Report of a recurrent cerebral venous thrombosis in a young athlete

Abstract

Background: Reports of occurrence of deep vein thrombosis during intensive sport are scarce. While a few cases have been described in the cerebral territory, these are only in the context of traumatism or anabolic agent consumption. Thus, causality with exercise remains uncertain and the mechanisms hypothetic. We present the case of a young athlete who experienced two episodes of severe cerebral venous thromboses (CVT), both during intensive training, in the absence of any other known thrombogenic factor.

Case presentation: A healthy 26-year-old man presented a thrombosis of the superior sagittal sinus during recent intensive training for a triathlon. Investigation at the time found no drug or anabolic steroid consumption, or any hematologic or coagulation disturbance. Anticoagulation therapy was initiated for 10 months with good outcome. One year later, soon after returning to intensive exercise, mainly running, the patient presented a thrombosis of the straight sinus complicated by bithalamic hyperintensities observed on T2 magnetic resonance imaging sequences. Anticoagulation treatment was reinitiated and led to repermeabilization of the cerebral vein and reversibility of thalamic abnormalities. Four months later, the patient was free of headache and had no cognitive impairment. He continues to practice intensive sport with vitamin K antagonist as preventive treatment.

Conclusion: This is the first case report of recurrent CVT in a context of intensive sport, without any other thrombogenic features, suggesting a causal link. Intensive exercise should be considered as a potential promoting factor of CVT and investigated during routine examination.

Figure 1

Computed tomography angiography (a) showing an extended superior sagittal sinus thrombosis (arrow) and T1 weighted sagittal magnetic resonance imaging (b) showing thrombosis of the straight sinus (arrow).

Figure 2

Fluid attenuated inversion recovery axial magnetic resonance imaging showing bithalamic hyperintensities (a), reversible with anticoagulation therapy (b).