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Keywords:

  • brain;
  • cortical malformation;
  • gyration;
  • MRI;
  • prenatal diagnosis;
  • Sylvian fissure;
  • ultrasound

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients And Methods
  5. Results
  6. Discussion
  7. References

Objective

To illustrate and determine the significance of abnormal Sylvian fissure development (or abnormal operculization) in cases in which prenatal cerebral imaging is suggestive of underlying cortical dysplasia.

Methods

This was a retrospective study of 15 fetuses at 24–34 weeks in which abnormal operculization was identified on prenatal cerebral imaging and for which follow-up data were available. The imaging findings were correlated to macro- and microscopic neuropathological data (n = 11) or to postnatal clinical and imaging findings (n = 4).

Results

On microscopic examination of fetuses from 11 terminated pregnancies, abnormal operculization was associated with cortical dysplasia in four cases and the cortex was normal in seven. Abnormal operculization was associated with cortical dysplasia in only one of the four liveborn infants. Cases of abnormal Sylvian fissure development with normal cortical architecture were classified, according to associated anomalies of the central nervous system, into one of five groups: those with neural tube defects, microcephaly or frontal hypoplasia, glutaric aciduria, other cerebral abnormalities, and extracerebral anomalies.

Conclusion

Abnormal operculization on prenatal imaging does not systematically reflect underlying cortical dysplasia. It may be related to extracortical factors such as abnormal cerebral volume or other developmental anomalies of the central nervous system. An understanding of the significance of abnormal Sylvian fissure development could be useful in integrating its analysis into a more general one of the whole central nervous system. Copyright © 2008 ISUOG. Published by John Wiley & Sons, Ltd.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients And Methods
  5. Results
  6. Discussion
  7. References

One of the major maturational processes of the human brain is gyration which leads to a significant increase of the cerebral surface. A major landmark of the dynamic changes of the brain surface is the development of the Sylvian fissure on the lateral convexities of the cerebral hemispheres, the so-called ‘operculization process’1. This process, studied initially by neuropathologists2, 3, can be followed using prenatal imaging; this was described first using ultrasound4–7, and more recently in fetal cerebral magnetic resonance imaging (MRI) atlases8, 9. We have shown that operculization is a dynamic process, with a precise timetable, that can be studied and followed on a reference axial plane during routine ultrasound examination10.

This reference axial plane and timetable have been included systematically in our unit's ultrasound and MRI analysis of fetal cerebral development. The hypothesis of the current study was that abnormal Sylvian fissure development is the main marker of abnormal gyration, which should be scrutinized particularly when cerebral abnormalities are suspected. It has been suggested in the literature that abnormal operculization results from underlying cortical dysplasia (defined as abnormal histological architecture of the cerebral cortex) and that affected fetuses are at increased risk of refractory epilepsy or developmental delay in the postnatal period11–13. In this article, we studied retrospectively the charts of fetuses in which abnormal Sylvian fissure development was identified on the reference axial plane during prenatal imaging. Our objectives were to illustrate and determine the significance of abnormal Sylvian fissure development and to determine whether it reflects underlying cortical dysplasia.

Patients And Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients And Methods
  5. Results
  6. Discussion
  7. References

This was a retrospective study of 15 fetuses, ranging in age from 24 to 34 gestational weeks, in which abnormal Sylvian fissure development was identified on prenatal cerebral imaging in our unit between 2001 and 2006. Abnormal operculization was identified in all cases by an ultrasound study performed in our department and was analyzed with cerebral fetal MRI in all cases except one. The mean gestational age at the time of referral was 27 weeks. Gestational age was established by last menstrual period and adjusted by first-trimester crown–rump length measurement. Patients were referred for the following main findings on ultrasound examination (Table 1): ventriculomegaly (n = 8), microcephaly (n = 2), posterior fossa abnormalities (decreased transcerebellar diameter) (n = 3), midline abnormalities (n = 1), neural tube defect (n = 2), abnormal gyration (n = 2), extracephalic morphological abnormalities (n = 3) and intrauterine growth restriction (n = 1).

Table 1. Summary of findings in 15 cases with abnormal fetal Sylvian fissure operculization on prenatal cerebral imaging
CaseGA (weeks)Indications for referralPrenatal CNS imaging findingsTOPFinal diagnosis: neuropathological data/postnatal MRI diagnosis
  1. CNS, central nervous system; GA, gestational age; IUGR, intrauterine growth restriction; MRI, magnetic resonance imaging; NTD, neural tube defect; TOP, termination of pregnancy; US, ultrasound.

128 (US, MRI)VentriculomegalyDiffuse cortical abnormalities (irregular bumpy gyral pattern suggestive of polymicrogyria)YesDiffuse polymicrogyria
227 (US, MRI)VentriculomegalyDiffuse cortical abnormalities (polymicrogyria)YesDiffuse polymicrogyria
  Abnormal operculization   
326 (US)Intestinal echogenicityMicrocephalyNoDiffuse polymicrogyria
 30 (MRI)Pericardial effusionDiffuse cortical abnormalities Abnormal white matter
   Suggestive of polymicrogyria Cerebellar hypoplasia and dysplasia  (cytomegalic infection)
   Cerebellar hypoplasia  
428 (US, MRI)VentriculomegalyLissencephalyYesLissencephaly Type 1
   Microcephaly Microcephaly
528 (US, MRI)VentriculomegalyLissencephalyYesCortical hypoplasia
  Corpus callosal agenesisAbnormal germinative zones Hyperplasia of the germinative zones
  Posterior fossa anomaliesCorpus callosal agenesis Pontocerebellar hypoplasia
  Multiple malformationsPontocerebellar hypoplasia Corpus callosal agenesis
627 (US)VentriculomegalyVentriculomegalyNoAbnormal operculization (without individualization of the insula)
 32 (MRI)NTDAbnormal operculization Ventriculomegaly
   Reduced cisterna magna Reduced cisterna magna, normal  cerebellum
   Sacral NTD  
727 (US, MRI)VentriculomegalyAbnormal operculizationYesAbnormal operculization (macroscopic)
  Occipital meningocele  (NTD)Occipital meningocele Normal cortical architecture  (microscopic)
   Midline anomalies Occipital meningocele
   Cerebellar hypoplasia Cerebellar hypoplasia
830 (US, MRI)MicrocephalyAbnormal anterior operculizationYesFrontal lobe hypoplasia
  IUGRMicrocephaly, trigonocephaly Trigonocephaly and facial  dysmorphia (monosomy 9p)
928 (US, MRI)MicrocephalyAbnormal anterior operculizationYesNormal operculum (macro- and microscopic)
   Microcephaly Severe microcephaly
   Cerebellar hypoplasia Facial dysmorphia
     Cerebellar hypoplasia
1024 (US)Cerebellar hypoplasiaAbnormal anterior operculizationYesNormal operculum (macro- and microscopic)
   Microcephaly Microcephaly
   Cerebellar hypoplasia Mild cerebellar hypoplasia
     Bilateral cataract
1134 (US, MRI)Abnormal operculizationAbnormal operculizationNoAbnormal operculization
  Enlarged pericerebral  spacesSevere macrocephaly Macrocephaly
   Bilateral subependymal cysts Bilateral subependymal cysts
   Enlarged pericerebral spaces Enlarged pericerebral spaces
1226 (US, MRI)VentriculomegalyAbnormal operculizationYesAbnormal operculization (macroscopic)
  Cerebellar hypoplasiaVentriculomegaly Normal cortical architecture  (microscopic)
   Cerebellar hypoplasiaInfra- and supratentorial heterotopia 
1328 (US, MRI)Midline anomaliesAbnormal operculization with an otherwise normal gyral patternNoAbnormal operculization (with an otherwise normal gyral pattern)
   Corpus callosal agenesis Corpus callosal agenesis
1427 (US, MRI)VentriculomegalyAbnormal operculization and abnormal central gyrusYesAbnormal operculization and deep sulci (macroscopic)
   Midline abnormalities with  asymmetrical frontal lobes Gross frontal lobe asymmetry
  Normal cortical architecture  (microscopic)   
1525 (US, MRI)Multiple malformations (dysmorphic limbs, heart)Isolated abnormal operculizationYesNormal operculization (macro- and microscopic)

Transabdominal neurosonography was performed in all planes using a Siemens Acuson Antares (Siemens AG Healthcare Sector, Erlangen, Germany) ultrasound system, equipped with a CH6-10 curved-array probe. Transvaginal sonography was not performed because the transabdominal examinations provided adequate visualization of the fetal head in all cases. Prenatal MRI was performed with a 1-T system (GE Healthcare Technologies, Milwaukee, WI, USA). As part of the evaluation of the cerebral structures, Sylvian fissure development was analyzed systematically on a reference axial plane using the methodology and timetable as previously reported (Figure 1)10.

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Figure 1. (a) Summary of timetable of fetal Sylvian fissure development as reported by Quarello et al.10, with line drawings representing the angle that the insula makes with the temporal lobe or the extent to which the temporal lobe overrides the posterior half of the insula at six gestational ages. Ultrasound reference plane (b) and corresponding T2-weighted fast spin echo magnetic resonance axial image (c) showing normal operculization at 28 gestational weeks.

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The imaging findings were correlated with fetal neuropathological data in 11 cases and to postnatal clinical and imaging findings (when the pregnancy was not terminated) in four cases. Fetopathological data included macro- and microscopic examination. All neuropathological studies were reviewed by J.C.L. and the pathologists involved in the study in order to reach a consensus concerning diagnosis. In all postnatal cases, a cerebral MRI study was performed and the examination, focusing particularly on analysis of the cortical architecture, was reviewed by both a neuropediatrician and a pediatric neuroradiologist. Our 15 informative cases were classified either according to the presence of cortical dysplasia or, in fetuses without evidence of cortical dysplasia, according to associated cerebral abnormalities.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients And Methods
  5. Results
  6. Discussion
  7. References

According to neuropathological data (n = 4) or postnatal imaging (n = 1), abnormal Sylvian fissure development was associated with cortical dysplasia in five cases (Cases 1–5; Table 1). Cortical dysplasia included polymicrogyria (n = 3) (Figures 2 and 3), lissencephaly (n = 1) and an exceptional cortical malformation described as cortical hypoplasia with hypertrophy of the germinative zones associated with pontocerebellar hypoplasia (n = 1) (Figure 4).

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Figure 2. Case 2. Ultrasound (a) and magnetic resonance (b, c) reference planes showing abnormal Sylvian fissure development (long arrows) in a 28-week fetus (compare with Figure 1). Axial (a and b) and coronal (c) images showed abnormal scalloped cortical ribbon suggestive of polymicrogyria (short arrows); this was confirmed on pathological examination.

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Figure 3. Case 3. (a) T2-weighted fast spin echo axial magnetic resonance (MR) image in a 36-week fetus showing abnormal gyration with abnormal operculization (long black arrow) and abnormal hyperintense white matter (short arrows) with microcephaly and cerebellar hypoplasia. (b) Postnatal MR imaging confirmed the prenatal diagnosis of abnormal operculum (arrow) with an underlying diffuse polymicrogyria, which was secondary to cytomegalovirus infection, associated with an abnormal signal of the white matter.

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Figure 4. Case 5. T2-weighted fast spin echo axial magnetic resonance images (a and b), including reference axial plane (a), showing a ‘lissencephalic’ cortical pattern with a thin cortical ribbon and abnormal Sylvian fissure development (long arrow) (compare with Figure 1) and hypertrophied germinative zones (short arrows) in a 28-week fetus. Macroscopic examination (c and d) showed abnormal triangular Sylvian fissure (long arrow) and hypertrophied germinative zones (short arrows). Microscopic examination revealed cortical hypoplasia and confirmed hypertrophied germinative zones.

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The cortex was found to be normal in 10 of the 15 cases at final diagnosis (Cases 6–15); this was assessed by microscopic neuropathological examination in seven cases and postnatal cerebral MRI in three. However, abnormal development of the Sylvian fissure could be identified macroscopically in only three of the seven cases assessed by microscopic neuropathological examination.

The 10 fetuses with a normal cortex but abnormal Sylvian fissure identified on prenatal imaging could be further subdivided into five groups according to associated central nervous system (CNS) abnormalities. Group 1 consisted of those with neural tube defects (Cases 6 and 7; Figure 5). Group 2 consisted of those with microcephaly (Cases 9 and 10) or frontal hypoplasia (Case 8). In these three cases, the abnormal development involved exclusively the anterior part of the operculum. These fetuses showed no anterior depression between the surface of the frontal lobe and the insula, resulting in absence of individualization of the anterior part of the insula. In contrast, the posterior part of the insula was normal for gestational age (Figure 6). Case 8, with frontal hypoplasia described on neuropathological examination, showed microcephaly associated with trigonocephaly on CNS imaging. Karyotyping revealed a monosomy 9p (46 XX, del(9) (p21)). Group 3 consisted of a fetus with macrocephaly with increased pericerebral spaces (Case 11). Association with an abnormal operculum was suggestive of glutaric aciduria Type 1, which was confirmed biologically in the postnatal period. Group 4 consisted of fetuses with abnormal cerebral organization, involving either the posterior fossa (cerebellar hypoplasia) (Case 12) or the midline structures, including agenesis of the corpus callosum (Case 13) (Figure7) and disorganization of the anterior part of the interhemispheric fissure with asymmetrical frontal lobe (Case 14) (Figure 8). Group 5 consisted of one fetus with no associated CNS abnormality but polymalformative syndrome (Case 15) (Figure 9).

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Figure 5. Case 6. Ultrasound (a) and magnetic resonance (MR) (b) reference planes showing abnormal Sylvian fissure development (long arrows) and ventriculomegaly (equation image) associated with reduced cisterna magna (short arrows) (c) related to a sacral neural tube defect. Postnatal axial MR imaging (d) confirmed the prenatal findings, showing abnormal operculization with no individualization of the insula (arrows) replaced by polygyria (with an otherwise normal cortical ribbon)

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Figure 6. Case 9. T2-weighted fast spin echo axial (a) and parasagittal (b) magnetic resonance images showing abnormal development of the anterior part of the Sylvian fissure (arrows) (compare with Figure 1) associated with severe microcephaly in a 28-week fetus; note the disproportion between face and brain (b). Neuropathological examination showed a normal Sylvian fissure with normal cortical architecture on microscopic analysis.

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Figure 7. Case 13. Ultrasound (a) and magnetic resonance (MR) (b) reference planes showing abnormal Sylvian fissure development (arrow) associated with corpus callosal agenesis (equation image) (c) in a 28-week fetus. These findings were confirmed on postnatal cerebral MR imaging (d, arrows), which also demonstrated a normal cortical ribbon.

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Figure 8. Case 14. Ultrasound reference plane (a) showing abnormal operculization, with a Sylvian fissure similar in shape to a triangle (arrow) associated with abnormal anterior midline (equation image) in a 28-week fetus. These findings were confirmed on macroscopic examination (b) but microcopic examination showed normal cortical architecture.

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Figure 9. Case 15. Ultrasound (a) and magnetic resonance (b) reference planes showing abnormal Sylvian fissure development (arrows), which were associated with multiple malformations, in a 25-week fetus. This abnormal operculum was not found on either macroscopic or microscopic examination.

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Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients And Methods
  5. Results
  6. Discussion
  7. References

Analysis of gyration is essential to the evaluation of fetal cerebral anatomy on prenatal diagnostic neuroimaging in the second half of pregnancy. Gyration should be scrutinized particularly if an unexpected cerebral finding, such as unexplained ventriculomegaly or a posterior fossa or midline anomaly, has been diagnosed.

Sylvian fissure development or ‘operculization’ is one of the main landmarks of the gyration process and starts with individualization of the circular sulcus1–4, 8, 9. Initially, the circular sulcus is smooth at the margin of the insula, but it starts becoming angular after about 17 weeks as the parietal and temporal lobes grow over it. By 20 weeks' gestation the primitive parietal and temporal lobes around the posterior part of the insula, grow more rapidly than the frontal lobe. This discrepancy in growth explains the earlier development of the posterior compared with the anterior part of the Sylvian fissure2. The insular cortex is finally engulfed by the enlarged parietal, temporal, and frontal opercula. The anterior portion of the insula remains exposed until full term and full closure of the most anterior part of the Sylvian fissure does not occur until after delivery, usually within the first 2 years of postnatal life2.

We studied Sylvian fissure development on a reference axial plane on prenatal imaging and built a timetable of these dynamic changes10. Using this reference axial plane, we encountered fetuses in which Sylvian fissure development was obviously abnormal on ultrasound and MRI. Prior to this study, we used to suggest on prenatal counseling that abnormal operuculization was highly suggestive of cortical dysplasia with a high risk of refractory epilepsy or developmental delay in the postnatal period11–13. Therefore, we performed this retrospective study to understand the significance of abnormal Sylvian fissure development on prenatal imaging and to show if this abnormal operculization reflected underlying cortical dysplasia.

Unexpectedly, only one third (n = 5) of the cases in our series of 15 fetuses with abnormal operculization had underlying cortical dysplasia (Cases 1–5). Three of these fetuses had diffuse polymicrogyria, a cortical malformation rarely reported in the prenatal imaging literature14–17. The other two had a diffuse cortical malformation with a lissencephalic appearance, related to true lissencephaly Type 1 in one case; the other was an exceptional case of cortical hypoplasia with hyperplasia of the germinative zones. In all five cases, the cortical dysplasia involved the whole cortex diffusely. As suggested by Malinger et al.17, cortical malformations can be diagnosed by ultrasound in utero based on the presence of specific deviations from the normal pattern of development, especially Sylvian fissure development. However, a cortical malformation, either focal or more extensive, may occur without abnormal operculization, as reported by Righini et al. in a prenatally diagnosed case of focal polymicrogyria14. Therefore, especially in a fetal neurology clinic, prenatal evaluation of gyration should not be limited to the operculum. Operculization analysis should, however, be performed systematically especially in cases of ventriculomegaly or microcephaly, which are the main referral findings of diffuse cortical malformations such as lissencephaly Type 118–20.

The cortex was normal in two-thirds of the fetuses in our series. This should be emphasized because the majority of series have shown that abnormal gyration, especially abnormal Sylvian fissure development, is associated with disorders of neuronal migration12, 20, 21. Noteworthy is the report by Chen et al.22 of a series of abnormal operculization in a population of infants and children. They divided abnormal operculization into two categories, depending on whether the Sylvian fissure was malformed or underdeveloped. The group with malformed Sylvian fissure was divided into three subgroups, two representing neuronal migration disorders (one with lissencephaly (without operculum formation) and the other with pachygyria with abnormal operuculization). The third subgroup, with non- or abnormal formation of the Sylvian fissure, as well as the two subgroups with underdeveloped Sylvian fissure, showed no evidence of neuronal migration disorders. Our prenatal series confirmed the findings of Chen et al., in that abnormal operculization was found not to be necessarily associated with cortical dysplasia or abnormal neuronal migration.

We categorized our series of ten fetuses with abnormal operculization but an otherwise normal cortex into five groups according to the associated cerebral malformations.

Group 1: Neural tube defects (Cases 6 and 7)

Neural tube defects encompass different types of cortical abnormalities, including both true cortical dysplasia and histologically normal cortex with abnormal gross appearance. In his series of 25 patients with spinal dysraphism, Gilbert et al.23 investigated disorders of neuronal migration and found disordered cortical lamination in more than half of the cases, with polymicrogyria in 40%. In contrast, McLendon et al.24 described cerebral ‘polygyria’, the abnormal gross appearance of an otherwise histologically normal cortex. This abnormal cortical pattern, which has also been called ‘stenogyria’ to describe the small, closely spaced folds, was also observed by Kawamura et al.25 on MRI evaluation of cerebral abnormalities in a pediatric series (for which there was no histological verification of cortical architecture) of 24 children with lumbosacral neural tube defects. Our Case 6, with abnormal operculum formation but an otherwise normal cortical ribbon on postnatal MRI, was suggestive of such an abnormal cortical pattern. The abnormal Sylvian fissure of Case 7 with normal microscopic cortical architecture most likely represents a deformed Sylvian fissure related to microcephaly and loss of the pericerebral spaces, such as in the ‘banana sign’, which is the deformation of the cerebellum related to the reduced cisterna magna in a hypoplasic posterior fossa.

Group 2: Microcephaly or frontal hypoplasia (Cases 8–10)

In these three cases, the posterior part of the Sylvian fissure was normal and the abnormal development involved only its anterior part (Figure 6). This group was very similar to the group with underdeveloped insula (Type 4) described by Chen et al.22, in which the Sylvian fissure, and particularly the frontal lobe, was underdeveloped, resulting in a wide-open operculum with the insula exposed. In their series, four of the six patients in this group had microcephaly. This kind of abnormal operculum has also been associated with non-syndromic microencephaly26, 27. Interestingly, Barkovich et al.28 analyzed the cerebral cortex in cases of holoprosencephaly, paying particular attention to the Sylvian fissures, and found that the more severe cases of holoprosencephaly showed a single Sylvian fissure in the anterior midline. This fissure seemed to be composed of the posterior halves of the Sylvian fissures, with bilateral posterior opercula forming lateral borders, as if the anterior halves of the fissures had never formed due to reduction in growth of the frontal lobe. These observations suggest that development of the anterior part of the Sylvian fissure might be more dependent on the volume of the frontal lobe and more generally on the volume of the cerebral hemispheres than is the posterior part.

Group 3: Glutaric aciduria Type 1 (Case 11)

Prenatally, this case was suggestive of the diagnosis that was confirmed in the postnatal period, as we have discussed in detail previously29. The association of severe macrocephaly with abnormally wide Sylvian fissures, justifies a prenatal biological work-up for glutaric aciduria Type 1.

Group 4: Association with other cerebral abnormalities (Cases 12–14)

In this group, the associated malformations involved the midline (Cases 13, 14) and the cerebellum (Case 12). It should be noted that Chen et al.22 also reported that the most frequent anomaly associated with abnormal operculization is dysgenesis of the corpus callosum (except for neuronal migratory disorders). Of our two cases of midline anomalies, one had complete agenesis of the corpus callosum. In the second case, the corpus callosum was complete but the midline was abnormal, as suggested by deviation of the septum pellucidum and asymmetry of the frontal lobes; in this particular case, the abnormal operculum was also associated with other abnormal gyral development. This suggests that normal Sylvian fissure development might also be dependent on normal development of the entire cerebral structures.

Group 5: Multiple malformations with no other associated cerebral anomalies (Case 15)

This case was perplexing because no other associated cerebral abnormality was found on macroscopic and microscopic neuropathological examination, despite significant abnormal operculization on prenatal imaging. Chen et al.22 also reported absence of cerebral anomalies in a group of 58 patients presenting with underdeveloped Sylvian fissures (particularly the anterior part). Isolated abnormal operculum was also reported by Bingham et al.30 in two infants with interstitial deletion of chromosome 22 q11 and by Tatum et al.31 in two children with severe developmental delay. In our case, termination of pregnancy was elected by the parents because of multiple malformations. In our practice, we have encountered no previous cases in which abnormal operculization was an isolated finding. Prenatal counseling in such cases is very difficult. One should note that in cases of isolated abnormal operuculization, an abnormal posterior part of the Sylvian fissure increases the likelihood of developmental delays, while in most cases an abnormal anterior part represents a normal variant, particularly in the perinatal period22.

In the 10 fetuses in our series with normal cortex but abnormal Sylvian fissure identified on prenatal imaging, it is noteworthy that abnormal operculization was not found on macroscopic examination in four of the seven cases in which a neuropathological examination was performed. In contrast, the abnormal operculization was confirmed in all three cases in which postnatal MRI was performed. This lack of correlation between ‘in-vivo’ and ‘in-vitro’ analysis of the operculization was most likely due to the technical difficulties in preserving the fetal brain after termination, especially in cases of minor deformation of the brain surface, such as in abnormal Sylvian fissure development.

In summary, our series has confirmed that abnormal operculum development does not systematically reflect underlying ‘cortical dysplasia’, defined strictly as abnormal histological cortical architecture. Abnormal Sylvian fissure development can be related to extracortical factors. From a conceptual point of view, if operculization is induced by waves of migratory neurons arriving at the cortical plate, other ‘non-cortical’ parameters, such as the global volume of the brain and the integrity of the whole CNS, including development of the neural tube, the midline and the posterior fossa might play a major role in the gyration process. As stated by Barkovich et al., the etiological classification of abnormalities of cortical development is continually being updated as our understanding evolves32. From a practical point of view, the Sylvian fissure is usually readily visible on prenatal imaging when evaluating both the size of the lateral ventricles and performing other cephalic biometry. An understanding of the significance of abnormal Sylvian fissure development could be useful in integrating its analysis into a more general one of the whole central nervous system.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Patients And Methods
  5. Results
  6. Discussion
  7. References
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