MRI Station

Din – Nan – Wan – Gun

Tn. A / 29 tahun
CVA trombosis brain stem dd autoimun

 Acute Hipestesi N. V1, V2, V3 S (+) sejak Jumat pagi onset saat bangun tidur --> saat ini
perbaikan-
 perokok aktif (+) 1 pack/hari selama >15 tahun, alkohol (+)
 Status Neurologis
 NV: hipestesi N VI, V2, V3 Perbaikan --> (-)
 Lab (20/8/2)
 SE: 136/ 3.85/ 111
 DL: 17.2/ 9060/ 51.9%/ 231,000
 FH: 10.6/ 28.3/ 1.02
 Fibrinogen: 132.1
 D-Dimer 0.22
 OT/PT: 18/11Alb: 4.72
 Profil lipid: 99/ 295 / 20 / 25
CT Scan kepala + MRA
 Tampak lesi intraaxial punctat multipel non bordering deep subcortical isointens T1WI,
hiperintens T2FS/FLAIR
non restricted DWI, non blooming SWI, yang tidak menyangat pasca penambahan kontras pada
white matter lobus frontotemporoparietal kanan kiri
 ACA

MCA

A. Basilaris

A. Vertebralis
Kesimpulan

• Suspek demyelinating disease (autoimun dd vasculitis dd metabolic)

• Tidak tampak aneurisma, stnesosis, maupun malformasi vaskuler
Teaching point:

 Mengenali hyperintense punctiform pada white matter:

 vascular pattern  microvascular lesions
 perivascular pattern  sugestif multiple sclerosis
 nonspecific pattern  atipikal mikrovaskuler disease
White matter disease

 can be approached by taking into account the anatomy of cerebral microcirculation and its
interstitium, specifically by determining the most affected elements in the different
leukoencephalopathic groups
 For the radiologic approach of a case of HPIWM, the semiological elements to be
analysed are distribution and location, shape, size, enhancement after contrast
administration, presence of haemorrhage or microhaemorrhage, and grey matter
involvement
 Supratentorial

Distribusi Subcortical Periventrikular Deep area Corpus

infratentorial area area collosum
dan lokasi
bordering
Supra- • PvP subcortical 
infratentorial subcortical U- • VP VP
Juxtacortical
Bentuk / fibres
Oval/fusiform  non-bordering
Morfologi deep
PvP PvP subcortical
Punctate/ VP NsP
HPIWM roundish  NsP
Perifer  PvP
Amorphous  NsP
Ukuran PvP
>10---15 mm  PvP Central  VP

Kontras
(+)  PvP (MS) Vascular Perivascular Non-specific
enhance
pattern (VP): pattern (PvP): pattern (NsP):
• arterial • multiple • Vasculitis
Ada Microbleeding (+)  VP hypertensio sclerosis • Other
tidaknya (arterial n (MS) demyelinatin
perdarahan hypertension and • amyloid • Autoimmun g diseases
amyloid angiopathy e disease • toxicmetaboli
angiopathy • Migraine • Sarcoidosis cdiseases
Keterlibatan • Vasculitis • Infections
grey matter
Three main patterns can be defined on the basis of several semiological
elements:

 A vascular pattern  A perivascular pattern  A non-specific pattern

(VP) or microvascular
pattern, which is
usually caused by an
arteriolar lesion, and is
the most prevalent
(PvP), which is usually (NsP), when neither of
caused by perivascular the previous patterns
inflammation, among can be identified, and
other less common which is normally
causes. The paradigm of caused by microvascular
this pattern is MS, for disease
which an autoimmune
perivenular
inflammation has been
reported that causes
demyelinization
Vascular pattern

 foci of microbleeding is observed

in T2  arterial hypertension
(AH) and amyloid angiopathy
(AA)
 foci of leukoencephalopathy
confluent in the periventricular
white matter
 involvement of the basal ganglia
and the subcortical white matter
 no involvement of the U-fibres
Perivascular
pattern
 Juxtacortical lesion
 periventricular ovoid lesions 
Dawson’s fingers
 peripheral infratentorial lesions
 peripheral incomplete ring-
enhancement
Distribution

 HPIWM may present with a

predominantly supratentorial,
infratentorial or supra- and
infratentorial distribution.

Distribution. A mainly supratentorial distribution with frontoparietal prevalence is typical of the

vascular pattern. The infratentorial involvement with peripheral distribution suggests a
perivascular pattern. The infratentorial involvement with central distribution suggests a vascular
pattern
Location

 (1) juxtacortical; (2) sub-U subcortical; (3) non-

bordering deep subcortical; (4) bordering
subcortical; (5) periventricular, and (6) corpus
callosum. A predominantly juxtacortical
involvement or involvement of the corpus
callosum is not indicative of a vascular pattern
(VP); the rest of locations favour a VP or a non-
specific pattern, and thus, suggest a microvascular
cause. Periventricular lesions may be indicative of
a VP or a perivascular pattern depending on the
shape of the lesion
 Morphology
 There are several lesion types according to their shape: oval or fusiform, punctate or
roundish, and amorphous
Size

 Localization of an isolated lesion (not several confluent lesions) >10---15 mm in size is

suggestive of a PvP (lacunar infarctions are acknowledged to reach 15 mm).
 Smaller lesions are non-specific, and can be indicative either of a microvascular or a
perivascular lesion
Enhancement after
contrast administration

 In contrast, the active

inflammatory stage of the disease
usually involves an increase in
permeability or absence of the
blood---brain barrier and
gadolinium enhancement of the
lesion.

Enhancement following contrast administration. Absence of enhancement is a non-specific semiological

finding. Peripheral incomplete ring-enhancement favours a perivascular pattern caused by multiple
sclerosis. Patient with multiple juxtacortical lesions showing typically associated incomplete ring-
enhancement.