with additional features such as renal cysts, ocular abnormalities, liver fibrosis, hypothalamic hamartoma and polymicrogyria have been classified with this anomaly, so that detection of the typical midbrain changes should prompt additional investigation for these. The cardinal feature of the Joubert malformation is the presence of a ‘molar tooth’ sign which is created by a combination of midbrain hypoplasia with an abnormally deep interpeduncular fossa and a failure of the superior cerebellar peduncles to decussate across the midline (Fig. 82-8). On axial imaging the fourth ventricle is abnormally shaped with a ‘batwing appearance’, there is cerebellar hypoplasia and there is a midline vermian cleft and dysplastic small vermis. The midbrain is small.16 Rhombencephalosynapsis is a very rare cerebellar malformation in which the cerebellar hemispheres, deep cerebellar nuclei and superior cerebellar peduncles are fused across the midline and there is hypoplasia or aplasia of the vermis (Fig. 82-9).17 It may be associated with hydrocephalus typically due to aqueduct stenosis, as well as fusion of midbrain colliculi and other midline supratentorial anomalies such as absence of the septum pellucidum, and corpus callosum. The diagnosis of pontine tegmental cap dysplasia is made on the basis of characteristic imaging findings in children presenting with multiple cranial neuropathies and evidence of cerebellar dysfunction. There is a characteristic ‘cap’ or projection on the dorsal surface of the pons which projects into the fourth ventricle. This is continuous with the middle cerebellar peduncles and diffusion tensor imaging studies suggest this is caused by failure of decussation and abnormal axonal pathways at this level. There is also a ‘molar tooth’ appearances of the superior cerebellar peduncles which fail to decussate. The cerebellar vermis and hemispheres are all small as well as the pons distal to the dorsal pontine ‘cap’. The vestibulocochear nerves are absent, there is a cochlea dysplasia and there is a duplicated internal auditory canal for the facial nerve (Fig. 82-10). Lhermitte-Duclos or dysplastic cerebellar gangliocytoma is a developmental lesion with a distinctive radiological appearance in which there is enlargement of the cerebellar cortex, usually affecting one hemisphere. On MRI there is a non-enhancing mass with diffusely enlarged cerebellar folia.18 Pial enhancement may be demonstrated. There are many other forms of non-specific cerebellar dysgenesis for which as yet there are no universally accepted classification systems. The Chiari malformations are discussed separately as they represent separate entities. This is a true hindbrain malformation which is clinically, radiologically and embryologically distinct from the Chiari I malformation described below. The Chiari II malformation is aetiologically and epidemiologically intimately related to the myelomeningocele with an association that is close to 100%. It is therefore part of a spectrum of consequences of open spinal dysraphism or other failures of closure of the neural tube during fetal development. The clinical presentation is usually at birth or by earlier in utero detection of a lumbosacral meningocele. This entity is discussed in more detail in the ‘Disorders of Dorsal Induction’ section. This may be considered a form of hindbrain deformation rather than a true malformation and is characterised by cerebellar tonsillar descent through a normal-sized foramen magnum. It may be an acquired condition and has occasionally been observed either to improve or worsen over time without intervention. Clinical symptoms are more likely when there is greater than 5 mm descent below the foramen magnum, and therefore descent below this level is considered to be clinically significant. However, neuroimaging does not reliably predict those who are symptomatic. Children between 5 and 15 years have greater tonsillar descent up to 6 mm as a normal finding compared to children under 5 years or adults. There may be an associated syringomyelia. Symptoms including cough-induced headache, lower cranial nerve palsies and disassociated peripheral anaesthesia have been described. The earliest malformations to appear relate to the formation of the neural tube, and are described as abnormalities of dorsal induction or cranial dysraphism (occurring at 3–4 weeks’ gestation). Anencephaly, cephaloceles and Chiari II (Arnold–Chiari) malformation are generally considered to be consequences of abnormalities of dorsal induction. The events which follow the formation of the neural tube are known as ventral induction, when the two separate cerebral hemispheres are formed (5–8 weeks). The holoprosencephalies are all abnormalities of ventral induction. The structures in the posterior fossa are also formed during this period. Neurons form and proliferate in the subependymal layer of the lateral ventricles known as the germinal matrix and subventricular zone from around 7 weeks’ gestation. The neurons subsequently migrate peripherally along radially oriented microglia to form the layers of the cerebral cortex from 2 to 5 months’ gestation, the deeper layers forming first. Anencephaly is the most common cerebral malformation in the fetus and is incompatible with life. Most anencephalics are stillborn, but a few survive for a few days. A cephalocele is an extracranial protrusion of intracranial structures through a congenital defect of the skull and dura mater (Fig. 82-11). Some authors consider this to be a failure of neurulation or ventral induction (or primary neural tube closure) while others consider this as a post-neurulation event in which brain tissue herniates through a mesenchymal defect in the future dura and cranium. The cephalocele may be clinically palpable. Unlike myelomeningoceles in the spine, there is usually no skin defect. When the cephalocele contains only leptomeninges and CSF it is a meningocele, and when it also contains neural tissue, typically abnormal and non-functioning with areas of necrosis, calcification and cerebral malformation, it is an encephalocele. The herniation may also include part of the ventricle when it is known as an encephalocystocele. These congenital cephaloceles mainly occur in the midline and at predictable and consistent points, assumed to be multiple closure points of the neural tube to produce frontonasal, parietal, occipital or cervico-occipital cephaloceles. As expected, the bigger the extent of herniating brain, the more microcephalic the affected child is and the more cognitive impairment is present. Occipital cephaloceles are often syndromic. Cephaloceles are named by the bones which border the bone defect. In nasofrontal cephaloceles the bone defect lies between the frontal and the nasal bones at the level of the ‘fonticulus frontalis’, a small developmental communication that usually regresses during the fetal period. These lesions can be midline or just off the midline and can be associated with other midline defects such as callosal agenesis and callosal lipomas. If the communicating channel persists, there may be a cephalocele. If the more proximal part eventually obliterates, there may be a dermoid or ectopic brain tissue along the residual track but without intracranial communication. Frontoethmoidal (‘sincipital’), nasoethmoidal, naso-orbital, transethmoidal, sphenoethmoidal and sphenonasopharyngeal cephaloceles are also seen, although they are less common. The primary role of imaging is to establish the presence of neural tissue, other intracranial malformations and hydrocephalus as well as the bone defect. This requires a combination of MRI and CT. Small meningoceles that do not have an intracranial connection may not require surgery, since their size may decrease with time, producing the appearance of an ‘atretic meningocele’. As well as the detection of persistent intracranial connection, the detection and localisation of vascular structures is important before any neurosurgical intervention. This is discussed here as a congenital malformation of the hindbrain that is almost always associated with a neural tube defect, usually a lumbosacral myelomeningocele (open neural tube defect). Affected children may have hydrocephalus at birth (25%) but if not most (80%) will develop hydrocephalus following closure and repair of the lumbar myelomeningocele after birth. Other symptoms of complications of the malformation include upper airway problems, such as apnoea and stridor, and feeding problems, such as dysphagia due to brainstem compression or underdevelopment and which occur in about a third of patients. Patients can be developmentally normal or may have delay or seizures. Urinary retention may occur as well as congenital hip dislocations and feet deformities. The Chiari II malformation is characterised by a small posterior fossa and downward displacement of the cerebellum, pons, medulla oblongata and cervical cord through an enlarged foramen magnum. Associated features include medullary kinking, an inferiorly displaced, elongated and slit-like fourth ventricle, beaking of the tectum of the midbrain, flattening of the ventral pons and low attachment of the tentorium.19,20 The tentorial incisura is enlarged and the cerebellum herniates superiorly into the supratentorial space. The falx is partially absent or fenestrated, resulting in interdigitation of gyri across the midline, and the massa intermedia of the thalami is enlarged. The foramen magnum is enlarged and ‘shield-shaped’ (Fig. 82-12). Other malformations that may be associated with the Chiari II malformation but are less consistent include a lacunar skull dysraphism (luckenschadel), disorders of neuronal migration, malformation of the corpus callosum, dorsal midline cyst and absence of the septum pellucidum. The diagnosis can be readily made with CT by identifying the wide tentorial incisura, typical configuration of the wide foramen magnum and the small fourth ventricle and posterior fossa. Interdigitation of the cerebral hemispheres may be also identified. MRI is the best investigation to show complications, which include hydrocephalus, an isolated fourth ventricle, hydrosyringomyelia and compression of the craniocervical junction. The fourth ventricle in Chiari II malformation should be slit-like: a normal or enlarged ventricle suggests hydrocephalus or that the ventricle may be isolated (Fig. 82-13). A spinal cord syrinx may be present. The term ‘Chiari III’ malformation has been used by some authors to describe the association of the brain anomalies commonly seen in Chiari II malformation (inferior cerebellar, medulla and spinal cord displacement, medullary kinking and tectal beaking, etc.) plus an occipital or cervical encephalocele with occipital bone defect. Holoprosencephaly is a relatively common structural abnormality of the human forebrain, occurring in up to 1 in 10,000 live and stillbirths. It results from a disturbance in the usual signalling pathways required for separation of the embryonic prosencephalon into two separate cerebral hemispheres. Holoprosencephaly is found in association with chromosomal abnormalities, and various teratogenic factors including maternal diabetes. At least 13 different holoprosencephaly loci on chromosomal regions, nine of which are on known holoprosencephaly genes such as sonic hedgehog, ZIC2 and TGIF are recognised. The primary pathway involved in midline developmental anomalies is the sonic hedgehog pathway. This malformation is seen in trisomy 13, 18 and in triploidy. Other abnormalities of midline development are frequently also found. Classification of holoprosencephaly is based on the degree of separation of the cerebral hemispheres and it appears this is a continuous spectrum of failure of separation. The most severe form is alobar holoprosencephaly in which there is complete or nearly complete failure of separation of the cerebral hemispheres. Many infants are either stillborn or do not survive until term, while infants who do survive are very abnormal with abnormal reflexes, tone and seizures in the neonatal period as well as severe midline facial deformities. The facial deformities can include cyclops or a single eye on a stalk, midline clefts and hypotelorism. Only a minority of patients survive beyond the first year. The medial and ventral parts of the brain have not formed in these patients and the septum pellucidum is absent. On imaging there is a crescent-shaped holoventricle continuous with a large dorsal cyst and the cerebrum consists of a pancake-like mass of tissue with no interhemispheric fissure, corpus callosum or falx cerebri (Fig. 82-14). The hypothalamic and basal ganglia are fused. There is no normal circle of Willis and the arterial supply comes directly from the internal carotid and basilar arteries without normal anterior, middle and posterior cerebral arteries. Despite the underlying microcephaly, hydrocephalus often develops and CSF diversion with a shunt may be required as a palliative procedure to help manage head size for nursing. Holoprosencephaly should be distinguished from gross hydrocephalus in which there is a very thin, barely visible cerebral cortical mantle and from hydranencephaly caused by a global early in utero insult (thought to be ischaemic) in which much of the cerebral hemisphere parenchyma is destroyed, leaving a fluid-filled cavity but with relative preservation of mesial temporal occipital lobes, deep grey matter and brainstem (Fig. 82-15). Semilobar holoprosencephaly is less severe; although posteriorly the interhemispheric fissure is partially formed, anteriorly the hemispheres fail to separate. As the brain is less dysmorphic, the midline facial abnormalities are also mild or absent. These children present later with developmental delay or concerns over reduced or increasing head size due to hydrocephalus. The frontal lobes are fused, but the thalami are partially separated. There is still a single ventricle instead of the two lateral ventricles seen normally but the failure of separation of the hypothalami, thalami and basal ganglia is less severe compared to the alobar form and there may be an indication of a third ventricle. The posterior corpus callosum is partially formed. The temporal horns are rudimentary and the hippocampi are underdeveloped.
Paediatric Neuroradiology
Normal Brain Maturation
Normal Myelination
Normal Gyral Development
Other Postnatal Maturational Changes
Brain Malformations and Developmental Abnormalities
Posterior Fossa Abnormalites
Cerebellar Hypoplasia
Dandy–Walker Malformation and Its Variants
Joubert’s Syndrome and Related Disorders (JSRD)
Other Posterior Fossa Malformations or Developmental Disorders
Rhombencephalosynapsis.
Pontine Tegmental Cap Dysplasia.
Lhermitte-Duclos or Dysplastic Cerebellar Gangliocytoma.
Chiari II Malformation
Chiari I Malformation
Supratentorial Abnormalities
Disorders of Dorsal Induction
Anencephaly.
Cephalocele.
Chiari II Malformation (Arnold–Chiari).
Disorders of Ventral Induction
Holoprosencephaly.
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