Malformations of cortical development (MCDs) are neurodevelopmental disorders that result from abnormal development of the cerebral cortex in utero secondary to genetic, infectious or vascular causes.

Abstract: Malformations of cortical development (MCDs) are neurodevelopmental disorders that result from abnormal development of the cerebral cortex in utero secondary to genetic, infectious or vascular causes. Individuals may experience lifelong drug-resistant epilepsy, cerebral palsy, feeding difficulties, intellectual disability and other neurological and behavioral anomalies. The neurological outcome is extremely variable depending on the type, extent and severity of the malformation and the involved genetic pathways of brain development. Both fetal MR and US can diagnose MCD, but their diagnosis remains challenging due to the late gestational appearance of the typical morphologic features and the expertise required to perform a multiplanar, preferably transvaginal, neurosonogram. Although disruption can occur at multiple stages of cortical development resulting in significant overlap between the different types of cortical malformations, in this review we will focus only on the Group 2 (Barkovich Classification) malformations, including lissencephaly, cobblestone malformation and heterotopia, all of which result from abnormal neuronal migration.

Key words: cortical malformation, Lissencephaly, Cobblestone Malformation, Heterotopia, PVH, subcortical.

Authors: Shiri Shinar1 and Susan Blaser2

Reviewer: Karen Fung-Kee-Fung

1 Ontario Fetal Centre, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynaecology, Mount Sinai Hospital, University of Toronto, Toronto, ON, Canada.

2 Department of Diagnostic Imaging, Hospital for Sick Children, Department of Medical Imaging, University of Toronto, Toronto, ON, Canada.

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Classification of malformations of cortical development

The original classification scheme for MCD by Barkovich in 1996 was based upon the earliest developmental step at which the process was disturbed. Since then, the classification scheme has been revised multiple times due to the identification of many new genes and syndromes resulting in MCD 1, 2. Although overlap exists between the three groups, cortical abnormalities in Group 1 are malformations secondary to proliferative disorders, abnormal neuronal and glial proliferation or apoptosis.  Included in Barkovich Group 1 are microlissencephaly (decreased proliferation), megalencephaly and hemimegalencephaly (increased proliferation) and focal cortical dysplasia (abnormal proliferation). Group II malformations are due to abnormal neuronal migration and is further divided into four sub-categories. The first of these is related to abnormalities of the neuroependyma (ventricular epithelium), which result in the formation of periventricular nodular heterotopias. The second describes generalized abnormalities of trans-mantle migration, mainly lissencephalies. The third describes localized abnormalities of trans-mantle migration, mainly subcortical heterotopias; and the fourth describes abnormalities due to abnormal terminal migration/defects in pial limiting membrane, mainly cobblestone malformation3. Group III malformations are secondary to abnormal post-migrational development, such as polymicrogyria and schizencephaly.

Definition and pathophysiology of Group 2 disorders


The term “lissencephaly” is derived from the Greek words lissos, meaning “smooth”

and enkephalos, meaning “brain”. Lissencephaly is caused by neuronal under-migration.

Lissencephaly spectrum includes agyria (complete lack of gyri), pachygyria (few broad gyri and shallow sulci) and subcortical band heterotopia (SBH, see below)4. The most common, known as classical lissencephaly or Type 1 lissencephaly, features a very thick and smooth cortex (10–20 mm) and no other major brain malformations5. It can be isolated or can accompany multiple congenital anomaly syndromes, including Miller-Dieker, Baraitser-Winter cerebrofrontofacial syndrome and X-linked lissencephaly with abnormal genitalia or XLAG6-8. Miller-Dieker (17p13.3 mutation) is the most severe of these, with typical facies and a lack of sulcation.  The other known genes responsible for lissencephaly Type 1 include LIS1, ARX, RELN, VLDLR, ACTB, ACTG1, DCX, DYNC1H1, KIF2A, TUBA1A, TUBB2B, and TUBG19

Since the Barkovich classification was last revised, several additional types of lissencephalies have been recognized. Not only the pattern and gradient of gyral anomaly, but cortical thickness, callosal anomalies and posterior fossa involvement can be utilized in phenotype-genotype classification. This expanded classification attempts to offer linkage of various lissencephaly phenotypes to certain genotypes 10, 11.

Cortical thickness is an important characteristic of lissencephaly. While the normal cortex is comprised of six layers with an overall thickness of 4 mm, in lissencephaly there are two to four layers9, resulting in either a thick (10-20 mm), thin (5-10mm) or variable cortex, with the former being most common.

Gradient is another important feature of lissencephaly, with posterior predominant lissencephaly more common than anterior predominant or diffuse lissencephaly6.

The gradient of involvement in the gyral pattern can help differentiate the other LIS disorders. Involvement may be partial or demonstrate pachy/agyria with frontal or posterior severity reflecting the mutation. Frontal pachygyria and posterior agyria is the most common pattern and suggests mutations of the LIS1 gene. For example, the two most common causal genes, DCX (Doublecortin) and LIS1 can be differentiated on imaging as the former results in amore severe anterior  than posterior gradient of gyral abnormality, while the latter should be suspected with a  more severe posterior  than anterior gradient. The less involved lobes may have a more normal 6-layer cortex, with a transitional zone between that and the more involved,  disorganized lobes, which exhibit 4-layers.

Gender related differences also occur. DCX mutations lead to classic lissencephaly in males, but may exhibit subcortical band heterotopia in females6, 10, 12. The band or double cortex, as can be seen in DCX mutations, would be difficult to confirm on prenatal imaging, although the dysgyria and vermian hypoplasia are helpful prenatal imaging features5.

The cerebellum may also be involved in lissencephaly13.  For example, a RELN gene mutation should be suspected when lissencephaly is associated with cerebellar hypoplasia10, 14, while an ARX gene mutation should be suspected in chromosomal males with X-linked lissencephaly and ambiguous genitalia (XLAG).Vermian hypoplasia may be seen in DCX mutations, while thin, asymmetric or bent brainstem in association with callosal deficiency, abnormal basal ganglia and hypoplastic cerebellum should suggest a tubulinopathy.

Brainstem involvement can also be seen in the dystroglycanopathies and features may overlap with the tubulinopathies (Di Donato 2017). Cobblestone lissencephaly (formerly called Type 2 lissencephaly) is genetically, embryologically, and pathologically distinct from type 1 lissencephaly. It results from defects in dystroglycan glycosylation, which affects linkage of radial glial cells with the pial limiting membrane, leading to neuronal over-migration through pial gaps3. The dystroglycanopathies with brain and eye anomalies, include Walker–Warburg syndrome (WWS), muscle–eye–brain disease (MEB), and Fukuyama muscular dystrophy. In these conditions the brain surface lacks normal sulcation and has an uneven appearance, thus the name cobblestone cortex. Many patients have cerebellar and ocular abnormalities and congenital muscular dystrophy. WWS is considered the most severe of the disorders, but there is considerable overlap. The currently known genes responsible for Cobblestone malformation include FKTN, POMT1, POMT2, POMGnT1, FKRP, CRPPA, TMEM5, ISPD and LARGE 3, 15.


Heterotopia occurs when neurons originating in the periventricular (subependymal) region fail to migrate, leaving tracks or nodules of normal neurons in abnormal locations adjacent to the ependymal lining (periventricular nodular heterotopia) or in subcortical topography (SBH)16. In subcortical band heterotopia (SBH), bilateral bands of grey matter are found interposed in the white matter between the cortex and the lateral ventricles17. This may appear as a solid band of heterotopic tissue or as numerous islands of radially oriented grey matter separated by white matter18. SBH always have a genetic origin, and abnormalities in the DCX and LIS1 genes account for the majority of cases 19. Again, the predominant location (anterior or posterior) is helpful in suggesting the mutation involved.

Periventricular nodular heterotopia (PNH), consists of nodules of grey matter located along the walls of the lateral ventricles. PNH can be highly variable in extent, ranging from isolated single nodules to confluent bilateral lesions. These neurons failed to migrate into the cortex2 usually due to a clastic event and not secondary to a motility defect3. Consequently, the majority are not linked to a gene mutation. Two genes have been identified – x linked PNH due to Filamin A (FLNA) gene mutation and the rarer autosomal recessive ARFGEF2 gene mutation20. An additional form, not yet related to known mutations, consists of peri-atrial PHN in association with cerebellar dysplasia21.

Prevalence and timing of development

All types of lissencephaly and heterotopias are rare. The fetal prevalence is unknown. Classical lissencephaly has a reported prevalence of about 12 per million births22.

The prevalence of WWS is unknown but it is estimated to affect 1 in 60,500 newborns. It is equally distributed between males and females. Fukuyama congenital muscular dystrophy is the second most common form of muscular dystrophy in the Japanese population and is caused by mutations in the fukutin (FKTN) gene23.

Malformations of neuronal proliferation and migration occur between gestational weeks 8 and 2524.

Imaging diagnosis

Cortical maturation and gyral formation follow an age specific temporo-spatial schedule. Familiarity with this schedule allows for the diagnosis of abnormal maturation. Both dedicated neurosonography and MRI can depict fetal cortical malformations.  Neurosonography is the most important imaging tool for prenatal malformation screening as it is widely available and safe for both mother and fetus. It can detect lissencephalies and PNH, but MRI is a superior imaging modality for this purpose thanks to its optimal delineation of grey and white matter25 and topographical characterization of development of cortical gyri and sulci. Most cortical abnormalities will be detected after 24 weeks, but some, particularly the severe lissencephaly seen in Miller-Dieker patients, can be diagnosed prior to 24 weeks26, 27. With high resolution ultrasound transducers focused on the cortical rim, the more severe malformations can be detected even prior to 20 weeks.28, 29

Lissencephaly type 1

The diagnosis of lissencephaly type 1 can be suspected already at 23 weeks with appearance of mild ventriculomegaly and delayed operculization 30, 31. This diagnosis however is usually made after 27 weeks, due to absence of the Rolandic fissure which should be visualized from 26 weeks 32. Other fetal neuroimaging signs that can be seen include a smooth and thick cortex and abnormal lamination33, ventriculomegaly, a sulcation gradient, and associated cerebellar and/or callosal anomalies. The cortical findings are usually symmetric34. The symmetrically abnormal opercular formation is responsible for a “figure-eight” shaped brain30.

Cobblestone malformation

The diagnosis of Cobblestone malformation should be suspected when typical findings are present. An early diagnosis in the beginning of the second trimester can be suspected after 14 weeks with demonstration of a kinked brainstem and a cephalocele35, as well as a hyperechogenic cortical rim. This diagnosis should also be considered in cases of early onset ventriculomegaly, irregular ventricular wall and a hyperechogenic cortical rim or echogenic band28, 29. Additional features may include hydrocephalus, posterior pachygyria/agyria, anterior polymicrogyria-like appearance, abnormal operculization, and cerebellar dysplasia/hypoplasia and cysts. Myelination is a known feature, but would not be assessable on fetal MRI or sonography. Cobblestone lissencephaly in the dystroglycanopathies is also associated with fused colliculi, a small pons, a dysmorphic mesencephalon, a dorsal pontomedullary kink, vermian hypogenesis, and cerebellar hypoplasia. Microphthalmia and retinal dysplasia (small and dysplastic globe) are commonly seen as are posterior cephaloceles9, 16, 36.

Lissencephaly due to Tubulinopathies

Fetal neuroimaging signs that can be associated with lissencephaly due to tubulinopathies include microcephaly, corpus callosum agenesis, hypoplastic brainstem and cerebellum, large germinal zones and ganglionic eminences and polygyria. The more severe mutations of TUBA1A and less often TUBB2B have 2-layered cortex37, while the less severe mutations of TUBA1A or TUBB2B, or most mutations of TUBB and TUBB3 show distinct features intermediate between thick lissencephaly, ventricular asymmetry and polymicrogyria.



Subcortical band heterotopia

SBH is generally associated with a normal or mildly simplified gyration pattern, broad gyri, and an increased cortical thickness. SBH is difficult to identify on prenatal ultrasound. 

Periventricular nodular heterotopia (PNH)

Irregular lateral ventricular walls are the clue to the sonographic diagnosis. On MR multiple small nodular subependymal foci of low signal intensity, isointense to the germinal matrix can be seen. Irregular ventricular walls due to heterotopias should not be confused with ventricular wall irregularity secondary to clastic events, such as CMV infection, ischemia or hemorrhage. Heterotopic nodules may be single, multiple, unilateral or bilateral (string-of-pearls appearance) and appear in various locations along the ventricular wall. Single nodules may be found following subependymal disruption as seen with hydrocephalus. “String-of-pearls” lesions along the lateral ventricular walls may be seen with FLNA mutations.  Multiple nodules can be associated with ACC and mega cisterna magna. A posterior or trigonal location is associated with hippocampal, cerebellar and brainstem anomalies36.

Implications of standard examination 

Although the diagnosis of lissencephaly requires a dedicated multiplanar sonographic evaluation of the brain, initial suspicion can arise from the standard ultrasound examination through evaluation of the sylvian fissure. The maturation of the fetal Sylvian fissure during the second half of gestation is a major landmark of normal cortical development.

Typical patterns of the Sylvian fissure operculization in the standard axial trans-thalamic

plane have been described according to gestational weeks38. These patterns are based on the degree of coverage of the insula by the temporal lobe and the angulation between the insula and the parietal and temporal opercular margins, normally demonstrating an acute angle after 24.5 gestational weeks. If a delay in maturation is suspected at this time, a dedicated neurosonogram should be carried out.

Implications of targeted exam 

The available experience suggests that even expert ultrasound in pregnancies at risk will fail to diagnose fetal MCD in many cases. Multiplanar transvaginal high resolution brain imaging with adjunct MRI should be carried out in any case of suspected abnormal cortical development. A cortical malformation should be suspected in cases of earlier or later than expected sulci and gyri development, hemispheric or focal cortical asymmetry, irregularity or disruption along the cortical mantle, or an hyperechogenic cortical rim.

Obstetrical management 

Following the suspicion of MCD by dedicated neurosonography and/or MRI, when appropriate and possible (depending on gestational age), the imaging diagnosis is supplemented by genetic

studies (CMA and whole exome sequencing of the fetus and both parents). When multiple PNH are seen in a female fetus, FLNA should be suspected and brain MR imaging of the mother should be completed.

In some instances, no further studies are required during pregnancy due to the clear and dire prognosis (i.e non development of cortical landmarks at an advanced gestational age, association of other CNS or systemic anomalies) and then the genetic evaluation can be deferred until after delivery or termination of pregnancy.


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This article should be cited as: Shinar S, Blaser S: Disorders of neuronal migration: Lissencephaly, Cobblestone Malformations and Heterotopia. Visual Encyclopedia of Ultrasound in Obstetrics and Gynecology,, February 2023.

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