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2.2 · Stroke Diseases and Syndromes
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. Fig. 2.2.12 Axial FLAIR image in the region of the medulla in a
patient with Wallenberg syndrome ( arrowhead ) shows hyperintense
signal intensity lesion in the lateral portion of the right medulla
oblongata ( arrowhead )
Subclavian Steal Syndrome
Subclavian steal syndrome (SSS) is a disease characterized
by subclavian stenosis or occlusion at the segment between
its origin from the aortic arch and the origin of the vertebral artery. is stenosis or occlusion causes reverse blood
diversion (stealing) from the basivertebral arteries through
the vertebral artery at the same side of subclavian occlusion to supply the ipsilateral arm (blood ow from the
head and neck to supply the arm, rather than ow normally
from the aortic arch toward the head via the vertebral
artery).
Most patients with SSS are asymptomatic. However,
symptomatic patients present with brain stem ischemia or
stroke at rest or a er exercise due to increased arm blood
demand. Also, patients o en complain from dizziness,
cerebral dysfunction, and drop attacks when the disease is
severe. Symptoms in the a ected arm ranged between
decrease pulses, coldness to claudications.
SSS doesn’t appear when the stenosed subclavian artery is
accompanied by vertebral artery arising separately from the
aortic arch (6 % of population). Angiography is the gold standard to establish the diagnosis of SSS.
Coronary-subclavian steal syndrome ( CSS ) is a disease
seen in patients with previous history of coronary artery
bypass gra surgery (CABG). e internal thoracic (mammary) artery, which is a branch of the subclavian artery, is
commonly used as a gra for the le anterior descending
artery (LAD). Severe stenosis of the subclavian artery that
compromised the arm blood supply causes the blood ow to
reverse in direction. e blood is withdrawn (stolen) from
the coronary arteries via the internal thoracic artery gra to
supply the arm. Patients typically present with exertional
angina precipitated or exacerbated by arm exercise. Diagnostic keys of CSS include history of CABG (mandatory), di erence in blood pressure between the two arms >20mmHg,
and angina produced by activity of the a ected arm, while
activity of the contralateral normal arm produces no
symptoms.
75
Signs on Angiography
Stenosis of the subclavian artery is seen in arch
aortography. After injecting the contrast within the
normal vertebral artery, the contrast is seen fl owing
within the contralateral vertebral artery via the
vertebrobasilar system in a retrograde pattern to supply
the arm when the patient is asked to exercise his arm
(. Fig. 2.2.13 ).
. Fig. 2.2.13 Selective right subclavian artery angiogram
shows retrograde fl ow in the left vertebral artery to supply the
left arm via the brachial artery ( arrowheads ). The direction of the
contrast fl ow is demonstrated by the arrows
Signs on Doppler Sonography
5 The earliest manifestation of stealing phenomenon
is a transient sharp deceleration of blood flow after
the first systolic peak. This deceleration is observed
as a systolic peak with a median notch, creating
two systolic peaks of the vertebral artery with
stealing phenomenon. The nadir of the notch
becomes progressively lower until it reaches and
crosses the baseline.
5 On rest, the vertebral artery flow shows double
peak systolic waveform with a median notch. The
waveform is classified according to the velocity of
the nadir into a nadir velocity greater than that of
end diastole (type 1), a nadir velocity equal to the
level of end diastole (type 2), a nadir velocity that
reaches the baseline (type 3), and a nadir velocity
that crosses the baseline (type 4).
5 After asking the patient to exercise his ipsilateral
arm or applying brachial artery blood pressure cuff
and then deflating it to induce the stealing
phenomenon, the arterial flow waveform of the
vertebral artery is reversed, and it is seen below
the baseline, confirming the reversal blood flow.
2
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Chapter 2 · Neurology
Krasnianski M, et al. Babinski-Nageotte’s syndrome and
Signs on MRI
In axial sections of 2D time-of-fl ight sequence, the
2
vertebral artery with stealing phenomenon shows fl ow
void signal compared to the contralateral vertebral
artery and both internal carotid arteries ( localizer sign ),
which indicates reversal of fl ow.
Hemimedullary (Reinhold’s) syndrome are clinically and
morphologically distinct conditions. J Neurol.
2003;250:938–42.
Krasnianski M, et al. Between Wallenberg syndrome and
hemimedullary lesion. Cestan-Chenais and BabinskiNageotte syndromes in medullary infarctions. J Neurol.
2006;253:1442–6.
Luxenberg EL, etal. Locked-in syndrome from rosto-caudal
herniation. J Clin Neurosci. 2009;16:333–4.
Further Reading
Benito-Leon J, etal. “Man-in-the-barrel” syndrome: MRI and
SPECT imaging. Eur J Radiol. 1997;24:260–2.
Cuisset T, et al. Coronary-subclavian steal syndrome: an
usual cause of refractory unstable angina. Int J Cardiol.
2008;127:e181–2.
Deleu D, etal. “Man-in-the-barrel” syndrome as delayed
manifestation of extrapontine and central pontine myelinolysis: bene cial e ect of intravenous immunoglobulin. J
Neurol Sci. 2005a;237:103–6.
Elting JW, etal. Predicting outcome drome coma: man-in-
the-barrel syndrome as potential pitfall. Clin Neurol
Neurosurg. 2000;102:23–5.
Ferrari G, et al. Foix-Chavany-Marie syndrome: CT study
and clinical report of three cases. Neuroradiology.
1979;18:41–2.
Girija AS, etal. Neurological complications of chickenpox.
Ann Indian Acad Neurol. 2007;10:240–6.
H o mann HJ.Moyamoya disease and syndrome. Clin Neurol
Neurosurg. 1997;99 Suppl 2:S39–44.
Holz A, etal. Moyamoya disease in a patient with hereditary
Marquardt F, etal. e coronary-subclavian-vertebral steal
syndrome (CSVSS). Clin Res Cardiol. 2006;95:48–53.
Masuzawa H, etal. Pontine gliomas causing locked-in syn-
drome. Childs Nerv Syst. 1993;9:256–9.
Prasad BKD, etal. Cerebral amyloid angiopathy. Ind J Radiol
Imag. 2006;16:745–7.
Roldan-Valadez E, etal. Imaging diagnosis of subclavian steal
syndrome secondary to Takayasu arteritis a ecting a le side subclavian artery. Arch Med Res. 2003;34:433–8.
Sheehy N, et al. Contrast-enhanced MR angiography of
subclavian steal syndrome: value of the 2D time-to- ight
“localizer” sign. AJR Am J Roentgenol. 2005;185:1069–73.
Trattnig S, etal. Colour Doppler imaging of partial subcla-
vian steal syndrome. Neuroradiology. 1993;35:293–5.
Van Son JAM, et al. Diagnosis and management of the
coronary- subclavian steal syndrome. Eur J Cardiothorac
Surg. 1998;3:565–7.
Yamada I, etal. Moyamoya disease: diagnostic accuracy of
MRI.Neuroradiology. 1995;37:356–61.
Zakaria T, etal. Locked-in syndrome resulting from bilateral
cerebral peduncles infarctions. Neurology. 2006;67:1889.
spherocytosis. Pediatr Radiol. 1998;28:95–7.
Hsu C-Y, etal. Moyamoya disease: the clue from computer
tomography. J Emerg Med. 2004;26:339–42.
2.3 Intracranial Hemorrhage
Hurwitz ES, etal. A cluster of cases of Reye syndrome associ-
ated with chickenpox. Pediatrics. 1982;70:901–6.
Kaneko A, etal. Color-coded Doppler imaging of the subcla-
vian steal syndrome. Intern Med. 1998;37:259–64.
Kim I-O, etal. Mitochondrial myopathy- encephalopathylactic
acidosis and strokelike episodes (MELAS) syndrome: CT
and MR ndings in seven children. AJR Am J Roentgenol.
1996;166:641–5.
Kinoshita T, et al. Reye’s syndrome with cortical laminar
necrosis: MRI.Neuroradiology. 1996;38:269–72.
Kliewer MA, et al. Vertebral artery Doppler waveform
changes indicating subclavian steal physiology. AJR Am J
Roentgenol. 2000;174:815–9.
Komiyama M, etal. Serial MR observation of cortical laminar
necrosis caused by brain infarction. Neuroradiology.
1998;40:771–7.
Intracranial hemorrhage is a condition characterized by the
presence of free blood within the cranium. e free blood
can be collected in the epidural space, subdural space, subarachnoid space, intrabrain parenchyma, or intraventricular
spaces.
Intracranial hemorrhage can be caused by head trauma,
anticoagulants use, ruptured aneurysms, vascular malformations, and hypertension. e most common areas of intracranial hemorrhage are the temporoparietal region and the
cerebellum. Native, nonenhanced CT is the diagnostic
modality of choice as an initial diagnostic modality to detect
intracranial bleeding.
Blood exhibits di erent densities on CT or signal intensities on MRI according to the age of the hemorrhage (acute,
subacute, or chronic) (
. Fig. 2.3.1 ).
2.3 · Intracranial Hemorrhage
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. Fig. 2.3.1 Illustration
demonstrates the diff erent
hematoma ages and
manifestations on CT. ( a ) Acute
blood (Deoxygenated Hb). CT:
bright (hyperdense). MRI: low T1/
low T2 signal intensity. ( b )
Subacute blood
(Methemoglobin). CT: gray
(isodense). MRI: high T1/high T2
signal intensity. ( c ) Chronic blood
(Hemosiderin). CT: dark
(hyperdense). MRI: low T1/low T2
signal intensity
77
Blood signal on CT and MRI
a
Acute blood (Deoxygenated Hb)
CT: bright (hyperdense)
MRI: low T1 / low T2 signal intensity
b
Subacute blood (Methemoglobin)
CT: gray (isodense)
MRI: high T1 / high T2 signal intensity
c
Chronic blood (Hemosiderin)
CT: dark (hypodense)
MRI: low T1 / low T2 signal intensity
2
Epidural Hematoma
Epidural hematoma is a free blood collection located between
the inner skull table and the dura matter. It is a life- threatening
emergency that usually results from trauma to the middle
meningeal artery (85 % of cases).
Patients usually present with nausea, vomiting, and
altered consciousness.
Signs on CT
5 The CT typically shows semi-convex-shaped,
hyperdense blood collection usually located in the
parietotemporal area (. Fig. 2.3.2 ).
5 The collected blood does not cross suture lines as
the dura matter is firmly attached to the clavaria.
5 There is significant mass effect over the ventricles
and the brain parenchyma in the acute phase.
5 It is almost always acute. However, acute on top of
chronic epidural hematoma can occur
uncommonly, and it is seen as a semi-convex blood
collection with hypodense and hyperdense
component (. Fig. 2.3.2 ) .
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Chapter 2 · Neurology
a
b
2
. Fig. 2.3.2 Axial CT images of two diff erent patients show acute epidural hematoma ( a , arrowhead ) and acute on top of chronic
hematoma ( b , arrow ). Notice the mass eff ect on the left lateral ventricle in ( a ) when the hematoma is acute and lack of the pressure eff ect
on the lateral ventricles in ( b ) when the hematoma is chronic
Q: When can you nd a black (hypodense) hematoma
although the bleeding is acute?
is is a rare condition that is seen when the hemoglobin
level in the blood is less than 4mg/dL, because the hyperdense density that re ects the X-ray photon absorption by
the iron in the blood is inadequate.
subdural space to be trapped in little or no absorption. e
most common symptom is headache with or without nausea
and vomiting; in the acute phase, subdural hygroma behaves
like an enlarged intracranial hemorrhage, and in the chronic
phase, it behaves like a space-occupying lesion. A er traumatic head injury, development of subdural hygroma is noted
6–46 days a er the initial trauma.
Subdural Hematoma
Subdural hematoma is a free blood collection located
between the dura matter and the arachnoid. Subdural hematoma usually arises due to emissary vein tear from a minor
trauma or due to uncontrolled anticoagulant therapy. Acute
subdural hematoma is a clinical emergency, where patients
present with signs similar to epidural hematoma. In contrast,
chronic subdural hematomas present with less severe symptoms, such as headache, nausea, and vomiting.
D i ff erential Diagnoses and Related Diseases
Subdural hygroma is a collection of cerebrospinal uid or
serum in the subdural space (. Fig. 2.3.4 ). It is believed to be
caused by chronic subdural hematoma in the elderly or due
to intracranial infections in children. Up to 30 % of cases
arise a er head trauma. e condition is self-limited and is
thought to be caused by a tear in the arachnoid that functions
as a one-way valve, allowing cerebrospinal uid to enter the
Signs on CT
5 Crescent-shaped, hyperdense blood collection
usually located in the frontoparietal region
(. Fig. 2.3.3 ). It can be bilateral in 15 % of cases.
5 The bleeding is not bounded by the sutures.
5 There is significant mass effect over the ventricles
and the cisterns.
5 Subdural hematoma can be acute (hyperdense),
subacute (isodense), and chronic (hypodense)
(. Fig. 2.3.3 ). Acute on top of chronic subdural
hematoma can occur, and it is seen as
crescent-shaped blood collection with hypodense
and hyperdense components (sedimentation
subacute subdural hematoma).
5 Subdural hygroma is seen as a cerebrospinal fluid
collection in the subdural space (. Fig. 2.3.4 ) .
2.3 · Intracranial Hemorrhage
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a
79
b
2
. Fig. 2.3.3 Axial CT images of two diff erent patients show acute subdural hematoma ( a , arrowhead ) and chronic subdural hematoma
( b , arrow ). Again notice the pressure eff ect over the lateral ventricles in the acute subdural hematoma ( a ) compared to the chronic subdural
hematoma ( b )
Subarachnoid Hemorrhage
Subarachnoid hemorrhage is characterized by the presence
of free blood within the subarachnoid space and the arachnoid cisterns. It most commonly occurs as a complication of
ruptured arterial aneurysms and trauma to the head. Patients
typically present with sudden severe headache, nausea, and
vomiting with neck sti ness.
Signs on CT
5 The cerebrospinal fluid spaces and cistern will be
seen hyperdense (white) due to blood mixed with
cerebrospinal fluid (. Fig. 2.3.5 ).
5 There is no midline displacement.
. Fig. 2.3.4 Axial brain CT of a patient with a history of
posttraumatic brain injury shows large left frontal subdural
h y g r o m a
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Chapter 2 · Neurology
a
b
2
. Fig. 2.3.5 Sequential axial CT images ( a ) & ( b ) of a patient with subarachnoid hemorrhage show hyperdense suprasellar cistern ( a ) and
Sylvian fi ssures ( b ) ( arrowheads ) due to subarachnoid bleeding
Intracerebral/Intraparenchymal
Hemorrhage
Intracerebral hemorrhage is the presence of free blood within
the gray or the white brain matter. It commonly arises due to
stroke, embolic vascular occlusion, and tumors or a er vascular rupture due to head trauma. Hypertension causes
bleeding into the basal ganglia in 60 % of cases.
Signs on CT
5 There is hyperdense blood collection within the
brain parenchyma that usually follows a vascular
territory (. Fig. 2.3.6 ).
5 When the bleeding is due to stroke, it is
surrounded by a halolike edema (cytotoxic
edema), while when it is due to a tumor, a
fingerlike edema is seen surrounding the blood
collection (vasogenic edema).
. Fig. 2.3.6 Axial brain CT of a patient with intraparenchymal
bleeding in the region of the right middle cerebral artery shows
large area of intraparenchymal bleeding surrounded by
cytotoxic edema exerting mass eff ect over the right anterior and
posterior horns of the right lateral ventricle ( arrowhead )
2.3 · Intracranial Hemorrhage
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Intraventricular Hemorrhage
Intraventricular hemorrhage is bleeding into the ventricles.
Commonly, it occurs secondary to parenchymal or subarachnoid hemorrhage and associated with di use axonal injury of
the corpus callosum. Arteriovenous malformation is the
most common cause for spontaneous intraventricular hemorrhage in adults. ere are two types of intraventricular
hemorrhage:
5 Ependymal intraventricular bleeding : the blood is seen
xed to the ventricular walls.
5 Free intraventricular blood : the blood is seen located in
the posterior horns (gravity dependent).
Signs on CT
There is hyperdense blood within the ventricles, either in
a free form lying in the posterior horns or encapsulated
within the ependymal ventricular wall (. Fig. 2.3.7 ).
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2
Signs on MRI
Chronic bleeding can be detected on T2* images as
hypointense intraparenchymal areas (. Fig. 2.3.8 ).
a
. Fig. 2.3.7 Axial brain CT of a patient with severe
intraventricular hemorrhage shows dilated both ventricles due
to bleeding, with subependymal ( arrowhead ) and free ( arrow )
intraventricular bleedings also seen
b
. Fig. 2.3.8 Axial T2W ( a ) and T2* MRI of a patient with previous intraparenchymal bleeding in the left temporal lobe shows area of focal
hypointense signal intensity on ( b ) due to hemosiderin. Notice the same area is visible on ( a ) but not as clearly seen as in the T2* image
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Chapter 2 · Neurology
Hemorrhage into Malignancy
Hemorrhage into neoplasms accounts for 10 % of spon-
2
taneous intracranial hemorrhage. It can be seen in 14 % of
metastases from melanoma and bronchogenic carcinoma
and in 5 % of cases of gliomas. Bleeding occurs because
abnormal tumor vascularity usually occurs in higher-grade
malignancies.
2.4 Meningitis
Meningitis is a disease characterized by in ammation of the
meninges due to infections or in ammatory disease (e.g., sarcoidosis). Infectious meningitis can be bacterial (e.g., pneumococcus) or viral (e.g., Haemophilus in uenzae ).
Patients with meningitis classically present with fever,
neck sti ness, and neurological symptoms. Rarely, meningitis
may lead to suprarenal gland suppression, causing patient
death due to adrenal gland insu ciency. Infection of the
Signs on CT
5 Atypical location for bleeding in a patient with
known primary or secondary brain malignancy.
5 The signal intensity of the blood is more
heterogeneous than that of nonneoplastic
hemorrhage. This heterogeneous texture is
attributed to the multiple episodes of bleeding
with different ages (mixed hypodense and
hyperdense pattern).
Further Reading
Dincsoy MY, etal. Intracranial hemorrhage in hypothalamic
low-birth-weight neonates. Child’s Nerv Syst. 1990;6:
245–9.
Gross A, etal. Intraventricular hemorrhage originating from
choroids plexus angioma in a road accident victim. Z
Rechtsmed. 1989;102:409–13.
meninges occurs due to hematogenous spread (e.g., bacteremia) or from direct extension from local infectious pathology (e.g., otitis media). Imaging in meningitis is mainly
performed to evaluate complications.
Signs on CT and MRI
5 Meningitis is detected typically as thickened
meninges with contrast enhancement. Meningeal
enhancement is divided into pachymeningeal and
leptomeningeal enhancement. The pachymeninges
are the dura matter, with its thick inner meningeal
component, and its inner table of the skull
(periosteum) component. The leptomeninges are the
pia and the arachnoid matters. Pachymeningeal
enhancement is seen as enhancement of the inner
skull table and meningeal refl ections (e.g., falx
cerebri) (. Fig. 2.4.1 ). In contrast, leptomeningeal
Heros RC, etal. Cerebral vasospasm a er subarachnoid hem-
orrhage: an update. Ann Neurol. 1983;14:599–608.
Koc RK, etal. Acute subdural hematoma: outcome and out-
come prediction. Neurosurg Rev. 1997;20:239–44.
Laguna P, etal. Intracranial hemorrhage in a boy with severe
haemophilia A and factor VIII inhibitor. Child’s Nerv Syst.
2006;22:432–5.
Masuzawa T, etal. Computed tomographic evolution of post-
traumatic subdural hygroma in young adults.
Neuroradiology. 1948;26:245–8.
Masuzawa T, etal. Computed tomography evolution of post-
traumatic subdural hygroma in young adults.
Neuroradiology. 1984;26:245–8.
Moster ML, etal. Chronic subdural hematoma with transient
neurological de cits: a review of 15 cases. Ann Neurol.
1983;14:539–42.
Park CK, etal. Spontaneous evolution of post-traumatic sub-
dural hygroma into chronic subdural hematoma. Acta
Neurochir (Wien). 1994;127:41–7.
Schellinger PD, etal. Intracranial hemorrhage, the role of
magnetic resonance imaging. Neurocrit Care. 2004;
1:31–45.
Schwartz DT. Sensitivity of computed tomography for
subarachnoid hemorrhage. Ann Emerg Med. 2009;53(1):
160–1.
Xi G, etal. Intracerebral hemorrhage, pathophysiology and
therapy. Neurocrit Care. 2004;1:5–18.
. Fig. 2.4.1 Axial T1W postcontrast brain MRI shows right
frontal pachymeningeal enhancement with epidural abscess
formation ( arrow )
2.4 · Meningitis
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2
enhancement is seen as thin linear enhancement that
follows the pial surfaces, the cortical gyri, and fi lls the
subarachnoid spaces (. Fig. 2.4.2 ).
5 Ventriculitis is seen as an enhancement of the
subependymal surface of the ventricles after contrast
injection.
5 Subdural pus collection (empyema) is an extra-axial pus
collection that usually results from untreated or
chronic meningitis (crescent sign).
5 Abscess is seen as an area of low density on CT or low
T1 and high T2 signal intensities on MRI with uniform
rim enhancement after contrast injection (. Fig. 2.4.3 ).
The abscess is commonly surrounded by vasogenic
edema.
5 Subdural hygroma is a sterile collection of fluid located
in the subdural space usually as a sequela of meningitis
in children.
5 Hydrocephalus may arise due to inflammation of the
basal meninges blocking the fourth ventricle. It is seen
in advanced stages of meningitis. Dilatation of the
temporal horns is a definite sign of hydrocephalus.
5 Post meningioencephalic sequela is a severe advanced
stage of meningitis characterized by loss of brain tissue
(encephalomalacia) and parenchymal calcification with
hydrocephalus (. Fig. 2.4.4 ).
5 Superior sagittal sinus thrombosis may be seen as a
triangular fi lling defect on axial images ( delta sign ) .
. Fig. 2.4.3 Axial postcontrast brain CT shows right temporal
abscess with thin rim enhancement and vasogenic edema
( arrowhead ) that exerts mass eff ect over the anterior horns of
the lateral ventricles
. Fig. 2.4.2 Axial postcontrast brain CT shows enhancement
of the leptomeninges around the ambient cisterns ( arrowheads )
. Fig. 2.4.4 Axial nonenhanced brain CT shows
postmeningoencephalic parenchymal and meningeal (falx)
calcifi cation ( arrowheads )
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Chapter 2 · Neurology
D i ff erential Diagnoses and Related
Diseases
2
5 Multiloculated hydrocephalus is a clinicopathological
condition characterized by enlarged, loculated ventricles
with paraventricular porencephalic cavities. e
condition is seen in neonates, commonly as a sequel of
ventriculitis complicating neonatal meningitis. Neonates
present with hydrocephalus, neurological deterioration,
and seizures. Mortality rate is high (>70 %). CT and MRI
typically show multiloculated ventricles with irregular
borders and internal septae (. Fig. 2.4.5 ).
5 Canalis basilaris medianus is a congenital anomaly
characterized by a well-de ned channel seen in the
midline of the basiocciput, very close to the anterior
rim of the foramen magnum. It is seen on CT or MRI as
a linear defect in the midportion of the clivus
(. Fig. 2.4.6 ). Although it is an asymptomatic anomaly,
it can be the source of recurrent meningitis in children
due to transmission of bacteria from the superior
nasopharynx into the central nervous system through
this basiocciput defect.
5 Vogt–Koyanagi–Harada syndrome is a rare, sporadic, and
systemic disorder mostly seen in adults and characterized
by acute panuveitis, meningitis, and cutaneous
. Fig. 2.4.6 Axial CT illustration of the base of the skull shows a linear
median bony defect of the clivus (canalis basilaris medianus)
manifestations. e disease arises due to a widespread
pathology a ecting the melanin-forming cells in di erent
organs, typically in dark-skinned people. Uveitis is
in ammation of the uvea, which supplies nutrition to the
globe and is composed of the iris, ciliary body, and
choroid. Any part of the uvea can be involved in the
in ammation (e.g., iritis), and patients typically present
with a painful eye, with pain in the distribution of the
trigeminal nerve (because the ciliary body is supplied by
the ophthalmic division of the trigeminal nerve). e
disease has three phases: a prodormal phase characterized
by fever, severe headache, and tinnitus; an ophthalmic
phase characterized by bilateral uveitis and optic disk
hyperemia; and a convalescent phase seen weeks a er the
ophthalmic phase, characterized by premature graying of
hair (poliosis), vitiligo, alopecia, painful hearing
(dysacousia), tinnitus, and vertigo. Diagnostic criteria
include the absence of ocular trauma with the following:
(a) bilateral chronic iridocyclitis, (b) posterior uveitis
including retinal detachment, (c) neurological signs with
signs of meningitis (e.g., neck sti ness), and (d)
cutaneous ndings of alopecia, vitiligo, or poliosis. Signs
on orbital CT or MRI may show choroidal and scleral
thickening due to chronic in ammation on postcontrast
images or retinal detachment with typical (V-shaped
sign) on severe cases (
. Fig. 2.4.7 ). Uncommonly, the
disease can present with optic neuritis, seen as enhanced
optic nerve on postcontrast images on both CT and MRI.
. Fig. 2.4.5 Axial nonenhanced brain CT of a neonate shows
multiloculated hydrocephalus
Further Reading
Albanese V, etal. Neuroradiological ndings in multilocu-
lated hydrocephalus. Acta Neurochir. 1982;60:297–311.
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