2. Diffusion-tensor magnetic resonance (MR) imaging
(DTI) and fiber tractography (FT) - new methods to
demonstrate the orientation and integrity of white matter
fibers in vivo
Developmental central nervous system (CNS) diseases,
both congenital and postnatal, can be a spotlighted field of
DTI due to the potential for generating a fiber pathway and
aberrant connections in the case of a blockage of normal
white matter formation
Axonal damage caused by a chronic infarct or motor
neuron disease , a direct insult to axonal fibers such as
multiple sclerosis or acute disseminated encephalomyelitis
3. single-shot spinecho echo-planar imaging (EPI) and parallel
imaging techniques to achieve motion-free and higher signal-to-
noise ratio (SNR) DTI
The total imaging time for DTI and FT was 7–9 minutes
according to the section numbers, which was added to the routine
MR imaging examinations.
six-channel sensitivity encoding (SENSE) head coil
4. Anisotropy was calculated by using orientation-
independent fractional anisotropy (FA), and diffusion-
tensor MR imagingbased color maps were created from
the FA values and the three vector elements.
The vector maps were assigned to
red (x element, left-right),
green (y, anterior-posterior), and
blue (z, superior-inferior) with a proportional intensity
scale according to the FA.
6. Connects cortex with other areas of brain such as deep
nuclei, cerebellum, spine
Efferent or afferent tracts
CORTICOSPINAL TRACT
CORTICOPONTINE TRACTS
CORTICOBULBAR TRACT
MEDIAL LEMNISCUS
OPTIC RADIATION/ GENICULOCALCARINE
TRACT
7. FT image of the corticospinal tract (left) is generated from the fibers connecting two ROIs in the
longitudinal pontine fibers and the posterior limb of the internal capsule (right).
8. Intrahemispheric connections
1. Long range fibres and
2. Short range U fibres
ARCUATE FASCICULUS- connect frontal parietal
temporal lobes
SUPERIOR AND INFERIOR FRONTO-OCCIPITAL
FASCICULI
CINGULUM
UNCINATE FASCICULUS- orbitofrontal cortex to anterior
temporal lobes
SUPERIOR AND INFERIOR LONGITUDINAL
FASCICULI
9.
10. Cross the midline connecting same cortical area in
opposite hemispheres
CORPUS CALLOSUM
ANTERIOR COMMISSURE
HIPPOCAMPAL COMMISSURE
HABENULAR COMISSURE
POSTERIOR COMMISSURE
11. FT images of the
corpus callosum (left
and bottom right) are
generated from a
single ROI at the
precise anatomic
locations on the
sagittal color map (top
right).
12. FT image of the
middle cerebellar
peduncles (left) is
generated from single
ROIs on the coronal
view (right). These
fiber tracts form a
midline crossing by
means of the red
transverse pontine
fibers (thick arrow),
and some extend to
cortical connections
superiorly (thin
arrows).
13. FT images of
the superior
(yellow) and
inferior (blue)
cerebellar
peduncles (left
and bottom
right) are
generated from
single ROIs on
axial color
maps (top
right). RAO
right anterior
oblique.
14. Between 8 and 20 weeks gestation, the corpus callosum
is formed by development of the callosal precursors and
the fibers from the hemispheric cortex.
These callosal precursors secrete the chemoattractant
axonin-1 to guide the developing axons across the midline
.
Therefore, each region of the hemispheric fibers is
connected to the contralateral side through the corpus
callosum.
15. Agenesis of the corpus callosum (ACC) is characterized
by typical MR imaging findings such as a “cartwheel
configuration” of the interhemispheric sulcal markings,
absence of the cingulate gyrus, and colpocephalic features
of the lateral ventricles.
At DTI-FT, fibers from the hemispheric cortex fail to
cross the midline and form a thick bundle running
anteroposteriorly (ie, the Probst bundle) .
16.
17.
18.
19. Prenatally diagnosed ACC in a newborn girl. (a) Midline sagittal MR
image shows absence of the corpus callosum and cingulate gyrus
and a radial configuration of the sulcal markings (arrows). (b) FT
image shows a thickened bundle of anteroposteriorly running fibers
(green andblue fibers), which is the Probst bundle. Note the normal
corticospinal tract (yellow fibers).
20.
21. The corpus callosum develops from the genu portion
followed by the body, the splenium, and lastly the rostrum.
Therefore, the posterior part or rostrum is hypoplastic in the
case of partial ACC.
A high FAvalue and strong fiber connection through the
remaining portion of the corpus callosum are demonstrated in
partial ACC.
The white matter fibers from the parieto-occipital lobe form a
back-to-front bundle and enter into the remaining genu
portion. Fibers from the frontal lobe also join the connection
through a partially formed corpus callosum, forming an H-
shaped configuration of hemispheric fibers on axial views
22. Partial ACC in a 9-year-old boy with seizure disorder. (a) Axial inversion-recovery image
shows partial ACC with a remaining genu portion and colpocephalic configuration of the
lateral ventricles (arrows). (b) FT image shows anteroposteriorly running Probst bundles
(green fibers) (arrowheads). These converge into the small remaining genu portion (arrow),
which connects fibers from not only the frontal lobe but also from other regions of the brain.
23. HSP manifests as a progressive spastic gait in the second
decade, and dementia, muscle rigidity, and cerebellar
ataxia can occur in combination.
At MR imaging, thinning of the corpus callosum is
demonstrated, particularly of the anterior part, which
suggests prgressive atrophy after the complete formation
of the corpus callosum.
At DTIandFT,the decreased fibers through the anterior
part of the corpus callosum are demonstrated with intact
splenial fibers
24. a) Sagittal T1-weighted MR image shows thinning of the genu and
anterior body of the corpus callosum (arrows). (b) FT image shows loss
of the callosal fibers through the genu and anterior body (arrows),
whereas the fibers through the rostrum, splenium, and posterior body are
normal. Note that the corticospinal tract is normal (arrowheads) even
though the patient has spastic motor dysfunction.
25. In the developing brain, neuronal migration occurs from
the ependymal portion to the cortex by means of a radial
growth pattern with the guidance of the radial glial fiber
system .
In a premature brain, a highly anisotropic cortical ribbon
appears, which reflects the directivity of neuronal
migration
29. Evaluation of the gray matter with DTI is not of great
value because of the low FA of the gray matter and a
partial volume effect by cerebrospinal fluid in the sulcus.
Hence, DTI and Ft can be used to evaluate the integrity
of the white matter adjacent to the dysplastic cortex.
DTI and FT allow perfect visualization of decreased FA
around the corticomedullary junction and fiber
connection between deep white matter and dysplastic
cortex in comparison with the normal contralateral side.
In the case of severely dysplastic white matter, an
aberrant course of the underlying white matter tract can
be detected with DTI-FT
30. Axial T2-weighted MR image
shows slightly increased
signal intensity in the white
matter of the left temporo-
occipital lobe with blurring of
corticomedullary
differentiation (arrows). (b)
Interictal axial single photon
emission computed
tomographic (SPECT) scan
shows decreased perfusion in
the abnormal area (arrows)
31. Ictal axial SPECT scan shows
increased perfusion in the same
area (arrowheads). (d) Axial FT
image, generated from an ROI in
the posterior part of the corona
radiata and the inferior
longitudinal fasciculus, shows
decreased fiber connections
around the subcortex of the
affected temporo-occipital lobe
(arrowheads) compared with the
branching pattern of the normal
contralateral occipital cortex.
32. Axial T2weighted MR images show a thickened
and dysplastic cortex (left) with signal intensity
changes in the underlying white matter
33. Axial FA map shows decreased anisotropy in the
affected white matter (arrows); the gray matter change
could not be adequately evaluated
34. Axial functional MR images of the brain show that the
region activated by movement of the left hand (bottom) is
displaced inferiorly and laterally in comparison with the
region activated by movement of the normal contralateral
side (top)
35. FT image shows a curved course of the corticospinal tract
along the inferior margin of the dysplastic white matter, an
appearance that matches the findings on the functional MR
images.
36. In the case of heterotopic gray matter in the white
matter, the arrested neurons exist in the white matter
bundles and might have some degree of directivity like
the normal white matter tracts and show increased
anisotropy.
Gray matter in the white matter, that is, nodular or band
heterotopia, showed a higher anisotropic value compared
to the normal cortex with statistical significance
37. subependymal nodules of gray matter (GM) line the
lateral walls of the ventricles
Nodules of PVNH follow GM in density/signal
intensity and do not enhance following contrast
administration
38. Axial T2WI in a patient with corpus callosum agenesis shows multiple nodules of
subependymal heterotopic gray matter st. Cortex shows perisylvian areas of
pachy- and polymicrogyria . (37-33B) More cephalad image in the same patient
shows additional foci of subependymal heterotopic GM st and cortical dysplasia
.
39. malformations in which large, focal, mass-like
collections of neurons are found in the deep cerebral
white matter anywhere from the ependyma to the
cortex .
The involved portion of the affected hemisphere is
abnormally small, and the overlying cortex appears thin
and sometimes dysplastic
Occasionally ribbon-like bands of heterotopic GM
(subcortical band heterotopia) form partway between
the lateral ventricles and cortex
41. Axial FA map
shows that
heterotopic
gray matter has
high anisotropy,
a finding
suggestive of its
radial
orientation and
of arrested
neuronal
migration.
42. d) FT image
obtained in a norm
child shows norma
subcortical U-fibe
(arrows) and fiber
connectivity
between the deep
white matter and t
cortex.
43. c) FT image shows
failure of the normal
connection between
the deep white
matter and the
cortex and absence
of cortico-cortical
connections
(arrows). cc corpus
callosum, cst
corticospinal tract.
44. The most commoncause of childhood cerebral palsy is
hypoxic brain injury and periventricular leukomalacia
(PVL) in premature births
45. From the middle of the third trimester of pregnancy through the
40th postconceptional week, the dorsal brainstem, thalami, basal
ganglia, and perirolandic cortex exhibit high metabolic activity.
As a rule, in the setting of mild to moderate HII, blood is shunted
to preserve flow to the basal ganglia, thalami, brainstem, and
cerebellum.
Damage is reflected in the interarterial (watershed) boundary or
border zones and cerebral cortex
severe or profound HII, the injury pattern is global with injury to
the deep nuclei (thalami and globi pallidi) posterior brainstem,
hippocampi, superior cerebellar vermis, and sensorimotor regions
of the cerebral cortex.
In the 2nd trimester ischemic injury leads to liquefaction and in
the third trimester leads to astrogliosis.
46. Severe HII affects mostly thalami;
less severe HII causes GMH, IVH, PVL, and cerebellar
injury
Oligodendrocyte precursor cells vulnerable;
periventricular, near trigones and frontal horns 2/3 have
coexisting hemorrhages (GMH-IVH)
Early on US: periventricular hyperechoic "flares"
Subacute: ± cysts, then resolve → gliosis, ventricular
dilation
47. Coronal US of grade I germinal matrix hemorrhage (GMH) in a 33-week preterm
newborn at 5 days of age shows an expansile hyperechoic germinal matrix
hemorrhage at the left caudothalamic groove st. (8-67B) Sagittal US shows grade
I GMH. Focal hemorrhage is demonstrated at the caudothalamic groove st, which
represents the location of the greatest aggregation of germinal matrix tissue.
48. Linear hyperechoic foci within frontl and temporal horns
Sag plane shows clot within lv and seen approaching
choroid plexus
49. Coronal US shows grade III GMH. Clot fills, distends the lateral ventriclesSagittal
US shows grade III GMH. Posterior fontanelle US shows distending clot within
lateral ventricle. Clot is encompassing the choroid plexus within the trigone . The
posterior fontanelle approach to US allows clear visualization of the lateral ventricle
and trigonal regions.
50. Axial graphic depicts profound, severe, or central HII in a term infant with preferential
involvement of the posterior putamina and ventrolateral thalami . (8-78B) Axial
NECT in acute profound HII demonstrates loss of the normal GM attenuation of basal
ganglia st and thalami st. This image shows diffuse loss of GM/WM discrimination and
ventricular and sulcal effacement from cerebral edema.
51. Axial T2WI in a term newborn with total or
diffuse HII shows peripheral edema (reversal
sign) and patchy thalamic edema. T2WI
underestimates HII changes.
52. Coronal cranial US in acutely asphyxiated term newborn shows diffuse "salt and
pepper" pattern of heterogeneous echogenicity and lateral ventricular
compression secondary to diffuse cerebral edema. NECT shows term neonate
with total or diffuse pattern of HII and loss of central and peripheral GM/WM
differentiation. Lateral ventricles are compressed, prominent normal torcula st
due to surrounding edema.
53. Axial T2WI
shows the same
patient, 6
months
following
diffuse or total
HII event.
Multicystic
encephalomalaci
a and patchy
thalamic
hyperintensity st
are shown.
54. In PVL, with either spastic quadriplegia or diplegia,
severe atrophy of the periventricular fibers is
demonstrated at DTI and FT due to previous germinal
matrix hemorrhage.
The corticospinal tract is usually normal, and sensory
fibers are decreased
The connecting fibers between the thalamus and
parietal cortex, the posterior thalamic radiations, are
also absent.
Thinning of the corpus callosum due to volume loss of
periventricular white matter (PVWM)canbeobserved.
The severity of spasticity (diplegic vs quadriplegic) is
not well correlated with the degree of PVWM volume
loss, but In hemiplegic, the motor dysfunction is well
correlated with the DTI and FT findings.
55. Axial T2-weighted
MR image shows
loss of
periventricular
white matter and
dilatation of the
lateral ventricle,
findings typical of
periventricular
leukomalacia.
56. (b) Lateral FT image
shows thinning of
sensory fiber tracts
(sf) and absence of
posterior thalamic
radiations. All fibers
to and from the
thalamus were
generated from the
left thalamus (th)
(pink area). The
corticospinal tract is
normal.
57. (c) Lateral FT
image obtained in
a normal child
shows the fibers
connected to the
thalamus (th).
Note the abundant
f iber bundles
from the thalamus
to the parieto-
occipital lobe,
posterior thalamic
radiations (ptr),
and sensory fibers
(sf) in comparison
with the findings
in periventricular
leukomalacia seen
in b.
58. Axial T2weighted MR image obtained at the level of
the basal ganglia shows changes of cerebromalacia
in the left internal capsule, thalamus, and putamen.
Axial magnified MR image of the mid pons shows
no abnormalities
59. Axial color-coded vector map shows decreased volume of the left
corticospinal tract as a faint blue area on the left side of the pons
(arrow). (d) Axial color-coded vector map obtained in an age-
matched control subject shows a symmetrical configuration of the
corticospinal tract (cst) and other major fibers passing through
the pons. mcp middle cerebellar peduncle, ml medial lemniscus,
tpf transverse pontine fibers.
61. Posterior fossa malformations such as ArnoldChiari syndrome
or Dandy-Walker malformation did not show remarkable
findings at DTI and FT.
Joubert syndrome is a subtype of posterior fossa malformation
and consists of vermian hypoplasia and derangement of the
cerebellar-brainstem connections or cerebellocortical
connections.
At MRimaging, the typical “molar tooth appearance” of the
superior cerebellar peduncle (SCP) is diagnostic, and partial or
complete absence of the vermis is demonstrated.
At DTI and FT, a thickened and elongated SCP with a
horizontal configuration can be seen and corticospinal tracts
fail to cross in the caudal medulla.
62. Anomalies of the kidneys, eyes, extremities, liver, and bile
ducts are common in the JSRD spectrum.
Six major JSRD phenotypic subgroups are recognized:
1. pure JS,
2. JS with ocular defect,
3. JS with renal defect,
4. JS with oculo-renal defects,
5. JS with hepatic defect, and
6. JS with oro-facio-digital defects.
COACH syndrome consists of cerebellar vermis
hypoplasia, oligophrenia, ataxia, ocular coloboma, and
hepatic fibrosis.
63. Axial graphic shows Joubert malformation. Thickened superior cerebellar
peduncles around an elongated 4th ventricle form the classic "molar tooth"
sign. Note cleft cerebellar vermis . (3647) Autopsy specimen of JSRD shows
foreshortened midbrain with narrowed isthmus , thick superior cerebellar
peduncles , "bat wing" 4th ventricle , and clefted superior vermis .
64. Sagittal T2WI in a patient with classic Joubert shows small misshapen
vermis , upwardly convex superior fourth ventricle , and rounded
enlarged fastigial point
Axial scan in the same patient shows "molar tooth" sign, foreshortened
midbrain with narrow isthmus st, thick superior cerebellar peduncles
surrounding an elongated fourth ventricle, and disorganized cleft
vermis
65. a) Axial T2weighted MR image shows a “molar tooth” appearance of the SCP (arrows)
and vermian hypoplasia, which are the typical findings of Joubert syndrome. (b) Axial
FA (left) and color vector (right) maps show high anisotropy and an anteroposterior
direction (green area) of the SCP with thickening (arrowheads). (c) FT image shows an
elongated SCP(arrowheads) with a strong connection from the cerebellum to both the
sensory and motor cortices (arrow). cst corticospinal tract.
66. FT image obtained in a normal age-matched
control subject shows normal volume of the SCP
and normal cortical connections compared with
those in Joubert syndrome seen in the 1st image
67. DTI-FT is a powerful anatomic imaging tool that can
demonstrate the gross fiber architecture but not the
functional or synaptic connection
the fiber tracking technique is quite operator dependent,
and the operator should have a detailed knowledge of the
neuroanatomy. The standard ROI location and placement
of the adequate threshold value for fiber tracking are
essential for achieving an objective and uniform fiber
tracking result
Editor's Notes
CORTICOPONTINE FIBRES: arise from all areas of cerebral cortex like frontopontine, parietopontine, occipitopontine, and temporopontine fibres
Carry info from cortex to ipsilateral pons and then via mcp into cerebellum
CORTICO BUBAR: Carries umn input to motor nuclei of 5,7,9,10,11,12 cranial nerves
ML: 2ND order neurons which carry sensory spinothalamic info
OR: runs from LGB to occipital lobe and carries visual input from retina on to occipital cortex
