key: cord-0814694-a74kwdmg
authors: Coline, Baudar; Thierry, Duprez; Amandine, Kassab; Nathalie, Miller; Pierre, Rutgers Matthieu
title: COVID-19 as triggering co-factor for cortical cerebral venous thrombosis?
date: 2020-06-27
journal: J Neuroradiol
DOI: 10.1016/j.neurad.2020.06.008
sha: b145985798b74fdc942a46817e2b33a58666bb63
doc_id: 814694
cord_uid: a74kwdmg

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Ethics approval and consent to participate: this case-report received the approbation of the President of the local ethics committee. Consent for publication : written informed consent for publication of their clinical details and clinical images was obtained from the patient. A copy of the consent form is available for review by the Editor of this journal.

Availability of data and materials : 'Not applicable'

Competing interests : MPR has received funding from Boehringer-Ingelheim for clinical trials and advisory board fees. All other authors declare no competing interests. We report a clinical case of an isolated cortical cerebral venous thrombosis (CVT), without any history of genetic or acquired thrombophilia, associated with COVID-19. Up to now, a few cases of sinus CVT have been reported to be possibly linked to a SARS-CoV-2 infection (1) (2) (3) (4) (5) . This is however, to our J o u r n a l P r e -p r o o f knowledge, the first description of a case with an associated cortical CVT. Other brain imaging abnormalities (arterial stroke or images compatible with acute disseminated encephalomyelitis) have been described (6) . The COVID-19 is caused by the SARS-CoV-2. This coronavirus activates inflammatory and thrombotic pathways by binding the angiotensin-converting enzyme 2 receptors of endothelial cells, leading to an endotheliitis and a diffuse procoagulant state (7) . Our case suggests that the cerebral venous system can also be affected by this pathologic process.

A 33 year old female patient, with a combined estrogen-progestin oral contraception (ethinylestradiol 0.02mg/day and gestodene 0.075mg/day; monophasic 21-day pills) developed an unusual, bilateral and moderate headache on March 22 th , 2020. The following day, she had a fever (39°c), diffuse myalgia, cough with increased headache intensity. One week later, the clinical picture was completed by a slight dyspnea, anosmia and dysgueusia. All symptoms and signs disappeared three weeks later, except for the headache, which persisted and progressively worsened. On April 27 th , 2020, she suffered from a partial complex epileptic seizure with secondary generalized convulsions, treated with levetiracetam (1g/day). On admission, general and neurological clinical examination was unremarkable. However we noted that she had a body mass index (BMI) of 34.6kg/m² (normal range 20-25). Usual blood tests were normal, except for a very slight increase of fibrinogen at 4.2g/L (normal range 2.0-4.0) and a more significant elevation of the D-Dimers (902ng/mL, normal <500). Other routine coagulation tests were normal. The Chest-CT scanner was rated as "no CT findings present to indicate pneumonia" (Cov19Neg) according to Radiological CVT is an uncommon cause of stroke. The incidence has been evaluated to 15.7 per million inhabitants per year (12) . Many medical conditions have been identified as risk factor of CVT, such as acquired or genetic thrombophilia, and either specific local causes including head, face or neck infections or some systemic diseases (13) . Cortical CVT is reputed to be more likely to induce seizures (14).

Our patient had two risk factors for developing a CVT: a high BMI and the use of a combined estrogen-progestin oral contraception. We did not find any genetic or acquired thrombophilia condition associated with CVT. No other conditions inducing hypercoagulability were detected, except for the COVID-19. Therefore, we hypothesize that COVID-19 has played a synergistic role as risk factor for the patient's cortical CVT. It needs to be highlighted that our patient suffered from a headache from the earliest onset of the disease course, without recovery, until the oral anticoagulation was initiated, almost 6 weeks after the onset of the headache. Importantly, all other Altough a causal relationship between the SARS-CoV-2 infection and the development of the cortical CVT of our patient cannot be definitely demonstrated, we suggest COVID-19 to be a risk factor based on the temporal relationship, the absence of another cause of hypercoagulability, and plausible pathophysiological mechanisms.

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