The numbness came on suddenly, down the right arm and leg, and had lasted an hour by the time he reached a hospital in Kurunegala, Sri Lanka. He was 23, with a blood pressure of 126 over 76, no smoking history, and no family history of clotting problems. His strength and reflexes were normal. The one recent change in his life was that he had started treatment for pleural tuberculosis 14 days earlier.
A scan showed bleeding deep in the left thalamus, a reading that would ordinarily send a team looking for a burst artery or a malformation. Instead, ten days later, a different scan found something almost nobody looks for: a clot in the basal vein of Rosenthal, a paired vein curling around the midbrain that drains the thalamus and nearby structures. Their case report appears in the Journal of Medical Case Reports.
Blocked Drainage Can Cause Bleeding, Not Just Clotting
The counterintuitive part is that a clot produced a hemorrhage. Understanding why drives everything else.
When a vein draining a part of the brain becomes blocked, blood continues to flow in through the arteries but has nowhere to go. Pressure builds in the capillaries, perfusion falls, and the blood-brain barrier breaks down. Fluid leaks out, tissue swells, and small vessels give way. The result looks like a bleed on a scan, but the cause is a downstream obstruction.
Cerebral venous thrombosis is an uncommon cause of stroke. The report puts it at under 1% of cerebrovascular events in one passage and 0.5% to 3% in another, and notes that the deep venous system is involved in fewer than 10% of those cases. Isolated clotting of the basal vein alone is rarer still, first documented on imaging in 2004.
The diagnostic trap is that it is easy to stop early. A plain CT shows the hemorrhage, and the hemorrhage is a satisfying answer. Here, CT angiography ruled out an aneurysm or malformation, and only when a contrast scan showed the left basal vein failing to light up was a dedicated venogram ordered. That venogram confirmed the clot. The authors note that the diagnosis was not initially suspected and that venography was performed on hospital day 10 due to persistent symptoms and resource constraints.
Everything That Should Have Flagged a Clotting Risk Came Back Normal
The workup was thorough and almost entirely unremarkable. Hemoglobin, white blood cell count, platelets, INR, and clotting times were normal. C-reactive protein was 3 mg/L and the erythrocyte sedimentation rate 12 mm in the first hour, both within range. Protein C and S were normal. Antiphospholipid antibodies, antinuclear antibody, homocysteine, HIV, and hepatitis B and C all came back negative.
Factor V Leiden testing, prothrombin gene mutation testing, and antithrombin III level testing could not be performed due to cost. The authors say so plainly rather than gloss it.
That normal panel is the point they press hardest. Standard inflammatory markers and routine coagulation studies do not reliably capture the clotting risk posed by active tuberculosis, and normal results can be falsely reassuring.
The proposed mechanism is inflammation-driven. Tuberculosis elevates cytokine levels, including tumor necrosis factor alpha and interleukin-6, prompting the liver to produce more fibrinogen and clotting factors and activating the vascular endothelium. Natural anticoagulants, including antithrombin III, protein C, and protein S, fall. A 2025 review in the Journal of Clinical Medicine covers this hypercoagulability in detail.
Two other factors are raised as possible contributors, both hedged. The early intensive phase of treatment kills bacteria rapidly, which can transiently spike inflammation, a pattern related to TB immune reconstitution inflammatory syndrome. And rifampicin-containing regimens have been linked in some studies to more venous thromboembolism, with a reported case of rifampicin-associated pulmonary embolism among the supporting literature. The authors present these as possible, not established.
Why This Matters in a Country Where TB Remains Elevated
Tuberculosis is not a foreign problem for American readers. The CDC's provisional 2025 data recorded 10,260 TB cases in the United States, a rate of 3.0 per 100,000. That is a slight decline from 2024, but counts remain above pre-pandemic levels, and the agency cautions that provisional figures may change when finalized.
Extrapulmonary tuberculosis, the kind this patient had, is the form most often linked to that inflammatory flare, with pleural and lymph node disease specifically noted. The clinical prompt is narrow and portable. A young adult on TB treatment who develops new neurological symptoms deserves consideration of venous thrombosis, and confirming or excluding it requires venography, not just an arterial study.
Blood Thinners for a Brain That Is Already Bleeding
The treatment decision here looks alarming and is, in fact, standard. Despite active intracerebral hemorrhage, the team started therapeutic anticoagulation with subcutaneous enoxaparin on day 10 and continued the TB drugs without interruption.
Anticoagulation is the cornerstone of cerebral venous thrombosis management even when bleeding is present, a position reflected in the 2024 American Heart Association scientific statement and the European Stroke Organization guideline. Stopping the clot from extending relieves the pressure causing the bleed.
Repeat imaging at three weeks showed no progression of the hemorrhage. He was bridged to warfarin, discharged on day 31, and switched to rivaroxaban six weeks later once thrombophilia had been excluded as far as local resources allowed. At three months, he had marked neurological improvement and no recurrent clots. Follow-up venography could not be performed again due to resource constraints.
This is one patient, and one case cannot establish how often TB treatment precedes this complication or whether rifampicin contributes. It documents a diagnostic sequence worth knowing: a young person with a brain bleed, no hypertension, no coagulopathy, and an active infection that quietly tilts the blood toward clotting. Anyone with sudden numbness, weakness, severe headache, or vision changes should seek emergency care regardless of age, and people on TB treatment should not stop their medication on their own.
Key Questions Answered
How does a blood clot cause bleeding in the brain?
The clot blocks a vein draining an area of brain tissue. Blood keeps flowing in through arteries but cannot exit, so pressure rises, the blood-brain barrier breaks down, tissue swells, and small vessels rupture. The bleed is a downstream consequence of the blockage.
What is the basal vein of Rosenthal?
A paired vein that runs along each side of the midbrain and drains deep structures including the thalamus, basal ganglia, and inner temporal lobe. Because it is small, it is easily missed on routine imaging unless a venogram is specifically ordered.
Why was tuberculosis considered the cause?
Active TB drives inflammation that raises clotting factors and lowers the body's natural anticoagulants. The authors judged this to be the most plausible unifying explanation after an extensive workup found no other cause, though genetic thrombophilia testing was not affordable.
Should people on TB treatment worry about blood clots?
Clots remain an uncommon complication, and this case does not change treatment recommendations. Stopping TB medication carries serious risks of its own. New neurological symptoms during treatment should prompt urgent evaluation rather than self-discontinuation.
Why give blood thinners to someone with a brain bleed?
In cerebral venous thrombosis, anticoagulation is standard even when hemorrhage is present, because preventing clot extension relieves the pressure driving the bleeding. Major guidelines support this, with close monitoring and repeat imaging.
What does one case report actually prove?
Very little on its own about frequency or causation. Its value is documenting a diagnostic pathway, showing that a deep venous clot can masquerade as a primary brain hemorrhage in a young patient with no conventional risk factors.
