58 DAVID SUTTON PICTURES INTRACRANIAL LESIONS (2)

58
INTRACRANIAL LESIONS (2)
DAVID SUTTON 58.23

DAVID SUTTON PICTURES
DR. Muhammad Bin Zulfiqar
PGR-FCPS III SIMS/SHL

• Fig. 58.1 (A) Massive capsular haematoma with
blood in the ventricles. (B) Spontaneous
haemorrhage into right fontal lobe, minor
extension into right lateral ventricle. Low density
around haematoma due to clot retraction.

• Fig. 58.2 (A) Axial unenhanced CT and (B) T2 -
weighted MR image demonstrating an acute
intrinsic pontine haemorrhage.

• Fig. 58.3 CT of resolving left thalamic
haemorrhage 10 days after onset. (A) Before
contrast there is some residual high density
centrally. (B) After contrast there is marginal
enhancement.

• Fig. 58.4 (A) MR of subacute posterior fossa haemorrhage. T 2 -
weighted, and 3 4 days after onset. Low signal lesion with some
marginal high signal. (B) MR T2-weighted, and 3-4 days after onset.
Low-signal lesion with some marginal high signal. (B) MR (T 2 -
weighted). Large haematoma in right temporal lobe 10 days after
ictus. Peripheral high signal (C) MR (T2 -weighted). Cortical
haematoma at 4 weeks. Note rim of low density.

• Fig. 58.4 (A) MR of subacute posterior fossa
haemorrhage. T 2 -weighted, and 3 4 days after onset.
Low signal lesion with some marginal high signal. (B)
MR T2-weighted, and 3-4 days after onset. Low-signal
lesion with some marginal high signal. (B) MR (T 2 -
weighted). Large haematoma in right temporal lobe 10
days after ictus. Peripheral high signal (C) MR (T2 -
weighted). Cortical haematoma at 4 weeks. Note rim of
low density.

• Fig. 58.5 (A) Subarachnoid haemorrhage. Congealed blood in the
basal cisterns, insulae and interhemispheric cleft. (B) Clot in both
frontal lobes from anterior communicating ruptured aneurysm. (C)
Subarachnoid haemorrhage from right middle cerebral aneurysm.
In addition to blood in the subarachnoid space, there is a local clot
in the anterior part of the right insula indicating the site of the
ruptured aneurysm. (D) Ruptured anterior communicating
aneurysm with blood between frontal lobes, in septal cyst and in
ventricles.

• Fig. 58.6 (A) Enhanced CT shows a right posterior
communicating aneurysm. (B) Large irregular
suprasellar aneurysm after enhancement. (C)
High-density rounded mass in suprasellar region.
(D) The mass enhances strongly with contrast
medium. Large aneurysm confirmed at
angiography (L36, W80).

• Fig. 58.6 (A) Enhanced CT shows a right posterior
communicating aneurysm. (B) Large irregular
suprasellar aneurysm after enhancement. (C) High-
density rounded mass in suprasellar region. (D) The
mass enhances strongly with contrast medium. Large
aneurysm confirmed at angiography (L36, W80).

• Fig. 58.7 (A) MRA axial study. Large aneurysm of the
right carotid artery bifurcation is shown protruding up
from the right cavernous sinus. There is also a small
occipital angioma supplied by the right posterior
cerebral artery. (B) Axial T 2- weighted MR image
showing a small anterior communicating artery
aneurysm. (C) Axial T2 -weighted MR showing a small
aneurysm of the distal left posterior cerebral artery.

• Fig. 58.7 (A) MRA axial study. Large aneurysm of the right carotid
artery bifurcation is shown protruding up from the right
cavernous sinus. There is also a small occipital angioma supplied by
the right posterior cerebral artery. (B) Axial T 2- weighted MR image
showing a small anterior communicating artery aneurysm. (C) Axial
T2 -weighted MR showing a small aneurysm of the distal left
posterior cerebral artery.

• Fig. 58.8 (A,B) Basilar aneurysms confirmed at angiography. Two different
patients with high-density enhancing rounded masses behind the sella and
extending into brainstem. (C) MRA shows left posterior communicating aneurysm.
(D) Giant right intracavernous carotid aneurysm (3D MRA, TOF). (E) Lateral (a) and
(b) views of giant basilar tip aneurysm. Flow arches up and over the invisible main
cavity. (F) MRA (compressed axial 3D TOF). Two angiomas, one temporo-occipital,
one anterior temporal. (G) MRA (3D TOF). Occluded right internal carotid artery
cross-filling from left to right.

• Fig. 58.8 (A,B) Basilar aneurysms confirmed at
angiography. Two different patients with high-density
enhancing rounded masses behind the sella and extending
into brainstem. (C) MRA shows left posterior
communicating aneurysm. (D) Giant right intracavernous
carotid aneurysm (3D MRA, TOF). (E) Lateral (a) and (b)
views of giant basilar tip aneurysm. Flow arches up and
over the invisible main cavity. (F) MRA (compressed axial
3D TOF). Two angiomas, one temporo-occipital, one
anterior temporal. (G) MRA (3D TOF). Occluded right
internal carotid artery cross-filling from left to right.

• Fig. 58.8 (A,B) Basilar aneurysms confirmed at angiography. Two
different patients with high-density enhancing rounded masses
behind the sella and extending into brainstem. (C) MRA shows left
posterior communicating aneurysm. (D) Giant right intracavernous
carotid aneurysm (3D MRA, TOF). (E) Lateral (a) and (b) views of
giant basilar tip aneurysm. Flow arches up and over the invisible
main cavity. (F) MRA (compressed axial 3D TOF). Two angiomas, one
temporo-occipital, one anterior temporal. (G) MRA (3D TOF).
Occluded right internal carotid artery cross-filling from left to right.

• Fig. 58.9 (A) Axial MR section (T2 -weighted) at base
of skull. The right carotid and both vertebrals (lateral
to the cord) show no signal due to normal flow. The
dilated left internal carotid shows dissection with high
signal in the false channel due to low or no flow
(arrow). (B) CT with coronal reformat shows kinked
vertebral artery arching high into left cerebellopontine
angle (arrows) and compressing 7th nerve in a patient
with facial tic.

• Fig. 58.9 (A) Axial MR section (T2 -weighted) at
base of skull. The right carotid and both
vertebrals (lateral to the cord) show no signal
due to normal flow. The dilated left internal
carotid shows dissection with high signal in the
false channel due to low or no flow (arrow). (B)
CT with coronal reformat shows kinked vertebral
artery arching high into left cerebellopontine
angle (arrows) and compressing 7th nerve in a
patient with facial tic.

• Fig. 58.10 (A) Large temporal angiomatous malformation.
Note mottled appearance. The dilated vessels are of slight
increased density and there are small 'cystic' and low-
density areas. (B) After contrast medium, the dilated
serpiginous vessels are well shown. Major drainage is to an
aneurismal vein of Galen. (C) Large occipital angioma. CT
shows mottled area of mixed high and low densities with
flecks of calcification. (D) After enhancement multiple
dilated vascular shadows are shown.

• Fig. 58.10 (A) Large temporal angiomatous malformation. Note mottled
appearance. The dilated vessels are of slight increased density and there
are small 'cystic' and low-density areas. (B) After contrast medium, the
dilated serpiginous vessels are well shown. Major drainage is to an
aneurismal vein of Galen. (C) Large occipital angioma. CT shows mottled
area of mixed high and low densities with flecks of calcification. (D) After
enhancement multiple dilated vascular shadows are shown.

• Fig. 58.11 Patient with proptosis and orbital
bruit due to dural AV fistula. CT shows
grossly dilated superior ophthalmic vein.

• Fig. 58.12 (A,B) MR T 2 -weighted image
shows an angioma lying with tortuous vessels
mainly in the left temporal lobe.

• Fig. 58.13 MR study (T,-weighted). (A) Midline sagittal
section. (B) Axial section. A large complex midline
angioma drains into an aneurismal vein of Galen, and there
is a dilated straight sinus and aneurysmal torcular. (C) MR
study (T,-weighted). Right temporoparietal angioma
supplied by hypertrophied middle cerebral artery. (D)
Coronal MR study (T,-weighted) of small left parasagittal
angioma showing cone-like extension into brain.

• Fig. 58.13 MR study (T,-weighted). (A) Midline sagittal section. (B)
Axial section. A large complex midline angioma drains into an
aneurismal vein of Galen, and there is a dilated straight sinus and
aneurysmal torcular. (C) MR study (T,-weighted). Right
temporoparietal angioma supplied by hypertrophied middle
cerebral artery. (D) Coronal MR study (T,-weighted) of small left
parasagittal angioma showing cone-like extension into brain.

• Fig. 58.14 (A,B) Extensive bilateral AVMs are
demonstrated on these two axial T 2 -weighted
MR images. There are multiple enlarged
superficial drainage veins. (C) Axial MR shows
transpontine venous angioma. (D) Angiogram
shows abnormal drainage veins.

• Fig. 58.14 (A,B) Extensive bilateral AVMs are
demonstrated on these two axial T 2 -
weighted MR images. There are multiple
enlarged superficial drainage veins. (C) Axial
MR shows transpontine venous angioma. (D)
Angiogram shows abnormal drainage veins.

• Fig. 58.15 (A) Sagittal midline MR (TI-weighted).
Cavernous angioma of pons appears as in
homogeneous mixed-signal lesion with
peripheral low-signal halo. (B) Axial section (T]-
weighted) shows the lesion equally well. (C,D)
Axial MR scans T2 -weighted show large
haematoma, which showed cavernomatous
features on histology, on the right frontal lobe.

• Fig. 58.15 (A) Sagittal midline MR (TI-weighted).
Cavernous angioma of pons appears as in
homogeneous mixed-signal lesion with peripheral
low-signal halo. (B) Axial section (T]-weighted) shows
the lesion equally well. (C,D) Axial MR scans T2 -
weighted show large haematoma, which showed
cavernomatous features on histology, on the right
frontal lobe.

• Fig. 58.16 CT shows
watershed infarct at
junction of LMCA and
ACA territory.

• Fig. 58.17 CT shows basal ganglia calcification in a child
with HIV/AIDS. There are also small established vascular
infarcts, the largest in the right frontal region.

• Fig. 58.18 Acute infarct. (A) Doubtful low-
density in the left occipital region. No mass
effect. (B) Strong enhancement with contrast
medium. (C) Middle cerebral infarct. Mixed low-
density and isodense lesion in right parietal
region. No mass effect. (D) Patchy enhancement
after contrast medium.

• Fig. 58.19 (A,B) MR axial sections showing infarcts in
two different patients (A) T2 -weighted. Right
cerebellar infarct appears as high signal. (B) T1-
weighted. Large areas of low signal in both
hemispheres from embolic infarcts in a patient with
hypertrophic cardiomyopathy. (C,D) MR axial sections
(T]-weighted) showing high signal from sagittal and
transverse sinuses which are thrombosed.

Fig. 58.19 (A,B) MR axial sections showing infarcts in
two different patients (A) T2 -weighted. Right
cerebellar infarct appears as high signal. (B) T1-
weighted. Large areas of low signal in both
hemispheres from embolic infarcts in a patient with
hypertrophic cardiomyopathy. (C,D) MR axial sections
(T]-weighted) showing high signal from sagittal and
transverse sinuses which are thrombosed.

• Fig. 58.20 (A) Axial section shows
thrombosed right transverse sinus with
evidence of venous infarcts in temporal lobe.
(B) Left cavernous sinus occluded shows high
signal around patent internal carotid; axial
MR section shows left proptosis.

• Fig. 58.21 MRA shows occlusion of left internal
carotid at its origin.

• Fig. 58.22 MRA shows atheromatous
irregularity of proximal segments and
trifurcation.

Fig 58.23 (A) Axial MR T-weighted child with
AIDS mature right ACA 2 - and right MCA
territory infarcts show as high-signal. (B)
Axial MR T 2 increased signal.

• Fig. 58.24 (A,B) Perfusion MR. Occlusion of
right internal carotid artery.

• Fig. 58.25 Diffusion MR shows recent small
left frontal cortical infarct.

• Fig. 58.26 (A) MRI shows large area of right
hemisphere with high signal. (B) MRA shows
occlusion of right internal carotid artery.

• Fig. 58.27 (A) Acute extradural haematoma.
High-density biconvex mass in right
occipitoparietal region with mass effect following
trauma (L34, W75). (B) Acute subdural
haematoma. Superficial high-density
concavoconvex lesion (arrows) with marked mass
effect.

• Fig. 58.28 Subdural haematoma 3 weeks after
onset. The clot is largely absorbed and the
subdural fluid is now of low density.

Fig. 58.30 (A) Isodense subdural. Note mass effect and
effacement of sulci which suggest diagnosis prior to
contrast medium. (B) Post enhancement scan of
another isodense subdural. The lesion stands out
against the enhanced surface of the brain.

• Fig. 58.31 (A) Subcortical traumatic
haematoma. (B) Haemorrhagic contusions in
right frontal region. (C-D) Multifocal
haemorrhages and contusions in both
hemispheres.

• Fig. 58.32 (A,B) Cerebral trauma. Contusions in left
temporal lobe. (C) Subcortical small haemorrhages
associated with shearing injury, and a few large
haemorrhages. (D) Head injury in a child. There is cerebral
oedema mainly on the right, associated with compression
of the ventricles and some shift to the right.

• Fig. 58.33 (A) Depressed fracture in the left
temporal region with underlying haemorrhagic
contusions (134, W75). (B) Same case at higher
level (L) to show bone detail (L128, W75). (C)
Frontal aerocele. (D) Bone window film showing
frontal fracture and connection with top of
frontal sinus.

• Fig. 58.34 Subdural haematoma shown by
MR (T1-weighted) as high signal overlying left
hemisphere. (A) IR 1400/400 (B) SE 1400/40
(Courtesy of Dr Graeme Bydder).

• Fig. 58.35 Post-traumatic porencephalic cyst
or encephalomalacia. Large cortical and
subcortical defect in the left frontal region
several years after a severe head injury.

• Fig. 58.36 CSF fistula. CT cisternography.
Direct corona) sections with patient prone.
Soft tissue (A) and bone (B) window. Contrast
medium has entered an empty sella. Pituitary
stalk is arrowed. Bone window shows level of
contrast fluid in the sphenoid sinus on the
left.

• Fig. 58.37 (A,B) Cerebral abscess. (A) Low-density lesion in occipital
region with some mass effect. (B) After contrast medium, note thin
ring of enhancement round the abscess with oedema anteriorly. (C)
Multiple abscesses in frontoparietal area showing capsular
enhancement after contrast medium (L34, W75). (D) Capsular
enhancement in bilocular abscess. (E,F) Otogenic abscess in left
posterior temporal region with thick enhancing capsule and
oedema posteriorly.

• Fig. 58.37 (A,B) Cerebral abscess. (A) Low-density
lesion in occipital region with some mass effect. (B)
After contrast medium, note thin ring of enhancement
round the abscess with oedema anteriorly. (C) Multiple
abscesses in frontoparietal area showing capsular
enhancement after contrast medium (L34, W75). (D)
Capsular enhancement in bilocular abscess. (E,F)
Otogenic abscess in left posterior temporal region with
thick enhancing capsule and oedema posteriorly.

Fig. 58.38 (A) Axial T2 - weighted image of a left parietal
abscess and associated vasogenic oedema. The central
contents are hyperintense but the low-signal rim is
thought to be secondary to the paramagnetic effects of
the free radicals present. (B) Axial post-contrast CT in a
child demonstrating bilateral low-density subdural
empyemas with enhancement of the inner
membranes.

• Fig. 58.39 Tuberculoma. (A) Isodense lesion with
surrounding oedema. on T, weighted images.
The lesion now shows ring-enhancement (B)
Mixed enhancement after contrast. (C)
Tuberculomas. Two small lesions with thick ring
enhancement ([40, W80). (D) Small brainstem
tuber- on both CT and MRI and perilesional
oedema remains. The radioculomas with ring
enhancement anterior to dilated fourth ventricle.

• Fig. 58.39 Tuberculoma. (A) Isodense lesion with surrounding
oedema. on T, weighted images. The lesion now shows ring-
enhancement (B) Mixed enhancement after contrast. (C)
Tuberculomas. Two small lesions with thick ring enhancement ([40,
W80). (D) Small brainstem tuber- on both CT and MRI and
perilesional oedema remains. The radioculomas with ring
enhancement anterior to dilated fourth ventricle.

• Fig. 58.40 Tuberculomas in right frontal
region with nodular enhancement (A) and
upper midbrain with ring enhancement (B).
(C) Sagittal reformat of midbrain lesion. Note
infundibulum and pituitary gland well shown.

• Fig. 58.41 Axial T2 -weighted image (A) showing a
hypo intense caseating tuberculous granuloma in the
right frontal lobe in association with vasogenic
oedema. The lesion is situated at the grey-white matter
junction and on the postcontrast T, axial image (B) has
a multiloculated ring enhancing appearance.

• Fig. 58.42 An irregular enhancing tuberculoma is shown within the pons
on the postcontrast axial T,-weighted MR image. (A) The lesion is of
relatively low signal on the T2 axial image (B) and there is extensive
vasogenic oedema and some modest mass effect with distortion of the
4th ventricle. Axial T 2 -weighted MR (C) demonstrating third and lateral
ventricular hydrocephalus with transependymal oedema around the
occipital horns. This was secondary to tuberculous meningitis. On the
coronal T, postcontrast image (D) there is nodular meningeal thickening
and enhancement around the brainstem and cerebellum.

• Fig. 58.42 An irregular enhancing tuberculoma is shown within the pons on the postcontrast axial
T,-weighted MR image. (A) The lesion is of relatively low signal on the T2 axial image (B) and there
is extensive vasogenic oedema and some modest mass effect with distortion of the 4th ventricle.
Axial T 2 -weighted MR (C) demonstrating third and lateral ventricular hydrocephalus with
transependymal oedema around the occipital horns. This was secondary to tuberculous meningitis.
On the coronal T, postcontrast image (D) there is nodular meningeal thickening and enhancement
around the brainstem and cerebellum.

• Fig. 58.43 (A,B) Bilateral basal ganglia
cryptococcomas, which have a slightly punctuate
appearance on the T 2 -weighted images. On the T,
coronal images, the lesions are slightly hypointense
and those on the right exert some mass effect on the
right frontal horn. (C,D) Axial and coronal sections T2-
weighted and T,-weighted show small enhancing
abscess impinging on the right ventricle.

• Fig. 58.43 (A,B) Bilateral basal ganglia cryptococcomas,
which have a slightly punctuate appearance on the T 2 -
weighted images. On the T, coronal images, the lesions are
slightly hypointense and those on the right exert some
mass effect on the right frontal horn. (C,D) Axial and
coronal sections T2-weighted and T,-weighted show small
enhancing abscess impinging on the right ventricle.

• Fig. 58.44 (A,C) Congenital toxoplasmosis.
Grossly dilated ventricles and calcified
granulomas in atrophic cortex and basal
ganglia.

• Fig. 58.45 (A) Toxoplasmic encephalitis in a patient with AIDS. Multiple small abscesses with ring
enhancement. A ring enhancing lesion proven to be a toxoplasmosis abscess is shown peripherally
in the left frontal lobe on the T2 axial (B) and T, coronal postcontrast image (C). The appearances
are non-specific and there is a large amount of associated vasogenic oedema. Multiple small
enhancing nodules are present predominantly at the grey-white matter junction in this T, axial
image (D). The associated perilesional oedema is clearly seen on the T 2 axial image (E); this patient
was known to have AIDS and these were multiple toxoplasmosis abscesses. on the degree of brain
destruction caused by the infection. There

• Fig. 58.45 (A) Toxoplasmic encephalitis in a patient with AIDS. Multiple
small abscesses with ring enhancement. A ring enhancing lesion proven to
be a toxoplasmosis abscess is shown peripherally in the left frontal lobe on
the T2 axial (B) and T, coronal postcontrast image (C). The appearances are
non-specific and there is a large amount of associated vasogenic oedema.
Multiple small enhancing nodules are present predominantly at the grey-
white matter junction in this T, axial image (D). The associated perilesional
oedema is clearly seen on the T 2 axial image (E); this patient was known
to have AIDS and these were multiple toxoplasmosis abscesses. on the
degree of brain destruction caused by the infection. There

• Fig. 58.45 (A) Toxoplasmic
encephalitis in a patient with
AIDS. Multiple small abscesses
with ring enhancement. A ring
enhancing lesion proven to be a
toxoplasmosis abscess is shown
peripherally in the left frontal lobe
on the T2 axial (B) and T, coronal
postcontrast image (C). The
appearances are non-specific and
there is a large amount of
associated vasogenic oedema.
Multiple small enhancing nodules
are present predominantly at the
grey-white matter junction in this
T, axial image (D). The associated
perilesional oedema is clearly
seen on the T 2 axial image (E);
this patient was known to have
AIDS and these were multiple
toxoplasmosis abscesses. on the
degree of brain destruction
caused by the infection. There

• Fig. 58.46 Enhanced CT in acute cysticercosis. (A) Multiple ring and
nodular lesions inconstantly accompanied by oedema. (B)
Another patient with chronic quiescent cysticercosis. The brain was
riddled with cysts and calcified nodules. (C) The axial T 2- weighted
MR in this patient who presented acutely with epileptic seizures
showed a small hypointense lesion in the medial right temporal
lobe associated with a small amount of vasogenic oedema. (D) On
the postcontrast T, coronal image, this lesion showed almost
uniform enhancement and resolved on treatment for cysticercosis.

• Fig. 58.47 Huge hydatid cyst in the left frontal
lobe. It is of CSF density and shows no capsular
enhancement of adjacent oedema. It expands the
overlying skull vault.

• Fig. 58.48 Multiple TZ hyperintense lesions in the basal
ganglia, thalami, internal capsules and periventricular
white matter are present in this patient with acute
disseminated encephalomyelitis (ADEM).

• Fig. 58.49 Herpes encephalitis. (A) Lowdensity
area in right temporal region with slight mass
effect. (B) Bilateral low-density areas in both
temporal lobes. Burr hole for brain biopsy on
right. (C) After contrast medium there is marked
irregular enhancement, mainly gyral.

Fig. 58.49 Herpes encephalitis. (A) Lowdensity
area in right temporal region with slight mass
effect. (B) Bilateral low-density areas in both
temporal lobes. Burr hole for brain biopsy on
right. (C) After contrast medium there is
marked irregular enhancement, mainly gyral.

• Fig. 58.50 MR (T,-weighted) shows high signal
in both temporal lobes. Herpes encephalitis.

• Fig. 58.51 Progressive multifocal leucoencephalopathy. (A)
Occipital lesions mainly on right. (B,C) Several weeks later, the
disease has progressed through both hemispheres but most
markedly on the right. Multifocal well-defined hyperintense lesions
confined to the white matter are shown on this T,-weighted axial
image (D) of an immunocompromised patient. The signal
abnormality extends into the gyral cores. The left frontal lesion
shown on the T, coronal postcontrast image (E) is markedly
hypointense, non-enhancing and despite its size is not associated
with any mass effect. These lesions are typical of progressive
multifocal leucoencephalopathy (PML).

• Fig. 58.52 (A) Axial T2 -weighted image in a
patient with AIDS showing widespread signal
abnormality in the white matter of HIV
encephalitis. There is also background atrophy
with ventricular enlargement and mild sulcal
widening. (B) AIDS encephalitis.

• Fig. 58.53 (A) Axial MR section with
gadolinium enhancement (T,-weighted)
shows superficial peduncular lesions (arrows).
Sarcoidosis. (B) Intracanalicular optic neuritis
secondary to sarcoid. Left optic nerve shows
high signal on T,-weighted MR. (C) Sarcoidosis
with marked meningeal thickening.

• Fig. 58.53 (A) Axial MR section with gadolinium
enhancement (T,-weighted) shows superficial
peduncular lesions (arrows). Sarcoidosis. (B)
Intracanalicular optic neuritis secondary to sarcoid. Left
optic nerve shows high signal on T,-weighted MR. (C)
Sarcoidosis with marked meningeal thickening.

• Fig. 58.54 Generalised atrophy. (A) Dilated
lateral ventricle. (B) Enlarged sulci and
interhemispheric fissure (L36, W80).

• Fig. 58.55 (A-D) Communicating
hydrocephalus complicating meningitis. All
four ventricles are dilated and the sulci are
effaced.

• Fig. 58.56 (A) Alzheimer's disease. Coronal MRI
showing bilateral symmetrical atrophy of each
hippocampus and parahippocampal gyrus. (B,C)
Frontotemporal dementia (non-Pick). Coronal MRI
showing severe atrophy of the anterior part of the left
temporal lobe and mild enlargement of the frontal
horn of the left lateral ventricle. (D) True Pick's disease,
showing more mild left temporal lobe atrophy.

• Fig. 58.56 (A) Alzheimer's
disease. Coronal MRI
showing bilateral
symmetrical atrophy of each
hippocampus and
parahippocampal gyrus. (B,C)
Frontotemporal dementia
(non-Pick). Coronal MRI
showing severe atrophy of
the anterior part of the left
temporal lobe and mild
enlargement of the frontal
horn of the left lateral
ventricle. (D) True Pick's
disease, showing more mild
left temporal lobe atrophy.

• Fig. 58.57 T2- weighted axial images in a patient with
CADASIL (cerebral autosomal dominant arteriopathy,
subcortical infarcts and leucoencephalopathy) showing
predominantly confluent signal hyperintensity in the
cerebral white matter, fairly symmetrical in
distribution. The changes are particularly marked in the
temporal lobes (A). The basal ganglia also exhibit a
lacunar state (B).

Fig. 58.58 Axial T2 – weighted image in a patient with
multisystem atrophy showing marked atrophy of the pons
and middle cerebellar peduncles. Abnormal T2 high signal
is present in the pons in the form of a cross (hot cross bun
sign) with more confluent signal hyperintensity in the
middle cerebellar peduncles. The cerebellum is also
atrophic and the 4th ventricle is consequently enlarged.

• Fig. 58.59 Cerebellar atrophy showing
widened sulci and fissures. The brainstem is
also atrophic.

• Fig. 58.60 T2-weighted axial images
demonstrating basal ganglia, thalamic and
midbrain lesions in Wilson's disease.

• Fig. 58.61 Calcification of the basal ganglia.

• Fig. 58.62 Axial CT scans demonstrating
extensive calcification in the basal ganglia,
thalami, subcortical white matter, brainstem and
dentate nuclei of the cerebellum in Fahr's
syndrome.

• Fig. 58.63 Axial T 2- and T,-weighted images
in Cockayne's syndrome demonstrating gross
supratentorial atrophy and diffuse signal
abnormality and reduction in bulk of the
white matter. T, high and Tz low signal in the
basal ganglia is indicative of calcification.

• Fig. 58.64 Multiple sclerosis. (A)
Paraventricular and white-matter low-density
areas. (B,C) Enhancing paraventricular and
white-matter low-density areas. (D) Axial MRI
section J, -weighted). Multiple sclerosis
plaques are seen as areas of high signal.

• Fig. 58.64 Multiple sclerosis. (A) Paraventricular and
white-matter low-density areas. (B,C) Enhancing
paraventricular and white-matter low-density areas.
(D) Axial MRI section J, -weighted). Multiple sclerosis
plaques are seen as areas of high signal.

• Fig. 58.66 (A-C) Axial CT scans demonstrating
confluent and symmetrical low-density change in
the deep and peripheral supratentorial white
matter in metachromatic leucodystrophy. (D) Axial
MR Tz W shows widespread low density in white
matter.

• Fig. 58.66 (A-C) Axial CT scans demonstrating
confluent and symmetrical low-density change
in the deep and peripheral supratentorial white
matter in metachromatic leucodystrophy. (D)
Axial MR Tz W shows widespread low density in
white matter.

• Fig. 58.69 (A) Axial T2 and (B) T, coronal postcontrast
images in a patient with Alexander's disease showing
signal abnormality in the white matter, which has a
predilection for the frontal lobes. There is some basal
ganglia involvement and enhancement postcontrast.

• Fig. 58.70 (A) Axial T2 -weighted MRI showing
bilateral parietal periventricular signal
abnormality in a patient with classical
phenylketonuria. (B) Axial CT showing extensive
very low density change in the cerebral white
matter and thalami in maple syrup urine disease.

• Fig. 58.71 (A) Multiple dilated perivascular spaces are present on
the T 2 -weighted axial image in this patient with
mucopolysaccharidoses. (B) Tz sagittal image through the
craniocervical junction in Morquios' syndrome showing a small
foramen magnum and some cervical cord impingement. There is
odontoid hypoplasia and ligamentous and dural thickening
contributing to the small foramen magnum.

• Fig. 58.72 (A,B) CT of elderly demented
patient. Cortical atrophy is mild but there are
extensive areas of patchy low density in the
deep cerebral white matter. Binswanger's
disease.

• Fig. 58.73 (A) Axial T2- and (B) coronal T1 -weighted
images showing extensive signal abnormality in the
cortex and white matter of the right cerebral
hemisphere in MELAS. There is some mass effect and
note that the signal change involves all three vascular
territories, although is largely posterior in
distribution. There is also cerebellar atrophy.

• Fig. 58.74 Bilateral mature cystic cleft-like
lesions have occurred in the lentiform nuclei
in this patient with a mitochondrial cytopathy.
(A) Axial MR T2 W. (B) Coronal MR T2 W.

• Fig. 58.75 Mitochondrial cytopathy. Four-year-old boy
with ataxia, myoclonus and drowsiness. MRI (T 1 -
weighted) reveals loci of high signal in the lentiform
nuclei and parietal white matter extending into
posterior limbs of internal capsule.

• Fig. 58.76 (A) Diagram of hippocampus and its relationships. A.
Lateral aspect of left temporal lobe. B-E Coronal sections from
before backward at levels shown in A. Ch F = choroidal fissure; F =
fimbria; MD = margo denticulatus (dentate gyrus); HFi =
hippocampal fissure; TH = temporal horn; CAI = four regions
within hippocampus itself; PHG = parahippocampal gyrus; UN =
uncus; EC = entorhinal cortex; UG = uncinate gyrus; SLG =
semilunar gyrus (part of amygdala); GA = gyrus ambiens; HF =
hippocampal formation; OF = uncal fissure; CS = collateral sulcus;
UN = uncal notch; SUB = subiculum. (B) Coronal MRI section
through left medial temporal lobe at level of C above. T,-weighted.

• Fig. 58.76 (A) Diagram of hippocampus and its relationships. A. Lateral aspect of
left temporal lobe. B-E Coronal sections from before backward at levels shown in
A. Ch F = choroidal fissure; F = fimbria; MD = margo denticulatus (dentate gyrus);
HFi = hippocampal fissure; TH = temporal horn; CAI = four regions within
hippocampus itself; PHG = parahippocampal gyrus; UN = uncus; EC = entorhinal
cortex; UG = uncinate gyrus; SLG = semilunar gyrus (part of amygdala); GA =
gyrus ambiens; HF = hippocampal formation; OF = uncal fissure; CS = collateral
sulcus; UN = uncal notch; SUB = subiculum. (B) Coronal MRI section through left
medial temporal lobe at level of C above. T,-weighted.

• Fig. 58.77 (A) Corona) MRI sections, T2 -weighted,
through hippocampal bodies, corresponding to level E
of Fig. 58.76A. The left hippocampus is smaller than
the right and shows higher signal. Hippocampal
sclerosis. (B) Coronal MRI (FLAIR) image at level of
hippocampal body accentuating high signal in left
hippocampus. (C) T,-weighted image at similar level
from a 3D accumulation, showing the left
hippocampus to be much smaller than the right.

• Fig. 58.77 (A) Corona) MRI sections, T2 -weighted, through
hippocampal bodies, corresponding to level E of Fig.
58.76A. The left hippocampus is smaller than the right and
shows higher signal. Hippocampal sclerosis. (B) Coronal
MRI (FLAIR) image at level of hippocampal body
accentuating high signal in left hippocampus. (C) T,-
weighted image at similar level from a 3D accumulation,
showing the left hippocampus to be much smaller than
the right.

• Fig. 58.78 Coronal MRI (T 2 -weighted).
Abnormal vessels are shown in the right
medial temporal lobe involving the
hippocampus. Angioma.

• Fig. 58.79 Diagram showing three standard
sagittal sections (A) and six coronal sections
(B).

• Fig. 58.80 A coronal section in the third
position showing the bodies of the lateral
ventricles (V) and the sylvian fissures (SF).
Lying between the lateral ventricles is the
cavum septi pellucidi (CSP).

• Fig. 58.81 A coronal section in the fourth
position showing the prominent landmark of
the parahippocampal gyri (HG). V = lateral
ventricles.

• Fig. 58.82 A coronal section in the sixth
position showing the characteristic echogenic
choroid plexus (CP).

• Fig. 58.83 A sagittal section in the midline
showing the echogenic cerebellum and the
fourth ventricle (arrow) posteriorly.

• Fig. 58.84 An angled sagittal section showing
the full sweep of one lateral ventricle around
the caudate nucleus and thalamus.

• Fig. 58.85 (A) A coronal section showing the
typical appearance of hydrocephalus involving
the lateral and third ventricles. The section is
through the foramen of Monro. Echogenic
haemorrhage is within the ventricle. (B) A
ventricular shunt in position more posteriorly.

• Fig. 58.86 (A) A coronal section. (B) A sagittal
section showing the characteristic findings of the
Dandy- Walker syndrome. There is cystic
dilatation of the fourth ventricle filling the
posterior fossa. A shunt is in place.

• Fig. 58.87 (A) A coronal section. (B) A sagittal
section showing the findings of a retrocerebellar
arachnoid cyst for comparison. Note that in the
sagittal section the cerebellum (Cb) and the
fourth ventricle (iv) can be seen compressed
forward by the cyst.

• Fig. 58.88 Coronal section showing the single
fused ventricle typical of holoprosencephaly.

• Fig. 58.89 A coronal section in a premature infant
showing a typical reflective haemorrhage (H) from the
germinal matrix. A mass effect from the haemorrhage
is distorting and elevating the lateral ventricle on this
side.

• Fig. 58.90 A posterior coronal section
showing asymmetric enlargement of one
choroid plexus (H) typical of haemorrhage.

• Fig. 58.91 A sagittal section showing the
characteristic appearances of advanced
periventricular leucomalacia (PML) as
periventricular cystic spaces.

• Fig. 58.93 A transcranial section showing a
large crescentic subdural haematoma.

• Fig. 58.94 99 "Tc-exametazime brain SPECT: axial (A),
Coronal (B), right parasagittal (C) and left parasagittal (D)
sections in a patient with massive infarction of the right
middle cerebral artery territory. Note severe ischaemia o5
the Srontai, tempura% and panetai cortex and also oI the
basal ganglia on the right.

• Fig. 58.95 99 ", Tc-exametazime brain SPECT:
axial, coronal and right parasagittal images
showing very extensive perfusion deficits
during the acute ischaemic phase (top row)
and substantial improvement several months
later after clinical recovery (bottom row).

• Fig. 58.97 19mTc-exametazime brain SPECT: axial
(top row) and left and right parasagittal (bottom
row) sections in a patient with suspected
Alzheimer's disease. The distribution is primarily
posterior but quite asymmetric, unlike Fig. 58.96.

• Fig. 58.99 99 -Tc-exametazime brain SPECT: axial (top row) and left
and right parasagittal (bottom row) sections in a patient with
dementia of frontal lobe type. Note the marked frontal and
temporal ischaemia with central atrophy as well.

58 DAVID SUTTON PICTURES INTRACRANIAL LESIONS (2)

58 DAVID SUTTON PICTURES INTRACRANIAL LESIONS (2)

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