Open Access

Case report
Cerebral venous sinus thrombosis in HIV-infected patients: report of 2 cases
Julius Chacha Mwita1,2,&, Kgomotso Baliki1,2, Ludo Tema1
1

Department of Internal Medicine, University of Botswana, Gaborone, Botswana, 2Department of Internal Medicine, Princess Marina Hospital,

Gaborone, Botswana
&

Corresponding author: Julius Chacha Mwita, Department of Internal Medicine, University of Botswana, Private Bag 0022, UB, Gaborone Botswana

Key words: Cerebral venous sinus thrombosis, HIV, cerebrovascular diseases, stroke
Received: 21/08/2013 - Accepted: 25/08/2013 - Published: 04/09/2013
Abstract
Infection with the human immunodeficiency virus (HIV) is associated with increased risk of cerebrovascular disease; however Cerebral Venous
Sinus Thrombosis (CVST) is rarely associated with HIV-related cerebrovascular events. We describe two cases of HIV-positive patients who, at the
same time, presented to our hospital with deep cerebral venous thrombosis and stroke.

Pan African Medical Journal. 2013; 16:4. doi:10.11604/pamj.2013.16.4.3252

/

This article is available online at: http://www.panafrican-med-journal.com/content article/16/4/full/
© Julius Chacha Mwita et al. The Pan African Medical Journal - ISSN 1937-8688. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original
work is properly cited.

Pan African Medical Journal – ISSN: 1937- 8688 (www.panafrican-med-journal.com)
Published in partnership with the African Field Epidemiology Network (AFENET). (www.afenet.net)

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Introduction

smoking or using illicit drugs. There was no family history of
strokes, sudden deaths or clotting disorders.

Cerebral venous sinus thrombosis is a rare cause of stroke that
often affects young adults and children [1]. About 75% of the
affected adults are women, and direct causes or predisposing risk
factors can be identified in up to 85% of patients [1]. They include
local trauma and infection, prothrombotic states like nephrotic
syndrome, anti-thrombin III deficiency, pregnancy, malignancy and
the use of oral contraceptives[1-3]. Although venous thrombotic
events (VTEs) are frequent among HIV patients, few cases of CVST
have been reported[4,5]. The mechanism of HIV-related thrombosis
is complex and involves the intersection of HIV infection, highly
active antiretroviral therapy (HAART) and traditional prothrombotic
factors [1,5,6]. We report two HIV-positive females who presented
with stroke secondary to cerebral venous sinus thrombosis. They
were both on antiretroviral therapy that constituted zidovudine,
lamivudine and nevirapine.

Examination after convulsion revealed an afebrile and anxious
patient with a regular pulse rate of 127 beats/minute, a respiratory
rate of 28/minute and a blood pressure of 131/43 mmHg. She had
no lymphadenopathy and there were no bleeding or discharge from
both ears. She had nuchal rigidity but without any neurological
deficits. Examination findings of the abdomen, cardiovascular and
respiratory systems were unremarkable. The patient’s initial
investigations revealed normal full blood count, renal and liver
function tests. Her random blood glucose was 4.9mmol/L and she
had negative antinuclear antibody test results. Cerebrovascular fluid
examination revealed a slightly turbid fluid with 6 white cells/mm3
and 75 red blood cells/mm3. A computed tomography of the brain
with contrast showed diffuse meningeal enhancement, white matter
oedema of the left brain hemisphere and a filling defect at the
confluence of the transverse cerebral veins suggestive of thrombosis
of the sagittal vein. The patient was admitted for anticonvulsants

Patients and observations

and anticoagulation on the wards.
One day after admission she had about 10 episodes of sided

Case report 1

convulsions, with residual right sided hemiparesis. The power of all
the muscle groups in the right upper and lower limbs was grade

A 17-year-old female presented with new onset right sided focal

2/5. A Magnetic Resonance venography established superior sagittal

seizures that started on the day of presentation. She had three

and left transverse sinuses thrombosis (Figure 1). Furthermore,

episodes prior to being seen at our casualty, each lasting about 5-10

there were venous infarction with haemorrhagic component and

minutes and was associated with confusion. At the casualty, she had

oedema in the left frontal, temporal, occipital and parietal lobes. In

a right sided tonic-clonic seizure that involved the face, upper and

addition to continuation of anticoagulation, anticonvulsants were

lower limbs. Four days prior to presentation, the patient started

optimized to control convulsions. There was a reduction of seizure

having a global headache that was associated with photophobia and

episodes over the subsequent five days and the patient’s

painful eyes. She denied any fever, nausea, vomiting or a recent

neurological deficit slowly normalized inthe next three weeks. She

head trauma. Two weeks before, she had a tympanoplasty on the

was then discharged home with mild hemiparesis and her

right ear for chronic suppurative otitis media without any immediate

subsequent outpatient visits showed no neurologic deterioration.

post-procedure complications. Her past medical history revealed a
left ear tympanoplasty in 2011. She is HIV positive, acquired from

Case report 2

her mother, and she has been on a combination of zidovudine,
lamivudine and nevirapine since the age of 5 years. Her last CD4

A 44-year old female presented with a constant, throbbing and

cell count was 198cell/µL. Her mother died of HIV/AIDS when she

worsening headache over the past three days. The headache was

was about 4 years old leaving her alone with her busy father. This

generalized in nature, associated vomiting, photophobia, dizziness

has made her vulnerable to sexual abuses and she has had about

and diplopia. There was no history convulsion, limb weakness or

eight reported episodes of rape since the age of 12 years. As a

parasthesia. She denied any history of trauma, fever or any loss of

result, she was put on oral contraceptives (OCPs) since the age 13

consciousness. Her past medical history was significant of HIV

years and was switched to injectable contraceptive Depo-Provera 4

disease for the past 10 years. She was on Zidovudine, Lamivudine

months ago. She denied any history of alcohol intake, cigarette

and Nevirapine treatment, and her last CD4 count was 293 cell/µl

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two months ago. She did not smoke cigarettes and had never used

factors associated with CVST, and it is not uncommon to find

contraceptive pills. There was no family history of strokes, sudden

multiple factors in a single patient [1]. Aetiological factors include

deaths or clotting disorders. On examination, the patient was teary,

hypercoagulable states, inflammatory and infectious diseases such

in obvious discomfort, afebrile and with normal vital signs. Her

as facial infections, dental abscesses, otitis media, mastoiditis,

Glasgow coma scale was GCS 15/15 with normal pupils and extra-

endocarditis and septicaemia [1, 2]. The present cases occurred in

ocular muscle movement. There were signs of meningism without

female patients, and one of them had a recent tympanoplasty due

any neurological deficits. Examinations of other systems were

to chronic otitis media. Although venous thrombotic events (VTEs)

unremarkable and she had normal baseline blood tests. Lumbar

are frequent among HIV patients, few cases of CVST have been

puncture had an opening pressure of 23 cm H2O with a closing

reported [4, 5]. Mechanisms for the observed hypercoagulability in

pressure of 10 cmH2O and normal laboratory cerebrospinal fluid

HIV infected patients are multifactorial and include the presence of

results. The patient was admitted for observation in the ward and

antiphospholipid antibodies and deficiency of natural anticoagulants

discharged three days later when her CSF culture results were

such as protein C, protein S, heparin cofactor II, and antithrombin

negative. Two days after discharge, she was readmitted with

[5]. Some studies have reported a high prevalence of antibodies

worsening headache, photophobia and diplopia. On examination she

against protein S among HIV infected patients, leading to

had normal vital signs, neck stiffness and bilateral lateral rectus

significantly low protein S activity in about 31%-76% of patients

muscle weakness. A repeat lumbar puncture showed opening and

[8]. Although protein S deficiency is not correlated with HIV disease

closing pressures of 30cm and 15cm of H2O respectively. The

severity it appears that thrombosis is highly correlated with low CD4

headache improved after lumbar puncture, and her cerebrospinal

counts (3), the presence of opportunistic infections, malignancies, or

fluid microscopy and culture results were once more negative. A

autoimmune disorders [9, 10]. Our patients had no opportunistic

non-contrast computed tomography showed ill-defined sulci and

infections and only one of them had CD4 count of less than

hyper-density along the sagittal, right transverse and sigmoid

200/mm3. Nevertheless, we could not determine their protein C and

sinuses. With intravenous contrast, filling defects were noted in the

protein S levels. While one patient had a prothrombotic state

above sinuses. There were no obvious haemorrhages, infarcts or

because of contraceptives use and otitis media, the second patient’s

mass effect noted. We made a diagnosis of thrombosis of the

thrombosis risk could only be attributed to her HIV seropositivity.

superior sagittal, right transverse and left sigmoid sinuses. The

Both patients used HIV antiretroviral regimen that contained

patient was started on low molecular weight heparin and

Zidovudine, Lamivudine and Nevirapine. Although the absolute risk

subsequently continued on oral warfarin. Few days later, she had

of thrombosis in patients not using combination antiretroviral

five

therapy is about 6-fold in comparison with a healthy population of

episodes

neurological

of

generalised

deficits.

seizures

without

Fundoscopy revealed

any

residual

papilloedema

that

comparable age, there is additional risk of thrombosis in patients on

subsequently improved with intravenous Manitol. Similarly, her

HAART

[6,10,11].

The

prothrombotic

effect

of

HAART

is

seizures were controlled by phenytoin and she was discharged

nevertheless more pronounced when a combination that includes

about three weeks later without any neurologic deficit.

protease inhibitors (PIs) is used [6, 12]. Protease inhibitors based
therapy promotes thrombosis by inducing platelets and endothelial
dysfunction [12]. It is however remains unclear whether non-

Discussion
Cerebral venous sinus thrombosis is a rare condition that often
presents with thrombosis in the cerebral venous or dural sinuses,
and rarely in the cortical (superficial) veins [2]. As in our patients,
the superior sagittal and left transverse sinuses are the most
affected sinuses [7]. CVST affects young adults and children, and
represents about 1% of all strokes[1, 2]. It occurs in about 3-4
cases per million population, mainly in women due to the use of oral
contraceptive pills and the postpartum state[1]. There are several

protease inhibitors are prothombotic [11].
The clinical presentations of CVST are quite variable and result from
mass effect of the enlarging thrombus as well as the consequential
increased intracranial pressure[1]. As a result, swollen veins,
oedema haemorrhages and infarction are typically found on
imaging[1]. Headache is the commonest symptom, present in 95%
of CVST patients [13]. Seizures occur in about 47%, and may be
focal in about half of the patients [1, 13]. Other reported symptoms
include hemiparesis, aphasia, coma and papilloedema [1, 13].Our
patients presented with headache, seizures, hemiparesis and

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papiloedema. The diagnosis of CVST is usually done by the

Authors contributions

Computerized tomographic (CT) and magnetic resonance imaging
(MRI) scans[1]. However, magnetic resonance venography is
preferred as it outlines the occluded sinuses as well as associated
cerebral oedema and venous infarctions [14]. Initial management
involves patient’s stabilization and prevention or reversing cerebral

All the authors contributed to the management of the patients and
in the writing up of the manuscript. All the authors have read and
approved the final version of the manuscript.

herniation by the use of mannitol or surgery[1]. Despite the risk of
haemorrhage, anticoagulation is advised to stop the propagation of
thrombosis and prevent pulmonary thrombosis [1]. Even in patients

Figures

with evidences of haemorrhagic brain infarction, anticoagulation has
safely been used [1, 7]. The prognosis of CVST is generally good,

Figure 1: Magnetic Resonance Venography demonstrating

with more than 80% of all patients having full neurologic recovery

thrombosis of the superior sagittal sinus

[1]. Our patients were given lower molecular weight heparin for five
days and subsequently continued on warfarin. They both had
remarkable clinical improvement, and were discharged on warfarin

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Figure 1: Magnetic Resonance Venography demonstrating thrombosis of the superior sagittal sinus

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