Sudden 'Stroke-Like' Onset of
Hemiparesis Due to Herpetic Encephalitis
Mohammad AbdulJabbar, Ibrahim Ghozi, Anwar Haq and Hanz Korner

ABSTRACT: Background/Objective: Herpes simplex encephalitis usually has a progressive cause.
Sudden neurological deficits are unusual. Method: Case study. Results: A 17-year-old girl presented
with an acute onset focal neurological deficit followed one week later by the more classical feature of
altered level of consciousness, fever and focal seizures. The diagnosis of hepetic encephalitis was made
by magnetic resonance imaging (MRI) and by the significant increase in cerebrospinal fluid titres of
antibodies against herpes simplex type I. Conclusion: Herpetic encephalitis should be considered in the
differential diagnosis of acute stroke in young patients even in the absence of encephalitic features, if
common etiological factors such as embolization and intracerebral bleed are excluded.

RESUME: Hemiparesie a debut subit due a une encephalite herpetique. Introduction et objectif: Nous
decrivons un cas d'encdphalite, due au virus de l'herpes simplex, dont le mode de presentation clinique a 6t6
inhabituel par le d6but subit de l'hfimiparesie, a la fa?on d'un ictus ceY6bral. Methode: Une jeune fille de 17 ans a
pr&ente' un deficit neurologique suivi, une semaine plus tard, par les manifestations plus classiques: une alteration
de la conscience, de Phyperthermie et des convulsions focales. Resultat: Le diagnostic reposait sur les manifestations
observers a 1'imagerie par resonance magnetique (MRI) et sur l'augmentation significative des titres d'anticorps
contre le virus de l'herpes simplex I dans le liquide cephalo-rachidien. Conclusions: L'enc6phalite herp6tique
devrait etre incluse dans le diagnostic differentiel de l'ictus cerebral aigu chez le jeune patient, m6me en l'absence
de manifestations d'encfiphalite, si les principaux facteurs dtiologiques courants, tels l'embolie ou l'h6morragie
intracerebrale, ont 6te exclus.
Can. J. Neurol. Sci. 1995; 22: 320-321

Herpes simplex virus (HSV) infections are distributed worldwide.1 HSV infection of the central nervous system is among the
most severe of all human viral infections of the brain,2 and causes an acute necrotizing encephalitis with edema, necrosis and
hemorrhage that selectively affects the temporal and frontal
lobes.3 The usual clinical presentation is with fever, headache,
focal neurological deficit and focal seizures, with progression to
confusion, disorientation and possibly coma within a few days.3
In this report, we describe a case presenting like an acute stroke.
CASE REPORT

A 17-year-old girl was admitted to Security Forces Hospital with the
complaint of headache and left-sided weakness. The patient was
healthy until ten hours prior to admission, when she developed severe
right hemicranial throbbing headache, associated with nausea, and followed one hour later by sudden weakness of the left upper and lower
limbs with deviation of the mouth to the right side. The headache
improved with the onset of the weakness. The patient had no other medical problems and was taking no medication. There was no history of
migraine, nor of heart disease, nor any history of recent travel or exposure
to toxins. She was newly married, and not on contraceptive medication.
Physical examination revealed a conscious, oriented young lady
with normal vital signs. The fundus examination showed sharp disc
margins and no vascular changes. The neck was supple. Cranial nerve
examination showed an upper motor neuron facial nerve palsy on the
left side. Motor system examination revealed weakness on the left side
with power 0/5 in the arm and 2/5 in the leg, hypotonia, hyporeflexia
and an extensor plantar response on the left. There were no cerebellar

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https://doi.org/10.1017/S0317167100039573 Published online by Cambridge University Press

signs and no signs of meningeal irritation; the skin and the mucous
membranes of the oropharynx were normal. Chest, heart and abdominal
examination showed no abnormality.
Laboratory data included hemoglobin of 12.5 g/dL; white blood
count of 6,400/mm3 (67% neutrophils + 26% lymphocytes and 5%
monocytes); platelet count of 272,000/mm3. Serum sodium (140
mmol/L); potassium (4.2 mmol/L); calcium (2.3 mmol/L); phosphate
(1.05 mmol/L); total protein of (76 g/L); creatine kinase (106 u/L); and
arterial blood gas studies were normal. VDRL test was non-reactive
and thromboplastin time was normal. Protein C, protein S, and
antithrombin III were normal; antinuclear antibodies, antiDNA, ESR,
C3 and C4 were also normal. Brucella serology was negative.
Echocardiography showed a normal heart. A contrast-enhanced brain
CT scan was normal. The CSF examination done on admission showed
clear colorless fluid with no WBCs but 400 RBCs, protein 0.49 g/L and
sugar 3.4 mmol/L. Gram stain and stains for acid fast bacilli were negative. Antibodies against herpes simplex virus were not found in the CSF
or the blood (less than 30 ELISA units).
The patient's condition remained stable for five days after admission
while she was receiving supportive measures. On the 6th day, she
became febrile and confused with a temperature of 38°C; a focal
left-sided seizure which became generalized then occurred and recurred
three times with deterioration of consciousness and respiratory compromise. She received 10 mg i.v. diazepam and 500 mg phenytoin but
despite this, she had two additional seizures resulting in marked hypoxia.

From the Division of Neurology, Khalid University Hospital (M.A.) and Division of
Neurology, Security Forces Hospital (I.G., A.H., H.K.), Riyadh, Saudi Arabia.
RECEIVED NOVEMBER 8 , 1 9 9 4 . ACCEPTED IN FINAL FORM APRIL 1 3 , 1 9 9 5 .

Reprint requests to: Dr. Mohammad AbdulJabbar, Associate Professor, Neurology Unit,
King Khalid University Hospital, P.O. Box 7805[38], Riyadh 11472, Saudi Arabia

LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES

She was intubated and ventilated, and received an additional 500 mg
phenytoin which controlled the seizures. An urgent brain CT scan done
on the same day showed an enhancing lesion with a small bleed mainly
in the right temporal lobe with marked edema (Figure 1). EEG showed
slow waves with occasional sharp waves over the right centre—temporal
region suggestive of herpes simplex encephalitis. Although the presentation was atypical, treatment with acyclovir and dexamethasone was
initiated. Lumbar puncture was thought to be contraindicated because of
the temporal lobe swelling. The patient was extubated after three days
after regaining consciousness and being seizure-free. A gadoliniumenhanced MRI (Figure 2) on the tenth day showed the same picture as
did the CT scan. A follow-up CT scan snowed resolution of the brain
edema and the temporal lobe swelling. A second CSF examination
showed clear colorless fluid with 22/mm lymphocytes, RBCs, 45/mm,
protein 0.55 g/L and glucose 3.9 mmol/L (blood glucose 5.9 mmol/L).
Antibodies against herpes simplex type I was elevated in both CSF and
serum; 210 ELISA units in CSF and 1986 in the serum, results strongly
suggestive of herpes simplex encephalitis.
Subsequently, the patient's neurological status showed progressive
improvement. She was discharged from the hospital after 14 days walking unsupported with residual weakness of the left upper limb.
DISCUSSION

Herpes simplex virus is the commonest cause of severe focal
encephalitis in man,4 with an approximate annual incidence, in
the USA, Sweden, England and other western countries of 1 in
250,000. 56 ' 7 It accounts for up to 10-20% of encephalitic viral
infections of the CNS worldwide.8 Such data are not available
from any Arab country.

The clinical findings of herpes, simplex encephalitis (HSE)
are non-specific and do not allow for empirical diagnosis of the
disease based solely on the clinical presentation. 9 HSE is the
only viral CNS infection for which therapy has proved useful in
rigorously controlled trials; 710 successful therapy depends on a
high level of suspicion. As noted before, the clinical diagnosis is
often presumptive and supported by evidence of focality on
physical or radiologic evaluation.10
The diagnosis in our case was eventually made by the MRI
findings and by the significant increase in CSF antibody titres from
0 to 210 ELISA units over 10 days. MRI is thought to be the most
sensitive noninvasive test in the diagnosis of HSE, especially in the
early stages.3 The detection of a rise in CSF antibody titres has
been considered as a useful diagnostic test but only retrospectively;
the finding has a sensitivity ranging from 70% to 90% and a specificity ranging from 81% to 88% depending on the type and number of serologic tests used. 4 The definitive diagnosis of HSE
depends on either a positive brain biopsy result or (increasingly)
on polymerase chain reaction amplification of HSB DNA from the
CSF. Neither of these studies could be done in our centre. The difficulty in diagnosis in our case was due to the atypical presentation, not previously recorded in the literature. The stroke-like
onset, without any encephalitic features appearing for a week is
unusual, especially with no evidence of bleeding on the CT scan.
Normal CSF findings on admission have been reported
previously.1112 Early MRI examination could be of great help in
delineating the pathology at presentation.
We conclude that HSE should be considered in the differential diagnosis of acute stroke in young patients with no obvious
embolic source, evidence of carotid artery dissection, nor evidence of intracerebral bleeding even in the absence of
encephalitic features, since effective antiviral therapy improves
the outcome and decreases the high mortality and morbidity.10
REFERENCES

Figure 1: CT brain done 6 days after admission showing enhanced
right temporal lobe lesion with oedema and small bleed.

Figure 2: A Gadolinium-enhanced MRI image done on the 10th day
showing the same lesion seen in the CT scan.

Volume 22, No. 4 — November 1995
https://doi.org/10.1017/S0317167100039573 Published online by Cambridge University Press

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