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2.3 Intracranial Hemorrhage 59
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Fig. 2.3.3. Axial CT images of two different patients show acute
subdural hematoma ( a , arrowhead ) and chronic subdural hema-
toma ( b , arrow ). Again notice the pressure effect over the lateral
ventricles in the acute subdural hemaotoma ( a ) compared to the
chronic subdural hematoma ( b )
Fig. 2.3.4. Axial brain CT of a patient with a history of posttraumatic brain injury shows large left frontal subdural hygroma
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Fig. 2.3.5. Sequential axial
CT images of a patient with
subarachnoid hemorrhage
show hyperdense suprasellar
cistern and sylvian fi ssures
( arrowheads ) due to
2.3
subarachnoid bleeding
Signs on CT
There is hyperdense blood collection within the brain
parenchyma that usually follows a vascular territory (Fig.
2.3.6 ).
When the bleeding is due to stroke, it is surrounded by a
halo-like edema (cytotoxic edema), while when it is due to a
tumor, a fi nger-like 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 effect over the right anterior and posterior
horns of the right lateral ventricle ( arrowhead )
2.3 Intracranial Hemorrhage 61
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Fig. 2.3.7. 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
Intraventricular Hemorrhage
Intraventricular hemorrhage is bleeding into the ventricles. Commonly, it occurs secondary to parenchymal
or subarachnoid hemorrhage, and associated with diffuse axonal injury of the corpus callosum. Arteriovenous
malformation is the most common cause for spontaneous intraventricular hemorrhage in adults. There are
two types of intraventricular hemorrhage:
Ependymal intraventricular bleeding : the blood is
seen fi xed to the ventricular walls.
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. 2.3.8 ).
Signs on MRI
Chronic bleeding can be detected on T2* images as hypointense
intraparenchymal areas (Fig. 2.3.7 ).
Fig. 2.3.8. Axial brain CT of a patient with severe intraventricular hemorrhage shows dilated both ventricles due to bleeding,
with subependymal ( arrowhead ) and free ( arrow ) intraventricu-
lar bleedings also seen
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2.3
Hemorrhage into Malignancy
Hemorrhage into neoplasms accounts for 10% of spontaneous 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.
Signs on CT
Atypical location for bleeding in a patient with known
primary or secondary brain malignancy.
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
diff erent ages (mixed hypodense and hyperdense pattern).
For Further Reading
3 . Laguna P et al Intracranial hemorrhage in a boy with severe
haemophilia A and factor VIII inhibitor. Child’s Nerv Syst.
2006;22:432–5
4 . Dincsoy MY et al Intracranial hemorrhage in hypothalamic
low-birth-weight neonates. Child’s Nerv Syst. 1990;6: 245–9
5 . Heros RC et al Cerebral vasospasm after subarachnoid
hemorrhage: an update. Ann Neurol. 1983;14:599–608
6 . Koc RK et al Acute subdural hematoma: outcome and out-
come prediction. Neurosurg Rev. 1997;20:239–44
7 . Gross A et al Intraventricular hemorrhage originating from
choroids plexues angioma in a road accident victim. Z
Rechtsmed. 1989;102:409–13
8 . Schwartz DT. Sensitivity of computed tomography for sub-
arachnoid hemorrhage. doi:10.1016/j.annemergmed. 2008.
06. 471
9 . Moster ML et al Chronic subdural hematoma with transient
neurological defi cits: a review of 15 cases. Ann Neurol. 1983;
14:539–42
10 . Masuzawa T et al Computed tomographic evolution of
post-traumatic subdural hygroma in young adults.
Neuroradiology. 1948;26:245–8
11 . Park CK et al Spontaneous evolution of post-traumatic
subdural hygroma into chronic subdural hematoma. Acta
Neurochir (Wien). 1994;127:41–7
12 . Masuzawa T et al Computed tomography evolution of post-
traumatic subdural hygroma in young adults. Neuroradiology. 1984;26:245–8
1 . Xi G et al Intracerebral hemorrhage, pathophysiology and
therapy. Neurocrit Care. 2004;1:5–18
2 . Schellinger PD et al Intracranial hemorrhage, the role of
magnetic resonance imaging. Neurocrit Care. 2004;1: 31–45
2.4 Meningitis 63
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2.4
Meningitis
Meningitis is a disease characterized by infl ammation
of the meninges due to infections or infl ammatory disease (e.g., sarcoidosis). Infectious meningitis can be
bacterial (e.g., Pneumococcus ) or viral (e.g., Hemophilus
infl uenza ).
Patients with meningitis classically present with
fever, neck stiffness, and neurological symptoms.
Rarely, meningitis may lead to suprarenal gland suppression, causing patient death due to adrenal gland
insuffi ciency. Infection of the 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
after contrast injection (Fig. 2.4.3 ). The abscess is commonly
surrounded by vasogenic edema.
Subdural Hygroma : is a sterile collection of fl uid located in the
subdural space usually as a sequela of meningitis in children.
Hydrocephalus may arise due to infl ammation of the basal
meningies blocking the 4th ventricle. It is seen in advanced
stages of meningitis. Dilatation of the temporal horns is a
defi nite sign of hydrocephalus.
Post meningio-encephalic sequela : is a severe advanced stage
of meningitis characterized by loss of brain tissue (encephalomalacia) and parenchymal calcifi cation with hydrocephalus
(Fig. 2.4.4 ).
Superior sagittal sinus thrombosis may be seen as a triangular
fi lling defect on axial images ( delta sign ).
Meningitis is detected typically as thickened meningies 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 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 ).
Ventriculitis is seen as an enhancement of the subependymal
surface of the ventricles after contrast injection.
Subdural pus collection (empyema) : is an extra-axial pus
collection that usually results from untreated or chronic
meningitis (crescent sign).
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
Fig. 2.4.1. Axial T1W postcontrast brain MRI shows right frontal pachymeningeal enhancement with epidural abscess formation ( arrow )
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2.4
Fig. 2.4.2. Axial postcontrast brain CT shows enhancement of
the leptomeningies around the ambient cisterns ( arrowheads )
Fig. 2.4.3. Axial postcontrast brain CT shows right temporal
abscess with thin rim enhancement and vasogenic edema ( arrow-
head ) that exerts mass effect over the anterior horns of the lateral
ventricles
Fig. 2.4.4. Axial nonenhanced brain CT shows postmeningoencephalic parenchymal and meningeal (falx) calcifi cation
( arrowheads )
D i ff erential Diagnoses and Related Diseases
Multiloculated hydrocephalus: is a clinicopathologi-
cal condition characterized by enlarged, loculated
ventricles with paraventricular porencephalic cavities. The condition is seen in neonates, commonly as
a sequel of ventriculitis complicating neonatal meningitis. Neonates presents with hydrocephalus, neurological deterioration, and seizures. Mortality rate
is high (>70%). CT and MRI typically show multiloculated ventricles with irregular boarders and
internal septae (Fig. 2.4.5 ).
Canalis basilaris medianus: is a congenital anomaly
characterized by a well-defi 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
2.4 Meningitis 65
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children due to transmission of bacteria from the
superior nasopharynx into the central nervous system through this basiocciput defect.
Vogt–Koyanagi–Harada syndrome : is a rare, spo-
radic, and systemic disorder mostly seen in adults
and characterized by acute panuveitis, meningitis,
and cutaneous manifestations. The disease arises due
to a widespread pathology affecting the melaninforming cells in different organs, typically in dark
skinned people. Uveitis is infl 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 infl 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). The
disease has three phases: a prodormal phase characterized by fever, severe headache, and tinnitus; an
ophthalmic phase characterized by bilateral uveitis
and optic disc hyperemia; and convalescent phase
seen weeks after the ophthalmic phase, characterized by premature graying of hair (poliosis), vitiligo,
Fig. 2.4.5. Axial nonenhanced brain CT of a neonate shows
multiloculated hydrocephalus
alopecia, painful hearing (dysacousia), tinnitus, and
vertigo. Diagnostic criteria include absence of ocular
trauma with four of the following: (a) bilateral
chronic iridocyclitis, (b) posterior uveitis including
retinal detachment, (c) neurological signs with signs
of meningitis (e.g., neck stiffness), and (d) cutaneous
fi ndings of alopecia, vitiligo, or poliosis. Signs on
orbital CT or MRI may show choroidal and scleral
thickening due to chronic infl 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. 2.4.6. Axial CT illustration of the base of the skull shows a
linear median bony defect of the clivus (canalis basilaris
medianus)
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Fig. 2.4.7. Orbital CT
postcontrast ( a ) and
nonenhanced ( b ) illustra-
tions of a patient show left
eye choroidal/scleral
thickening and enhancement
2.4
due to uveitis in ( a )
( arrowhead ), with V-shaped
sign of retinal detachment in
the left eye in ( b )
For Further Reading
1 . Bilaniuk LT et al Computed tomography in meningitis.
Neuroradiology. 1978;16:13–4
2 . Splendiani A et al Contrast-enhanced FLAIR in the early
diagnosis of infectious meningitis. Neuroradiology. 2005;
47:591–8
3 . Smirniotopoulos JG et al Patterns of contrast enhancement
in the brain and meninges. RadioGraph. 2007;27:525–51
4 . Albanese V et al Neuroradiological fi ndings in multilocu-
lated hydrocephalus. Acta Neurochir. 1982;60:297–311
5 . Kamra P et al Infectious meningitis: prospective evaluation
with magnetization transfer MRI. Brit J Radiol. 2004;77:
387–94
6 . Jacquemin C et al Canalis basilaris medianus: MRI. Neuro-
radiology. 2000;42:121–3
7 . Gilbert JA et al Vogt-Koyanagi-Harada syndrome: case
report and review. J Emerg Med. 1994;12:615–9
8 . Rao NA et al Vogt-Koyanagi-Harada disease diagnostic cri-
teria. Int Opthalmol. 2007;27:195–9
9 . McGehee BE et al Bilateral retinal detachment in a patient
with Vogt-Koyanagi-Harada syndrome. Emerg Radiol. 2005;
11:366–71
2.5 Encephalitis 67
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2.5
Encephalitis
Encephalitis means infl ammation of the brain parenchyma. Brain infl ammation can result from different
etiologies, most commonly viruses and autoimmune
infl ammation.
Patients with encephalitis typically present in early
stages with headache or fl ue-like illness, followed by
alteration in consciousness, drowsiness, confusion,
fever, and seizures. Coma may result in severe cases.
This topic discusses the different kinds of encephalitis with their characteristic radiological features.
Limbic Encephalitis
The brain can be divided into regions according to
functions. The fi rst part is the brain stem, which plays
a role in the basic attention, consciousness, arousal,
heart and respiration adjustment, temperature control,
and sleep–wake cycle control. The second part is the
limbic system, which controls the behavior related to
food, hormones and sex, jealousy, sadness and love,
pleasure, and fl ight or fi ght responses. The limbic system is composed of the hippocampus, thalamus, hypothalamus, and amygdale. The third part is the rational
brain (neocortex), which controls logic, thoughts,
speaking, planning, and writing.
Limbic encephalitis (LE) involves infl ammation of
one structure or more related to the limbic system. LE
can be caused by infections (e.g., herpes simplex
virus), or auto-immune response.
Herpes encephalitis ( HSE ) is caused by herpes sim-
plex virus type 1 or type 2. HSE type 1 is often seen in
children and young adults. It starts as an orofacial
infection (gingivostomatitis), which lasts for 1–2
weeks, followed by fl u-like symptoms. Patients present with fever, headache, and change in mental status.
The virus spreads in retrograde fashion along the
trigeminal nerve course or the olfactory bulb into the
brain. In the brain, the virus has affi nity to infect the
meningies, temporal lobes, and the inferior frontal
lobe. HSE type 1 is the most common cause of encephalitis (95%). HSV type 2 is a genital form of HSE that
affects neonates delivered by mothers, with herpes
infection in the birth canal. It is an uncommon type of
encephalitis (15%), and clinical diagnosis is usually
confi rmed by cerebrospinal fl uid (CSF) analysis that
reveals high leucocytes and protein content, and detection of the herpes virus DNA by serology.
Autoimmune LE has two forms. The fi rst form is
called paraneoplastic limbic encephalitis ( PLE ), which
is seen in patients with particular cancers with paraneoplastic manifestations, such as thymus, lung, breast,
and testes cancers. PLE is confi rmed by detecting
paraneoplastic antibodies in the patient blood like
immunoglobulin G antibodies, ANNA 1, PCA 1, CV2,
MA 2, and ANNA 2 antibodies.
The other form of autoimmune LE is nonPLE,
which has the same picture as PLE in the absence of
the serum paraneoplastic antibodies. The most common subsyndrome of the nonPLE is voltage-gated
potassium channel ( VGKC ) antibody-associated
encephalitis . This syndrome is commonly undiagnosed
due to the lack of awareness about its existence. The
diagnosis of autoimmune LE is important because it
responds well to immunosuppressive drugs.
Signs on CT
Initially, the scan may be normal, or shows hypodense lesions
aff ecting the medial temporal lobes mainly in a bilateral
asymmetrical pattern with mass eff ect and edema (Fig. 2.5.1 ).
Areas of necrosis and hemorrhage may be seen on nonenhanced contrast images. Postcontrast images show patchy
enhancement. The explanation for the temporal lobes
aff ection lies in the reactivation of the virus from the
trigeminal ganglia within Meckle’s cave.
Postencephalitic sequel includes parenchymal calcifi cation
and dilatation of ventricles.
In HSE, the basal ganglia are often spared.
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Fig. 2.5.1. Axial sequential
T2W MR-Images show
bilateral symmetrical
hyperintense signal intensities affecting the region of the
temporal lobes (both white
2.5
and gray matters) in a patient
with herpes encephalitis
(HSE)
Signs on MRI
In HSE, hyperintense, ill-defi ned cortical and white matter
areas on T2W sequences with edema, mass eff ect, and gyral
enhancement (Fig. 2.5.1 ) are seen. Later in the course of the
disease, meningeal enhancement after contrast may be seen
due to spread of the virus to the meningies.
Autoimmune LE shows the same picture like HSE. Bilateral
temporal and hippocampal lesions are typically seen. The main
diff erence is based on the CSF analysis detecting the virus
antibodies, or the autoimmune antibodies. Also, the history of
cancer favors the autoimmune encephalitis.
Acute Demyelinating Encephalomyelitis
(ADEM)
ADEM is an autoimmune demyelinating encephalitis
that arises typically as an immune reaction 2 weeks
after viral infection with MMR (measles, mumps,
rubella), whooping cough infection (pertussis), or after
immunization with MMR vaccine.
In ADEM, there is a hypersensitivity reaction affecting myelin and brain vessels (vasculitis). Patients classically present with sudden onset of neurological symptoms
refl ecting a wide central nervous system disturbance 2
weeks after viral infection or immunization.
ADEM has the same MRI picture as multiple sclerosis (MS). Unlike MS, which has multiple relapsing episodes, ADEM occurs once in life (monophasic course).
Acute hemorrhagic leukoencephalitis ( AHL ) is a
severe form of ADEM characterized by intraparenchymal hemorrhage. AHL often arises after an upper
respiratory tract infection or allergic reaction. The
patient will show features of encephalitis, fever, and
impaired consciousness.
Signs on MRI
Large multifocal periventricular lesions with mild mass eff ect
giving high signals in T2 (demyelinating areas) exactly like MS
plaques, with asymmetric involvement of cerebral hemispheres (Fig. 2.5.2 ). MS plaques are often found bilaterally.
The demyelinating plaques show ring enhancement after
gadolinium injection in a similar fashion like acute MS
plaques.
Involvement of spinal cord and the cortical gray matter is
common.
Contrast enhancement is not always a feature.
Typically, ADEM does not involve the corpus callosum.
Bilateral optic neuritis may occur.
In AHL, signs of hemorrhagic plaques are found on nongado-
linium enhanced images.
How can you differentiate between MS and ADEM?
MS has an acute and chronic phase, while ADEM
has only one acute stage.
MS affects white matter only, while ADEM affects
white and gray matters.
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