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Diffuse or patchy T2-hyperintense signal changes in the deep hemispheric and

subcortical white matter are probably the most common abnormal findings on
MRI in the adult and elderly patient population. The terms microvascular ischemic
changes or chronic small vessel disease are frequently used to describe these
lesions on imaging studies. Their etiology and clinical significance have been
debated extensively.

Certain hyperintense signal changes are considered normal incidental findings,


with no clinical relevance. A uniformly thin, linear, T2 hyperintensity that has a
smooth outer border along the border of the body of the lateral ventricles is often
seen in the elderly population and likely represents fluid or gliotic changes in the
subependymal zone. It tends to be more pronounced at the tips of the frontal horns
(ependymitis gran- ularis). This finding is thought potentially to be due to focal
loss of the ependymal lining with gliosis and/or influx of interstitial fluid into
these regions.

Patchy signal changes within the white matter of the cere- bral hemispheres
beyond a relatively low threshold (generally, one white matter hyperintensity per
decade of life is felt to fall within the normal range) are pathological and are most
com- monly of ischemic origin. According to the most accepted hypothesis, these
hyperintensities are the result of gradual narrowing or occlusion of the small
vessels of the white matter, the diameters of which are less than 200 micrometers
(hence the terms microvascular lesions or small vessel disease). Patho- logically,
these lesions are composed of focal demyelination and gliosis. The lumen of the
involved vessels is narrow or occluded; their walls may exhibit arteriosclerotic
changes and commonly amyloid deposits. On imaging studies, they have a chronic
appearance, with diffuse borders and no surrounding edema or evidence of mass
effect. They are generally associ- ated with some degree of central atrophy, which
tends to worsen with higher lesion loads. The distribution of these lesions changes
only very gradually on serial scans, often showing minimal to no significant
difference on studies spaced several years apart.

While age by itself can cause such changes, and the inci- dence of these lesions
increases with age in people 40 years or older, there are several other risk factors
that can make them more numerous. These include hypertension, diabetes, hyper-
cholesterolemia, and smoking. Indeed, patients with these medical problems are
more likely to have an elevated number of ischemic white matter lesions.

Chronic ischemic white matter lesions are hypodense on CT, but MRI is much
more sensitive and reveals more exten- sive lesions (Fig. 33A.38; Fig. 33A.38, B-
C available online only). On MRI, the lesions are hyperintense on T2 and FLAIR
sequences. They may or not be visible as T1 hypointensities. It is possible that
only lesions visible on T1-weighted images may be clinically significant.
Common locations are the peri- ventricular (PV) and more commonly, the deep
white matter, but subcortical lesions are also common, with sparing of the U-
fibers. The lesions can be isolated, scattered, or more con- fluent, especially in the
PV zone. Morphologically, individual lesions generally exhibit indistinct borders
with a diffuse cotton-wool appearance and range in size from punctate to small.
Regions of confluent lesions may appear large and more commonly affect the deep
white matter anterior and posterior to the bodies of the lateral ventricles,
symmetrically within the parietal and frontal lobes. Deep white matter lesions also
often occur in a distribution parallel to the bodies of the lateral ventricles on axial
views, with an irregular band-like or beads- on-string appearance often
separated from the PV lesions by an intervening band of relatively unaffected
white matter. Involvement of the external capsules is also characteristic. These
patterns of lesion distribution and morphology are often best seen on FLAIR.
Contrary to the lesions of multiple sclerosis (MS), microvascular ischemia tends
not to involve the temporal lobes or the corpus callosum. Besides the hemi-
spheric white matter, microvascular ischemic lesions often also involve the basis
pontis.

The clinical significance of ischemic white matter lesions depends on their extent
and location. The presence of a few small, scattered, ischemic white matter lesions
on T2-weighted images is clinically meaningless, and these are usually consid-
ered a normal imaging manifestation of aging. Patients may feel more comfortable
with descriptions such as age spots of the brain to convey their benign nature
when verbally discuss- ing results. More extensive lesions also visible on T1-
weighted sequences, however, are more likely to be associated with neurological
abnormalities such as abnormal gait, dementia, and incontinence. In ischemic
arteriolar encephalopathy or Binswanger disease, there is pronounced, widely
distributed, and confluent PV and deep white matter signal change. In more severe
cases, the confluent hyperintensity also involves the internal and external capsules
or subcortical white matter. Besides confluent lesions, coexisting multiple
scattered T2 hyperintensities are also very common. Ischemic white matter lesions
are often intermixed with lacunar ischemic strokes and generalized cerebral
volume loss is also frequently noted.

Scattered small, nonspecific-appearing, seemingly micro- vascular white matter


hyperintensities have a broader differ- ential diagnosis in the younger patient
population. Multiple small T2 hyperintense lesions in the hemispheric white
matter can be caused by migraine, trauma, inborn errors of metabo- lism,
vasculitis (including Sjgren syndrome, lupus, Behet disease, and primary CNS
vasculitis), Lyme disease, and MS. Since the MRI appearance of these is
nonspecific, clinical cor- relation is always warranted. In many instances, these
white matter lesions are idiopathic, and future serial imaging studies are needed
for follow-up.
Fig. 33A.38 Microvascular ischemic white matter changes. A, Axial FLAIR image reveals
extensive hyperintense areas in the hemispheric white matter bilaterally. Some are confluent at
the borders of the ventricles, others are scattered in other regions. Note the band of
hyperintensity in the left hemisphere parallel to the border of the lateral ventricle. B-C, On axial
FLAIR and T2-weighted images, faint hyperintense signal changes are seen in the pontine
tegmentum bilaterally, exhibiting the typical imaging appearance of microvascular ischemia
(arrows) (for images, see online version of this chapter).
Perubahan sinyal hiperintens T2 diffus atau patchy pada substansia alba
subkortikal dan hemisfer dalam adalah temuan abnormal paling sering pada MRI
populasi pasien dewasa dan usia lanjut. Istilah perubahan iskemik mikrovaskular
atau penyakit pembuluh darah kecil kronik sering digunakan untuk
mendeskripsikan lesi ini pada studi pencitraan. Etiologi dan signifikansi klinis
telah didebatkan secara luas.

Perubahan sinyal hiperintens dianggap sebagai penemuan insidental normal, tanpa


relevansi klinis. Hiperintens T2, tipis, linier yang memiliki batas luar yang halus
sepanjang perbatasan badan ventrikel lateralis sering terlihat pada populasi usia
lanjut dan mungkin merupakan perubahan cairan atau gliotik pada zona
subependimal. Hal ini terlihat lebih jelas pada ujung kornu frontal (granularis
ependimititis). Temuan ini terjadi karena hilangnya fokus lapisan ependim dengan
gliosis dan atau masuknya cairan interstitial ke daerah ini.

Menurut hipotesis yang paling diterima, hiperintensitas terjadi karena penyempitan


bertahap atau oklusi dari pembuluh darah kecil substansia alba , diameter kurang
dari 200 mikrometer (istilah lesi mikrovaskular atau pembuluh darah kecil). Secara
patologi, lesi ini terdiri dari demyelinasi fokal dan gliosis. Lumen pembuluh darah
yang terlibat sempit atau oklusi, dindingnya menunjukkan perubahan
ateriosklerotik dan umumnya terdapat deposit amiloid. Pada pencitraan, terlihat
gambaran kronis dengan batas difus dan tidak terdapat edema disekitarnya maupun
bukti efek massa. Umumnya dikaitkan dengan beberapa tingkat atrofi sentral, yang
cenderung lebih buruk dengan banyaknya jumlah lesi. Distribusi dari perubahan lesi
ini bertahap pada serial scan , sering menunjukkan perbedaan minimal atau tidak
signifikan pada studi yang terpisah beberapa tahun.

Sementara usia itu sendiri menyebabkan beberapa perubahan, dan insidensi dari
lesi ini mengalami peningkatan pada orang usia 40 atau lebih, terdapat beberapa
faktor resiko lainnya yang dapat meningkatkan insidensi. Termasuk hipertensi,
diabetes, hiperkolesterolemia, dan merokok. Pasien dengan masalah kesehatan
cenderung memiliki peningkatan lesi iskemik substansia alba.

Lesi iskemik substansia alba kronis adalah hipodens pada CT tetapi MRI lebih
sensitif dan mengungkapkan lesi lebih luas ( gambar 33A.38; gambar 33A.38, B-C).
Pada MRI lesi terlihat hiperintens pada sekuen T2 dan FLAIR. Mereka mungkin atau
tidak terlihat sebagai hipointens T1. Kemungkinan hanya lesi yang terlihat pada T1
yang mempunyai makna klinis yang signifikan.

Lokasi yang umum adalah periventrikular dan lebih sering pada substansia alba,
namun lesi subkortikal juga sering, dengan U-fiber yang terpisah. Lesi dapat
terisolasi, tersebar, atau lebih konfluen, khususnya di zona PV. Secara morfologi,
lesi umumnya menunjukkan batas yang tidak jelas dengan gambaran cotton
wool dengan ukuran bervariasi dari punctat sampai kecil. Area dari lesi konfluen
terlihat besar dan lebih sering mengenai substansia alba corpus ventrikel lateralis
anterior dan posterior, simetris dalam lobus parietal dan frontal. Lesi substansia
alba juga sering terjadi dengan distribusi parallel korpus ventrikel lateralis pada
potongan axial , dengan gambaran irregular band like atau beads-on-stringyang
sering dibedakan dengan lesi PV oleh intervening band dari substansia alba yang
tidak terkena. Keterlibatan kapsula externa juga karakteristik. Pola dari distribusi
lesi dan morfologi terlihat baik pada FLAIR. Berbeda dengan lesi MS, iskemia
mikrovaskular cenderung tidak melibatkan lobus temporal atau korpus kalosum.
Selain melibatkan substansia alba hemisfer , lesi iskemik mikrovaskular juga
melibatkan basis pons.

Signifikansi klinis dari lesi substansia alba tergantung luas dan lokasi yang
terkena. Adanya lesi substansia alba iskemik , kecil, tersebar pada T2-weighted
secara klinis tidak bermakna dan biasanya dipertimbangkan sebagai manifestasi
normal dari penuaan. Pasien mungkin merasa lebih nyaman dengan deskripsi
seperti age spots of the brain dalam menyampaikan perjalanan klinis saat
mendiskusikan hasil. Lesi lebih luas juga terlihat pada sekuen T1-weighted namun
sering berkaitan dengan gaya berjalan yang abnormal, demensia, dan
inkontinensia. Pada ensefalopati arteriolar iskemik atau penyakit binswanger
terdapat konfluen PV, tegas, terdistribusi luas dan perubahan sinyal substansia
alba. Pada beberapa kasus yang berat, hiperintensitas konfluen juga melibatkan
kapsula interna dan eksterna atau substansia alba subkortek. Selain lesi konfluen,
hiperintensitas T2 yang tersebar multiple juga sangat umum. Lesi iskemik
substansia alba juga sering tumpang tindih dengan stroke iskemik lakunar dan
penyusutan volume otak .

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