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. 2023 Apr 25;13(3):319–320. doi: 10.1177/19418744231173085

Isolated Cortical Vein Thrombosis

Galina Gheihman 1,2,, Christopher Cashman 1,2, Joshua P Klein 1
PMCID: PMC10334060  PMID: 37441207

Case Description

A 52-year-old female with a family history of Factor V Leiden mutation and a personal history of migraines and Chiari I malformation status post suboccipital craniotomy three weeks prior presented with clumsiness and paresthesias of the right hand. CT head demonstrated left parietal edema, and brain MRI suggested an adjacent, isolated cortical vein thrombosis. No other venous or sinus thrombosis was noted. Her course was complicated by focal seizures. She was started on apixaban and levetiracetam. A workup for underlying hypercoagulability was negative. A brain MRI two months later showed resolution of cerebral edema and normalization of the appearance of the cortical vein, supporting the diagnosis of isolated cortical vein thrombosis (Figure 1). Cortical vein thrombosis most often arises from extension of thromboses of dural sinuses 1 ; isolated cortical vein thrombosis is rare and has been reported in only 116 patients previously. 2

Figure 1.

Figure 1.

Axial (A) and coronal (B) head CT showing a focal area of abnormal hypoattenuation in the left parietal lobe (arrows). Axial T2-FLAIR (C) and susceptibility weighted (D-E) MRI of the brain showing left parietal edema (C) and adjacent abnormally enlarged and hypointense thrombosed cortical vein (D-E, arrows). A subsequent MRI showed resolution of the cerebral edema on axial T2-FLAIR imaging (F) and normalization of the appearance of the cortical vein on susceptibility weighted images (G-H, arrows), consistent with its recanalization.

Cerebral cortical vein thrombosis may be misdiagnosed due to its non-specific symptoms. Clinically, cortical vein thrombosis—like cerebral venous sinus thrombosis—presents most often with headache, and focal neurological deficits follow in hours or days in about half of patients. Seizures occur in a third of patients within the first week. 1 Symptoms do not conform to the vascular territories involved in arterial strokes, further hindering rapid diagnosis. Diagnosis may be aided by brain MRI with specific sequences. T2*-weighted gradient-echo (GRE) sequences 3 detect blood products and calcifications; susceptibility-weighted imaging (SWI) 4 is more sensitive and can distinguish between hemorrhage/hemosiderin and calcifications. Contrast-enhanced CT or MR venography may demonstrate a filling defect in a large cortical vein, but these techniques are limited in their ability to detect thrombosis of smaller cortical veins and in their overall sensitivity due to variable anatomy of the cortical veins.

Treatment depends on etiology; in unprovoked cases, anticoagulation is usually continued for 3-6 months.

Footnotes

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iDs

Galina Gheihman https://orcid.org/0000-0003-1599-3271

Christopher Cashman https://orcid.org/0000-0003-1019-004X

Joshua P. Klein https://orcid.org/0000-0001-6139-8081

References

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