Вот как бывает: Normal MRI findings in herpes simplex virus encephalitis [Архив] - медицинская консультация врача онлайн бесплатно - форум

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Evdoshenko
20.05.2007, 18:15
Peter Höllinger Lukas MatterMatthias Sturzenegger
Normal MRI findings in
herpes simplex virus
encephalitis
Received: 21 December 1999
Received in revised form: 13 April 2000
Accepted: 2 May 2000
Sirs: Signs and symptoms of herpes simplex virus encephalitis (HSVE)
are manifold and do not allow a firm diagnosis based on clinical findings
alone [10]. Diagnosis remains a challenge despite several refined methods
of investigation, including magnetic resonance imaging (MRI), electroencephalography (EEG), and analysis of cerebrospinal fluid (CSF) with
polymerase chain reaction (PCR) and antibody titers. The former gold standard of diagnosis was brain biopsy, which nowadays has largely been replaced by PCR [6]. Due to the ease of performance and widespread availability of the method, there is agreement that PCR analyses of CSF specimens will redefine the spectrum of HSV infections of the CNS [2, 5]. Cerebral MRI is believed to be the most sensitive neuroimaging method for the diagnosis of HSVE [1, 8, 9]. Definite diagnosis of HSVE relies on
a synopsis of clinical findings and additional investigations, which all have
limited sensitivity and specificity [6,10]. Establishing a firm diagnosis remains
an important issue, since the effective treatment of HSVE with
acyclovir is associated with remarkable costs [3]. On the other hand,
prompt initiation of treatment is essential for improvement in outcome
[10]. A 21-year-old farmer suffered
from bifrontal headache with slightly elevated body temperature and
malaise for approximately 2weeks.
One day before admission involuntary
jerking of the right cheek occurred
for about 30 s. The following
day he suddenly noticed myoclonic
jerks of his right arm with rapid progression
to a generalized tonic-clonic
seizure of about 1 min duration. On
admission he was febrile (up to
39°C), with slight somnolence and a
motor hemisyndrome on the right
side with mixed aphasia. Results of
laboratory investigations are listed in
Table 1. CSF essentially showed
mononuclear pleocytosis and a positive
PCR for HSV–1. This is an
unnested PCR amplifying a 200-bplong
fragment of 5-regulatory DNA
sequences of the thymidine kinase
gene with an analytical sensitivity of
five DNA-copies (Institute for Medical
and Molecular Diagnostics,
Zurich). In addition, normal values in
blood were obtained for antibodies
against Mycoplasma pneumoniae,
varicella zoster virus, cytomegalovirus,
human immunodeficiency
virus 1, Treponema pallidum, Borrelia
burgdorferi, rubella, measles, and
mumps. MRI (1.5T, Siemens, Germany)
of the brain was performed on
the second hospital day and included
the following sequences: T1 axial
(TR 528/TE 12) and sagittal
(440/12), T2 axial (3176/98) and
coronal (3640/96), proton weighted
axial (3176/16), contrast-enhanced
T1 in three planes and axial fluidattenuated
inversion recovery images.
Careful examination of temporal
lobes, opercular regions, and the
cingulate gyri revealed no signal abnormalities.
EEG on that day showed
bifrontotemporal delta waves with
preponderance on the left side without
periodic complexes.

Evdoshenko
20.05.2007, 18:17
Approximately 7 h after the generalized seizure antiviral therapy with
intravenous acyclovir (10 mg/kg)
every 8 h was started and continued
for 12 days. Under a prophylactic
treatment with 100 mg diphenylhydantoin
three times daily no further
clinical seizure activity was observed.
On the second hospital day
only a palsy of the right corner of the
mouth and slightly elevated body
temperatures persisted. Cerebral MRI
performed on the sixth hospital day
remained completely normal. CSF
1 week after admission showed regression
of pleocytosis and negative
PCR. Serum IgA antibody titers
against HSV at that time remained
positive without a significant titer
change. After 2 weeks in the hospital
the patient was discharged without
any focal neurological deficit. CSF
1 month later showed 12 mononuclear
cells with negative PCR. One
year after the initial encephalitic
episode he complained of persistently
reduced physical performance and
excessive daytime sleepiness. The
Epworth Sleepiness Score was 17,
polysomnography revealed a normal
result, and the multiple sleep latency
test was clearly pathological with an
average sleep latency of 4 min 42 s
and one sleep-onset REM episode.
CSF, EEG, and MRI at that time
were normal. The HLA-DRB1*15
antigene (associated with narcolepsy)
was not found. Under a symptomatic
treatment with methylphenidate
sleepiness could be overcome when
necessary.
Our patient presented with fever
and a secondarily generalized tonicclonic
seizure followed by an acute
neurological deficit for several hours,
which therefore perhaps corresponds
to a postictal paresis of Todd. This
focal neurological sign together with
mononuclear CSF pleocytosis allowed
the clinical diagnosis of focal
encephalitis [10]. EEG showed focal
slowing over temporal regions of
both hemispheres with intermittent
epileptic discharges, findings which
are not specific but typical of HSVE
[4]. PCR from CSF performed on the
day of admission was positive for
HSV–1 and therefore allowed an etiological
diagnosis to be established.
Repeated PCR after 8 days of ongoing
acyclovir treatment was negative,
which is in good agreement with the
findings of previous studies [5, 10].
Antibody titers were suggestive of
HSV reactivation; however, they did
not show a course over time with the
encephalitic syndrome. Intrathecal
antibody production was not documented
since there were no detectable
IgA antibodies against HSV
in the CSF. Diagnostic antibody titer
changes in HSVE have been reported
only in about 66–80 % of definite
cases [5, 10].
Interestingly, our patient had normal
cerebral MRI, including T2-
weighted and fluid-attenuated inversion
recovery images in axial and
coronal planes as well as diffusionweighted
imaging performed on days
2, 6, and again14 months after the
acute onset of symptoms. This is in
contrast to previous studies reporting
a high sensitivity of MRI in the early
diagnosis of HSVE [1, 2, 8, 9]. However,
to our knowledge, the sensitivity
and specificity of the various
imaging modalities in the diagnosis
of human HSVE have not been quantified
or related to the time point with
respect to disease course. Especially,
there are no comparisons with virological
methods such as brain biopsy
or PCR [10]. From animal experiments
with nasal inoculation of HSV
it is known that cerebral MRI can remain
normal in about 5% [7]. Reports
on human HSVE generally describe
clearcut pathological findings
on cerebral MRI, but a patient with
normal MRI, CSF pleocytosis, and
positive HSV-PCR has obviously not
yet been described [2]. We think that
our patient falls into this rare category
and fulfills those diagnostic criteria.
As outlined above the firm diagnosis
of HSVE is based on several elements
of clinical presentation and
additional investigations, which must
be integrated for a firm diagnosis.
These various findings in our patient
allowed the diagnosis of HSVE, despite
the normal MRI. Another typical
but rare element is the occurrence
of organic hypersomnia 1 year after
the acute encephalitic episode.
In the acute phase of HSVE a
rapid decision concerning acyclovir
therapy must be taken due to the favorable
prognostic consequences of
early treatment [10]. HSVE with at
least initially normal CSF cell count
is well known from the literature [2].
We would like to emphasize that
even normal MRI of the brain can occur
throughout the course of confirmed
HSVE. MRI as a structural
imaging method is a secondary tool
in the diagnosis of HSVE, but never a
proof of this entity. On the other
hand, normal MRI should not prevent
the clinician from initiating acyclovir
therapy.

reywal
14.11.2009, 01:21
а в двух словах, об чем там говорится?
насколько мне помагает мой бессловарный инглишь, вроде как у больного на МРТ ничего такого не обнаружили?