CT Scan

World Journal of Medicine and Medical Science Research Vol. 2 (5), pp.
071-107, August 2014

Available online at http://wsrjournals.org/journal/wjmmsr
ISSN 2331-1851 2014 World Science Research Journals
Case Review
Comparison of the diagnostic accuracy of CT scan and

MRI techniques in detecting herpes simplex virus
encephalitis (HSVE)
Mufarreh Musallem Alazmi
1
Unit 34/ 35 Ashridge Road, suburb:Darra, City: Brisbane, State: Queensland 4067, Australia.
Accepted 21 July 2014
The objective of this retrospective study is to examine and compare the diagnostic accuracy of CT scan
and MRI techniques in detecting type 1 and type 2 of herpes simplex virus encephalitis (HSVE). HSVE
remains the most devastating and fatal viral infection of the brain despite available antiviral treatment.
The gold standard diagnostic method for HSVE is the identification of HSVE DNA in the cerebrospinal
fluid (CSF) by utilizing polymerase chain reaction (PCR). The computed tomography (CT) scan ,
magnetic resonance imaging (MRI), and diffusion-weighted imaging (DWI) initial and follow-up imaging
findings in the presented cases of HSVE type 1 and HSVE type 2 were assessed. CT images were
normal or depicted few abnormalities in the initial stages of the HSVE. Conventional MRI examinations
may be normal in the initial stages of the HSVE. Initial detection of the HSVE lesions were seen by using
diffusion weighted imaging. Diffusion-weighted imaging can show scattered tiny high intensity lesions
in both hemispheres after early hours of the onset of seizures and symptoms. Sequential DW imaging
depicted that the diffusion abnormality started to disappear and normal diffusion pattern appear in the
late course of the HSVE. Thus, DW imaging is an important imaging technique for early diagnosis and
detection of HSVE type 1 and HSVE type 2.
Key words: Keywords: HSVE-type 1, HSVE-type 2, CT scan, MRI, DWI..
INTRODUCTION
Encephalitis is an inflammatory process that occurs in the
brain parenchyma. It is controlled by a clinical proof of
brain dysfunction. Encephalitis is caused by either
infectious or non-infectious processes (Steiner et al.,
2010), thus it is classified based on whether it is
infectious (e.g., viruses, bacteria or fungus) or non-
*Corresponding author. E-mail: finjal2013@hotmail.com.
infectious (e.g., chemical drugs or other health problems).

Most types of viral encephalitis are acute (that is, chronic
or sub-acute expositions), and are characterised by
particular pathogens, especially in the immunecompromised system (Kneen et al., 2012). Six types of
herpes virus family can infect humans and lead to
neurological diseases; they are varicella-zoster (VZV),
herpes simplex encephalitis type -1 (HSVE-1), herpes
simplex encephalitis type-2 (HSVE-2), Epstein-Barr
(EBV), human herpes virus six (HHV 6) and
World J. Med. Med. Sci. Res. 072
cytomegalovirus (CMV). In cases where a herpes virus

infects the central nervous system (CNS), the clinical
findings may be confusing and un-definitive (Baskin and
Hedlund, 2007). There are two types of HSVE: HSVE-1
and HSVE-2. HSVE-1 is usually linked with mucosa of
the face and skin; HSVE-2 is usually linked with
infections in the genital area. Because the infections in
neonates are usually acquired at birth, neonatal herpes
can lead to CNS and is typically secondary to HSVE-2. In
non-neonatal children, reactivation of HSVE-1 is the most
common aetiology of HSE (Baskin and Hedlund, 2007).
Herpes simplex virus encephalitis (HSVE) is the most
common type of viral encephalitis diagnosed in industrial
countries; 1 in 250,000 to 500,000 people are diagnosed
annually, with the highest percentages in the elderly and
youths (Solomon et al., 2012). Herpes simplex virus
encephalitis type-1 (HSVE-1) is found to be the most
typical cause of encephalitis in immune-competent
patients (Steiner et al., 2010) while Herpes simplex
encephalitis type 2 (HSVE-2) typically occurs in immunecompromised individuals and neonates (Solomon et al.,
2012). HSVE is the cause of 45% of the cases diagnosed
with focal encephalitis (Reuter et al., 2007). Indeed,
HSVE is considered the most fatal viral encephalitis
(Shaikh et al., 2013). About ninety percent of HSVE
cases result from HSVE-1, and 10% of the cases result
from HSVE-2 (Solomon et al., 2012). HSVE-1 is usually
found in the frontal and temporal lobes of the brain
(Mekan et al., 2005). HSVE-2 is the predominant type of
HSVE found in neonates. It is more diffused and has
severe effects on the brain (Pelligra et al., 2010). When
untreated, both types of HSVE have mortality rates of
70% and < 3% return to normal neurologic function (Abel
et al., 2010; Bonkowsky et al., 2006). In people treated
for HSVE-1, neurologic sequels occur in < 28% of adults
and children (> three months old). In the treated group
(mainly neonates and immune-compromised patients)
with HSVE-2, 15% of infants die and 17 to 32% percent
experience moderate to severe long term intellectual and
motor impairments (Bonkowsky et al., 2006). The
detection and diagnosis of HSVE are difficult. Although a
number of different diagnostic tests can be conducted to
diagnose
HSVE,
they
have
advantages
and
disadvantages. One reason why HSVE is difficult to
diagnose accurately and rapidly is that some defects of
the CNS can imitate HSVE (Noguchi et al., 2010). Some
of these defects have features similar to HSVE; they are:
intracranial tumours, trauma, toxic encephalopathies,
metabolic encephalopathies, cerebrovascular disease,
intracranial
haemorrhage,
subacute
sclerosing
panencephalitis, intracranial abscesses, rocky mountain
spotted fever, meningitis and togavirus (Graber et al.,
2011). General symptoms of HSVE are fever, confusion,
headache, vomiting and nausea, loss of appetite,
lethargy, fatigue, disorganized speech, uncontrolled
movements, ravings, convulsions, loss of consciousness
and neck stiffness (Hasan et al., 2010).
Aim of the project

The aim of this research project is to compare the
diagnostic accuracy of magnetic resonance imaging
(MRI) and computed tomography (CT) scan technologies
for the detection of both types of HSVE (HSVE-1 and
HSVE-2). To achieve this objective, the developments of
both modalities in detecting HSVE will be investigated.
Hypotheses of the project

This research project tests and demonstrates the
superior advantages of MRI techniques to CT scanning in
the detection of HSVE. Two hypotheses are formulated:
Hypothesis 1: MRI has superior advantages over CT in
detecting HSVE type 1 (HSVE-1).
Hypothesis 2: MRI has superior advantages over CT
scan in detecting HSVE type 2 (HSVE-2).
DATA SOURCE
A comprehensive review of the literature involved six
electronic databases: the University of Queensland
library, ScienceDirect, CINaHL, MEDLINE, Wiley Online
Library, The Cochrane Library SpringerLink and OvidSP.
The criteria for including these sources are that they were
published not earlier than 2004. References published
earlier than 2003 may have some outdated information
about herpes simplex encephalitis and hence was
excluded from this study. Moreover, the terms used in the
search preferably have the phrases CT scan and herpes
simplex viral encephalitis, MRI and herpes simplex viral
encephalitis, CT scan and MRI in diagnosing herpes
simplex viral encephalitis, SPECT and herpes simplex
viral encephalitis, EEG and herpes simplex viral
encephalitis, laboratory investigations of herpes simplex
viral encephalitis, or herpes simplex viral encephalitis in
their title and/or in their text. These search terms were
chosen because it is essential that MRI and CT scans are
differentiated from other types of methods or modalities
that are used in the detection of herpes simplex viral
encephalitis.
LITERATURE REVIEW
Although early detection of HSVE leads to early
treatment and desirable cognitive outcomes (Caksen et
al., 2007), significant mortality and morbidity can be
caused by HSVE infection in neonates. A rough
estimation shows that only 1 neonate out of 3200 born
alive has HSVE infection. Early detection of HSVE
infection by using the most accurate modality and prompt
commencement of the most appropriate treatment
Alazmi
073
destruction of the epithelial layer. Widespread

inflammatory cells develop and infiltrate the underlying
dermal layer as well as the surrounding rim (Gupta et al.,
2007). Lesions associated with HSVE-1 and HSVE-2
includes impetigo, which often affects adjacent and
perioral facial skin. Aphthous ulcers occur only on nonkeratinized mucosa (e.g., tongue, lips, alveolar mucosa,
cheeks, oral pharynx and soft palate). Erythema
multiform, iris, and target lesions often appear on visible
skin in herpes labialis and pathognomonic bulls eye
(Figures 1 and 2) (Tyring, 2006).
Figure 1. Herpetic lesions at the lower lips vermilion
border.
method will definitely help in treating and minimising

many of the harmful effects that HSVE infection can have
on the CNS (Husyin et al., 2007; Karsen et al., 2013).
Non-infectious encephalitis
The non-infectious causes of this type of encephalitis are
associated with autoimmune disease cases and/or
neoplastic cases, vasculitis, metabolic cases, stroke
cases, drug reactions and other disorders (Glaser et al.,
2006).
Infectious encephalitis
In cases where encephalitis is caused by infections, it is
very common that viral pathogens are detected, followed
by parasitic, bacterial, fungal aetiologies and prion.
Encephalitis can also be caused by several viruses, such
as HSVE-1, HSVE-2, varicella zoster virus (VZV), West
Nile virus and cytomegalovirus (CMV), as well as certain
members of the Bunyavirus genus and the Flavivirus
family (Glaser et al., 2006).
Herpes simplex virus encephalitis (HSVE)
HSVE causes severe destruction and necrosis of frontal
and temporal lobe structures, which include amygdala,
hippocampus and limbic mesocortices Human bodies are
the only natural reservoir for this infection (Glaser et al.,
2006). After entering through cracks or breaks in the skin
or mucosa, HSVE attaches to epithelial cells where it
begins its replicating process. It is then carried by the free
sensory nerve endings on the dermis. The nucleocapsid
that contains the viral genome is then carried over to the
sensory ganglions nucleus by the retrograde axonal flow.
Skin indications may include vesicular lesions that are on
an erythematous base. These lesions result in the focal
Herpes simplex virus encephalitis type -1 (HSVE-1)

The main symptoms and clinical symptoms of HSVE-1
include acute febrile encephalopathy and disordered
mentation, severe headache, focal cerebral deficits and
cerebrospinal fluid findings. Despite therapy, HSVE-1 is
severe and develops rapidly. Less than 5% of survivors
regain normal brain function (Reuter et al., 2007). HSVE1 infection can be transmitted via direct contact with
person who has infectious secretions, such as a viralinfected orolabial vesicular fluid; it can also be
transmitted by respiratory droplets (Whitley, 2006).
HSVE-1 is considered the most common perioral and oral
viral infection (Tyring, 2006).
Herpes simplex Virus encephalitis type -2 (HSVE-2)

Clinical findings include mild headache, low grade fever,
and mild to moderate alterations in mental condition.
Although neonatal HSVE-2 is a rare disease, it is a
devastating one. It has a high rate of severe neurological
complications and mortality. HSVE-2 is less common and
relatively less severe than HSVE-1. HSVE-2 is not
commonly reported in elderly people, but it is reported in
older persons, especially those with impaired immunity
(Reuter et al., 2007).
HSVE-2 infection is usually
transmitted via genital routes (also in labour from mother
to infant). In such cases, the virus reproduces on penile
skin sites or in the vaginal tract, by the seeding of the
sacral ganglia. Although HSVE-2 is typically a genital
infection, oral lesions were also detected in some cases
(Whitley, 2006).
In Herptic whitlow, lesions occur on a thumb or finger.
This lesion can be caused by either HSVE-1 or HSVE-2
during the primary stage of infection. It usually occurs in
young adults and children (Figure 2). In adults, oral
secretions are also a source of infection; therefore, health
care employees and athletes who are engaged in contact
during sports (e.g., wrestlers or players of rugby) are at
high risk for exposure to viral infection (Hoff and Gerber,
2012). Genital herpes is the common causative pathogen
of genital ulcers. Some lesions in genital herpes caused
by HSVE-1 have been reported in developed countries
Figure 2. (a) Redness and swelling with several vesicular lesions and pustulation on the right forefinger of a
fourteen-month-old girl. (B) The patient also presented with gingivitis and stomatitis, showing as vesicles with a
red halo and distinguished ulcers on her tongue and lower lip. Source: Hoff and Gerber (2012).
(Hoff and Gerber, 2012).
INVESTIGATIONS OF HERPES SIMPLEX VIRUS

ENCEPHALITIS PATIENTS FOR BOTH TYPES (HSVE1 AND HSVE-2) PATIENTS
Many types of tests can be used to detect HSVE,
including physical and vital signs examinations,
laboratory investigations, electroencephalograph (EEG)
and
Neuro-imaging
methods.
Some
laboratory
investigations can be conducted in traditional laboratories
and some can only be conducted in modern centres.
These tests will be described in the following sections.
However, the focus will be on CT scan and MRI
modalities because these are the aim of the project.
Physical and vital signs examinations

The vital signs of the patient should be taken, including
body temperature, pulse rate, heart beats, oxygen
saturation level and respiratory rate. The patient should
be checked for the symptoms of HSVE. The ability of the
patient to respond to words or signs should be
investigated. The patient should also be checked for any
disorientation. The patients medical history and his or
her parents medical histories also should be reviewed
carefully (Kneen et al., 2012; Husyin et al., 2007; Karsen
et al., 2013; Salih et al., 2009; Steiner et al., 2005).
Laboratory examinations
Microscopes and laboratory machines are used in
investigations of the aetiology of illnesses. Specimens
and samples are taken from patients suspected of having
an HSVE infection.
Preliminary and regular laboratory tests

Laboratory investigations can involve blood film,
biochemical analysis, blood culture, full blood count, and
rectal swabs, as well as nasopharyngeal (viral cultures
from rectum, nasopharynx and throat). Stool, urine and
skin vesicles tests may be particularly effective in
detecting an infectious aetiology of HSVE (Bloch, 2007;
Solomon et al., 2012).
Lumbar puncture analysis

After conducting preliminary tests and investigations, the
cerebrospinal fluid of the suspected patient can be tested
for glucose and protein contents, and cellular analysis of
the cerebrospinal fluid (CSF) can be performed (Steiner
et al., 2005). The lumbar puncture technique can also be
used to detect any red blood cells caused by bleeding
and therefore xanthochromia in CSF, as well as in CSF
culture. Lumbar puncture is used only when prior CT or
MRI imaging techniques exclude any mass-effect lesion
in the spine. Steiner et al. (2005) reported that CSF
glucose was within acceptable limits in all cases.
However, recent CSF findings in patients diagnosed with
HSVE were determined by the polymerase chain reaction
(PCR) method of HSVE-DNA detection.
Polymerase chain reaction (PCR) amplification test

Viral DNA can be detected by the PCR test on specimens
taken from patients with suspected HSVE infection. The
samples are taken from gingivostomatitis, skin eruptions,
blood and cerebrospinal fluid (CSF) (through the lumbar
puncture procedure). These specimens and the lumber
puncture procedure are preferred because of their high
specificity and accuracy, compared to other procedures
Alazmi
075
Figure 3. PCR test for detection of HSVE DNA type 1 and type 2 (Source: Schmutzhard et al., 2004).
Figure 4. Electroencephalography (EEG) showing periodic lateralized epileptiform

discharges in a HSVE patient (Source: Halperin, 2008).
(Figure 3) (Enomoto et al., 2005; Schmutzhard, 2004).

DNA detection of HSVE in the CSF through PCR is the
most common modality used to diagnose HSVE;
however, PCR was reported as yielding some negative
results in both children and adults. Hence, the recognition
of HSVE imaging is essential (Salih et al., 2009).
Although PCR is preferable to brain biopsy and is
considered an excellent test, false negatives can occur
early after the inception of illness (Whitley, 2006). The
detection specificity and sensitivity of HSVE-DNA using
cerebrospinal fluid (CSF) with the PCR method in
diagnosis of HSVE are acceptable at 94100% and 98%,
respectively (Hasan et al., 2010).
Brain biopsy
Brain biopsy is an invasive-specific and sensitive means
of diagnosis. It isolates HSVE from the brain tissue
obtained in the operating room. The isolated tissues are
then tested for HSVE infection by microscope in the
laboratory. However, this method of diagnosis was
replaced by the PCR detection of HSVE-DNA in the CSF
(Whitley, 2006).
EEG
EEG was commonly used in diagnosing encephalitis
because it shows untypical, abnormal conditions in the
detection of HSVE. EEG provides sensitive and early
indications of cerebral involvements. In most cases, it can
show abnormalities prior to initial evidence of
parenchyma involvements on neuro-imaging (Steiner et
al., 2005). The main features of the EEGs focal changes
are slow-wave and spike activity, as well as periodic
discharges of lateralized epileptiform arising from the
temporal lobe (Figure 4). In the early stages of the
disease, abnormal electric activity occurs at one temporal
lobe, but then spread towards the contralateral temporal
lobe in later stages when the disease develops (during 7
to 10 days). The EEGs sensitivity is approximately 84%;
however, its specificity does not exceed 32.5% (Whitley,
2006).
Neuroimaging methods
Neuroimaging plays an important role in detecting
inflammatory lesions on the brain and meninges (Ferrari
Figure 5. SPECT images showing a broad increasing uptake within the left insula, the left frontal lobe and the right cerebellar
hemisphere (pointing arrow) at 7 days after onset (Source: Ametani et al., 2005).
et al., 2009). Structural data are presented by MRI and

CT scan. Metabolic and functional data are presented by
magnetic resonance spectroscopy (MRS), functional
magnetic resonance imaging (FMRI), single photon
emission computed tomography (SPECT) and photon
emission tomography (PET) (Steiner et al., 2005).
it remains a costly, complex and relatively unavailable

technique (Steiner et al., 2005).
ROLE AND ACCURACY OF CT SCAN AND MRI

INVESTIGATIONS IN DETECTING BOTH TYPES OF
HERPES SIMPLEX VIRUS ENCEPHALITIS (HSVE-1
AND HSVE-2)
Single photon emission computed tomography

Single photon emission computed tomography (SPECT)
is a nuclear medicine tomographic imaging modality
based on the gamma rays technique. It is similar to
conventional nuclear medicine planar imaging, which
uses a gamma camera. Moreover, SPECT provides
increased uptake images for the affected areas using
technetium 99 m hexamethyl propyleneamineoxime
(technetium 99 m HMPaO), which is important for early
diagnosis during the acute stage. Ametani et al. (2005)
reported the case of 69-year-old woman who 7 days after
the onset of symptoms of HSVE underwent a SPECT
scan using technetium 99 m HMPaO. The image
presented wide and increased uptake in the left temporal
lobe, left frontal lobe. It also presented an increasing
uptake in the contralateral right cerebellar hemisphere
(Figure 5). The findings indicated that sequential SPECT
studies are very important in understanding the
pathophysiology of HSVE (Ametani et al., 2005).
Photon emission tomography

Photon emission tomography (PET) is a technique used
in nuclear medicine imaging. It can produce threedimensional images and functional images. Although it is
the highest standard in providing functional imaging data,
Although the MRI has many advantages, such as

improved soft tissue contrast capabilities, high anatomic
resolution, non-ionizing radiation and multi-planer
imaging capability, CT scans are reported as the best
preliminary process for neurological examination (Kubota
et al., 2007; Steiner et al., 2005). CT scanning and MRI
have strengths and weaknesses in detecting HSVE.
Hence, they are very important imaging modalities for this
particular application. In addition, other MRI sequences
improve the utility of MRI in HSVE detection. These will
be discussed in detail in this project (Steiner et al., 2005).
Computed tomography scan (CT scan)

The computed tomography (CT) scan is used as a firstinstance neurological examination. It uses a special array
of x-rays to produce two-dimensional (2-D) or threedimensional (3-D) images of the brain. It is considered a
standard practice in the acquisition of imaging modality.
In HSVE, CT scan shows areas with low density as a
mass effect located at the temporal lobe; these can
develop to haemorrhagic lesions and/or radiolucent
(Figures 6 and 7) (Whitley, 2006). One to two weeks after
the disease onset, a follow-up CT scan screens more
progressive and wide-spread structural and vascular
abnormalities that involve insula and cingulate gyri and
Alazmi
077
Figure 6. Two days after the onset of

HSVE symptoms. Brain CT scan depicting
slight hypo dense area and obscured
sulcus in the medial side of the right
temporal lobe (Source: Takeuchi and
Takasato, 2011).
the contra lateral temporal lobe. Changes in subacute

haemorrhage and contrast enhancement may also be
demonstrated at this stage (Steiner et al., 2005).
Computed tomography angiogram

The three-dimensional CT angiogram (3DCTA) is an
effective technique for evaluating vascular cerebral
defects. It can demonstrate cerebral defects and bony
structures. In addition, 3DCTA is very helpful in detecting
cerebral aneurysms of 5 mm in diameter or larger;
however, as the vessel diameter increases, the accuracy
of 3DCTA decreases. A problem with 3DCTA is its low
isotropic spatial resolution. However, with the
development of multi-detector row CT angiography
(MDCTA) techniques, such as four-detector CT, sixteendetector CT and 64-detector CT, isotropic spatial and
temporal resolution increase as the number of detectors
increases (Kock et al., 2007). Since the 320-detector row
CT scanner, with its 16 cm wide detectors, was
introduced, it has been possible to obtain time-resolved
CT angiography (CTA) for the whole brain. Using this
new generation of CT scanners to conduct continuous
scanning during the bolus passage of the iodinated
contrast medium makes it possible to acquire
hemodynamic information 4-D data without being limited
to the intracranial vasculature structural 3-D data. The
pathologies that change cerebral hemodynamics might
be facilitated by this technique (Figure 8) (Siebert et al.,
2012). However, it is reported that CTA is effective in
evaluating large vessels, whereas mall vessels are better
Figure 7. Ten days post-onset of HSVE

symptoms. Brain CT scan showing a
hematoma in the right medial temporal lobe,
without
obvious
mass
effect.
Source:Takeuchi and Takasato (2011).
evaluated by MRA because it has better sensitivity than

CTA has (Kker, 2007). In addition, the most significant
disadvantage of MDCTA is its restricted ability to
evaluate lumen of extensive calcified arteries, which can
lead to false positive diagnoses. In contrast to CTA, MRA
can differentiate between MRI contrast agents and
calcification in the lumen of vessels or in soft tissues
(Kock et al., 2007).
Perfusion computed tomography

Perfusion CT is a newly introduced technique that
enables fast quantitative and qualitative evaluations of
cerebral perfusion by generating cerebral blood flow
(CBF) maps and mean transit time (MTT), as well as
cerebral blood volume (CBV). The main principle of this
technique is the central volume principle (CBF-CBVMTT). It needs software that employs complex algorithms
to generate the perfusion maps (Hoeffner et al., 2004).
Compared to MRI perfusion, CT perfusion has the
limitations of less sensitivity to perfusion abnormalities
and restricted anatomical coverage. In addition, larger
coverage affects temporal resolution. CT perfusion uses
high doses of ionizing radiation and mainly depends on
operator skills and knowledge (Figures 9 to 12) (Hoeffner
et al., 2004).
Advantages of CT scan
CT scanning of the brain in children and adults usually
takes a few seconds, which reduces the risk of negative
Figure 8. (a) Sagittal; (b) coronal. 4DCTA whole-brain maximum

intensity projections (MIP) (one image per second) showing capillary
phase, venous outflow and arterial inflow. Source: Siebert et al. (2012).
Figure 9. Axial CT image showing a part of the anterior cerebral artery (ACA), which was selected to
be the input artery (white-arrow). The torcularherophili was selected to be the input vein (black-arrow);
time concentration curves were produced for the vein (red line) and the input artery (green line).
(Source: Hoeffner et al., 2004).
effects on the results of reactional movement of the

patients body. It also reduces the need for sedation or
general anaesthesia (GA) (Rao et al., 2013). Moreover,
the cost of a CT scan is usually 50% less than the cost of
a MRI. The intensive monitoring of very ill or
unconsciousness patients, which may include metallic
and ferromagnetic equipment, can be done without any
restriction because x-rays are used. No magnetic fields
are used in the imaging process (Corno and Festa,

2009). Some HSVE patients are very ill and need close
observation and continuous intensive care, which makes
the CT scan very suitable. The scan duration is very short
compared to the MRI examination. The CT scan may be
used in the localization of a biopsy site for definitive
diagnosis when PCR and MRI are not available. The
conventional cerebral angiogram can be replaced by CT
Alazmi
079
Figure 10. Various colour ramps were employed to illustrate the MTT, CBV and CBF maps in the above axial CT perfusion maps of an
adult healthy patient showing normal perfusion. Source: Hoeffner et al. (2004).
Figure 11. CBF map and axial CT image of an adult healthy patient showing the circular ROIs in place (purple circles). (Source:
Hoeffner et al., 2004).
cerebral angiogram (CTA) to detect vascular

involvement. Although vascular abnormality of HSVE
usually develops late, CTA is still helpful in detecting and

diagnosing vascular abnormalities that may associate
Figure 12. Acute infarction in a 76-year-old woman who was unresponsive. Initial axial CT image of the brain
illustrates slight hypoattenuation in left insula (arrows), frontal lobe and temporal lobe. Axial CBF map
demonstrates reduced CBF (arrows) in anterior middle cerebral artery (MCA) and left anterior cerebral artery
(ACA) territories. Axial CBV map reveals reduced CBV (arrows). Axial MTT map demonstrates slightly elevated
MTT (arrows). Follow-up axial CT scan illustrates wide infarct (arrows) within MCA and left ACA regions.
Source: Hoeffner et al. (2004).
with HSVE infections of both types (Mekan et al., 2005).
Disadvantages of CT scan
The CT scan uses x-rays, which are ionizing radiation
that poses risks to patients when they are exposed to
them, including cancers in tissues. Children and
neonates are more sensitive to the risks of x-rays than
adults are. Contrast-enhanced CT scan studies require
the use of iodinated contrast materials, which increase
the risks of exposing patients to allergic reactions
(Stoodley and Philip, 2011). The CT scan does not have
the same power and accuracy that MRIs have in
detecting and differentiating subtle abnormalities in soft
tissues (Rumboldt and Ebooks, 2012). CT scans of the
brain have only 50 percent sensitivity during the early
stages of HSVE. Moreover, the presence of abnormalities
is generally linked with poor prognosis and severe
damage. In addition, CTA and CT perfusion techniques
are less sensitive than MRA and PWI-MRI in detecting
tiny vascular defects (Hoeffner et al., 2004; Kock et al.,

2007). Normal CT scans cannot exclude the infection of
HSVE in the early or late phase of the disease, and it is
usually expected to be negative during the first five days
of the disease (Hseyin et al., 2007).
Magnetic resonance imaging

Magnetic resonance imaging (MRI) is crucial in detecting
HSVE. MRI now has a significant role in clinical imaging
(Steiner et al., 2005). The several MRI sequences include
gradient-echo imaging (GRE), diffusion tensor imaging
(DTI), fluid-attenuation inversion recovery (FLAIR)
sequence, perfusion weighted imaging (PWI), diffusionweighted
Imaging
(DWI),
magnetic
resonance
spectroscopy (MRS) and magnetisation transfer ratio
(MTR). In addition, conventional routine T1-weighted
(T1WI) and T2-weighted (T2WI) sequences improve the
utility of MRI accuracy. The accuracy of MRI scanning in
the detection of HSVE depends on the progression of the
Alazmi
081
Figure 14. Brain MRI illustrating diffused white matter high

signal on T2WI in two patients with HSVE-1. Patient 1 (A
and B): 7 years old, MRI 14 days after onset of HSVE.
Patient 2 (C and D): 13 years old, MRI 10 weeks after onset
of HSVE. Source: Schleede et al. (2013).
Figure 13. Brain MRI in a 44-day-old child with HSVE-2,

illustrating multifocal lesions on corresponding T1WI (A,
B) and T2WI (C, D). Age at onset of symptoms: 25 days.
The lesions impact bilateral cortical, white matter and
basal ganglia structures. Source: Schleede et al. (2013).
condition, its stage of development, and the MRI

sequence used in the MR investigation (Steiner et al,
2005).
T1 weighted imaging
In non-contrast T1 Weighted Imaging (T1WI) MRI, the
areas of the brain affected by both types of HSVE are
screened as general gyral oedema. It is also possible that
signals of hyper-intensity can be seen in cases of subacute haemorrhage (Steiner et al., 2005). T1 noncontrast and contrast-enhanced MRI imaging is usually
negative at early stage (three days) of HSVE in both
types, but it is frequently positive four days to three
months after the first onset of symptoms (Figures 13A,
15B and 19C) (Schleede et al., 2013).
T2 Weighted imaging
When using T2-weighted (T2WI) MRI, the areas of the
brain affected by HSVE are screened for hyper-intensity,
which is usually seen in HSVE-1 in children (> 3 months)
and adults (Figures 14A to 14D and 19B and 19D) and in
HVSE-2 in neonates (Figure13C and 13D). In cases of
sub-acute haemorrhage, the haemorrhagic spots will be
screened for hypointense. From day 1 of HSVE-1 onset,

T2WI often shows high signal changes and persists in all
follow-up T2WI examinations (Schleede et al., 2013). The
MRI diagnosis of HSVE-2 in neonates may be difficult
because of the high water content and incomplete white
matter myelination of the neonates brain, which may
obscure slight T2 abnormalities and reduce the accuracy
of T2WI sequences. Necrosis is demonstrated by
increased signalling within the first 48 h on T2WI or
FLAIR sequences, with decreased T1 signals and
variable enhancement (Vossough et al., 2008).
T2*WI Gradient-echo Imaging
The sensitivity of T2*WI gradient-echo imaging (T2* WI
GRE) MRI is higher than the sensitivity of spin-echo (SE)
T2WI in detecting cerebral micro-bleeds that appear as
hypointense lesions that resemble tiny dots (Figure 15)
(Werring et al., 2004). This sequence is very helpful in
cases where HSVE involves a haemorrhaging pattern,
which occurs mostly in older patients (Ametani et al.,
2005).
Fluid-attenuation inversion recovery sequence

The
fluid-attenuation
inversion
recovery
(FLAIR)
Figure 15. A: axial T2*WI FSE; and B: T2*WI GRE MRI of a 63-yearold patient. The T2*WI GRE in (B) illustrates several micro-bleeds as
low signal intensity mainly at the frontal regions and in the
parietooccipital areas; these micro-bleeds were not detected in (A)
using the standard T2WI-fast spin-echo (FSE) sequence. Source:
Werring et al. (2004).
Figure 16. FLAIR images showing hyperintense signals in both bilateral cingulate gyri, left and insular
medial temporal lobe (Source: Ametani et al., 2005).
sequence is another type of MRI sequence that is used to

detect HSVE (Figure 16). FLAIR has been proved
valuable in the MRI diagnosis of HSVE-1 in adults
because it increases the conspicuity of lesions. However,
the contrast of tissues presented by FLAIR in neonates is
of relatively low quality compared to those presented in
adults and older children. This is caused by the lack of
myelination in neonates, which reduces the accuracy of
FLAIR in detecting HSVE in neonates (Vossough et al.,
2008). Unfortunately, this technique is unable to
determine the timing of the HSVE onset; it is also unable
to differentiate between cytotoxic oedema and vasogenic
oedema (Steiner et al., 2005).
apparent diffusion coefficient map (ADC), presented a

restricted diffusion pattern in HSVE patients of both types
within the first three days after symptom onset (Figures
17, 18 and 19A) (Schleede et al., 2013). Unlike the
FLAIR sequence, DWI is able to differentiate between
cytotoxic oedema and vasogenic oedema, and can
determine the timing of the HSVE onset (Steiner et al.,
2005). DWI is even more sensitive than T2WI or FLAIR in
detecting early cortical lesions in HSVE, in both infants
and adults. Diffusion abnormalities disappear within 14
days after onset, whereas hyper intensities on T2WI
persist (Ferrari et al., 2009).
Magnetic resonance spectroscopy

Diffusion-weighted imaging
Diffusion-weighted Imaging (DWI) was recently found to
have a great advantage, especially during the first 72 h of
infection by both types of HSVE, as an early and first step
in diagnosis (Salih et al., 2009). DWI, including the
Magnetic resonance spectroscopy (MRS) can identify

and quantify brain metabolite concentration; it can also
provide a high level of brain-tissue specificity. Hence, it is
advanced in differentiating between pathological brain
tissues and normal brain tissues (Steiner et al.,
Alazmi
083
Figure 17. D and E axial DWIs illustrate increased signal

intensity (diffusion restriction) at left temporoparietal area
indicating recent HSVE-1 infection. Source: Salih et al.
(2009).
Figure 18. (A and B) axial and coronal DWIs at 20 h following onset of HSVE-2
symptoms. Dispersed tiny spotty lesions of high-intensity were screened within
the two hemispheres (Source: Kubota et al., 2007).
Figure 19. MRI of a nine-year-old patient brain with HSVE-1

infection. Five days post-onset of symptoms (A) restricted
diffusion pattern (ADC map) was seen in both insulae (A), which
coincided with the lesions of high signal on T2WI (right > left) (B).
Sixteen days later, both insulae depicted contrast enhancement
(C). At this time, coinciding high signal alterations were also seen
on T2WI (D) (Source: Schleede et al., 2013).
Figure 20. DT images showing some of its common coronal types. A: Mean diffusivity maps; B: fractional anisotropy maps; C:
Colour encoded maps of the essential eigenvector (red: left to right; green: anterior to posterior; blue: cranial to caudal).
Source:Paolo et al. (2007).
Figure 21. Tractography demonstrating frontotemporal fibre tracts

(red) coinciding to curved fasciculus (Source: Paolo et al., 2007).
2005).MRS discovers metabolic changes linked to

neuronal death in acute HSVE lesions; some of these
changes can include a decrease in N-acetyl aspartate
(NAA) signal. In addition, an increase in creatine and
inositol resonances is a reflection of a resultant gliosis
(Steiner et al., 2005).
Magnetization transfer ratio

The main advantage of Magnetization Transfer Ratio
(MTR) is that it can detect any changes in the water
content of cells, the level of cell destruction, and damage
to myelin (Steiner et al., 2005).
Diffusion tensor imaging

Diffusion tensor imaging (DTI) is an MRI technique that
enables the evaluation of the brains water microscopic
movement. DTI is also used to measure the tract integrity

of the fibres in the brains white matter. Although DWI has
been used in various brain pathologies, there are only a
few heterogeneous results, case studies, and researches
regarding its use in detecting HSVE. Compared to DWI,
DTI enables the differentiation in descriptions of brain
pathology. It also has additional directional diffusion data.
DTI enables the examination of the tissues of the brain
regarding its directionality and histological organization.
This is done by calculations of derived metrics, based on
the full diffusion tensors estimation (Figures 20 and 21).
DTI is used in the diagnosis of many neurological
disorders and has proved to be sensitive to minor
changes in the tissues that cannot be detected using
conventional MR images (Herweh et al., 2007). In
Herweh et al. (2007) study, which included six patients
with HSVE infection, DTI confirmed and extended
findings from previous investigations, proving HSVE
infection and providing detailed information about lesions
and their evolution.
Alazmi
085
Figure 22. Abnormality in the left MCA as visualized on TOF-MRA.

Source: Kker (2007).
Magnetic resonance angiogram

Some inflammatory changes can be detected and
screened as multiple microaneurysms which are rather
specific for vasculitis. Whatever the type of the affected
vessels is, brain parenchymal changes are detected on
MRI with a cerebral vasculitis in most patients. However,
the size of the affected vessels does affect the sensitivity
of vascular imaging. The disease in the large vessels is
screened best with magnetic resonance angiogram
(MRA) and MRI (Figure 22). Increasing the availability of
3T MRI scanners can be helpful in improving the time of
flight (TOF)-MRA because it may enable the generation
of diagnostic vascular imaging beyond the circle of Willis,
which usually cannot be properly screened at 1.5T. CT
has a lower sensitivity than MRI has in evaluating
changes in the cerebral vasculitis, with the exception of
cerebral haemorrhage. Furthermore, CT angiography on
multislice CT scanners is effective in evaluating vasculitis
in large vessels; however, small vessels are better
investigated by MRA (Kker, 2007).
Perfusion weighted imaging

The microscopic flow of blood through tissues can be
visualized in magnetic resonance perfusion. It can
measure the cerebral blood flow (CBF), cerebral blood
volume (CBV) and the mean transit time (MTT) of units of
blood through units of tissues. Two techniques are
commonly used: the technique of endogenous contrast
with arterial spin labelling of arterial water and the
gadolinium-based dynamic susceptibility technique.
There is a consistent decrease in CBV along with

hypoperfusion in cerebral vasculitis. Because no ionizing
radiation is involved, these techniques are very suitable
for measuring the efficacy of the treatment with a series
of examinations (Gomes, 2010).
Stracke et al. (2006) first tested whether magnetic
resonance perfusion weighted imaging (MR-PWI) could
show abnormal perfusion patterns in the early stage of
HSVE. The study presented a case of 64-year-old female
patient with personality changes and symptoms of HSVE
that began five days earlier. Her initial CT scan was
normal, but a conventional MRI showed abnormalities
signal (Figure 23). PWI was used to get rid of any
distortions in the blood brain barrier and any increase in
leptomeningeal enhancement. No obvious abnormality of
cerebral perfusion was illustrated in the perfusion maps.
However, these differences were not sufficiently
pronounced to be visible on conventional perfusion maps.
Region of interest (ROI) measurements did not
demonstrate any changes in MTT or time-to-peak (TTP),
but there was a significant increase in relative cerebral
blood volume (rCBV) caused by changes in the affected
areas with regard to vascular regulation (Figure 24). This
study showed that inflammatorily affected areas in the
insula and temporal lobe of HSVE patients can be
demonstrated by MR-PWI throughout the early stages of
infection.
Advantages of MRI
The MRI technique is very precise in detecting tiny
abnormalities in soft tissues, particularly in the central
Figure 23. MR-FLAIR images and T2-weighted TSE images

showing signal elevation in the insular region, temporomesial
structures and frontobasalgyri ( Source: Stracke et al., 2006).
Figure 24. ROI measurements localization in both insular and

temporomesial regions as illustrated on EPI source image (left). Right
insular cortex (L5) and right temporal lobe (L1) illustrate an increase in
negative integral in comparison to the left side (right). Source: Stracke et
al. (2006).
Alazmi
087
nervous system. MRI provides many sequences, such as

DWI, DTI, GRE-T2* WI, MRS, FLAIR, T2 WI, T1WI, T1WI
post contrast and PWI, all of which provide sensitivity to
HSVE pathological changes. MRI using EPI sequences is
very helpful in reducing the length of scans in very ill
patients and in reducing the incidence of artefacts caused
by voluntary and involuntary motions. EPI sequences are
also very helpful in perfusion and dynamic imaging. In
addition to two-dimensional (2-D) imaging, MRIs also can
provide 3-D imaging and temporal imaging (Semelka et
al., 2010). The MRI technique uses non-ionizing
radiation, which has no biological impact on tissues if
safety guidelines and specific absorption rate (SAR) limits
are met (Coskun, 2011).
MRI and DWI in particular are very sensitive to brain
abnormalities in the early onset of HSVE-1 and HSVE-2
infection, which makes it very helpful in preventing bad
prognoses of both types of HSVE. Conventional MRI
sequences and other specific MRI techniques can
provide structural and functional information about the
brain, which provides an excellent reflection of the
evolution of HSVE (Kker et al., 2004).
Disadvantages of MRI
The MRI technique is an expensive system. It needs
liquid helium, which is also expensive and requires
continuous cooling. MRI uses high magnetic field
strength, which poses many hazards for ferromagnetic
objects that can harm patients, such as projectiles and/or
burns. Patients with non-conditional pacemakers cannot
undergo an MRI scan because these pacemakers will not
function properly and can induce burns. Moreover,
patients with ferromagnetic implants may not undergo
MRI examination unless these implants are removed.
Patients who are very ill and/or unconscious (artificialrespiration dependent) need continuous care and close
observation.
These patients cannot undergo an MRI scan unless
safe or conditional medical machines for monitoring and
respiration are available. MRI can induce peripheral
nerve stimulation (PNS) (Coskun, 2011). MRI rise needs
sedation or GA because of the long duration of the scan
and therefore the high possibility of patients motion (Rao
et al., 2013). The MRI technique needs homogenous
radiofrequency (RF) field, a gradient field, and a main
magnetic field to produce clear images. Any error in the
RF coil, the gradients, or main magnet can produce
useless images or false diagnoses. Moreover, any
ferromagnetic or metallic object close or in the vicinity of
the RF, the gradient field, or the main magnet field may
produce artefacts and unusable images. Conventional
MRI sequences were reported by several studies of
normal scans in early stages of HSVE diagnosed in
patients, which was confirmed by PCR testing (Salih et
al., 2009).
STUDIES FOR DETECTING HERPES SIMPLEX TYPE1(HSVE-1) BY MRI AND CT SCAN

Study 1
Tonomura et al. (2010) reported the case of 30-year-old
symptomatic woman that was confirmed by PCR test to
have HSVE-1. Her initial brain T2-weighted MRI showed
an increase in signal intensity within the bilateral regions
in the amygdaloid and hippocampus body, medial
temporal and frontal lobes, and the insular (Figures 25A
and B). The CT scan of her brain performed on day 5
showed lesions with low intensity bilateral within the
temporal and frontal lobes and haemorrhagic foci within
the left amygdaloid body (Figures 25C and D). On day 11
after the onset of symptoms, intracranial haemorrhage
was obvious on CT scan (Figure 25C). On day 26, there
was a decrease in her level of consciousness that was
linked with tachycardia and desaturation. Thrombosis of
her right pulmonary artery trunk with pulmonary embolism
was obvious in an improved CT scan of her chest (Figure
25F). CT of the brain also revealed intraventricular and
subarachnoid bleeding (Figure 25E). On day 54, the CT
scan of the brain demonstrated that the intracranial and
subarachnoid bleeding had resolved. Improved CT
angiography illustrated an avascular region within the left
temporal lobe; however, no other venous or arterial
abnormalities, such as irregular vascular distribution or
aneurysm formation were illustrated.
Study 2
Salih et al. (2009) conducted a study on 18 patients (9
female, 9 male) with confirmed diagnosis of HSVE-1.
Cranial CT scans were done in 14 patients, and 11
patients were evaluated with MRI. Serial cranial CT
scans revealed unilateral or bilateral hypodensity in the
temporal lobes with or without involvement of other areas
(frontal, parietal or occipital) in eight patients. In two
patients, the abnormalities were confined in either frontal
or occipitoparietal lobes. Of these patients, the initial CT
scan on days 1 to 8 from onset of symptoms was normal
in five patients. Hyperdense lesions of haemorrhage were
observed in six patients. Follow-up CT brain scans in the
chronic stage of the disease in three patients revealed
encephalomalacia and brain atrophy.
On MRI during the acute stage, hyperintense signal on
T2WI and/or restricted diffusion abnormalities on DWI
were seen in 10 of 11 patients. These corresponded to
oedematous changes in the temporal lobes in eight
patients, whereas in two patients, localization was either
in the frontal lobe or parietooccipital region. MRI scans
revealed no abnormality in only one of 11 patients. This
was performed four days after symptom onset. In this
patient, examination of CSF (taken on day 5 from onset
of symptoms) revealed positive PCR for HSVE. Subacute
Figure 25. Brain T2WI (A and B) demonstrated left-predominant bilateral areas of

increasing intensity of signal in the amygdaloid and hippocampus body, the medial
frontal, medial temporal and insular lobes. Brain CT scan (C) showed lesions with
highly intensity within the left amygdaloid body. Lesions with low intensity within
the bilateral temporal and frontal lobes. Intraventricular and subarachnoid bleeding
was also reported (D and E). An enhanced CT of the chest showed massive right
pulmonary artery trunk thrombosis (F). Source: Tonomura et al. (2010).
haemorrhagic lesions, as revealed by high signal

intensities on T1WIs, were detected in two patients. In a
6-month-old boy with HSVE, the initial CT (done on day 5
after the onset of symptoms) showed bilateral
hypodensity in the temporal lobes. Cranial MRI done 12
days later showed temporal lesions, as well as subacute
haemorrhage at the pons (Figure 26). Both lesions
showed remarkable resolution on a follow-up MRI about
18 months later. MRI discovers disease in T1 signal and
increased T2 signal within the medial insulae, temporal
lobes and orbital frontal lobes. Irregularities appear more
frequently and earlier than in CT of the brain. The initial
CT scans done on days 1 to 8 from onset of symptoms
were normal in 50% of patients, compared to one (9%) of
eleven MRI scans done during the acute stage. The
results are in agreement with other studies, which
confirmed the superiority of MRI to CT scan as a
neuroimaging modality for detecting lesions of HSVE.
The DWI was found to play a major role as the first and
early diagnostic step (Salih et al., 2009).
Study 3
Hasan et al. (2010) presented four cases diagnosed with
HSVE-1 by PCR test.
Case 1: Male patient aged 21 years. His initial CT brain
showed no pathology. Because of a prosthetic aorta
valve in the patient, brain MRI could not be performed.

Case 2: Male patient aged 19 years. His initial brain CT
did not reveal any pathology, and there was no pathology
on initial conventional brain MRI.
Case 3: Male patient aged 26 years. The initial brain CT
was evaluated as normal. Brain MRI was taken the next
day and revealed marked lateral ventricle temporal horns,
especially in the right side. Five days later, brain CT
discovered infarcts in the left pons and hemisphere, shift
to right from left, and pressure to the left ventricle.
Case 4: Female patient aged 27 years. After 6 days of
complaints, her brain CT showed moderate oedema in
both hemispheres. On the fifth day of her hospitalisation,
MRI demonstrated widespread increases in signals on
both hemispheres, especially in the left temporal region.
MRI of the brain on the 15th day of hospitalisation
showed increased signal intensities in subcortical and the
cortical white matter in the left temporal lobe. Contrast
involvement was also observed after intravenous (IV)
contrast substance injection and signal increases on the
right frontal anterior lobe. Compared to two MRIs,
regression was partly observed in lesions on the left
temporal lobe and the result was evaluated as HSE. This
study found that pathological signs were revealed in the
brain CT only on the fifth day, whereas they were
revealed in the MRI on the second day (Hasan et al.,
2010).
Alazmi
089
Figure 26. (A and B) axial CT study showing small hypodense

lesions on both sides of the pons (arrows in A) and hypodense
lesions at temporal lobes (arrows in B). (C) Axial SE T1WI
shows high signal intensity (arrows) on the pons indicating
subacute haemorrhagic lesions and (D) Axial T2WI on the
same date shows high signal lesions at temporal lobes
(arrows). (E) Axial SE T1WI shows small resolving low signal
lesions at the pons (arrows). (F) Axial T2WI shows smaller
resolving high signal lesions at temporal lobes (arrows).
Study 4
Kker et al. (2004) presented three cases with HSVE-1.
All cases underwent conventional MRI and DWI. Only
Case 2 underwent a CT scan.
Case 1: Three MRI scans were performed in a man aged
73 years. The first MRI scan was performed 40 h after
the onset of complaints. The MRI finding in T1WI
sequence post-contrast administration of gadolinium (GdDTPA) showed no cerebral contrast uptake. The T2WIFLAIR sequence showed tiny hyper intensities lesions in
the left frontal operculum and on the two sides of the

insular cortex. DWI with a single shot EPI sequence
showed moderate hyper intensities within the left frontal
operculum and on both sides of insular cortex. No
abnormal hyper intensities were seen in the white matter.
Forty hours after the onset of complaints, the DWI
sequence was most sensitive in depicting abnormalities.
The second MRI scan in this patient was performed 9
days post-onset of symptoms. T1WI sequence with post
contrast administration of Gd-DTPA showed cortical
contrast uptake in areas of the cingulate gyri and the
insula. The T2WI-FLAIR sequence showed more
Figure 27. Case-1(ai): Serial MRI images after 40 h (column on left side), after 9 days (middle column) and after
19 days (right column). Source: Kker et al. (2004).
pronounced and extensive signal hyper intensity changes

than in the first scan of the same areas. DWI single shot
EPI sequence showed stronger hyper intensities in both
sides of insular cortex and in left frontal operculum. Nine
days after onset all sequences performed in second scan
were of equal sensitivity to abnormalities.
The third MRI scan was done 19 days after the
complaints onset. T1WI sequence with post contrast
administration of Gd-DTPA showed cortical contrast
uptake in areas of the cingulate gyri and the insula.
T2WI-FLAIR sequence showed more pronounced and
extensive signal hyper intensity changes than in the first

scan of the same areas. DWI single shot EPI sequence
showed slight hyper intensities in the left frontal
operculum and both sides of insular cortex. In the last
MRI scan, the T2WI and T1 + Gd were most sensitive to
abnormality (Figure 27).
Case 2: A man aged 82 years developed severe
dysarthria and aphasia. MRI disclosing T2 hyper
intensities of HSVE was performed 96 h after onset of the
symptoms. No pathology was revealed by the CT scan
Alazmi
091
performed earlier. HSVE-DNA was found by PCR in the

CSF. This patient underwent two MRI scans. The first
MRI scan performed 96 h post onset showed in the post
contrast (Gd-DTPa) T1WI hypointensity lesions and no
cortical enhancement. T2WI FLAIR sequence showed
slight or invisible hyper intensities. DWI single shot EPI
sequence showed moderate hyper intensities; this
sequence was the most sensitive sequence to
abnormalities in this scan.
The second MRI scan was performed 17 days post
onset of the symptoms. The T1WI sequence with contrast
(Gd-DTPa) injection showed cortical contrast uptake.
T2WI-FLAIR sequence showed moderate hyper
intensities. DWI single shot EPI sequence showed slight
hyper intensity lesions. In this scan, T1WI+ Gd was more
sensitive to abnormalities than the other sequences.
Case 3: The MRI screening of a woman aged 62 years
48 h following admission was reported for a left
temporobasal hypo intensity that was linked to a left
temporal focal dysrhythmia on the electroencephalogram.
This patient underwent one MRI scan and the T1WI
sequence with post contrast (Gd-DTPa) injection showed
no cortical enhancement. T2WI-FLAIR sequence showed
high hyper intensity lesions.
DWI single shot EPI
sequence showed moderate hyper intensity lesions. In
this scan, T2WI-FLAIR sequence was the most sensitive
to abnormalities.
HSVE primarily affects neurons, which is correlated
with the HSVE cortical distribution with only secondary
involvement of the white matter. Therefore, the
discrimination of cytotoxic oedema in the cerebral cortex
and the interstitial oedema separation in the surrounding
white matter utilizing DWI can be highly important in
diagnosing HSVE. Serial imaging was conducted starting
40 h from the appearance of symptoms in two of the
patients in this study. MRI screenings were performed
after two days (1st and 3rd patient) and four days (2nd
patient), which plotted cortical hyper intensity in the
T2WI. In all patients, DWI revealed cortical hyper
intensity using a single-shot EPI sequence in the early
stage. The areas where restricted diffusion was found
were screened in regions of T2 hyper intensity and in
other cortical regions with relatively slight T2 signal
alteration. MRI screening was next conducted nine days
later on patient 1. By then the T2 diffusion restriction and
signal abnormality had increased both in intensity and
extension. Moreover, contrast enhancement was
reported within the affected cerebral cortex. MRI
screenings were conducted 19 days later on patient 1
and 17 days later on patient 2. Both demonstrated
cortical T2 hyper intensity in the affected areas. However,
the signal changes in DW images were relatively less
conspicuous than in the earlier scanning. Persistent
contrast uptake was illustrated in areas of T2 signal
change. The conclusion of this study was that MRI, as
well as diffusion-weighted images was able to reveal
signs of HSVE-T1 as early as 40 h after the appearance

of symptoms. DWI also showed diffusion abnormality in
the cerebral cortex and may have been more precise
than T2WI sequences were. The diffusion abnormality
was more likely to disappear after 14 days, whereas T2
signal changes and contrast endured beyond 2 weeks
(Kker et al., 2004).
(a) DWI utilizing a single-shot EPI sequence. Hyper
intense cortical lesions are present on the two sides
within the left frontal operculum as well as within the
insular cortex without the involvement of the white matter.
(b) DWI performed 9 days later demonstrates new
changes in signal within the bilateral cingulate gyri and
development of lesions on both sides.
(c) 19 days later, most of the diffusion irregularities have
vanished. The slight hyper intense changes in the insular
cortex were a result of T2 shine-through; this was further
proved by ADC calculation.
(d) T2WI FLAIR image taken 40 h following the early
stage of the disease reveals faint hyper intense lesions
on the two sides within the insular cortex, in the same
area as the diffusion irregularities.
(e) 9 days later, the changes in signal within this T2WI
FLAIR image were more detailed and thorough than they
were in the first scan as the lesions in the two cingulate
gyri were not illustrated in the first scan.
(f) 19 days later, the changes in signal within this T2WI
FLAIR sequence did not change greatly compared to the
scan performed 10 days earlier.
(g) T1-weighted image following administration of GdDTPA at 40 hrs illustrates moderate leptomeningeal
enhancement without any uptake of cerebral contrast.
(h) contrast-enhanced T1WI MRI image 9 days later
distinctly illustrates cortical enhancement in the regions
involved within the cingulate gyri and the insula.
(i) 19 days later there was no change in the contrast
uptake compared to the scan performed 10 days earlier.
Source: Kker et al. (2004)
Study 5
Damsgaard et al. (2012) reported discrepancies in
findings of proton MRS and conventional MRI in female
aged 67 with HSVE-1. On day 3 after the onset of
symptoms, a brain CT scan revealed no abnormalities.
The patient began treatment with acyclovir-10, mg/kg IV
every 8 h. On day 7, the patient underwent MRI and MRS
on a 1.5T unit. A conventional MRI was performed using
axial gradient 3D T1-weighted, axial turbo spin echo
T2WI and coronal T2WI-FLAIR fat-saturated (FatSat)
sequences. DWI was also performed and an ADC map
was calculated. An intravenous contrast-enhanced axial
gradient 3D T1 sequence was obtained. The MRI
demonstrated subcortical white matter hyper intensity on
T2-WI and T2WI-FLAIR FatSat in the ventral part of left
temporal lobe (Figure 28A and 28B); this was interpreted

as encephalitis. No extra-temporal involvement was
found, but the right frontal lobe showed hyper intensive
areas representing older ischemic lesions. There was no
enhancement on the post-contrast T1WI and no affected
water diffusion on DWI and ADC. Proton MRS was
performed on the bilateral temporal lobes by the single
voxel method. On MRS, peaks of choline (Cho), N-acetyl
aspartate (NAA) and creatine could be observed. The
MRS findings in HSVE patient were as follows: (1) a mild
decrement of the N-acetyl aspartate (NAA)/Creatine (Cr)
scale-proportion in the unaffected right temporal lobe; (2)
a large decrement of the NAA/Cr scale-proportion in the
affected left temporal lobe; (3) a raised Choline (Cho)/Cr
ratio bilaterally in the temporal lobes, but within normal
ranges. The decrease in NAA/Cr ratio was ascribed to
neuronal damage or loss and the replacement by
astrocytes, while the increase in Cho/Cr ratio was caused
by the inflammatory process of macrophage infiltration or
demyelination. The high and broad peak at 0.8 1.5 ppm
was an unspecific combination of lactic acid, lipids, and
low molecular weight proteins, and was seen in many
pathological processes (Figure 20C and 20D). It was
shown that the decrement in NAA/Cr scale-proportion
was a result of neuronal damage, and the increase in
Cho/Cr ratio reflected the demyelination associated with
the neuronal damage.
The findings indicated that the abnormalities on proton
MRS are nonspecific, but they could be a helpful
parameter in the assessment of cerebral lesions with
associated prognostic features.
Study 6
Taylor et al. (2007) presented 31-year-old female patient
with PCR amplification of CSF that resulted in positive
HSVE-1. The initial CT scan of her brain without and with
contrast enhancement was normal. Her initial MRI
illustrated T2 hyper intense lesions with restricted
diffusion in the bilateral anterior cingulate gyri and within
the left frontal region gyri (Figure 29). MRI screening was
repeated after two days, following onset of leg weakness.
It illustrated very slight lesion evolution on diffusion
images. The spinal cord MRI was normal. Three days
after the first MRI, new lesions were reported in the
subcallosalgyri and in the left medial temporal lobe.
These lesions were enhanced with gadolinium (Figure
30). The findings of this study demonstrated that CT
scanning had markedly decreased sensitivity for HSVE
lesions compared to MRI (Taylor et al., 2007).
Study 7
Markoula et al. (2009) studied two patients, one male
aged 52 years and one female aged 46 years; both were
confirmed to have HSVE-1 by PCR in the CSF. The brain

CT scan of the female patient in the acute stage was
normal. MRI of the brain demonstrated abnormalities of
high intensity on T2WIs in the right insular cortex and the
right temporal lobe (Figure 31A). The T1WI, following
contrast administration, illustrated gyriform enhancement
within the right insula and the right temporal lobe (Figure
31B). After six months, a follow-up visit and MRI
screening were arranged for re-examination. Although
the patient was asymptomatic, the T2WI scans illustrated
an increase in the number of hyper intensity lesions in the
periventricular white matter close to the horns of the
lateral ventricle and the insula (Figure 31C). The
abnormal contrast enhancement, although reduced, was
still existent in the right temporal lobe on the postcontrast T1WIs, which displayed no noticeable atrophy
(Figure 31D). The patient was then hospitalised for one
day. A new lumbar puncture showed a normal cell count,
slightly higher level of protein, and regular glucose level.
PCR was negative for HSVE-1 DNA. Brain CT scan in
the acute stage for the male patient illustrated hypointense regions with benign enhancement after contrast
administration in the right temporal lobe. A brain T2WIMRI illustrated hyper intensity lesions on the right
temporal lobe, cingulate gyrus and right insular cortex
(Figure 32A and 32B), with abnormal contrast
enhancement on images of post contrast scanning
(Figure 32C). At 6 months, a follow-up visit was arranged
for the male patient following the encephalitis abuse. A
new MRI of the brain was also conducted and T2WIs
revealed expansion and development of the lesions
within the right temporal lobe, cingulate gyri, and insula,
as well as the presence of white matter hypersensitivities
in the right frontal lobe (Figure 32D and 32E). The postcontrast T1WIs showed the enhancement was decreased
in size (Figure 32F) compared with the T1WIs of the
earlier MRIbut still existent without atrophy. This study
asserted the value of PCR and MRI in the investigation
process of HSVE. MRI investigations are highly important
for precisely defining HSVE severity and also for
detecting morphologic irregularities in HSVE, showing
white and grey matter lesions throughout early stages of
infections when CT scans are unable to detect them
(Markoula et al., 2009).
Study 8
Elbers et al. (2007) presented a study that included 16 of
322 patients with acute encephalitis that fulfilled the
criteria for HSVE (8 males and 8 females). Of the 16
patients, 12 (75%) had HSVE detected in the CSF by
PCR. In 10 (83%) of the 12 patients, the virus detected
by PCR was HSVE-1, while the virus detected for 2
(17%) patients was HSVE-2. In this study, 15 (94%) of
the 16 patients underwent a brain CT scan, and 13 (81%)
underwent MRI screening. Neuroimaging irregularities
Alazmi
093
Figure 28. On day 8 after onset of symptoms, MRI axial T2WI (A) depicts white matter hyper intensity in the ventral part
of the temporal lobe due to oedema. MRI coronal T2WI-FLAIR FatSat (B) depicts white matter hyper intensity in the
ventral part of the temporal lobe caused by oedema. Hyper intensive areas in the right frontal lobe represent older
ischemic lesions. Proton MRS at 1.5T was performed in the right (C) and left (D) temporal lobes by single voxel method
(TE _ 35, TR _ 2000, NSa _ 128). MR spectroscopic voxels were with cubic shape. Assignment of peaks: choline 3.2
ppm; creatine 3.0 ppm; N-acetyl aspirate 2.0; lactic acid 1.3 ppm; lipid 0.9-1.2 ppm. Source: Damsgaard et al. (2012).
consistent with HSVE (that is, high/low-density lesions,

haemorrhage, mass effect, or localized oedema on either
MRI or CT scans) were recognized in 14 (88%) of the
cases. The results showed that 4 (25%) of the cases

involved subsequent haemorrhage and infarction. All
were reported with positive CSF PCR for HSVE-1. Of the
Figure 29. Initial MRI, coronal FLAIR. (A) Coronal FLAIR image illustrates patchy T2 hyper
intensity foci in the left cingulate gyrus and over the left frontal lobe in the superior frontal gyrus
with white and grey matter involvement. (B) Coronal FLAIR image more anteriorly demonstrating
the involvement of bilateral cingulate gyrus that extends upwards within the left frontal lobe. (C)
Diffusion trace image illustrates bilateral restricted diffusion within the cingulate gyri. (D) Illustrates
decreased ADC within the left frontal cortex suggesting severe cellular swelling, hyper cellularity, or
cytotoxic oedema. (E) Diffusion trace image demonstrates a tiny focus of diffusion abnormality in
the right insula (arrow) which is not easy to evaluate on the ADC map. (Source: Taylor et al.,
2007).
15 CT scans, 6 (40%) were diagnosed as normal,

whereas of 13 MRI scans, only one patient did not show
any evidence of HSVE infection. Of the 6 cases with
negative CT results, 4 patients (67%) showed
irregularities consistent with HSVE on MRI scans. The
findings indicated that MRI is a more sensitive and
effective diagnostic imaging process for discovering
irregularities correlated with HSVE than CT scan is.
Hence, MRI should be the first preference for HSVE
evaluation and diagnosis (Elbers et al., 2007).
STUDIES ON DETECTING HSVE-2 BY MRI AND CT

SCAN
Study 1
Vossough et al. (2008) conducted a study of 12 neonatal
patients (8 girls and 4 boys) over an eight-year period.

They all had HSVE-2, which had been proven by
serological or virological processes, and had undergone
brain MRI and CT studies.
The imaging output for neonatal HSVE-2 was variable.
In eight patients (67%), the disease was multifocal and
limited to the brainstem or temporal lobes and cerebellum
in four (33%) other patients. In 8 patients (67%), the
temporal lobes were involved. In 3 of 11 patients (27%),
the first CT scan was negative whereas two other
patients (18%) were under subsections of hypo densities
in the pons and thalami. In 9 of 11 patients (81%),
conventional MRI images revealed more extensive
irregularities than CT images did. In two patients (20%),
lesions were first seen only on DWIs, while conventional
MRI and CT images were normal (Figure 33). DWIs
revealed a rather more extensive disease than was first
seen on conventional MRI or CT images in five other
Alazmi
095
Figure 30. Follow-up MRI three days after the first MRI. Coronal FLAIR
images (A and B) with involvement within the right insular (A) coinciding
to the region of diffusion abnormality illustrated on the earlier DWI (Figure
29E); larger involvement of the cingulate gyri (B) in comparison to the
previous scan with subcallosal region and left mesial temporal lobe
involvements (B, arrow-heads), which is typical representation for HSVE.
T1 axial pre-gadolinium (C), and post-gadolinium (D), demonstrating
enhancement within the region of T2 abnormality in the left frontal lobe
(arrowhead). Source: (Taylor et al. (2007).
patients (50%). On the other hand, DWI revealed more

conspicuity of lesions but did not add any more
information to that given by conventional MRI images in
three patients (30%).
Most of the regions that were normal on conventional
MRI images displayed restricted diffusion on follow up
imaging, and they indicated encephalomalacia and
necrosis (Figures 33 and 34). In one patient, the
diagnosis was based on restricted diffusion in the left
temporal lobe; however, conventional MRI images were
negative. At three months, follow-up imaging revealed
only slight focal encephalomalacia with remaining
products of blood or calcification in the left temporal lobe,
and the patient was neurologically normal (Figure 33). A
haemorrhage was suspected or seen on the initial
imaging studies in eight patients (66%), while the initial
finding upon presentation was a temporal lobe bleed in
one of the patients. The deep grey matter structures were
distinctly involved in seven patients (58%) (Figure 34A
and 34B).
The appearance of neonatal HSVE-2 end-stage with
relative
prominence
and
extensive
cystic
encephalomalacia of the deep structures of grey matter in
relation to the damaged cortex and subcortical white
matter may lead to the erroneous assumption that the
deep grey nuclei are not included in the neonatal herpes
(HSVE-2) (Figure 35). In 8 patients (67%), the temporal
lobes were involved. In three patients (25%), the illness
was limited and restricted to the inferior frontal and
temporal lobes. In five patients (42%), regions of loss of
grey-white discrimination, cortical grey matter blurring
regions, or leptomeningeal or gyral enhancement were
shown on MRI images (Figure 36). In addition to areas
that were previously assumed to be necrotic because of
direct herpetic involvement, four patients who underwent
diffusion imaging (40%) showed infarcts and restricted
diffusion in the brains watershed regions away from the
infection site. Thus, the chance of hypoperfusion damage
in these patients was heightened (Figure 37).
This study found that neonatal HSVE-2 can be either
limited to the temporal lobes, cerebellum, or brainstem or
it can be multifocal. Neonatal HSVE-2 is a more diffused
on the first MRI images were the only discoveries in two

of the patients. Vossough et al. (2008) reported that DW
imaging plays a substantial role in the detection of HSVE2.
Study 2
Reuter et al. (2007) presented the case of a man aged 85
years who was immune-competent symptomatic. The
PCR test of CSF was positive for HSVE-2. CT scan of the
brain revealed peripheral and central parenchymal loss
caused by aging. Brain MRI revealed tiny T2 bright areas,
one in the right inferior frontal lobe and the other one in
the left temporal lobe cortex. They were understood as
chronic
focal
infarcts.
Extensive
perivascular
demyelination was also reported.
In another study, Reuter et al. (2007) reported that MRI
abnormalities were existent in 21 of 24 examined cases
of HSVE-2 which were proven by PCR in adults.
Discoveries of high T2 signal intensities contained focal
abnormalities in the orbital surface of the frontal lobe and
the medial region of the temporal lobe, which were
associated with oedema. The limbic region (involving the
insula, parahippocampalgyrus, and hippocampus) are
areas in the temporal lobe that were particularly damaged
in some patients. Compared to T1T2 weighted imaging
sequences, parietal lobe involvement was also reported.
FLAIR-MRI may be a preferable imaging sequence
(Reuter et al., 2007).
Study 3
Figure 31. The female patients axial T2WI (A), and coronal postcontrast T1WI (B) while still in the acute stage of HSVE. After 6months, the T2WI shows an expansion and development of the
initial of hyper intensity lesions in the periventricular white matter
and the insula (C), and the coronal post-contrast T1WI illustrates the
presence of abnormal contrast enhancement within the right
temporal lobe, however, it reduced in size (D). No noticeable
atrophy has developed (C and D) (Source: Markoula et al., 2009).
process than HSVE-1 in adults. The CT scan was

negative in many cases, or the irregularity was hard to
distinguish in patients who had symptoms earlier than
expected in the early stage of the disease. Conventional
MRI had an important advantage over CT in illustrating
locations of irregularity, but DWI scanning showed the
largest utility in defining diseased locations that were
normal on CT scan or conventional MRI sequences. The
watery nature of the neonatal brain complicates
distinguishing between locations of infection and normal
brain on conventional MRI images. For many of the
patients in this study, DWIs were capable of revealing
early changes that were not detectable on CT or
conventional MR images. Locations of restricted diffusion
Harrison et al. (2003) presented an incident of chronic

atypical HSVE-2 in a man aged 68 who was
immunocompromised and displaying symptoms of HSVE.
The CT scan and conventional MRI of the brain revealed
only slight atrophic changes (Figure 38). No DWI was
done for this patient and conventional MRI screenings of
the brain at the presentation or even in the late course of
the encephalopathy were unremarkable. In the late
course of the disease, the patient was found to have
HSVE-2 by PCR test. These results showed that PCR
test should be performed very early in the course of the
disease with DWI to confirm diagnosis and indicate
antiviral medication.
Study 4
Pelligra et al. (2007) reported the case of a 16-day-old
infant with a cerebellar and brainstem involvement
secondary to HSVE-2 infection. DW-MRI conducted three
days following the commencement of symptoms showed
restricted diffusion primarily in pons, middle cerebellar
peduncles, brainstem and cerebellar structures (Figure
Alazmi
097
Figure 32. The male patients axial T2WI (A and B) and post contrast T1WI (C) in the acute
stage illustrate lesions within the cingulate gyrus, right temporal lobe and insula. After 6 months
(D and E), expansion and development of the white matter alterations are noticed in the right
temporal lobe, cingulate gyri and insula; as well as the new appearance of hyper intensities in
white matter of the right frontal lobe. The post-contrast images illustrate that the abnormal
contrast enhancement in the cingulate gyri and right insula is still present, though reduced, six
months later (F). No noticeable atrophy has developed in this case (D, E and F). Source:
Markoula et al. (2009).
Figure 33. Usage of DW imaging to diagnose HSVE-2. (a) Normal axial FLAIR image in
13-day-old patient 6. No irregularities were seen on any of the conventional MRI images;
the first CT scan was also normal. (b) Axial DWI reveals the focus of restricted diffusion
(arrow) within the medial anterior left temporal lobes uncal region, proved on ADC maps
(not shown). Because of these results, acyclovir was instantly commenced in the MRI
room. (c) Axial T1WI gained after 11 weeks illustrates a region of calcification or blood
bodies (arrow) with infarction at the location of diffusion abnormality. (Source: Vossough
et al., 2008).
39). No abnormality was seen on conventional MRI (T2,

T1, and post MR contrast agent administration
sequences). On day seven, another MRI was conducted
on the brain, which revealed an analogous pattern of
restricted diffusion at the same locations demonstrated in
the antecedent study. T1WI illustrated bright signal of T1shortening in these areas that were not noticeable in the
first study (Figure 40). The administration of gadolinium

showed leptomeningeal enhancement over the surface of
the cerebellar folia and around the pons. On day 18, the
third MRI of the brain demonstrated damage to brain
development. T1 shortening was detected in the
corticospinal tracts bilaterally, extending to the left
Rolandic cortex (Figure 41A). There were expanded
Figure 34. Involvement of brainstem, deep grey matter structures and

cerebellum by neonatal HSVE- 2 as illustrated in different patients. (a)
Axial DWI shows restricted diffusion in the right lentiform nucleus (arrow)
and the left caudate nucleus head (arrow) in addition to the right and left
occipitotemporo parietal regions and confirmed on ADC maps (not
shown). Normal basal ganglia were demonstrated on the first
conventional MRI images and CT scan (patient 3). (b) Axial CT image of
the same patient in (a) taken three years later illustrates cystic
encephalomalacia in the left occipitotemporo parietal region (asterisk).
The arrows show hypoattenuation in the left caudate nucleus head and
the right lentiform nucleus and they indicate old necrosis. (c) Axial DWI of
another patient (patient 9) illustrates restricted diffusion in the deep
cerebellar hemispheres (arrow) and pons (arrow). The only irregularity on
this patients first CT scan was questionable hypoattenuation in the upper
medulla and the pons (not shown). (d) Axial T2WI taken in the same
patient as in (c) after 18 days illustrates cystic encephalomalacia in
cerebellar hemispheres (arrowheads) and the medulla (arrows). (Source:
Vossough et al., 2008).
abnormal T1 and T2 signals with tissue loss associated

with the ventral medulla and pons, the grey and white
matter of the cerebellar hemispheres, and the middle
cerebellar peduncles (Figure 41B).
This study also highlighted the significance of
performing DW-MRI sequences to discover CNS
involvement at early stages of HSVE infection and then
using serial MRI scans to follow up on the formation and
development of CNS lesions.
Study 5
Brown et al. (2010) reported an uncommon case of an
immune-competent girl who contracted HSVE-2 infection
as an infant. At eight years, she was discovered to have
an active, chronic form of the same disease with a lack of
clinical symptoms and neurologic deficits. Her newborn
examination included normal brain CT and MRI scans
and an abnormal EEG. Viral and bacterial cultures of
Alazmi
099
Figure 35. Neonatal HSVE-2 at end-stage

(patient 2). The above non-contrast axial CT
image shows significant necrotic alterations
and encephalomalacia associating with the
parietal and frontal lobes bilateral. The
relative clarity of the thalami (arrows) and
basal ganglia (arrowheads) in association
with the ruined cortex has previously led to
the wrong assumption that neonatal HSVE-2
does not include the deep structures of grey
matter. (Source: Vossough et al., 2008)
Figure 36. Watershed region ischemic defect in neonatal HSVE-2

(patient 11). (a) DW axial image illustrates restricted diffusions
various foci (arrows) in the brains watershed region. The maps of
ADC (not shown) proved the existence of restricted diffusion. (b)
Axial T2WI taken after 3 weeks demonstrates that the areas
illustrating restricted diffusion have developed infarction (arrows).
The findings imply a sign of hypo perfusion defect in addition to
the initial herpetic necrosis. (Source: Vossough et al., 2008).
cerebrospinal fluid were normal, and PCR for HSVE was

not conducted. The newborn patient was discharged. At
eight years, a CT scan was arranged after a lightweight
head trauma complicated head pain. She was
coincidentally discovered to have various calcifications in

the intracerebral parenchyma, right temporal lobe
encephalomalacia, and extensive bilateral white matter
hypo densities (Figures 42A and 42B). Mental status and
Figure 37. Cortical blurring and leptomeningeal/gyral enhancement in different HSVE2 neonatal patients. (a) Axial T2WI (patient 11) illustrates decreased cortical
differentiation of white/grey matter (arrowheads) within the right temporal lobe. (b)
Leptomeningeal/gyral contrast enhancement (arrows) within the right temporal area on
coronal image post contrast administration also in (patient 11). (c) Axial CT image of
(patient 11) taken two weeks after, illustrates extensive liquefactive necrosis (arrow).
(d) Gyriform contrast enhancement in bilateral frontoparietal areas on the axial image
following administration of gadolinium (patient 3). This was the only irregularity
detected on conventional MRI images. (e) Sagittal TWI following administration of
contrast in another patient, (patient 9), reveals leptomeningeal enhancement (arrows)
over the brainstem. There was no cortical irregularity detected on any of the scans,
including DWIs. (f) Sagittal T1WI taken after three weeks on the same patient as in (e)
demonstrates the existence of calcification and/or blood bodies (arrow) and reduced
volume of the pons. (Source: Vossough et al., 2008).
Figure 38. MRI screening of the brain conducted 11 days following the
commencement of symptoms. Axial T2WI reveals slight atrophy, but no
intracerebral lesions noted. Source: Harrison et al. (2003).
thorough neurologic inspection results were completely

normal. MRI of the illustrated brain was considerably
abnormal (Figure 43, column 1), with several intense

enhancing lesions that were cortically based (Figure 42C
Alazmi
101
Figure 39. Axial EPI-DWI three days following the

commencement of symptoms reveals hyper intensity led by
restricted diffusion in the pons (a arrows); the (b arrow)
points at cerebellar peduncles, and (c arrow) points at right
medial cerebellar hemisphere. (Source: Pelligra et al., 2007).
Figure 40. Axial spin-echo T1WI eight days following the

commencement of symptoms demonstrates hyper intensity
of T1-shortening in the pons (a arrows); (b arrows) points
at cerebellar peduncles. Low signal of oedema is also
illustrated in the cerebellar white matter. (Source: Pelligra et
al., 2007).
and 42D).
Sever signal abnormality was noted, particularly within
the right hemisphere and specifically in the temporal and
frontal lobes (Figures 43B-1 and 43E-1) with some
involvement of the parietal lobe in addition to a slighter
grade of signal abnormality within the anterior left frontal
lobe (Figure 43A-1). There were some susceptibility
artefacts noted on GRE sequences that corresponded
with the different densities on CT scans (Figures 42C,
42D and 43).
Study 6
Kubota et al. (2007) presented the case of an 18-day-old
girl with neonatal HSVE-2, in which DWI was performed
repeatedly. Although there were no abnormal findings on
conventional MRI at 20 h after the inception of the illness,
DWI detected an area of high intensity in the left
frontotemporal lobe and dispersed small spotty high
intensity lesions in both hemispheres. Performed 72 h
after the inception of illness, the second DWI detected a
Figure 41. A. Coronal T1WI performed 18 days following the

commencement of acyclovir therapy reveals T1-shortening
bilaterally in the basal ganglia along the side of the corticospinal
tracts (a arrows), with unilateral radiation to the left Rolandic
cortex (b arrow). B. Midline sagittal T1WI demonstrates
abnormal signal and loss of volume in the pons, ventral medulla
(b arrow), and cerebellar vermis (c arrow) (Source: Pelligra et
al., 2007).
new area of high intensity in the right temporal lobe,

expansion of dispersed hyper intensity lesions in the
bilateral hemispheres, and a lesion of hyper intensity
signal in the left frontotemporal lobe. In this case, early
DWI was beneficial for early discovery and analysis of
neonatal HSVE. this findings showed that in comparison
with conventional MRI, DWI could be more sensitive in
demonstrating the lesions in HSVE because the changing
movement of water molecules in the neonatal brain
occurs earlier than structural changes do (Figure 44)
(Kubota et al., 2007).
FINDINGS
From the literatures review it was found that in adult
immune-competent patients and patients more than 3
months old with HSEV-1, the abnormalities are quite
characteristic, involving the inferolateral frontal lobes, the
medial temporal lobes, and the insular cortex. It is usually
associated with hemorrhagic patterns. Involvement can
be more generalized in immunocompromised HSVE-2
patients (including neonates < 3 months old) and is more
likely to involve the brainstem. It is also important to
Alazmi
103
Figure 42. Axial CT images (A and B) and MRI images (C and D) at

first examination illustrating extensive abnormalities in right
hemispheric white matter with bilateral frontal (A) and right temporal
(B) calcifications. These post-contrast T1WIs illustrating contrast
enhancement (C and D) (Source: Brown et al., 2010).
highlight that the pattern of abnormality in adults and

children is different from neonatal HSVE. In addition, the
extra-limbic involvement is more common in children than
in adults (HSVE-1) and is seen most commonly in the
parietal lobe, sparing the basal ganglia.
Early diagnosis by CT scan is difficult in both types of
HSVE (type 1 and type 2). The findings usually consist of
subtle low density within the medial and anterior parts of
the temporal lobe and the insular cortex. The changes
can become more apparent and can even develop
to hemorrhage if scanned at a later stage. Contrast
enhancement in CT scan is not common throughout the
first week of the disease. Patchy low level enhancement
may be seen after this period. On the other hand, MRI
has proved to be the most specific and sensitive imaging
method for both types of HSVE, especially during the
early stage of the disease.
However, normal MRI findings were also reported
during the later stages of the disease. The appearance of
the affected areas is similar in both types of HSVE in
terms of signal characteristics in main MRI sequences. In
T1WI without contrast media injection, the affected region
appears as general oedema, and if it is complicated by

sub-acute haemorrhage, a hyper intense signal will be
seen.
In T1WI with contrast (Gd), in the acute stage of the
disease enhancement rarely appears. However, later
enhancement will have variable patterns: leptomeningeal
enhancement,
gyral
enhancement,
diffused
enhancement, and ring enhancement.
In T2WI, the affected white matter and cortex appear
with hyperintensity pattern. The more established
haemorrhagic components appear as hypo intense
areas. GRE sequences may demonstrate blooming if
there are haemorrhagic lesions (uncommon in neonates,
but common in older patients).Several recent studies
indicated that MRI with DWI is very helpful early in the
detection of HSVE-1 and HSVE-2 in adults, children, and
neonates; however, DWI is not superior to conventional
MRI in follow-up imaging. DWI/ADC has higher sensitivity
to abnormalities than T2WI does. The restricted diffusion
in the brains of patients with HSVE infection is common
because of cytotoxic oedema. T2 signal shining through
DWI is common because of vasogenic oedema.
Figure 43. Serial axial FLAIR MRI images demonstrating development of HSVE-2 throughout
period of 48 months. The number of months since the first examination is registered at the
bottom-right corner of each image. The first column of images illustrates the appearance of the
brain at the time of examination. Every row of images from A to E illustrates the brain at the
same anatomical level: (A) Superior to the corpus callosums body. (B) Genu of the corpus
callosum with bifurcation of the fornix and lateral ventricles at the splenium. (C) Through the
genu of the internal capsule and the thalamic nuclei. (D) Through the superior cerebellar
cistern and basal ganglia, and (E) Mesencephalic red nuclei and temporal lobes (Source:
Brown et al., 2010).
Conclusion
HSVE is a devastating CNS infection with high mortality
rates and neurological complications. There are two
types of HSVE, type 1 and type 2. Type 1 is typically
detected in adults and children, whereas type 2 is
detected mostly in neonates (< 3 months old) and in
immune-compromised patients. Both types of HSVE are
not specific and can vary in their presentation.
Furthermore, many brain infections and defects mimic the
radiological appearance of HSVE, which make diagnosis
very difficult. Many methods and techniques are used in
combination to detect HSVE of both types. Early
detection of the disease increases the opportunity to
prevent the occurrence of harmful effects of this disease

on the central nervous system. In acute HSV encephalitis
of both types, damage to brain tissues commonly
becomes apparent on conventional MRI and CT scans
within a few days after the onset of symptoms. Temporal
lobe abnormalities in brain imaging are considered strong
evidence for both types of herpes simplex virus
encephalitis. Brain abnormality involvement in patients
with HSVE-1 usually includes insular cortex, temporal
lobes, and inferolateral frontal lobes, and it is commonly
associated with hemorrhagic patterns. Brain abnormality
involvement in patients with HSVE-2 is usually more
generalized and commonly involves the brainstem.
Although both CT scan and MRI may reveal focal hypo
Alazmi
105
Figure 44. MRI axial and Coronal DWI at 20 h following the

commencement of seizures (A and B). There are dispersed
tiny spotty lesions of high intensity in both hemispheres.
Axial and coronal DWI 72 h following the early stage of the
disease (C and D).Expansion of small high intensity lesions
and new lesions are shown in the right temporal lobe. ADC
map of the brain is seen 72 h after the seizure (E). ADC
values were considerably decreased in the lesions seen on
DWI. Axial FLAIR scans 30 days following the
commencement of the disease (F). Cystic changes were
screened in the right temporal and the left frontotemporal
regions. Source: Kubota et al. (2007).
densities, oedemas, haemorrhages and changes in

ventricle size, MRI is more sensitive in early
demonstration of the HSVE pathology. CT scans of the
brain have only 50% sensitivity at early stages of the
disease. The presence of abnormalities is generally
correlated with poor prognosis and severe damage.
Nevertheless, in the early clinical stage of the disease,
conventional MRI findings may be negative. However, a
negative MRI does not rule out HSVE, so it is
recommended that treatment be empirically continued
until laboratory tests and other diagnostic modalities
definitely exclude the presence of HSVE. This can be
confirmed with a PCR test if it is available. In neonatal
patients, the alterations caused by the movement of
water molecules in brain tissues with HSVE infection
appear earlier than structural changes do. These
changes are obvious in DWI. Hence, DWI is superior to
conventional MRI in early stages of both types of HSVE.
This study found that MRI is more reliable than CT scan
in detecting the characteristic radiological changes

correlated with HSVE. MRI and DWI sequences in
particular are recommended as the most effective means
of investigation and detection in patients with suspected
HSVE of both types. Thus, it has been asserted that
hypothesis one and two have been proved correct.
REFERENCES
A Review of Common Pediatric Lip Lesions (2003).
Herpes Simplex/Recurrent Herpes Labialis, Impetigo,
Mucoceles, and Hemangiomas. Clinical Pediatrics, 42,
475-482.
Ametani M, Ogawa T, Tanabe Y, Sugihara S, Kinoshita
F, Kinoshita T (2005). 'Sequential Mr Imaging and
Spect Studies in Herpes Simplex Encephalitis with
Crossed Cerebellar Hyperperfusion'. Annals of Nuclear
Medicine, vol. 19, pp. 151-155.
Baskin HJ, Hedlund G (2007). 'Neuroimaging of Herpes

Virus Infections in Children', Pediatric Radiology,
37:949-963.
Bonkowsky JL, Filloux FM, Byington CL (2006). 'Herpes
Simplex Virus Central Nervous System Relapse During
Treatment of Infantile Spasms with Corticotropin',
Pediatrics, 117:E1045-E1048.
Brown WD, Bearer EL, Donahue JE (2010). 'Chronic
active Herpes Simplex Type 2 Encephalitis in an
Asymptomatic Immuno-competent Child. J. Child
Neurol.,
U6
Ctx_Ver=Z39.882004&Ctx_Enc=info%3aofi%2fenc%3autf8&Rfr_Id=info:Sid/Summon.Serialssolutions.Com&Rft_
Val_Fmt=info:ofi/Fmt:Kev:Mtx:Journal&Rft.Genre=articl
e&Rft.atitle=Chronic+active+Herpes+Simplex+Type+2+
Encephalitis+in+an+asymptomatic+Immunocompetent+
Child&Rft.Jtitle=Journal+of+Child+Neurology&Rft.au=B
rown%2c+William+D&Rft.au=Bearer%2c+Elaine+L&Rft
.au=Donahue%2c+John+E&Rft.Date=2010-0701&Rft.Eissn=17088283&Rft.Volume=25&Rft.Issue=7&Rft.Spage=901&Rft
_Id=info:Pmid/20179002&Rft.Externaldocid=20179002
&Paramdict=En-Us U7 - Journal article U8 - FetchLogical-P512B482435d64952dc23e8cde1b64b7ad5bfce808fc3399f7
6ee8aec3d23f978b511, vol. 25, p. 901.
Corno AF, Festa GP (2009). Introduction to CTscan
and MRI, Steinkopff, Heidelberg:
Coskun O (2011). 'Magnetic Resonance Imaging and
Safety Aspects', Toxicol. Industrial Health, 27, 307313.
Damsgaard J, Marinovskij E, Leutscher PDC (2012).
Discrepant Findings Between Proton Magnetic
Resonance Spectroscopy and Magnetic Resonance
Imaging in an Immunocompetent Patient with Herpes
Simplex Virus Type 1 Encephalitis. Scandinavian J.
Infect. Dis., 44, 315-319.
Elbers, JM, Macgregor D, Bitnun A, Richardson SE,
Ford-Jones EL, Tellier R, Wald RM, Petric M, Kolski
H, Heurter H (2007). A 12-Year Prospective Study of
Childhood Herpes Simplex Encephalitis: Is There a
Broader Spectrum of Disease?' Pediatrics, 119, E399E407.
Ferrari S, Toniolo A, Monaco S, Luciani F, Cainelli F,
Baj A, Temesgen Z, Vento S
(2009).
'Viral
Encephalitis: Etiology, Clinical Features, Diagnosis and
Management', The Open infect Dis J., 3, 1-12.
Glaser CA, Honarmand S, Anderson LJ, Schnurr DP,
Forghani B, Cossen CK, Schuster FL, Christie LJ,
Tureen JH (2006). 'Beyond Viruses: Clinical Profiles
and Etiologies associated with Encephalitis', Clin. Infect
Dis, 43, 1565-1577.
Gomes LJ (2010). 'The Role of Imaging in the Diagnosis
of Central Nervous System Vasculitis', Current Allergy
and Asthma Reports, 10, 163-170.
Graber JJ, Rosenblum
MK, Deangelis LM (2011).
'Herpes Simplex Encephalitis in Patients with Cancer'.
J Neuro-Oncol., 105, 415-421.

Gupta R, Warren T, Wald A (2007), 'Genital Herpes.
Lancet', 370, 2127-2137.
Halperin
JJ (2008)., Encephalitis: diagnosis and
treatment, New York U6 - Ctx_Ver=Z39.882004&Ctx_Enc=info%3aofi%2fenc%3autf8&Rfr_Id=info:Sid/Summon.Serialssolutions.Com&Rft_
Val_Fmt=info:ofi/Fmt:Kev:Mtx:Book&Rft.Genre=Book&
Rft.Title=Encephalitis&Rft.au=Halperin%2c+John+J&Rf
t.Series=Neurological+Disease+and+Therapy&Rft.Date
=2008-0101&Rft.Pub=informa+Healthcare&Rft.Volume=94.&Rft.
Externaldbid=N%2fa&Rft.Externaldocid=B27522222&P
aramdict=En-Us U7 - Ebook U8 - FetchUq_Catalog_B275222221, Informa Healthcare.
Harrison NA, Macdonald BK, Scott G, Kapoor R (2003).
'Atypical Herpes Type 2 Encephalitis associated with
Normal MRI Imaging', J Neurol, Neurosurg, and
Psychiatr., 74, 974-976.
Hasan K, Cengiz D, Mustafa Kasim K, Mahmut S,
Hayrettin A (2010). 'Herpes Simplex Encephalitis',
Eastern J. Med., 15 : 34.
Herweh C, Jayachandra MR, Hartmann M, Gass A,
Sellner J, Heiland S, Nagel S, Hhnel S, MeydingLamade U (2007). 'Quantitative Diffusion Tensor
Imaging in Herpes Simplex Virus Encephalitis', J
Neurovirol., 13, 426-432.
Hoeffner EG, Mukherji SK, Case I, Jain R, Gujar SK,
Shah GV, Deveikis JP, Carlos RC, Thompson BG,
Harrigan MR (2004). 'Cerebral Perfusion Ct: Technique
and Clinical Applications', Radiology, 231, 632.
Hoff NP, Gerber PA (2012). 'Herpetic Whitlow', Cmaj:
Canadian Medical Association Journal = Journal De
L'Association Medicale Canadienne, 184, E924.
Huseyin , zkan , Cahide Y, Ahmet Sami G, zlem
(2007). 'Cranial Ct/Mri Findings in Children with Acute
Herpes Simplex Encephalitis', J Pediatr Neurol, 5, 133.
Kneen R, Carrol E, Solomon T, Michael BD, Menson E,
Mehta B, Easton A, Hemingway C, Klapper PE, Vincent
A, Lim M (2012). National Encephalitis Guidelines, D.
& Stakeholder, G.. Management of Suspected Viral
Encephalitis in Children, Association of British
Neurologists and British Paediatric allergy, Immunology
and Infection Group National Guidelines, The J infect.,
64, 449.
Kock MCJM, Dijkshoorn ML, Pattynama PMT, Myriam
Hunink MG (2007). 'Multi-Detector Row Computed
Tomography Angiography of Peripheral arterial
Disease', Euro Radiol., 17, 3208-3222.
Kubota T, Ito M, Maruyama K, Kato Y, Miyajima Y,
Ogawa A, Kuno K, Okumura A, Watanabe
K
(2007).'Serial Diffusion-Weighted Imaging of Neonatal
Herpes Encephalitis: a Case Report', Brain and
Development, 29, 171-173.
Kuker W (2007). 'Cerebral Vasculitis: Imaging Signs
Revisited', Neuroradiology. 49, 471-479.
Kuker W, Ngele T, Schmidt F, Heckl S, Herrlinger U
Alazmi
107
(2004). Diffusion-weighted MRI in herpes simplex

encephalitis: a report of three cases. Springer-Verlag,
Berlin/Heidelberg.
Markoula
S,
Giannopoulos
S, Pelidou S-H,
Argyropoulou M, Lagos G, Kyritsis AP (2009). 'MRI
Deterioration in Herpes Simplex Encephalitis Despite
Clinical Recovery', The Neurologist, 15, 223-226.
Mekan SF, Wasay M, Khelaeni B, Saeed Z, Hassan A,
Sheerani M (2005). 'Herpes Simplex Encephalitis:
Analysis of 68 Cases from a Tertiary Care Hospital in
Karachi, Pakistan', J Pakistan Med Assoc., 55, 146148.
Paolo GPN, Ragini V, Seung-Koo L Elias RM (2007).
'Diffusion-Tensor Mr Imaging and Tractography:
Exploring Brain Microstructure and Connectivity 1',
Radiology, 245, 367.
Pelligra G, Lynch N, Miller SP, Sargent MA, Osiovich H
(2007).'Brainstem Involvement in Neonatal Herpes
Simplex Virus Type 2 Encephalitis', Pediatrics, 120,
E442-E446.
Rao P, Bekhit E, Ramanauskas F, Kumbla S (2013). 'CT
Head in Children', Eur J. Radiol., 82, 1050.
Reuter MD, Manian FA, Kershaw MA, Alpert MA (2007).
'Herpes Simplex Virus Type 2 Encephalitis in an Elderly
Immunocompetent Male', Southern Med. J., 100, 11431146.
Rumboldt Z, Ebooks C (2012). Brain imaging with Mri
and CT: an image pattern approach, Cambridge
University Press, Cambridge.
Salih MA, El Khashab HY, Hassan HH, Kentab AY, Al
Subaei SS, Zeidan RM, Al-Nasser, MN, Othman SA
(2009). 'A Study On Herpes Simplex Encephalitis in 18
Children, Including 3 Relapses, Open Pediatr. Med. J.,
3, 48-57.
Schleede L, Kraus V, Van Baalen A, Skopnik H,
Hartmann H, Rostasy K, Lucke T, Schara U, Husler
M, Bueter W, Baumgartner-Sigl S, Opladen T, WeigtUsinger K, Stephan S, Smitka M, Leiz S, Kaiser O
(2013). 'Pediatric Herpes Simplex Virus Encephalitis: A
Retrospective Multicenter Experience', J. Child Neurol.,
28, 321-331.
Schmutzhard J, Merete Riedel H, Zweygberg Wirgart B,
Grillner L (2004). 'Detection of Herpes Simplex Virus
Type 1, Herpes Simplex Virus Type 2 and VaricellaZoster Virus in Skin Lesions: Comparison of Real-Time
Pcr, Nested Pcr and Virus Isolation', J Clin. Virol: The
Official Publication of the Pan American Society For
Clinical Virology, 29, 120-126.
Semelka RC, Brown MA, Ebooks C (2010). MRI: basic
principles and applications, Wiley-Blackwell/John Wiley
& Sons, Hoboken, NJ.
Shaikh AG, Termsarasab P, Riley DE, Katirji B (2013).
'The Floccular Syndrome in Herpes Simplex Type 1
Encephalitis', J. Neurol. Sci., 325, 154.
Siebert E, Diekmann S, Masuhr F, Bauknecht H-C,

Schreiber S, Klingebiel R, Bohner G (2012).
'Measurement of Cerebral Circulation Times Using
Dynamic Whole-Brain Ct-angiography: Feasibility and
initial Experience', Neurol. Sci., 33, 741-747.
Solomon T, Kneen R, Beeching NJ, Michael BD, Smith
PE, Sanderson F, Davies NWS, Hart IJ, Holland M,
Easton A, Buckley C, National Encephalitis Guidelines
D, Stakeholder G (2012). 'Management of Suspected
Viral Encephalitis in Adults--Association of British
Neurologists and British Infection Association National
Guidelines', J. Infect., 64, 347-373.
Steiner I, Budka H, Chaudhuri A, Koskiniemi M, Sainio
K, Salonen O, Kennedy P (2005). Viral encephalitis: a
review of diagnostic methods and guidelines for
management. Eur. J. Neurol., 12, 331 - 343.
Steiner I, Budka H, Chaudhuri A, Koskiniemi M, Sainio K,
Salonen O, Kennedy P (2010). Viral encephalitis: a
review of diagnostic methods and guidelines for
management. Eur. J. Neurol., 17, 999 - 1009.
doi:10.1111/j.1468-1331.2010.02970.x
Stoodley, N & Philip, S 2011, 'CT Scan: Friend Or Foe?'
Clinical Risk, vol. 17, pp. 134-136.
Stracke CP, Meister IG, Mller-Hartmann W, Krings T
(2006). 'Mr Perfusion Imaging in Acute Herpes Simplex
Encephalitis: A Case Report', Clin. Neuroradiol., 16,
127-130.
Takeuchi S, Takasato Y (2011). Herpes simplex virus
encephalitis complicated by intracerebral hematoma,
Medknow Publications & Media Pvt. Ltd., India:
Taylor SW, Lee DH, Jackson AC (2007). 'Herpes
Simplex Encephalitis Presenting with Exclusively
Frontal Lobe Involvement', J. Neurovirol., 13, 477-481.
Tonomura Y, Kataoka H, Yata N, Kawahara M, Okuchi K,
Ueno S (2010). 'A Successfully Treated Case of
Herpes Simplex Encephalitis Complicated By
Subarachnoid Bleeding: a Case Report', J. Med. Case
Reports, 4, 310-310.
Tyring SK (2006). Mucosal immunology and virology,
Springer, London.
Vossough A, Zimmerman RA, Bilaniuk LT, Schwartz EM
(2008)., 'Imaging Findings of Neonatal Herpes Simplex
Virus Type 2 Encephalitis', Neuroradiology. 50, 355366.
Werring DJ, Frazer DW, Coward LJ, Losseff NA, Watt H,
Cipolotti L, Brown MM, Jger HR (2004). 'Cognitive
Dysfunction in Patients with Cerebral Microbleeds On
T2-Weighted Gradient-Echo Mri. Brain', J. Neurol., 127,
2265-2275.
Whitley RJ (2006). 'Herpes Simplex Encephalitis:
Adolescents and Adults', Antiviral Research, 71, 141148.

CT Scan

Încărcat de

Informații document

Titlu original

Drepturi de autor

Formate disponibile

Partajați acest document

Partajați sau inserați document

Opțiuni de partajare

Vi se pare util acest document?

Este necorespunzător acest conținut?

Drepturi de autor:

Formate disponibile

CT Scan

Încărcat de

Drepturi de autor:

Formate disponibile

World Journal of Medicine and Medical Science Research Vol. 2 (5), pp.

071-107, August 2014

Comparison of the diagnostic accuracy of CT scan and

*Corresponding author. E-mail: finjal2013@hotmail.com.

infectious (e.g., chemical drugs or other health problems).

World J. Med. Med. Sci. Res. 072

cytomegalovirus (CMV). In cases where a herpes virus

Aim of the project

Hypotheses of the project

destruction of the epithelial layer. Widespread

method will definitely help in treating and minimising

Herpes simplex virus encephalitis type -1 (HSVE-1)

Herpes simplex Virus encephalitis type -2 (HSVE-2)

World J. Med. Med. Sci. Res. 074

(Hoff and Gerber, 2012).

INVESTIGATIONS OF HERPES SIMPLEX VIRUS

Physical and vital signs examinations

Preliminary and regular laboratory tests

Lumbar puncture analysis

Polymerase chain reaction (PCR) amplification test

Figure 4. Electroencephalography (EEG) showing periodic lateralized epileptiform

(Figure 3) (Enomoto et al., 2005; Schmutzhard, 2004).

World J. Med. Med. Sci. Res. 076

et al., 2009). Structural data are presented by MRI and

it remains a costly, complex and relatively unavailable

ROLE AND ACCURACY OF CT SCAN AND MRI

Single photon emission computed tomography

Photon emission tomography

Although the MRI has many advantages, such as

Computed tomography scan (CT scan)

Figure 6. Two days after the onset of

the contra lateral temporal lobe. Changes in subacute

Computed tomography angiogram

Figure 7. Ten days post-onset of HSVE

evaluated by MRA because it has better sensitivity than

Perfusion computed tomography

World J. Med. Med. Sci. Res. 078

Figure 8. (a) Sagittal; (b) coronal. 4DCTA whole-brain maximum

effects on the results of reactional movement of the

are used in the imaging process (Corno and Festa,

cerebral angiogram (CTA) to detect vascular

usually develops late, CTA is still helpful in detecting and

World J. Med. Med. Sci. Res. 080

with HSVE infections of both types (Mekan et al., 2005).

tiny vascular defects (Hoeffner et al., 2004; Kock et al.,

Magnetic resonance imaging

Figure 14. Brain MRI illustrating diffused white matter high

Figure 13. Brain MRI in a 44-day-old child with HSVE-2,

condition, its stage of development, and the MRI

screened for hypointense. From day 1 of HSVE-1 onset,

Fluid-attenuation inversion recovery sequence

World J. Med. Med. Sci. Res. 082

sequence is another type of MRI sequence that is used to

apparent diffusion coefficient map (ADC), presented a

Magnetic resonance spectroscopy

Magnetic resonance spectroscopy (MRS) can identify

Figure 17. D and E axial DWIs illustrate increased signal

Figure 19. MRI of a nine-year-old patient brain with HSVE-1

World J. Med. Med. Sci. Res. 084

Figure 21. Tractography demonstrating frontotemporal fibre tracts

2005).MRS discovers metabolic changes linked to

Magnetization transfer ratio

Diffusion tensor imaging