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2.5 Encephalitis 69
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Fig. 2.5.2. Axial T1W ( a )
and FLAIR ( b ) images in a
patient with acute demyelinating encephalomyelitis
(ADEM) after measles,
mumps, rubella (MMR)
vaccination shows multifocal
hyperintense areas in ( b )
affecting the posterior lobe
and the area around the
temporal horns of the lateral
ventricles ( arrowheads ). The
areas are patchy and
asymmetrically distributed
Clinical history of infection or immunization with
ADEM.
Corpus callosum is typically not affected in ADEM,
while it is commonly affected in MS.
ADEM causes bilateral optic neuritis, while MS typ-
ically causes unilateral optic neuritis.
Hashimoto’s Encephalitis
Hashimoto’s encephalopathy (HE) is defi ned as a syndrome of persistent or relapsing neurological or neuropsychiatric symptoms, even though the thyroid levels
are usually normal.
HE usually affects children in school age, with an
incidence of 1.2% of population. Asymptomatic thyroid goiter can be seen in 85% of patients.
Patients with HE typically present with different
unexplained neurological symptoms like epilepsy,
behavioral changes, ataxia, hallucinations, or dementia. Diagnosis needs high level of suspicion. The characteristic feature that confi rms HE in a patient with
unexplained encephalitis is to fi nd high levels of thyroid antibodies in the serum, which is always abnormally high. In contrast, the thyroid function levels
usually are within normal or lower than normal range.
The disease responds well to steroid therapy.
Signs on MRI
The signs on MRI in HE are nonspecifi c. The MRI can be normal,
or show nonspecifi c features of subcortical white matter
changes (not the normal changes seen in a patient with
epilepsy) (Fig. 2.5.3 ).
Rasmussen’s Encephalitis
(Rasmussen’s Syndrome)
Rasmussen encephalitis (RE) is a rare, pediatric disease of chronic encephalitis usually effecting one hemisphere. The disease is characterized by partial motor
seizures and progressive cognitive deterioration.
RE has an unknown cause, although viral and immunological causes have been suggested. Patients may
show high titers of Epstein-Barr virus and cytomegalovirus in the CSF, with high serum GluR3 antibodies
supporting the autoimmune and the viral theories.
RE is mostly seen in children (mainly pediatric disease), although few rare adult cases have been reported.
RE has three stages, initial, acute, and residual. In the initial stage, the patient suffers from few partial motor seizures. Later in the acute stage, there is increased frequency
of the seizures attack. The residual stage is characterized
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2.5
Fig. 2.5.3. Axial FLAIR MR-illustrations demonstrate different
brain affection pattern in different types of encephalitis disorders: ( a ) Hashimoto encephalitis, ( b ) measles encephalitis (ME)
by cortical atrophy and permanent neurological defi cits.
Histopathology features include gliosis and perivascular
cuffi ng in both the white and the gray matters.
The key to suspect and diagnose RE is to have a
pediatric patient with multiple attacks of epilepsy,
increasing in frequency, with serial MRI examinations
showing changes and atrophy in one cerebral hemisphere only. Brain biopsy may be needed to confi rm
the diagnosis in atypical cases. Treatment ranges
between antiepileptics, antiviral medications, corticosteroids and immunosuppressive agents.
( c ) subacute sclerosing panencephalitis (SSPE), ( d ) Japanese
encephalitis (JE), and ( e ) encephalitis lethargica
Criteria to Diagnose Rasmussen Encephalitis
Previously healthy child between 14 months and 14
years.
Patients present with drug-resistant seizure, usually
tonic-clonic or partial seizure.
There are progressive unilateral neurological defi cits
that might lead to paresis (bilateral involvement
occasionally).
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Signs on MRI
Hyperintense cortex is seen on T2W or FLAIR images on
noncontrast enhanced images aff ecting the parieto-frontal or
the temporal lobes in acute stages (Fig. 2.5.4 ). The MRI may
be normal initially, and then shows signs of unilateral cortical
atrophy. Classically, the contralateral hemisphere, basal
ganglia, and the posterior fossa are unaff ected. However,
head of the caudate nucleus may be aff ected.
In the residual stage, cortical atrophy, ventricular enlarge-
ment of the aff ected side (Evaccu dilatation), and caudate
nucleus atrophy can be seen with atrophy of the whole
cerebral hemisphere. Atrophic changes are predominantly
seen in the peri-sylvian area and the caudate nucleus.
Measles Encephalitis
Measles encephalitis (ME) is a brain infl ammation due
to an acute infection with measles virus. ME is considered rare due to the worldwide spread of MMR vaccine (0.05–0.4%), yet few sporadic cases are reported
in the literature occasionally.
ME starts on the second to sixth day after development of the rash, but it may precede the rash. Patients
present with the usual clinical picture of encephalitis.
Diagnosis is made on the basis of identifying high
antimeasles antibodies titers in the CSF.
Signs on MRI
MRI often shows bilateral T1/T2 hyperintense signal intensities
in the basal ganglia and the white matter (Fig. 2.5.3 ).
The fronto-temporal areas may be aff ected in an asymmetric
pattern bilaterally.
Subacute Sclerosing Panencephalitis (SSPE)
Fig. 2.5.4. Axial FLAIR image in a child with recurrent epilepsy shows moderate hyperintense cortices in the left temporooccipital region in a unilateral pattern ( arrowheads ). The patient
was diagnosed later as a case of Rasmussen encephalitis (RE)
SSPE is a well-recognized chronic complication of
measles virus, developing 6–12 years after initial measles infection.
SSPE is a rare disease, with an incidence of
1:1,000,000, and high mortality rate. The majority of
patients with SSPE are known to have a previous attack
of classical measles years before. Fifty percent of SSPE
cases occur after 2 years from the initial measles infection, and patients are between 5 and 15 years of age.
Patients with SSPE often present behavioral changes
with jerking movements know as myoclonic seizures.
The myoclonic jerking is exacerbated on excitement.
Later, grand-mal (tonic-clonic) seizure develops, with
problems in swallowing, speech, and vision. Some
patients may develop pyramidal signs with cerebellar
signs (e.g., ataxia). Cortical blindness due to occipital
lobe involvement or optic nerve edema may occur. The
diagnosis of SSPE should be considered in patients
with cortical blindness even when other classical fi ndings of SSPE are absent. The duration of the illness can
be short (e.g., 6 weeks), or very long (e.g., 10 years).
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Diagnosis of SSPE is based on the high serum and
CSF antimeasles antibody titers detection. Imaging is
helpful in establishing differential diagnosis.
Signs on MRI
Commonly, the periventricular and subcortical white matter
are aff ected in SSPE (Fig. 2.5.3 ), with bilateral high T2W and
FLAIR signal intensities seen on MRI.
The basal ganglia, cerebellum, spinal cord, and corpus
callosum are less frequently aff ected.
Japanese Encephalitis
Japanese encephalitis (JE) is acute viral encephalitis,
caused due to infection with JE virus. JE virus belongs
to the Flaviviridae family (Flavivirus). The virus is
transmitted to humans from its hosts via its carrier, the
Culex tritaeniorhunchus mosquito. The natural hosts
of the JE virus are pigs, birds, dogs, and horses.
Following bite on the human body from an infected
mosquito, the virus proliferates in the lymphatic system. From there, it enters the blood stream and crosses
the blood-brain barrier (BBB) to start brain parenchymal infl ammation. Patients with JE present with loss of
appetite (anorexia), fatigue, headache, and vomiting.
The initial stage of the disease is characterized by rapidly progressing fever and nonspecifi c central nervous
system symptoms. The neurological symptoms include
rigidity, Parkinson-like symptoms, altered mental status, and seizures. The fever and the systemic symptoms improve gradually after 7–8 days. In 10% of
patients, long-term sequelae may occur, including psychiatric symptoms, motor impairment, and epilepsy.
Diagnosis is confi rmed by detection of JE virus
antibodies, or isolation of the virus from the CSF.
Signs on MRI
The classical fi ndings in JE include bilateral symmetrical high signal
intensity lesions on T2W and FLAIR images located in both thalami
(Fig. 2.5.3 ). Similar lesions may be found in the basal ganglia,
substantia nigra, hippocampus, pons, and cerebral white matter.
Hemorrhagic lesions in the thalami may be found occasionally.
West Nile Encephalitis
West Nile encephalitis (WNE) is encephalitis caused
by acute infection with the West Nile virus (WNV).
WNW is a positive-strand RNA virus belonging to the
Flaviviridae family.
WNE is observed in the Middle East and African
countries. The virus is transmitted to humans from the
C. tritaeniorhunchus mosquito from its original hosts;
the hosts of the WNV are crows and pigeons. WNV is
an “arbovirus.” Arboviruses are viruses that are transmitted from one animal host to the next by insects
(anthropods). WNV is not transmitted from person to
person.
Patients with WNE present with nonspecifi c febrile
illness, lymphadenopathy, skin rash, headache, and
body ache. Encephalitis symptoms start when the virus
crosses the BBB, resulting in seizures, confusion,
paralysis, and behavioral changes that may be mistaken with hysteria.
Diagnosis is based on detecting high titers of WNV
antibodies in the CSF.
Signs on MRI
The scan shows bilateral symmetrical lesions in both thalami,
with hemorrhagic tendency. The MRI picture is similar to the JE
picture.
Tick-Borne Encephalitis
(Spring-Summer Encephalitis)
Tick-borne encephalitis (TBE) is encephalitis caused
by TBE virus, a virus that belongs to the Flaviviridae
family.
Patients with TBE commonly present with meningitis (49%), followed by meningoencephalitis (41%),
and meningoencephalomyelitis (10%). Patients may
present with polio-like symptoms with polyradiculitis
course. The virus has an affi nity to the anterior horn
cells in the spinal nerve roots.
Diagnosis is based on confi rming the virus antibodies in the CSF.
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Signs on MRI
The brain MRI shows same picture like JE and WNE.
Polyradiculitis is seen as marked contrast enhancement of the
spinal nerve roots on contrast-enhanced images (Fig. 2.5.5 ).
Fig. 2.5.5. Axial postcontrast spinal MR-illustration at the level
of L3/L4 shows enhanced cauda equine roots and spinal roots
representing polyradiculitis ( arrowheads )
Murray Valley Encephalitis
Murray valley encephalitis (MVE) is encephalitis
caused by MVE virus, another virus that belongs to the
Flaviviridae family.
Majority of patients with MV virus are asymptomatic, with only 1:1,000 infected persons developing
encephalitis. The symptoms are nonspecifi c, with neurological residua in 40% of survivors. Diagnosis is
based on detecting the virus antibodies in the CSF.
Signs on MRI
The brain MRI shows same picture like JE, TBE, and WNE.
St. Luis Encephalitis
St. Luis encephalitis is a disease caused by the St. Luis
virus, another virus that belongs to the Flaviviridae
family. The virus was named after it was isolated from
the human brain tissue in 1933 during a large epidemic
in St. Luis city, USA.
The disease ranges between fl ue-like illnesses to a lifethreatening central nervous system disease. Diagnosis is
based on CSF serology.
Signs on MRI
The brain MRI shows same picture like JE, TBE, MVE, and WNE.
The substantia nigra is commonly involved in St. Luis
encephalitis.
Encephalitis Lethargica
Encephalitis lethargica (EL) is a rare, mysterious form
of encephalitis that was responsible for epidemic disease that killed 500,000 people from about 1917 until
1940. Many investigators link EL with the notorious
Spanish fl ue infl uenza virus, which is responsible for
the infl uenza epidemic at the end of the First World
War. Although the disease is considered historical, few
sporadic cases are reported from time to time.
EL typically has three forms: irritable, lethargic,
and lethargic with paralysis. The irritable form is characterized by marked restlessness and excitability. The
lethargic stage is characterized by a drowsy state, and
expressionless, mask-like face, resembling Parkinson’s
disease. The third stage is characterized by drowsiness
with some form of motor paralysis in the lower extremities, and frequent convulsions.
Patients with EL present with characteristic gradual
onset of headache, lethargy and asthenia, low grade
fever, cranial nerve palsies, and vomiting, especially in
children. Other neuro-psychiatric symptoms include
Parkinsonian mask-face, catatonia, choreiform movements, insomnia, delirium, and profound sweating.
Children with EL present with a wide variety of
behaviors that can be regarded as psychopathic. These
include personality change, emotional instability,
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nervousness, restlessness, and destructive and impulsive mood.
EL is one of the causes of juvenile Parkinsonism,
mainly the rigid-akinetic form. This can be explained
by the fact that the basal ganglia are classically affected
in EL.
Criteria to diagnose EL include encephalitis with
three of the following major criteria, assuming all the
known causes of encephalitis have been excluded
Neuro-psychiatric symptoms.
Sleep disturbance (e.g., insomnia)
Signs of basal ganglia involvement (e.g., Parkinson-
like symptoms).
Ophthalmic symptoms.
Obsessive compulsive behavior.
Respiratory irregularity.
Signs on MRI
MRI of EL patients show bilateral basal ganglia lesions with high
signal intensities on T2W and FLAIR images (Fig. 2.5.3 ).
For Further Reading
1 . Urbach H et al Serial MRI of limbic encephalitis.
Neuroradiology. 2006;48:380–6
2 . Collison K et al Asymmetric cerebellar ataxia and limbic
encephalitis as a presenting feature of primary Sjögren’s
syndrome. J Neurol. 2007;254:1609–11
3 . Vilensky JA et al Children and encephalitis lethargica: a
historical review. Pediatr Neurol. 2007;37:79–84
4 . Beleza P et al From juvenile Parkinsonism to encephalitis
lethargica, a new phenotype of post-streptococcal disorders: case report. Euro J Paediatr Neurol. 2008;12:505–7
5 . Benneis C et al Encephalitis lethargica following Bartonella
henselae infection. J Neurol. 2007;254:546–7
6 . Alfaresi M et al West Nile virus in the blood donors in UAE.
Indian J Med Microbiol. 2008;26:92–3
7 . Bosanko CM et al West Nile virus encephalitis involving the
substantia nigra. Neuroimaging and pathologic fi ndings
with literature review. Arch Neurol. 2003;60:1448–52
8 . Bender A et al Sever tick borne encephalitis with simulta-
neous brain stem, bithalamic, and spinal cord involvement
documented by MRI. J Neurol Neurosurg Psychiatry. 2005;
76:135–7
9 . Pfefferkorn T et al Tick-borne encephalitis with polyradicu-
litis documented by MRI. Neuroradiology. 2007;68: 1232–3
10 . Grubbauer HM et al Tick-borne encephalitis in a 3-month-
old child. Eur J Pediatr. 1992;151:743–4
11 . De Tiège X et al The spectrum of herpes simplex encepha-
litis in children. Euro J Paediatr Neurol. 2008;12:72–81
12 . Senol U et al Subacute sclerosing panencephalitis: brain
stem involvement in a peculiar pattern. Neuroradiology.
2000;42:913–6
13 . Pedersen H et al Computed tomographic fi ndings of early
subacute sclerosing panencephalitis. Neuroradiology. 1982;
23:31–2
14 . van der Meyden CH et al Gadolinium ring enhancement
and mass effect in acute disseminated encephalomyelitis.
Neuro radiology. 1994;36:221–3
15 . Garg RK. Subacute sclerosing panencephalitis. J Neurol.
doi:10.1007/s00415-008-9932-6
16 . Feydy A et al Brain and spinal cord MR imaging in a case of
acute disseminated encephalomyelitis. Eur Radiol. 1997;7:
415–7
17 . Bermejo PE et al Hemorrhagic acute disseminated enceph-
alomyelitis as fi rst manifestation of systemic lupus erythematosus. J Neurol. 2008;255:1256–8
18 . Lacroix C et al Acute necrotizing measles encephalitis in a
child with AIDS. J Neurol. 1995;242:249–56
19 . Baba Y et al Acute measles encephalitis in adults. J Neurol.
2006;253:121–4
20 . Parmar RC et al Measles encephalitis: a case report of two
cases with variable manifestations. Pediatr Int. 2002;44: 90–2
21 . Lury KM et al Eastern equine encephalitis: CT and MRI
fi ndings in one case. Emerg Radiol. 2004;11:46–8
22 . Wong SH et al Murray Valley encephalitis mimicking her-
pes simplex encephalitis. J Clin Neurosci. 2005;12:822–4
23 . Kroeger MA et al Murray Valley encephalitis virus recom-
binant subviral particles protect mice from lethal challenge
with virulent wild-type virus. Arch Virol. 2002;147:
1155–72
24 . Parquet MC et al St. Louis encephalitis virus induced
pathology in cultured cells. Arch Virol. 2002;147:1105–19
25 . Abe T et al Japanese encephalitis. JMRI. 1998;8:755–61
26 . Paprocka J et al Diffi culties in differentiation of Parry-
Romberg syndrome, unilateral facial scleroderma, and
Rasmussen syndrome. Childs Nerv Syst. 2006;22:409–15
27 . Granata T. Rasmussen’s syndrome. Neurol Sci. 2003;24:
S239–43
28 . Rajesh B et al Putaminal involvement in Rasmussen
encephalitis. Pediatr Radiol. 2006;36:816–22
29 . Heo SH et al A case of unilateral hemispheric encephalitis.
Neurol Sci. 2007;28:185–7
30 . Deb P et al Neuropathological spectrum of Rasmussen
encephalitis. Neurol India. 2005;53:156–61
31 . Bertoni M et al Encephalopathy associated with Hashimoto’s
thyroiditis: an additional case. Euro J Intern Med. 2003;14:
434–47
32 . Vasconcellos E et al Pediatric manifestations of Hashimoto’s
encephalopathy. Pediatr Neurol. 1999;20:394–8
33 . Arain A et al Hashimoto’s encephalopathy: documentation
of temporal seizure origin by ictal EEG. Seizure. 2001; 10:
438–41
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Mesial hippocampal (temporal) sclerosis : is a dis-
2.6
Epilepsy
Epilepsy is a chronic neurologic disease characterized
by recurrent, spontaneous episodes of seizures, which
are defi ned as excessive abnormal neuronal activity of
the cortical neurons. Seizures originate either from a
localized area within the brain (partial/focal), or arise
from both hemispheres simultaneously (generalized).
Partial seizures can be associated with loss of con-
sciousness (complex), or occur without loss of consciousness (simple/Jacksonian). Partial seizures can
spread from one area to another, ending up in initiating
secondary generalized seizure. Patients with partial
simple seizures experience mental events like: confusion, mild hallucinations, jerking movements, or emotional events (déjà vu phenomenon). In contrast, partial
complex seizure patients experience uncontrolled
behavior, loss of judgment, and loss of consciousness.
Also, patients with partial complex seizures often
experience a warning sign such as aura, odd odor, or
visual or auditory hallucinations. Partial seizures are
resistant to antiepileptic drugs in up to 30% of cases.
Generalized seizures are divided into two types:
one type is characterized by episodes of rigidity (tonic)
followed by repetitive involuntary movements (clonic),
and it is called “Grand mal seizure.” The other type is
characterized by absence of seizure with sudden, brief
(seconds) episode of loss of physical movement, and it
is called “Petit mal seizure.”
Status epilepticus is a condition characterized by
continuous seizure attack that lasts more for than 5
min, and can extend up to 30 min. Status epilepticus
can occur as a withdrawal symptom of antiepileptic
medications. Todd’s paralysis is a form of temporary
motor weakness experienced by the patient after an
episode of seizure.
Epilepsy can be caused by a variety of clinical conditions. Any condition that insults the brain cortex is
capable of initiating seizure attacks and epilepsy.
Moreover, seizure attacks can be initiated by metabolic
abnormalities (e.g., hypercalcemia). The role of brain
imaging in epilepsy is to detect anatomical structural
abnormalities. It is practical to divide the common
causes of epilepsy into fi ve simplifi ed main groups:
ease characterized by atrophy and sclerosis of the
hippocampus. Most patients have a history of brain
injury before the age of 5 years in the form of febrile
convulsion or status epilepticus. Mesial temporal
sclerosis is the most common cause of epileptic seizures in adults (40–60% of cases).
Congenital cortical anomalies : constitute up to
50% of epilepsy cases in children, and up to 25% of
adult cases. Anomalies that fall into this group
include lissencephaly, pachygyria, polymicrogyria,
gray matter heterotopia, and phakomatosis. The
frontal lobe is commonly involved in congenital
cortical anomalies.
Neoplasms : constitute up to 4% of epilepsy cases,
and they are mostly cortical neoplasms like astrocytoma, ganglioglioma, desmoplastic neuroepithelial
tumor, and oligodendroglioma. The temporal lobe is
commonly involved in cortical neoplasms.
Vascular abnormalities : constitute up to 5% of epi-
lepsy cases, and commonly include arteriovenous
malformations and cavernous angiomas.
Gliosis : is the result of the previous insult to the cortex
like postinfarction, postinfection, and posttrauma.
D i ff erential Diagnoses and Related Diseases
Lafora disease : is a very rare, autosomal recessive
disease characterized by myoclonic jerks, generalized tonic-clonic seizures, and multisystemic manifestation. Myoclonus jerks are brief involuntary
contractions of a group of muscles (e.g., hiccups are
myoclonus jerks of the diaphragm). The disease is
caused by abnormal deposition of polyglucosan in
the central nervous system, liver, myocardium, skin,
and muscles. Diagnosis is confi rmed by skin biopsy
that identifi es polyglucosan inclusions ( Lafora bod-
ies ) by positive periodic acid Schiff (PAS) stain.
Patients present typically before 20 years of age,
complaining of multiple attacks of myoclonic, generalized tonic-clonic seizures, intellectual disturbance,
and severe progressive motor and coordination disturbance. Patients often show abnormal liver profi le
due to liver failure. The disease is frequently seen
in countries where consanguineous marriages are
common, like the Middle East, India, and Pakistan.
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2.6
Death occurs almost 6–10 years after the fi rst manifestation of the disease.
Ulegyria : is a disease characterized by destruction
and gliosis of the gray matter in the depth of the sulci
with relative preservation of the gyral surfaces, giving the gyri a “mushroom shaped-appearance.”
Ulegyria commonly arises as a late effect of perinatal and postnatal hypoxia. It tends to occur in a symmetrical fashion in the perisylvian areas.
Schinzel-Giedion syndrome : is a rare, autosomal reces-
sive disease characterized by seizures, mental retardation, and spasticity. Other manifestations include
characteristic facial features, bitemporal narrowing
giving the skull “fi gure of 8 shape,” choanal atresia,
congenital heart defects, wide occipital synchondrosis, distal phalangeal hypoplasia, and hypospadia.
Signs on CT and MRI
I n mesial temporal sclerosis , there is increased T2 signal
intensity of the hippocampus, ipsilateral atrophy of the
temporal lobe with dilatation of the temporal horn (Fig. 2.6.1 ).
The key diagnosis is atrophy and high T2 signal intensity of
the hippocampus.
In oligodendroglioma , there is a brain mass with calcifi cations
and minimal brain edema. The lesion is seen predominantly
located in the frontal lobe, and shows heterogenous contrast
enhancement (Fig. 2.6.2 ).
In ganglioglioma , there is a lesion that arises from the frontal
or the temporal lobes cortices. Usually, the patient has a
history of epilepsy. The lesion can be cystic, solid, or mix. It
may show heterogeneous contrast enhancement, and rarely
shows calcifi cation.
In desmoplastic neuroepithelial tumor , there is a hypodense
lesion located in the temporal lobe cortex on CT, with no specifi c
signal on MRI. Usually, the patient has a history of epilepsy. The
tumor shows no contrast enhancement (Fig. 2.6.3 ).
In gliosis , the cortex shows an area of low signal intensity on
T1W and T2W images due to parenchymal fi brosis (Fig. 2.6.4 ).
In cavernous angioma , there is a honeycomb-like lesion that
appears with no edema or mass eff ect (except in cases of fresh
bleeding). The lesion has an isointense signal on T1W and
T2W images, with mixed hyperintense (blood) and
hypointense (calcium/hemosiderin) signals within it, and
surrounded by a hypointense rim of hemosiderin (pathognomonic sign, Fig. 2.6.5 ). MR-angiography shows no vascular
malformation, usually because most of the lesion is
thrombosed.
In
Lafora disease , brain infarction in the frontal and parietal
subcortical white matter areas may be seen after severe
seizure attack. On MR-Spectroscopy, there is a characteristic
decrease in N -acetylaspartate (NAA)/Creatine ratio in the
frontal lobe and the basal ganglia.
In ulegyria , the MRI scan shows thin gyri in the perisylvian
area with abnormal high T2 signal in a bilateral, symmetrical
fashion (Fig. 2.6.6 ). Unilateral lesions can occur.
status epilepticus , the hippocampus shows unilateral or
In
bilateral high signal intensity signal on both T2W and FLAIR
images (Fig. 2.6.7 ). This sign is usually seen in the acute
phase, and can extend up to months after the initial attack.
Fig. 2.6.1. Coronal T2W brain MRI of a patient with recurrent
epilepsy shows mild atrophy of the right hippocampus with
higher T2 signal intensity ( arrow ) compared to the left side
(mesial temporal sclerosis)
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Fig. 2.6.2. Axial nonenhanced brain CT shows a right frontal
lobe tumor that abuts the lateral ventricles ( arrowheads ) and
shows areas of dense calcifi cations (oligodendroglioma)
Fig. 2.6.4. Axial T1W postcontrast MRI of a patient with previous brain infarction shows area ( arrowhead ) of hypointensity,
with dilatation of the right occipital horn of the lateral ventricle
adjacent to it (gliosis)
Fig. 2.6.3. Axial T1W
postcontrast ( a ) and T2W
( b ) brain MRI in a patient
with epilepsy show temporal
cortical hypointense lesion
with high T2 signal intensity
and no contrast enhancement
(desmoplastic neuroepithelial
tumor)
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2.6
Fig. 2.6.5. Axial T1W brain image shows a hypointense signal
intensity ring with multiple areas of different MR intensities
( arrowhead ) located within the right temporal lobe (cavernous
angioma)
Fig. 2.6.7. Coronal FLAIR brain MR-illustration demonstrates
the radiological fi ndings in status epilepticus
For Further Reading
Fig. 2.6.6. Coronal FLAIR brain MR-illustration demonstrates
the radiological fi ndings in ulegyria
1 . Deblaere K et al Structural magnetic resonance imaging in
epilepsy. Eur Radiol. 2008;18:119–29
2 . Urbach H. Imaging of epilepsy. Eur Radiol. 2005;15:
494–500
3 . Ramos A et al Uncommon epileptogenic lesions affecting the
temporal lobe. Semin Ultrasound CT MRI. 2008;29: 47–59
4 . Urbach H et al MRI of long-term epilepsy-associated
tumors. Semin Ultrasound CT MRI. 2008;29:40–6
5 . Vazquez E et al Developmental abnormalities of temporal
lobe in children. Semin Ultrasound CT MRI. 2007;29: 15–39
6 . Paesschen WV et al Qualitative and quantitative imaging of
the hippocampus in mesial temporal lobe epilepsy with hippocampal sclerosis. Neuroimag Clin N Am. 2004;14: 373–400
7 . Vattipally VR et al MR imaging of epilepsy: strategies for
successful interpretation. Neuroimag Clin N Am. 2004;14:
349–72
8 . Villanueva V et al MRI volumetry and proton MR spectros-
copy of the brain in Lafora disease. Epilepsia. 2006;47: 788–92
9 . Gómez-Garre P et al Hepatic disease as the fi rst manifesta-
tion of progressive myo clonus epilepsy of Lafora. Neurolog y.
2007;68:1369–73
10 . Sirven JI et al MRI changes in status epilepticus. Neurology.
2003;60:1866
11 . Al-Mudaffer M et al Clinical and radiological fi ndings in
Schinzel-Giedion syndrome. Eur J Pediatr. 2008;167:
1399–1407
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