This document summarizes various pediatric white matter diseases seen on imaging. It begins by describing normal myelination patterns in the neonatal brain. It then divides white matter diseases into dysmyelinating, demyelinating, and hypomyelinating categories. Several specific diseases are described in detail, including their characteristic imaging findings. Metachromatic leukodystrophy, Krabbe disease, mucopolysaccharidoses, peroxisomal disorders, adrenoleukodystrophy, Zellweger syndrome, and mitochondrial diseases like MELAS are discussed. Common imaging patterns include abnormal white matter signal, involvement of specific tracts, sparing of U-fibers, and enhancement patterns.
Its important to recognise the myelination pattern in neonates and infants. This presentation talks about the myelination pattern and imaging of white matter diseases in children.
Its important to recognise the myelination pattern in neonates and infants. This presentation talks about the myelination pattern and imaging of white matter diseases in children.
Neuroradiology in multiple sclerosis
MRI in diagnosis of MS
MRI in D.D. of MS
MRI in monitoring disease progression and response to DMT
New imaging techniques
In this presentation, i have explained different modalities available for radiological evaluation of cns tumors. How to approach to a radiographic image and how to approach to a patient of cns tumors radiologically.
MRI in evaluation of white matter diseases like multiple sclerosis, leukodystrophies, demyelination, dysmyelination, ADEM, leukoencephalopathies, van der knaap disease, ALD, MLD, Krabbes disease, Leighs disease, Vanishing white matter disease, Canavan disease, Alexander disease
Radiology Spotters collection by Dr Pradeep. Nice collection Radiology spotters mixed collection ppt made by or collected by Dr. Pradeep, this is a collection of confusing spotter and very important spotter commonly asked in exams, our references is radiopaedia, learning radiology and Aunt Minnie.. Thanks
Neuroradiology in multiple sclerosis
MRI in diagnosis of MS
MRI in D.D. of MS
MRI in monitoring disease progression and response to DMT
New imaging techniques
In this presentation, i have explained different modalities available for radiological evaluation of cns tumors. How to approach to a radiographic image and how to approach to a patient of cns tumors radiologically.
MRI in evaluation of white matter diseases like multiple sclerosis, leukodystrophies, demyelination, dysmyelination, ADEM, leukoencephalopathies, van der knaap disease, ALD, MLD, Krabbes disease, Leighs disease, Vanishing white matter disease, Canavan disease, Alexander disease
Radiology Spotters collection by Dr Pradeep. Nice collection Radiology spotters mixed collection ppt made by or collected by Dr. Pradeep, this is a collection of confusing spotter and very important spotter commonly asked in exams, our references is radiopaedia, learning radiology and Aunt Minnie.. Thanks
Diffuse astrocytomas, also referred to as low-grade infiltrative astrocytomas, are designated as WHO II tumours of the brain.
The term diffuse infiltrating means there is no identifiable border between the tumour and normal brain tissue, even though the borders may appear well-marginated on imaging.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
The increased availability of biomedical data, particularly in the public domain, offers the opportunity to better understand human health and to develop effective therapeutics for a wide range of unmet medical needs. However, data scientists remain stymied by the fact that data remain hard to find and to productively reuse because data and their metadata i) are wholly inaccessible, ii) are in non-standard or incompatible representations, iii) do not conform to community standards, and iv) have unclear or highly restricted terms and conditions that preclude legitimate reuse. These limitations require a rethink on data can be made machine and AI-ready - the key motivation behind the FAIR Guiding Principles. Concurrently, while recent efforts have explored the use of deep learning to fuse disparate data into predictive models for a wide range of biomedical applications, these models often fail even when the correct answer is already known, and fail to explain individual predictions in terms that data scientists can appreciate. These limitations suggest that new methods to produce practical artificial intelligence are still needed.
In this talk, I will discuss our work in (1) building an integrative knowledge infrastructure to prepare FAIR and "AI-ready" data and services along with (2) neurosymbolic AI methods to improve the quality of predictions and to generate plausible explanations. Attention is given to standards, platforms, and methods to wrangle knowledge into simple, but effective semantic and latent representations, and to make these available into standards-compliant and discoverable interfaces that can be used in model building, validation, and explanation. Our work, and those of others in the field, creates a baseline for building trustworthy and easy to deploy AI models in biomedicine.
Bio
Dr. Michel Dumontier is the Distinguished Professor of Data Science at Maastricht University, founder and executive director of the Institute of Data Science, and co-founder of the FAIR (Findable, Accessible, Interoperable and Reusable) data principles. His research explores socio-technological approaches for responsible discovery science, which includes collaborative multi-modal knowledge graphs, privacy-preserving distributed data mining, and AI methods for drug discovery and personalized medicine. His work is supported through the Dutch National Research Agenda, the Netherlands Organisation for Scientific Research, Horizon Europe, the European Open Science Cloud, the US National Institutes of Health, and a Marie-Curie Innovative Training Network. He is the editor-in-chief for the journal Data Science and is internationally recognized for his contributions in bioinformatics, biomedical informatics, and semantic technologies including ontologies and linked data.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
3. NORMAL MYELINATION
After normal myelination in utero, myelination of the neonatal brain is far from complete.
It does not reach maturity until 2 years or so. It correlates very closely to developmental milestones .
The progression of myelination is predictable and abides by a few simple general rules; myelination progresses
from:
1. central to peripheral
2. caudal to rostral
3. dorsal to ventral
4. sensory then motor
4.
5. White matter diseases are traditionally divided into two
categories:
• Dysmyelinating diseases
• Demyelinating diseases
• Hypomyelinating diseases
Dysmyelinating diseases - also known as leukodystrophies, result
from an inherited enzyme deficiency that causes abnormal
formation, destruction, or turnover of myelin.
Demyelinating diseases - involve destruction of intrinsically
normal myelin.
Hypomyelinating diseases - the WM may partially myelinate but
never myelinates completely.
8. TYPES
1. late infantile,
2. juvenile, and
3. adult.
• The most common type is late infantile metachromatic leukodystrophy, in
children between 12 and 18 months of age and is characterized by motor signs of
peripheral neuropathy followed by deterioration in intellect, speech, and
coordination.
• Within 2 years of onset, gait disturbance, quadriplegia, blindness, and decerebrate
posturing may be seen. Death occurs 6 months to 4 years after onset of symptoms
9.
10. Imaging Features:
• At T2-weighted MR imaging, metachromatic leukodystrophy manifests as
symmetric confluent areas of high signal intensity in the periventricular white
matter with sparing of the subcortical U fibers .
• Islands of normal myelin around medullary veins in the WM may produce a
striking "tiger" or "leopard" pattern with linear hypointensities in a sea of
confluent hyperintensity. No enhancement is seen on T1 C+.
• The corpus callosum, internal capsule, and corticospinal tracts are also frequently
involved.
• The cerebellar white matter may appear hyperintense at T2-weighted MR
imaging.
11. Metachromatic leukodystrophy. (a) T2-weighted MR image demonstrates bilateral
confluent areas of high signal intensity in the periventricular white matter. Note
the classic sparing of the sub-cortical U fibers (arrowheads). (b) Contrast material–
enhanced MR image shows lack of enhancement in the demyelinated white
matter, a finding that is characteristic of metachromatic leukodystrophy.
12.
13. Metachromatic leukodystrophy. (a) T2-weighted MR image shows numerous linear tubular
structures with low signal intensity in a radiating (“tigroid”) pattern within the demyelinated
deep white matter. (b) T2-weighted MR image shows a punctate (leopard skin) pat-tern in
the demyelinated centrum semiovale, a finding that suggests sparing of perivascular white
matter. (c) On a contrast-enhanced T1-weighted MR image, the tigroid pattern seen in a
appears as numerous punctate foci of enhancement (arrows) within the demyelinated white
matter, which is unenhanced and has low signal intensity (leopard skin pattern).
14. Metachromatic leukodystrophy with involvement of the corticospinal tract.
T2-weighted MR image shows bilateral high-signal-intensity areas in the periventricular white matter with posterior
predominance. The corpus callosum is also involved (arrows).
T2-weighted MR image obtained at a lower level shows involvement of the descending pyramidal tracts of the medulla
(arrows) and deep cerebellar white matter.
15. Krabbe Disease:
An autosomal recessive disorder caused by a deficiency of
galactocerebroside -galactosidase, an enzyme that degrades
cerebroside, a normal constituent of myelin. .
The diagnosis is made by demonstrating a deficiency of the enzyme in
peripheral blood leukocytes.
16. Clinical presentation:
• Infantile, late infantile, juvenile, and adult forms are recognized.
• The infantile form is the most common and manifests as hyperirritability,
increased muscle tone, fever, and developmental arrest and regression.
• Disease progression is characterized by cognitive decline, myoclonus and
opisthotonus, and nystagmus.
• Typically, Krabbe disease is rapidly progressive and fatal.
17. CT brain:
• CT performed during the initial
stage of the disease may
demonstrate symmetric high-
attenuation foci in the thalami,
caudate nuclei, corona radiata,
posterior limbs of the internal
capsule, and brainstem.
19. Krabbe Disease:CT findings in a 4-month-old boy with early-infantile GLD.The series
demonstrates the hyperdensities in the primary myelination zones: brain stem,cerebellum, posterior
limb of the internal capsule, thalamus, and central part of the corona radiata. At this stage the CT
appearance is almost diagnostic, and more characteristic than the MRI findings.
20.
21. Axial T2 weighted images show bilateral parietal, occipital, deep gray matter and
cerebellar white matter hyperintensities with spared subcortical white matter.
22. Mucopolysaccharidosis:
A deficiency of the various lysosomal enzymes involved in the
degradation of glycosaminoglycans.
• Brain imaging is usually performed when hydrocephalus or spinal
cord compression is suspected.
• CT and MR imaging usually reveal delayed myelination, atrophy,
varying degrees of hydrocephalus, and white matter changes.
• As the disease progresses, the lesions become larger and more
diffuse, reflecting the development of infarcts and demyelination.
23. • The major features of
Mucopolysacchroidosis are
• Macrocephaly,
• Enlarged perivascular spaces, A striking
sieve-like cribriform appearance in the
posterior cerebral WM.
• Pachymeningopathy.
25. A patient with MPS II at 21 years of age,
Brain T2-weighted axial MR image demonstrating WM, mainly
found in the retrotrigonal area of the brain, and cribriform
changes in both periventricular and subcortical white matter.
Note also the enlarged ventricles and cortical sulci in the
frontal lobe.
28. • The subcortical white matter is relatively spared in the early stage but often becomes involved in the later
stages.
• The affected cerebral white matter typically has three different zones.
The central or inner zone appears moderately hypointense at T1-weighted MR imaging and
markedly hyperintense at T2-weighted imaging. This zone corresponds to irreversible gliosis and
scarring.
The intermediate zone represents active inflammation and breakdown in the blood-brain barrier. At
T2-weighted MR imaging, this zone may appear isointense or slightly hypointense and readily
enhances after intravenous administration of contrast material .
The peripheral or outer zone represents the leading edge of active demyelination; it appears
moderately hyperintense at T2-weighted MR imaging and demonstrates no enhancement .
• Atypical cases with unilateral or predominantly frontal lobe involvement may occur .
29.
30. NECT scans demonstrate
hypodensity in the corpus
callosum splenium and WM
around the atria and occipital
horns of the lateral ventricles.
Calcification in the affected WM
is common.
33. ALD with preferential involvement of the internal capsule,descending
pyramidal tract,cerebellar white matter,(a.b)
C. Bilateral enhancement of internal capsule.
34. Atypical ALD
T2-weighted MR image shows
involvement predominantly of the
frontal lobe white matter, genu of the
corpus callosum, and anterior limbs of
the internal capsule (arrows).
Gadolinium-enhanced T1-weighted MR
image shows linear enhancement within
the involved white matter and the
anterior limbs of the internal capsule
(arrows).
35. Zellweger Syndrome
Zellweger syndrome, or cerebrohepatorenal syndrome, is an autosomal recessive disorder caused
by multiple enzyme defects and characterized by liver dysfunction with jaundice, marked
mental retardation, weakness, hypotonia, and craniofacial dysmorphism .
It may lead to death in early childhood. The severity of disease varies and is determined by the
degree of peroxisomal activity.
MR imaging : diffuse demyelination with abnormal gyration that is most severe in the
perisylvian region. The pattern of gyral abnormality is similar to that seen in
polymicrogyria or pachygyria. Subependymal germinolytic cysts are common finding.
36. Zellweger syndrome in a 5-month-old girl
T2-weighted MR image shows extensive areas of diffuse high signal intensity in the white
matter. The gyri are broad, the sulci are shallow, and there is incomplete branching of the
subcortical white matter, findings that suggest a migration anomaly with pachygyria.
On a T1-weighted MR image, the white matter abnormalities demonstrate low signal
intensity
39. MELAS Syndrome
(mitochondrial encephalopathy with lactic acidosis and stroke-like
episodes)
• Patients with MELAS syndrome usually appear healthy at birth with normal early development, then
exhibit delayed growth, episodic vomiting, seizures, and recurrent cerebral injuries resembling
stroke.
• These stroke like events may give rise to either permanent or reversible deficits.
40. Multiple infarcts involving multiple vascular territories.
Atrophy
MRI
chronic infarcts
• involving multiple vascular territories
• may be either symmetrical or asymmetrical
• parieto-occipital and parieto-temporal (most common)
acute infarcts
• swollen gyri with increased T2 signal
• subcortical white matter involved
• increased signal on DWI (T2 shine through) with little if any change on ADC: thought to
represent vasogenic rather than cytotoxic oedema 3
42. Sequential MR images of a female patient with MELAS at ages 8 and 13 years.
A, T2-weighted coronal image during an acute stroke like episode shows parasagittal bilateral
hyperintense lesions (arrows) at the age of 8 years.
B, T2-weighted coronal image 2 months later shows that lesions have almost entirely resolved.
Cerebellar atrophy is evident.
C, T2-weighted axial image 5 years later, during a prolonged seizure, shows a new hyperintense
lesion in the left parietooccipital region (arrow).
43. Leighs Disease
• Leigh disease, or subacute necrotizing encephalomyelopathy, is an inherited, progressive,
neurodegenerative disease of infancy or early childhood with variable course and prognosis .
• Affected infants and children typically present with hypotonia, psychomotor deterioration, ataxia,
ophthalmoplegia, ptosis, dystonia, and swallowing difficulties.
Typical MR imaging findings include symmetric putaminal involvement, which may be
associated with abnormalities of the caudate nuclei, globus pallidi, thalami, and brainstem and, less
frequently, of the cerebral cortex (Fig 13).
The cerebral white matter is rarely affected.
Enhancement may be seen at MR imaging and may correspond to the onset of acute necrosis.
44. • Leighs disease show
hypodensities in bilateral
putamens and globus pallidus.
47. Canavan Disease
Canavan disease, or spongiform leukodystrophy, is an autosomal recessive disorder
caused by a deficiency of N-acetylaspartylase, which results in an accumulation of N-
acetylaspartic acid in the urine, plasma, and brain.
It usually manifests in early infancy as hypotonia followed by spasticity, cortical
blindness, and macrocephaly.
Canavan disease is a rapidly progressive illness with a mean survival time of 3 years.
Definite diagnosis usually requires brain biopsy or autopsy.
48. • T1-weighted MR imaging symmetric areas of homogeneous, diffuse low signal intensity ,
whereas T2-weighted , homogeneous high signal intensity throughout the white matter.
• The subcortical U fibers are preferentially affected early in the course of the disease.
• In rapidly progressive cases, the internal and external capsules are involved, and the cerebellar
white matter is usually affected as well.
• As the disease progresses, atrophy becomes conspicuous.
49. Canavan disease in a 6-month-old boy with macrocephaly
T2-weighted MR image shows extensive high-signal-intensity areas throughout the white
matter, resulting in gyral expansion and cortical thinning. Striking demyelination of the
subcortical U fibers is also noted.
T1-weighted MR image shows demyelinated white matter with low signal intensity.
50. CANAVAN DISEASE
Axial T2 weighted image shows high signal in white matter
typically a diffuse bilateral cerebral involvement and sub
cortical U fibres.
51. Alexander Disease
• Alexander disease, or fibrinoid leukodystrophy, is characterized by massive deposition of Rosenthal
fibers in the subependymal, subpial, and perivascular regions (Fig 16b) (37).
• Three clinical subgroups are recognized.
• The infantile subgroup is characterized by early onset of macrocephaly, psychomotor retardation, and
seizure. Death occurs within 2–3 years. Definite diagnosis usually requires brain biopsy or autopsy.
• In the juvenile subgroup, onset 7 and 14 years of age. Progressive bulbar symptoms with spasticity are
common.
• In the adult subgroup, onset between the 2nd and 7th decades. The symptoms and disease course can
be indistinguishable from those of classic multiple sclerosis in the adult subgroup.
52. • Involvement of frontal lobes and subcortical white matter and hyperintensity at T2w image.
• Enhancement near the tips of the frontal horns early in the disease course
.
• These hyperintense areas progress posteriorly to the parietal white matter and internal and external
capsules .
• In the late stages of the disease, cysts may develop in affected regions of the brain.
68. Conclusions
There are many different white matter diseases, each of which has distinctive features.
MR imaging is highly sensitive in determining the presence and assessing the severity
of underlying white matter abnormalities.
Although the findings are often non-specific, systematic analysis of the finer details of
disease involvement may permit a narrower differential diagnosis, which the clinician
can then further refine with knowledge of patient history, clinical testing, and
metabolic analysis.
MR imaging has also been extensively used to monitor the natural progression of
various white matter disorders and the response to therapy.
T2-weighted MR image shows bilateral high-signal-intensity areas in the periventricular white matter with posterior predominance. The corpus callosum is also involved (arrows).
T2-weighted MR image obtained at a lower level shows involvement of the descending pyramidal tracts of the medulla (arrows) and deep cerebellar white matter.
T1-weighted MR image shows multiple well-defined areas of low signal intensity in the central and subcortical white matter.
T2-weighted MR image demonstrates multiple well-defined areas of high signal intensity in the deep and subcortical white matter.
Brain T2-weighted axial MR image demonstrating WMA, mainly found in the retrotrigonal area of the brain, and cribriform changes in both periventricular and subcortical white matter. Note also the enlarged ventricles and cortical sulci in the frontal lobe.
T2-weighted MR image shows symmetric confluent demyelination in the peritrigonal white matter and the corpus callosum.
On a T1-weighted MR image, the peritrigonal lesions appear hypointense.
Gadolinium-enhanced T1-weighted MR image reveals a characteristic enhancement pattern in the intermediate zone (arrows) representing active demyelination and inflammation.
ALD involving the corpus callosum splenium. T2-weighted MR image shows the corpus callosum splenium with diffuse high signal intensity (arrows). No abnormality of the periventricular white matter is seen.
(a, b) T2-weighted MR images show demyelination of the internal capsule, descending pyramidal tract (arrows in a, long arrows in b), and cerebellar deep white matter (short arrows in b).
(c) Gadolinium-enhanced T1-weighted MR image shows bilateral enhancement of the internal capsule and descending pyramidal tracts (arrows).
T2-weighted MR image shows involvement predominantly of the frontal lobe white matter, genu of the corpus callosum, and anterior limbs of the internal capsule (arrows).
Gadolinium-enhanced T1-weighted MR image shows linear enhancement within the involved white matter and the anterior limbs of the internal capsule (arrows).
T2-weighted MR image shows extensive areas of diffuse high signal intensity in the white matter. The gyri are broad, the sulci are shallow, and there is incomplete branching of the subcortical white matter, findings that suggest a migration anomaly with pachygyria.
On a T1-weighted MR image, the white matter abnormalities demonstrate low signal intensity.
MELAS: mitochondrial encephalopathy with lactic acidosis and stroke-like episodes
Follow-up MR images may show resolution and sub-sequent reappearance of the abnormal areas.
increased signal intensity due to T2 prolongation effects (so-called “T2 shine-through effect”).
Initial T2-weighted MR image shows a high-signal-intensity lesion in the left occipital lobe (arrows). Prominent cortical sulci are seen in the right occipital lobe, a finding that suggests cortical atrophy.
On a contrast-enhanced T1-weighted MR image, the lesion demonstrates no enhancement.
Follow-up MR image obtained 15 months later shows another lesion in the left temporal area (arrowheads).
A, T2-weighted coronal image during an acute stroke like episode shows parasagittal bilateral hyperintense lesions (arrows) at the age of 8 years.
B, T2-weighted coronal image 2 months later shows that lesions have almost entirely resolved. Cerebellar atrophy is evident.
C, T2-weighted axial image 5 years later, during a prolonged seizure, shows a new hyperintense lesion in the left parietooccipital region (arrow).
Leigh disease in a 2-year-old boy.
T2-weighted MR image shows bilateral high-signal-intensity areas in the putamen and globus pallidus (arrows).
On a T1-weighted MR image, the lesions demonstrate low signal intensity (arrows).
T2-weighted MR image shows symmetric demyelination in the frontal lobe white matter. The internal and external capsules and parietal white matter are also involved.
T2 weighted MR image shows symmetric demyelination in frontal lobe white matter.