I have enough material. Here's an exam-ready answer for CVT, structured exactly how DNB Medicine examiners expect a 10-mark long answer/short essay.
Cerebral Venous Thrombosis (CVT) — 10 Mark Answer
1. Definition
Cerebral venous thrombosis (CVT) is thrombotic occlusion of one or more of the cerebral veins and/or dural venous sinuses (superior sagittal sinus, transverse/sigmoid sinus, cortical veins, deep venous system, cavernous sinus), leading to venous outflow obstruction, raised venous/intracranial pressure, venous infarction and hemorrhage. It is an uncommon but important cause of stroke in young adults, especially women.
2. Etiology / Risk Factors (mnemonic: think Virchow's triad - Hypercoagulability, Stasis, Vessel wall injury)
A. Prothrombotic/Hypercoagulable states
- Pregnancy and puerperium (peripartum state)
- Oral contraceptive pills, hormone replacement therapy
- Inherited thrombophilia: Factor V Leiden, prothrombin gene mutation, protein C/S and antithrombin deficiency
- Antiphospholipid antibody syndrome
- Malignancy (especially adenocarcinomas), paroxysmal nocturnal hemoglobinuria
- Polycythemia, thrombocytosis, nephrotic syndrome
- Behçet disease
B. Local causes
- Infection: otitis media, mastoiditis, sinusitis, meningitis (classic infective route to lateral/cavernous sinus)
- Head injury, neurosurgical procedures, lumbar puncture
- Direct tumor invasion of sinus
C. Drugs: tamoxifen, bevacizumab, erythropoietin, L-asparaginase, heparin-induced thrombocytopenia
D. Others: dehydration, SARS-CoV-2 infection/vaccine-induced (VITT), idiopathic (up to 15-20%)
3. Pathophysiology
Two mechanisms operate, often together:
- Venous sinus occlusion → impaired CSF absorption via arachnoid villi → raised intracranial pressure → headache, papilledema, VI nerve palsy
- Cortical/deep vein occlusion → local venous hypertension → vasogenic and cytotoxic edema → venous infarction, often hemorrhagic, that does not respect arterial territories
4. Clinical Features
Highly variable, evolving over hours to days (subacute, unlike arterial stroke):
- Headache - commonest symptom (>90%), often diffuse, progressive, worse lying down
- Raised ICP: papilledema, vomiting, blurred vision, VI nerve palsy
- Seizures (focal or generalized) - much more common than in arterial stroke
- Focal neurological deficits: hemiparesis, aphasia (may fluctuate, or be bilateral in sagittal sinus thrombosis - bilateral leg weakness)
- Altered sensorium - coma if deep venous system involved (poor prognosis)
- Site-specific syndromes:
- Superior sagittal sinus - bilateral leg weakness/sensory loss, seizures
- Cavernous sinus - painful ophthalmoplegia, proptosis, chemosis (usually septic, from facial/sinus infection)
- Lateral/sigmoid sinus - mastoid pain, VI/VII/VIII palsies
- Cortical vein - focal seizures, hemorrhagic infarct
- Deep venous system (straight sinus, internal cerebral veins) - bilateral thalamic involvement, coma
5. Investigations
- CT head (plain): may show "cord sign" (hyperdense thrombosed cortical vein) or "dense triangle sign"; may be normal in 30%
- CT venography / MR venography - investigation of choice: filling defect, "empty delta sign" on contrast CT/MRI (triangular filling defect in superior sagittal sinus)
- MRI brain with venogram: T2*/SWI shows blooming due to thrombus; venous infarcts often hemorrhagic and don't match arterial territory
- Digital subtraction angiography (DSA) - gold standard, rarely needed now
- D-dimer - sensitive but not fully reliable to exclude CVT (can be normal, especially in isolated headache presentations)
- Thrombophilia workup: protein C/S, antithrombin, factor V Leiden, antiphospholipid antibodies, homocysteine (send after acute phase/anticoagulation, not during)
- Baseline: CBC, coagulation profile, LP (if no mass effect, to check opening pressure and exclude infection)
6. Treatment
- Anticoagulation - mainstay, started even in presence of hemorrhagic venous infarct
- Low molecular weight heparin (body-weight adjusted, subcutaneous) preferred over unfractionated heparin (associated with lower mortality in trials) OR dose-adjusted IV UFH if renal impairment/rapid reversal needed
- Followed by oral anticoagulation (warfarin, INR target 2-3) for at least 3-6 months; longer/indefinite if strong persistent prothrombotic state
- DOACs (e.g., dabigatran) show comparable efficacy/safety to warfarin in recent meta-analyses (PMID: 38772568) - increasingly used
- Treat raised ICP: head elevation, mannitol/hyperventilation (temporizing); acetazolamide; therapeutic LP if impending visual loss and no mass effect; decompressive hemicraniectomy in malignant edema with herniation
- Seizure control: antiepileptics for those with seizures (prophylaxis debated)
- Endovascular thrombectomy/thrombolysis - reserved for patients deteriorating despite adequate anticoagulation ("medically refractory" CVT); systematic reviews show no added benefit over medical therapy alone as first-line (PMID: 38329489, 36471504)
- Treat underlying cause: antibiotics if septic (mastoiditis/sinusitis-related), stop offending drug/OCP, manage malignancy
- Decompressive surgery for large hemorrhagic infarcts with herniation risk
7. Prognosis
Generally better than arterial stroke - overall good outcome in ~80%. Poor prognostic factors: coma/altered mental status, deep venous system thrombosis, intracerebral hemorrhage, malignancy as cause, age >37, male sex.
Diagram tip for exam
Draw a simple line diagram of the dural venous sinuses (superior sagittal sinus, straight sinus, transverse/sigmoid sinus, confluence of sinuses, cavernous sinus) with cortical/deep veins draining into them - examiners give extra marks for a labeled diagram in CVT questions.
Recent evidence note: Meta-analyses (2024) support DOACs as an alternative to warfarin for CVT with similar efficacy and possibly lower bleeding risk (PMID: 38772568), and systematic reviews on mechanical thrombectomy/thrombolysis found insufficient evidence to recommend it over standard anticoagulation except in refractory cases (PMID: 38329489, 36471504) - useful to mention briefly under "recent advances" for extra marks.
Sources: Adams and Victor's Principles of Neurology (12th ed.), Goldman-Cecil Medicine, Bradley and Daroff's Neurology in Clinical Practice.