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Barik B.K., Pardhan B,
Murmu M,
Sethy
R.C.,
Bhakta
S, Das
A.K.
ABSTRACT:
Herpes
simplex
virus (HSV)
encephalitis
usually
caused
by HSV1
is
gravest
and
commonest
form of
acute
encephalitis.
It is
usually
present
with
fever,
headache,
seizure,
confusion,
stupor
and
coma.
Psychosis
may be
associated
with
these
manifestations.
Here we
are
reporting
a case
of
clinico-radiologically
diagnosed
case of
HSV
encephalitis
that
present
predominantly
with
psychosis
and make
diagnostic
dilemma.
(The
Ind.
Pract
2005; 58
(1):38-39.
KEY WORDS:
Herpes Simplex Virus, Encephalitis,
Psychosis
INTRODUCTION:
Among
all
acute
encephalitis
10% of
cases
are due
to HSV.
It is
usually
present
like
other
acute
encephalitis.
Psychosis
is a
distinct
feature
due to
involvement
of
temporal
lobe,
medial
and
orbital
part of
frontal
lobe. CT
scan
imaging
may
identify
the
cerebral
lesion
at
temporal
and
frontal
lobe.
Fatality
rate
varies
between
30-70%.
Early
presumptic
diagnosis
with the
help of
clinical
examination,
C.S.F.
examination
and
radio
imaging
and
early
therapeutic
intervention
with
acyclovir
may save
the life
of the
patient.
C.S.F.
PCR is
the
diagnostic
approach
now for
herpes
simplex
encephalitis.
CASE REPORT:
A
38 year
old male
presented
with
psychotic
behavior
or last
20 days.
He was
febrile
for
about 6
days 2
weeks
back.
Fever
was
typically
low
grade,
contunuosu.
With the
onset of
fever he
starts
incoherent
talk.
He was also unable to recognize the
known
persons.
His
speech
frequency
was very
much
decreased
and he
was
reluctant
to take
food. He
was
admitted
to local
private
hospital
on days
of his
illness
where
his CS
examination
was
done. At
that
time his
CSF cell
count
was 296/cumm,
mostly
lymphocytes,
protein
72mg%
and
sugar
48mg%.
His
treatment
was
started
there in
the line
of TB
meningitis
but
patient
gradually
deteriorated.
Due to
his
uncontrolled
psychotic
behavior,
psychatric
consultation
was
done,
treated
with
haloperidol.
But
patient’s
psychosis
did not
improve.
Rather
his
bladder
and
bowel
control
was
lost.
On the day of our hospital admission
patient
was
febrile,
drowsy,
disoriented,
illusion
and
auditory
hallucination
were
present.
Sensory
aphasia,
inhoherent
talks
were
associated
with
those
features.
His
plantar
reflex
was B/L
extensor
and gait
unsteady.
Investigation
revealed
WBC
11100/cumm.
ESR 15mm
and RBS
127mg%
DC – N
51% and
L 49%.
Repeat
C.S.F.
examination
was done
which
revealed
total
WBC
count
76/cumm
mostly
lymphocytes,
protein
28 mg%
and
sugar 78
mg%. CSF
contained
plenty
of RBC.
CT scan
of brain
showed
hypodense
area at
B/L
temporal
and
fronto
medial
lobe
(Fig. 1
and Fig
2)
suggestive
of HS
encephalitis.
Treatment
was
started
with
acyclovir
500 mg
IV 8
hourly
with
monitoring
pf S.
Creatinine
level.
On 10th
day of
therapy
patient’s
psychosis
decreased,
was able
to
recognize
his wife
and son
and
plantar
become
flexor,
though
auditory
and
gustatory
hallucination
still
persisted.
DISCUSSION:
HSV 1 and 2 infection
can
manifest
a
spectrum
of
illness
from
stomatitis
and
progenitor
lesion
to
facial
nerve
palsy
and
encephalitis.
Encephalitis
is due
to HSV1.
The
unique
localization
of the
disease
in the
temporal
lobe may
be
explained
by the
virus
route of
entry
into the
CNS1.
The
lesion
takes
the form
of
haemorrhagic
necrosis
of
temporal
and
medial
part of
frontal
lobe2.
Lesion
of these
areas in
imaging
study
with CT
or MRI
is
highly
suggestive3.
Patients
with
Japanese
encephalitis
display
abnormalities
of
thalamus,
basal
ganglia
and
midbrain.
Other
forms of
viral
encephalitis
imaging
studies
are non-
specific.
Manifestations like
hallucination,
anosmia,
personality
changes,
bizarre
behavior
or
delirium,
aphasia
usually
observed
in H.S.
encephalitis.
Temporal
lobe
seizure
usually
seen in
ECG.
Affection
of
memory
can be
recognized
in the
convalescent
state.
CSF often cloudy due to
RBC as
well as
WBC
protein
may be
raised
but
sugar
usually
normal.
In
minority
of
cases,
low
sugar in
CSF may
confuse
with TB
or
fungal
meningitis.
Test for
detection
of HSV
in the
CSF by
PCR are
useful
in
diagnosis
while
virus is
replicating
in
first
few days
of
illness.
Our patient presented at
OPD
after 3
weeks of
illness
when the
absolute
ways to
establish
the
diagnosis
is
fluorescent
antibody
study
and
viral
culture
of brain
tissue
obtained
by
biopsy.
Avoiding
this
hazardous
procedure,
we
treated
the
patient
with
empirical
antiviral
agents
based on
compatible
clinical,
radiological
and CSF
findings.
Treatment
option
for HSE
is
acyclovir
in the
dose of
30 mg
/kg/day
for
10-14
days5.
Our
patient
was
responding
well
with
above
mentioned
treatment.
After
one
month
follow
up ,
patient
improved
with
mild
psychotic
behaviour,
gaustatory
hallucination
and
depression.
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