Case Report

Cerebral venous thrombosis: Atypical presentation of
COVID-19 in the young
David E. Klein, DO,* Richard Libman, MD,* Claudia Kirsch, MD,† and
Rohan Arora, MD*

Objective: Identify clinical and radiographic features of venous infarct as a presenting
feature of COVID-19 in the young. Background: SARS-CoV-2 infection causes hypercoagulability and inflammation leading to venous thrombotic events (VTE).
Although elderly patients with comorbidities are at higher risk, COVID-19 may also
cause VTE in a broader patient population without these risks. Neurologic complications and manifestations of COVID-19, including neuropathies, seizures, strokes and
encephalopathy usually occur in severe established cases of COVID-19 infection who
primarily present with respiratory distress. Case description: Case report of a 29-yearold woman, with no significant past medical history or comorbidities, presenting
with new onset seizures. Further questioning revealed a one-week history of headaches, low-grade fever, mild cough and shortness of breath, diagnosed as COVID-19.
Imaging revealed a left temporoparietal hemorrhagic venous infarction with left
transverse and sigmoid sinus thrombosis treated with full dose anticoagulation and
antiepileptics. Conclusion: Although elderly patients with comorbidities are considered highest risk for COVID-19 neurologic complications, usually when systemic
symptoms are severe, this case report emphasizes that young individuals are at risk
for VTE with neurologic complications even when systemic symptoms are mild,
likely induced by COVID-19 associated hypercoagulable state.
Key words: Cerebral venous thrombosis (CVT)—COVID-19—Venous thrombotic
events (VTE)—Stroke in young
© 2020 Elsevier Inc. All rights reserved.

Cerebral venous thrombosis (CVT), although an
uncommon form of stroke, usually occurs in women
approximately 75% of the time, with 80% being less than
50 years of age.1,2 While viral infections rarely directly
cause CVT, strokes associated with viruses including
COVID-19 have been reported.3 Postulated mechanisms
From the *Department of Neurology, Zucker School of Medicine at
Hofstra/Northwell Health, United States; and †Department of Radiology, Zucker School of Medicine at Hofstra/Northwell Health,
United States.
Received April 30, 2020; revision received May 17, 2020; accepted
May 18, 2020.
Address correspondence to Rohan Arora, MD, Hofstra Northwell
School of Medicine Forest Hills, United States E-mail:
rarora@northwell.edu.
1052-3057/$ - see front matter
© 2020 Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2020.104989

for the direct and indirect apoplectic nature of certain
viruses include systemic inflammation and endothelial
injury, both known stroke risk factors. Emerging data
suggest a novel highly virulent strain of a b-coronaviruses (CoV), coronavirus infectious disease (COVID-19),
may confer a particularly high risk of stroke.4 6 Severe
acute respiratory syndrome coronavirus 1 (SARS-CoV1), Middle Eastern Respiratory Syndrome coronavirus
(MERS-CoV) and now severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been linked to
para-infectious stroke.3 6
Hypercoagulability of SARS-CoV2, manifesting as
increase in D-dimer, lactate dehydrogenase (LDH) and
prolonged coagulation times is associated with more
severe disease and can help risk stratify patients on presentation.7 However, the resultant venous thrombotic
events (VTEs) including deep vein thrombosis (DVT) and

Journal of Stroke and Cerebrovascular Diseases, Vol. 29, No. 8 (August), 2020: 104989

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D.E. KLEIN ET AL.

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pulmonary embolism (PE), are more often reported to
occur later in COVID-19’s disease course.8 10
In addition to fever, dry cough, shortness of breath and
myalgias, neurologic signs and symptoms may occur due
to COVID-19. Neurologic sequelae such as anosmia, ageusia, headache, dizziness and altered sensorium may occur
due to direct viral infection or as secondary complications
of SARS-CoV2.11 13 This case report presents a 29-yearold woman with a Dural Venous Sinus Thrombosis
(DVST) early in the course of COVID-19.

Case description
A 29-year-old right-handed woman with no known
medical history presented with new onset generalized
tonic-clonic seizures with post-ictal confusion. She later
reported that prior to admission, she had over a week of
cough, low grade fever, mild shortness of breath and a
mild headache. She took no regular medications, including no hormonal contraceptives. On initial exam, she was
afebrile, mildly agitated, and complaining of neck pain.
She was breathing room air with an oxygen saturation of
100% and had a body mass index of 17.4. While in the
emergency department she had a third seizure, was given
Lorazepam 2 mg IV, loaded with Levetiracetam 1000 mg
IV and started on Levetiracetam 750 mg IV twice daily.
Initial neurologic exam was notable for decreased level of
arousal, global aphasia, decreased blink to threat on the
right and a mild to moderate right facial palsy. There was
spontaneous movement against gravity in all four limbs
with slightly less movement of the right upper extremity.
Initial non-contrast head CT demonstrated left temporoparietal hemorrhagic venous infarct with edema and
mass effect with 5mm rightward shift as well as venous
thrombosis in distal left transverse and sigmoid sinus
(Fig. 1). Nasal swab polymerase chain reaction (PCR) was
positive for COVID-19. She had a notable microcytic anemia with hemoglobin of 5.5 g/dL on admission, determined to be due to iron deficiency secondary to
menorrhagia, treated with two units of packed red blood
cells and started on ferrous sulfate 325 mg daily. Additional laboratory findings, consistent with COVID-19
included elevated LDH, CRP, and D-dimer levels. Laboratory values, including a normal coagulation profile, are
included (Table 1). Ferritin was low, likely from iron deficiency anemia. Hypercoagulable work up was notable for
elevated anticardiolipin IgM serum levels and possible
thalassemia trait. Post transfusion, hemoglobin levels stabilized and her DVST was initially treated with intravenous
heparin. Due to poor oral intake, oral anticoagulation was
avoided, and she was transitioned to enoxaparin 50 mg
subcutaneously every 12 h.
MRI brain showed hyperintense DWI signal of the left
temporoparietal hemorrhagic infarct with mass effect and
effacement of the left lateral and third ventricle with 4mm

Fig. 1. Non-contrast head CT demonstrating left temporoparietal hemorrhagic venous infarct with edema and mass effect causing 5 mm rightward
shift, red arrow pointing to increased attenuation and venous thrombosis in
distal left transverse and sigmoid sinus

rightward shift (Fig. 2). 2D time of flight MR venography
demonstrated absence of flow in the left transverse and
sigmoid sinus and left internal jugular vein secondary to
venous thrombosis. Additionally demonstrated flow
related signal in the right transvers and sigmoid sinus
extending to a patent right internal jugular vein (Fig. 3).
The day after admission, she continued to have a waxing
and waning level of arousal and complained of diplopia.
On exam, there were bilateral 6th nerve palsies and fundoscopy demonstrated bilateral papilledema. She was started
on acetazolamide 500 mg twice daily with accompanying
serial fundoscopic exams. Over the next seven days, she
improved clinically in alertness and had a moderate mixed
aphasia with persistent bilateral 6th nerve palsies.

Discussion
Hypercoagulability induced by COVID-19 has been
implicated in PEs, VTEs, disseminated intravascular coagulation (DIC) and recently in stroke.9,14,15 Postulated
mechanisms of hypercoagulability include disruptions in
the renin-angiotensin (RAS) system with reduction in
ACE2 and Ang-1-7 and alterations in the coagulation cascade leading to a consumptive coagulopathy and cytokine
storm including IL-1, IL-6 and TNF-a. This is a significant
consideration while evaluating stroke patients in the setting of COVID-19. In this patient’s case with no past medical history, she had potential competing mechanisms of
hypercoagulability, including iron deficiency anemia, a

CEREBRAL VENOUS THROMBOSIS: ATYPICAL PRESENTATION OF COVID-19 IN THE YOUNG

3

Table 1. Laboratory data.
Variable

Result (reference range)

Absolute lymphocyte count (per mL)
Absolute reticulocyte count (per mL)
Activated partial thromboplastin time (aPTT) (s)
Anisocytosis
Anticardiolipin antibody level, total
Anticardiolipin IgG, serum (GPL)
Anticardiolipin IgM, serum (MPL)
Antithrombin III assay with reflex (%)
Beta 2 glycoprotein 1 antibody screen
Cardiolipin antibody IgA (APL)
C-reactive protein (mg/L)
COVID-19 PCR
CRP high sensitivity (mg/L)
CT abdomen and pelvis without contrast

580 (1000 3300)
70,000 (25,000 125,000)
28.7 (27.5 36.3)
Marked
Positive (negative).
11.7 (0.0 12.5)
53.9 (0.0 12.5)
91 (76 140)
Negative (negative)
<5.0 (0.0 12.5)
37 (<5)
Detected (not detected)
111.74 (<3.0)
Pulmonary ground glass opacities consistent with known COVID 19.
Enlarged fibroid uterus.
2876 (<230)
95 (75 150)
10.40 (15 150)
166 (34 200)
22 (34.5 45.0)
5.8 (11.5 15.5)
93.1 (>90)
2.4 (2.4 3.5)
Normal HPLC pattern with low MCV, anemia and high RBC, suggestive of
thalassemia trait. Hemoglobin A2 is normal with mild elevation of hemoglobin F, suggestive of delta/beta thalassemia trait.
4.5 (0 1.5)
Moderate
1.10 (0.88 1.17)
44 (30 160)
287 (135 225)
63.4 (80.0 100.0)
Marked
335,000 (150,000 400,000)
Moderate
0.06 (0.02 0.10)
55.2 (3.4 24.1)
12.7(9.8 13.1)
21.0 (10.3-14.5)
1.9 (0.5 2.5)
24.9 (16.0 26.0)
308 (140 530)
263.8 (110 370)
1.2 ( 3 to +2)
25 (20 27)
48 (41 51)
7.36 (7.32 7.43)
43 (35 40)
8760 (3800 10,500)

D-dimer assay, quantitative (ng/L)
Factor V assay (%)
Ferritin, serum (ng/mL)
Haptoglobin, serum (mg/dL)
Hematocrit (%)
Hemoglobin (g/dL)
Hemoglobin A (%)
Hemoglobin A2 (%)
Hemoglobin electrophoresis comments

Hemoglobin F (%)
Hypochromia
International normalized ratio (INR)
Iron total, serum (mg/dL)
Lactate dehydrogenase (LDH), serum (U/L)
Mean corpuscular volume (MCV) (fL)
Microcytosis
Platelets (per mL)
Poikilocytosis
Procalcitonin (ng/mL)
Prolactin, serum (ng/mL)
Prothrombin time (PT), plasma (s)
Red blood cell distribution width (RDW) (%)
Reticulocyte percent (%)
Thrombin time assay (s)
Total iron binding capacity (TIBC) (mg/dL)
Unsaturated iron binding capacity (mg/dL)
Venous blood gas base excess (mmol/L)
Venous blood gas HCO3 (mmol/L)
Venous blood gas pCO2 (mm Hg)
Venous blood gas pH
Venous blood gas pO2 (mm Hg)
White blood cell count (per mL)

possible b or d thalassemia trait and increased anti-cardiolipin IgM serum titers. Anticardiolipin antibodies have
been shown to rise in acute hypercoagulable states, certain cases of systemic viral infections and even in acute
stroke.14 Thus, the anticardiolipin antibody increase in
our patient’s case may or may not have contributed to her

DSVT, and this cannot be determined without future retesting. This suggests advanced COVID-19 provoked
hypercoagulability likely contributed to her DVST.
The neurologic manifestations of COVID-19, including
stroke, are usually reported later in the disease course.46,10,11
Though both cerebral venous infarction and

D.E. KLEIN ET AL.

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COVID-19 can occur in the young, cerebral venous thrombosis and infarction is a rare documented early presentation of COVID 19. The patient did have fever, shortness of
breath and a cough, minor in severity, which were not
presenting complaints on admission.
Regarding treatment, the choice of anticoagulants in
COVID-19 associated VTEs is a matter of debate.16 Both
unfractionated heparin and low molecular weight heparins are used in acute DVST. Emerging evidence suggests
that various heparins can bind to the COVID-19 spike
proteins, help downregulate IL-6, and directly dampen
immune activation.17 Theoretically this may be of clinical
benefit. Alternative treatments that interact with the
ACE2 receptors are also being postulated, although clinical trials have not yet occurred.18,19

Conclusion

Fig. 2. 3T DWI MRI, yellow arrow pointing to hyperintense DWI signal of
evolving left temporoparietal hemorrhagic infarct, with mass effect and
effacement of the left lateral and third ventricle with 5 mm rightward shift.

Hypercoagulability is a known complication of COVID19. Although severe cases are usually reported in older
populations and in those with underlying comorbidities,
this case report emphasizes that this may occur in young
individuals without significant medical history. Furthermore, COVID-19 positive patients may have an atypical
presentation with primary cerebrovascular syndromes
such as DVST.

Conflict of Interest
The authors declare that they have no known competing
financial interests or personal relationships that could have
appeared to influence the work reported in this paper.

References

Fig. 3. 2D time of flight MR venography with red arrows denoting absence
of flow in the left transverse and sigmoid sinus and left internal jugular vein
secondary to venous thrombosis. Light blue arrows denoting normal flow
related signal in the right transvers and sigmoid sinus extending to a patent
right internal jugular vein.

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