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Malformations of Cerebral Cortical Development
Clinical and Imaging Features
Zafer Koc, MD,* Filiz Koc, MD,
w
and Haydar Kaderoglu, MD
z
Abstract: Malformations of cortical development (MCDs)
comprise a variable spectrum of clinical, neuroradiologic, and
histopathologic findings. MCDs are increasingly recognized as
significant causes of epilepsy, developmental delays, and
congenital neurologic deficits. The aim of this study was to
determine the types, relative frequencies, and clinical and
imaging features of MCDs. Data were collected in 2 hospitals
and a medical imaging center during a 9-year period. Twenty-six
patients (17 men and 9 women; age range, 5 mo to 29 y; mean
age, 10.8 y) with an MCD were evaluated. The results of
magnetic resonance imaging studies were retrospectively re-
viewed for type, extension, and classification of the malforma-
tions and for associated findings. Clinical findings were obtained
by a review of the patients’ medical records. Of the patients
studied, epilepsy was present in 65%, mental and/or motor
retardation was identified in 34.6%, and skin lesions were noted
in 15%. The following types of MCD were identified:
malformations of the heterotopic gray matter in 35% of the
subjects, focal cortical dysplasia (23%), subependymal and
cortical tubers (19%), pachygyria (15%), polymicrogyria (15%),
schizencephaly (15%), and type 1 lissencephaly (8%). Approxi-
mately, 27% of the subjects had the following other types of
cerebral malformation: callosal agenesis (8%), ventriculomegaly
(8%), or agenesis of the septum pellucidum (4%). Our study
indicated that the most common forms of MCD are heterotopia
and focal cortical dysplasia. Patients with an MCD tended to
have a higher prevalence of epilepsy, developmental delays, and
neurologic deficits. Most patients with heterotopia had other
malformations of cortical dysplasia. Some patients with an
MCD also exhibited other malformations of the brain.
Key Words: cortical malformation, cortical dysplasia, lissence-
phaly, clinical findings, magnetic resonance imaging
(Neurosurg Q 2007;17:23–28)
Malformations of cortical development (MCDs) are
rare disorders that represent patterns of aberrant
architectural organization of the cerebral cortex and
adjacent white matter. It is rare to diagnose those
malformations in utero until late in the pregnancy,
although the presence of microcephaly or abnormalities
of the corpus callosum, lateral ventricles, or cerebellum
may be the first detectable sign of a more extensive brain
malformation involving the cerebral cortex. Patients with
an MCD usually present during early childhood with
drug-resistant epilepsy, mental and/or psychomotor
developmental delay, or hemiparesis.
1–5
Magnetic resonance imaging (MRI) provides the
anatomic detail necessary for the diagnosis of MCDs,
which may appear as a focal lesion or multilobar lesions
manifested as increased thickness of gray matter, blurred
boundaries toward the near white matter, or an abnormal
gyral pattern.
6–8
The early identification and selection of patients
who may be candidates for the surgical treatment of
epilepsy are important in the diagnostic evaluation of
patients with an MCD. Surgical intervention at an
appropriate time in select patients offers a chance for
freedom from seizures and improved cognitive outcome.
2
MCDs are more often diagnosed now than before
the advent of MRI.
9,10
The aim of this study was to
determine the types, relative frequency, clinical findings,
and imaging features of MCDs.
MATERIALS AND METHODS
Data from 26 patients (17 men and 9 women; age
range, 5 mo to 29 y; mean age ± SD, 10.8 ± 8.3 y) with a
diagnosed MCD were retrospectively analyzed. Patients’
data were collected from 2 hospitals and a medical
imaging center during a 9-year period. The results of MRI
studies of the cerebral malformations in all patients were
obtained by means of 3 different MRI units. An
experienced radiologist analyzed each subject’s MRI scan
of the brain. The classification, morphologic type and
shape, and site of the MCD were recorded, as were the
presence and degree of associated malformations and
anomalies. An experienced neurologist reviewed and
recorded each patient’s presenting complaints, clinical
findings, results of neurologic evaluations, electroence-
phalographic reports, and results of follow-up.
RESULTS
The clinical features and MRI findings of the 26
patients are summarized in the Table 1. The patients’
presenting complaints were primarily as follows: seizure
Copyright r2007 by Lippincott Williams & Wilkins
From the *Department of Radiology, Baskent University School of
Medicine; wThe Department of Neurology, Cukurova University
School of Medicine; and zThe Neurotip Medical Imaging Center,
Adana, Turkey.
Reprints: Zafer Koc, MD, Department of Radiology, Baskent
University School of Medicine, Adana, Turkey (e-mail: zaferkoc@
superonline.com).
ORIGINAL ARTICLE
Neurosurg Q Volume 17, Number 1, March 2007 23
TABLE 1. Imaging and Clinical Findings in 26 Patients With Malformation of Cerebral Cortical Development
Imaging Findings (Brain MRI) Clinical Findings
Patient
No.
Age
(y)/Sex
Malformation of Cortical Development,
Location Additional Findings Presenting Complaints Associated Clinical Findings
1 6/F Classic type 1 lissencephaly and a diffuse, flail,
thickened cortex
Ventriculomegaly Seizures Myoclonic epilepsy, spastic
quadriparesis, MR
2 5 Mo/M Bilateral parietal open lip schizencephaly and
heterotopia
— Afebrile convulsions Infantile spasm and motor
retardation
3 16/M Right parietal polymicrogyria, cortical
dysplasia, heterotopia
— Seizures SPE
4 29/F Bilateral diffuse subependymal nodular
heterotopia
— Seizures CPE
5 11/M Right parietal focal cortical dysplasia and
subependymal heterotopia
Aqueductal stenosis and cerebellar
hypoplasia, Dandy-Walker variant
Seizures SPE
6 28/F Cortical hamartomas and TS Subependymal calcified nodules Skin lesions and
abdominal distension
Renal AML
7 3/M Bifrontal pachygyria (incomplete
lissencephaly
Focal conical thickening and relative loss
of gray-white matter interface
Developmental delay MMR, pyramidal signs, facial
dysmorphia
8 1/M Conical hamartoma and TS — Adenoma sebaceum None
9 24/F Left frontal focal conical dysplasia Focal conical thickening Seizures CPE
10 10/M Left parietal open-lip schizencephaly and
heterotopia
Callosal agenesis and left frontoparietal
hemispheric dysplasia
Seizures SGE, MR, dysmorphic changes
11 18/M Bilateral (right frontal and left parietal) open-
lip schizencephaly and heterotopia
Right temporal arachnoid cyst Development delay and
seizures
CPE, spastic quadriplegia, MMR,
abnormal conjugate gaze
12 I7/F Right parietal local conical dysplasia Agenesis of septum pellucidum Seizures SGE
13 5/M Bilateral (right parietal and left frontal) open-
lip schizencephaly, heterotopia, left frontal
polymicrogyria
— Seizures Myoclonic partial epilepsy
14 1/F Classical type I lissencephaly Ventriculomegaly Developmental delay MMR
15 1/F Conical hamartomas and TS Cortical and subependymal nodules Development delay None
16 15/M Conical hamartomas and TS Giant cell astrocytoma and cortical and
subependymal nodules
Skin lesions None
17 11/M Left frontal polymicrogyria and subcortical
heterotopia
— Seizures CPE
18 6 Mo/M Bitemporal pachygyria (incomplete
lissencephaly)
— Afebrile convulsions and
development delay
Myoclonic and generalized tonic
seizures, hypotonia
19 7/M Left temporal focal conical dysplasia Dysmorphic changes in the left temporal
area
Behavioral disorder and
seizures
Dysmorphic face. MR, CPE
20 5/M Left parietal focal conical dysplasia Left parietal corneal-subcortical lesion
high signal on T2-weighted images
Seizures SGE
21 15/F Bilateral subependymal nodular heterotopia — Seizures CPE
22 16/M Bilateral temporoparietal pachygyria and
occipital polymicrogyria (incomplete
lissencephaly)
— Developmental delay Pyramidal signs and MMR
23 11/M Conical hamartomas and TS Subependymal calcified nodules and a
mass adjacent to the foramen of Monro
Skin lesions Multiple retinal nodular hamartomas
24 12/M Right frontal focal conical dysplasia Dysplastic area of the right frontal and
anterior interhemispheric
Headache No
25 16/F Left subependymal focal nodular heterotopia — Seizures CPE
26 2/M Bilateral frontal pachygyri (incomplete
lissencephaly)
Callosal agenesis Status epilepticus Myoclonic and generalized tonic
seizures, MMR
AML indicates angiomyolipoma; CPE complex partial epilepsy; F, female; M, male; MMR, mental-motor retardation; MR, mental retardation; SPE, simple partial epilepsy; SGE, secondary generalized epilepsy;
TS, tuberous sclerosis.
Koc et al Neurosurg Q Volume 17, Number 1, March 2007
24 r2007 Lippincott Williams & Wilkins
in 14 patients, developmental delay,
6
afebrile convulsion,
2
skin lesions,
4
status epilepticus,
1
headache,
1
and beha-
vioral disorder.
1
A family history of epilepsy was negative
in all patients, although epilepsy was a major clinical
finding in 17 (65.4%) of the patients studied. Eleven of
those patients experienced partial seizures, and 3 ex-
hibited generalized epileptic seizures. Temporal lobe
seizures were thought to afflict 5 of those patients, and
the remaining 6 were thought to experience seizures from
extratemporal (frontal and parietal) foci.
Heterotopic gray matter, the most frequent type of
the MCD noted in the study, was identified in 9 (34.6%)
of the subjects. Subependymal (periventricular) hetero-
topic gray matter was identified in 4 (15.4%) of the
patients (Fig. 1). Heterotopia as an associated finding was
identified in 5 (19.2%) of the patients, most of whom had
schizencephaly. Schizencephaly with heterotopic gray
matter was identified in 4 (15.4%) of the patients
(Fig. 2), and agenesis of the septum pellucidum was
noted as an associated finding in 1 patient. Focal cortical
dysplasia (FCD) was identified in 6 (23%) of the patients,
4 (67%) of whom experienced seizures. Polymicrogyria
was identified in 4 (15.4%) of the patients (Fig. 3).
Subependymal and cortical tubers (tuberous sclerosis)
were identified in 5 (19.2%) of the patients. Classic type 1
lissencephaly (agyria-pachygyria complex) (Fig. 4A) was
identified in 2 (7.7%) patients, and pachygyria was
identified in 4 (15.4%) (Figs. 4B–D). Associated other
malformations of the brain were identified in 7 (26.9%)
of the patients studied. Callosal agenesis was identified in
2 patients, and ventriculomegaly was identified in
2 patients. Aqueductal stenosis and cerebellar hypoplasia
(the Dandy-Walker variant), a temporal arachnoid cyst,
and agenesis of the septum pellucidum were observed in
1 patient each.
DISCUSSION
MCDs represent patterns of aberrant architectural
organization of the cerebral cortex and adjacent white
matter.
11
Many of these malformations develop during
the neonatal period or infancy.
12–16
Embryologic devel-
opment of the cerebral cortex is a complex process that
can be summarized in 3 main steps: cell proliferation,
neuronal migration, and cortical organization.
11
Microcephaly is thought to result from decreased
FIGURE 2. A and B, Patient 2. A, Axial
T1-weighted spin echo and B, T2-
weighted turbo spin echo brain MRIs
show bilateral parietal open-lip schizen-
cephaly (black arrows, B) and hetero-
topic gray matter on both sides of the
fissures (open arrows, B).
FIGURE 1. A to C, Patient 4. A, Axial T1-weighted spin echo; B, axial T2-weighted turbo spin echo; and C, coronal T2-weighted
turbo spin echo brain MRIs show diffuse, subependymal, well-defined small nodules of heterotopic gray matter along the lateral
borders of the lateral ventricles (arrows, A–C) that appear isointense with normal gray matter.
Neurosurg Q Volume 17, Number 1, March 2007 Cerebral Cortical Malfunctions
r2007 Lippincott Williams & Wilkins 25
cell proliferation and increased apoptosis, and macro-
cephaly is attributed to increased cell proliferation and
decreased apoptosis. Cortical hamartomas of tuberous
sclerosis, cortical dysplasia with balloon cells, and
hemirnegalencephaly are thought to result from the
abnormal proliferation of neuronal cells.
11
Heterotopia
of the gray matter, lissencephaly and subcortical band
heterotopia, or cobblestone complex and congenital
muscular dystrophy are thought to result from abnormal
neuronal migration.
11
When there is a primary, limited,
pure deficit in neuronal migration onset, the remaining
neuroblasts may migrate normally to form the regular
cortex, and subependymal (periventricular) heterotopia
develops. When the later stage of neuronal migration and
cortical organization is impaired, polymicrogyria, schi-
zencephaly, cortical dysplasia without balloon cells, or
microdysgenesia may develop.
12
The causes of MCDs are heterogeneous and may be
genetic or acquired.
10
These malformations may be isolated
findings or associated with other cortical and brain
malformations such as callosal agenesis or dysgenesis,
hydrocephalus, cerebellar hypoplasia, or mega cisterna
magna.
12–15
In our study, associated other types of brain
malformations were observed in 27% of the patients.
MCDs are a frequent cause of symptomatic focal
epilepsy in childhood and adulthood.
1,5,9,10,16
Although
the exact prevalence of MCD is unknown, its incidence in
patients who undergo surgical treatment for epilepsy has
been shown to vary from 12% to 40% and is more
frequent in children.
17
In particular, FCDs are increas-
ingly diagnosed in epileptic patients as a result of
improved MRI techniques. About 76% of the patients
with FCDs are thought to suffer from drug-resistant
epilepsy.
18–21
Surgical treatment offers a promising
therapeutic option for those individuals.
22
Our study
revealed that most of the patients with an MCD present
with that disorder in the neonatal period or during
childhood and that most of those patients (65%) also had
had epilepsy. This finding is consistent with data in the
literature.
2,12,23
In their study, Leventer and colleagues
23
reported
no sex-related prevalence of MCDs in pediatric patients
but noted that among adult patients, more women than
men had an MCD. In our series, we noted MCDs in more
boys than girls, but we found a female predominance of
those disorders in adults.
In many individuals with FCD, epilepsy manifests
early. However, in a few such patients, epilepsy does
FIGURE 3. A to C, Patient 3. A, Axial T1-weighted spin echo; B, axial T2-weighted turbo spin echo; and C, coronal T2-weighted
turbo spin echo brain MRIs show right parietal polymicrogyria (open arrows, A–C). Cortical dysplasia extends to the posterior
frontal region. Right parietal gyral asymmetry can be seen clearly, especially when compared with the left side. Note the right
parietal subcortical linear hyperintensities representing indistinct cortex-subcortical white-matter boundaries (arrows, B).
FIGURE 4. A to D, Patient 14. A, Axial proton density intermediate MRI of a patient with type 1 lissencephaly shows a thin,
smooth outer layer (arrow) and a thick inner band of gray matter with distinct gray-white matter boundaries (open arrow).
Primitive shallow sylvian fissures give the brain a typical ‘‘hour-glass’’ configuration. Patient 22. B, Axial T1-weighted spin echo; C,
proton density intermediate; and D, T2-weighted turbo spin echo brain MRIs reveal temporoparietal pachygyria with shallow sulci
and flat gyri (open arrow, B–D) and polymicrogyria of the bilateral occipital cortex (white arrows, B).
Koc et al Neurosurg Q Volume 17, Number 1, March 2007
26 r2007 Lippincott Williams & Wilkins
appear until the second to sixth decade of life. In some
patients, epilepsy can be controlled over a certain period
of time by antiepileptic drugs. Factors contributing to the
epileptogenicity of FCDs or influence the pharmacologic
treatment of epilepsy are unknown. Although dysgenesis of
the cortex and misconnection resulting from neuronal
malpositioning are usually thought to cause epilepsy, a
modified hypothesis suggests that the primary cause of
epilepsy might be abnormal interneuronal connectivity
rather than simply neuronal malpositioning.
4,17
In our
study, most epileptic patients with FCD began to experience
the symptoms of epilepsy during their first decade of life.
It has been suggested that MCDs most frequently
develop in the frontal lobes of the brain, which account
for the largest volume of brain tissue.
23
However, another
investigator reported that MCDs most frequently affected
the extratemporal areas.
24
We found the frontal and
parietal lobe to be the areas most frequently affected by
an MCD.
Although enhanced computed tomography or MRI
is recommended for the routine imaging of epileptic
patients with a possible MCD, MRI is sufficient as sole
imaging modality in most patients.
25
MRI is the most
effective noninvasive imaging method for the in vivo
diagnosis of MCD; its reported sensitivity ranges between
50% and 70%.
12,26
MRI findings of MCDs reveal a
spectrum of cytoarchitectural abnormalities that affect
the cortical and subcortical structure.
3
Cortical thicken-
ing with or without signal change, abnormal gyral
formation, and focal subcortical signal changes have
been reported as common MRI findings in patients with a
focal MCD.
27
Periventricular nodular heterotopia is a malforma-
tion of cortical development characterized by single or
multiple nodules of gray matter along the external walls
of the lateral ventricles.
12
Those nodules usually bulge
into the ventricle and may be multiple, bilateral, or
unilateral. MRI findings of FCD include focal cortical
thickening, alterations in the sulci and gyri patterns,
blurred boundaries between gray-matter and white-
matter transition, and T2-signal elongation of the
subcortical white matter that tapers toward the ventri-
cle.
3,5
MRI findings of the pachygyria-polymicrogyria
(incomplete lissencephaly) include figure-of-8 brain mor-
phology, vertical shallow sylvian fissures, and a smooth
brain with a thick cortex.
28
Polymicrogyria can be seen as
an irregular cortical surface: a small, fine, undulating
cortex with normal thickness in patients younger than
12 months; a thick bumpy cortex in patients older than
12 months; and an indistinct cortical-white-matter junc-
tion.
28
Lissencephaly type 1 appears as a distinct gray-
white matter boundary or an ‘‘hour-glass’’ configuration
of the brain on the results of Tl-weighted and T2-
weighted MRI. Periventricular and subcortical white
matter calcification can be seen in patients with cyto-
megalovirus-related lissencephaly on T2-weighted gradi-
ent echo MRI.
28
Schizencephaly is seen as an infolding of
the gray matter, which may be nodular, pachygyric or
polygyric, along the transmantle clefts. Heterotopia or an
absence or partially deficient septum pellucidum may be
associated findings.
28
Because problems of connectivity may be important
in the clinical outcome of patients with epilepsy, diffusion
tensor imaging and white matter tractography are helpful
new tools for the assessment of brain connectivity via
high-field MRI.
29
It has been suggested that using voxel-
based morphometry to perform automated analysis of
MRI scans can reveal cortical abnormalities overlooked
during visual inspection.
5
Patients with MCD represent a heterogeneous
group, most of these patients present with epilepsy at
different age of onset. Greater knowledge about the
genetic basis of MCDs and the mechanisms of brain
development has resulted in a continual improvement of
the treatment of MCDs. MRI studies of the brain reveal a
wide spectrum of findings that represent different imaging
features of MCDs. With the progressive improvement of
MRI techniques, MCDs are being seen in vivo with
increasing frequency in patients with epilepsy, and
certain types of epilepsy previously considered crypto-
genetic are now recognized as being associated
with MCDs. More comprehensive and detailed MRI
characterization and determining the exact location of
these lesions can help in presurgical evaluations and in
modifying the surgical interventions that will improve the
patient’s prognosis.
CONCLUSIONS
The most common forms of MCD are heterotopia
and FCD. Patients with an MCD tend to have a higher
incidence of epilepsy, developmental delays, and neuro-
logic deficits. Some patients with an MCD also exhibit
other malformations of the brain, such as callosal
agenesia, cerebellar hypoplasia, or mega cisterna magna,
and most patients with heterotopia have other malforma-
tions of cortical dysplasia.
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