Epidemiology
Risk factors
=>Thrombophillic states:
* Pregnancy
* Hormone therapy- HRT/ OCPs
* Heriditary thrombophilic states
* Autoimmune diseases- APLA;
* Malignancy
* Drugs- Chemotherapy; Heparin
=>Head and Neck infections:
* Sinusitis
* Otitis media
* Mastoiditis
* Meningoencephalitis
* Cerebral abcess
=>Mechanical causes:
* Trauma- base of skull fractures
* EVD
* I J CVC
* Dural A-V fistula
Risk factors
=>Thrombophillic states
=>Head and Neck infections
=>Mechanical causes
Clinical Features
=>Presentation is often progressive rather than hyperacute (unlike arterial stroke).
Median delay to diagnosis ≈ 1 week
=>Evolution may be:
* Acute
* Subacute (several days)
* Chronic (>1 month)
Clinical Features
=>Depend upon the site of thrombosis
1️⃣=>Headache-> May worsin lying flat/ Valsalva
->Pain localization:
* Sigmoid sinus → occipital / neck pain
* Lateral sinus → mimics ear infection
2️⃣=>Features of raised ICP:
* Nausea, vomiting
* Vision changes
* Diplopia
* Papilledema (~30%)
* CN VI palsy
* Encephalopathy
3️⃣=>Focal Neurological Deficits
* Hemiparesis (most frequent)
* Dysarthria
* Aphasia
* Visual impairment
* Cranial neuropathies–>Especially with cavernous sinus thrombosis
4️⃣=>Seizures
* Usually focal ± secondary generalization
Seizures are more common than in arterial stroke.
5️⃣=>Diffuse Encephalopathy / Reduced LOC
->Mechanisms:
1. Communicating hydrocephalus
2. Deep venous system occlusion
* Bilateral thalamic dysfunction
* May cause:
* Mutism
* Amnesia
3. Intracranial hemorrhage
4. Cerebral edema → herniation
* Fever-+/-
Cavernous sinus thrombosis
Clinical Features
Symptoms in detail
1️⃣ Oculomotor palsies
* CN III→ Ptosis (CN III)
* CN IV
* CN VI
→ Ophthalmoplegia
→ Diplopia
CN VI is often affected early (medial position within the sinus).
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2️⃣ Trigeminal sensory loss–>Facial numbness due to involvement of:
* V1 (ophthalmic)
* V2 (maxillary)
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3️⃣ Headache->severe, periorbital pain common
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4️⃣ Ocular findings
* Orbital pain
* Conjunctival redness
* Proptosis
* Loss of visual acuity
Mechanism:
* Impaired venous drainage of orbit
* Raised orbital venous pressure
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5️⃣ Fever
* May occur in septic cavernous sinus thrombophlebitis
Causes of Cavernous Sinus Thrombosis
=>Most common:
* Infection- Facial infection, Sinusitis, Orbital cellulitis
=>Inflammatory / autoimmune
=>Structural / mechanical:
Trauma, Meningioma
Pathophysiology
=>Dural venous sinuses lack valves, allowing multidirectional flow.
* Venous anastomoses permit partial rerouting of blood around a thrombus, hence compensate to an extent
=>If venous pressure rises:
1). Cerebral edema
* Elevated capillary pressure
* Reversible if occlusion resolves
2). Ischemic infarction
* Due to tissue blood stasis
* May become irreversible
* Elevated venous pressure + infarct → hemorrhagic transformation
=>CSF physiology:
* Venous sinuses drain CSF via arachnoid granulations (into superior sagittal sinus).
* Sinus thrombosis → impaired CSF absorption.
* May cause communicating hydrocephalus (ventricular dilation + ↑ ICP).
* Most problematic with superior sagittal sinus thrombosis.
Invx for CVST
=>D dimer
=>Imaging-
->Non-enhanced CT / MRI
* Sensitivity ≈80%
* Non-enhanced MRI is superior to non-enhanced CT
->CT Venography (CTV)
* Sensitivity ≈ 99%
* Specificity ≈ 88%
->MR Venography (MRV)
* Slightly superior for:
* Isolated cortical vein thrombosis
* Deep venous thrombosis
* MRI/MRV = gold standard if available
Direct Signs of the Clot on Imaging
=>Non-contrast CT
* Dense triangle sign–>Superior sagittal sinus thrombosis
* Dense cord sign–>Cortical or deep vein thrombosis
=>CT Venography
* Filling defect
* Classic: Empty delta sign
* Acute clot may appear dense like contrast
=>MRI Normal: * Dural sinuses = flow voids (T2/FLAIR) Abnormal: * Loss of flow void → thrombosis
Tt
Specific Tt
1️⃣ Anticoagulation (Mainstay)
Initial therapy:
* Heparin anticoagulation
* Transition to warfarin or DOAC after ~5–15 days
=>Intracranial hemorrhage–> NOT a contraindication
* Hemorrhage extension uncommon
* Risk of thrombus extension without anticoagulation is greater
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=>UFH vs LMWH
* No robust evidence one is superior
->LMWH–>Preferred in mild cases if unlikely to need procedure
->UFH infusion
* Preferred in critically ill
* Easier reversal if EVD/craniectomy required
* Must avoid supra- or subtherapeutic levels
Seizure Mx
2️⃣ Seizure Management
=>Risk factors
* Supratentorial cortical lesions
* SAH
* Focal edema or infarct
* Focal neurologic deficits
=>Prophylaxis
* Generally not recommended
* Consider in high-risk individuals
=>EEG if:
* Altered mental status
* Possible non-convulsive seizures
If seizure occurs:
* Treat aggressively
* Even a single seizure → start antiepileptic
3️⃣ Communicating Hydrocephalus & Papilledema
=>Mechanism:
* Impaired CSF drainage into venous sinuses → ↑ ICP
=>Clinical:
* Papilledema
* Visual field deficits
=>Mx:
->Acetazolamide
* 500–1000 mg/day-> Reduces CSF production
Cautions:
* Causes bicarbonate wasting → may need supplementation
* Contraindicated in pregnancy
->CSF drainage:
* EVD–> Rarely required
* Lumbar puncture
* Only if no focal lesion on CT
* Often requires serial LPs
* Difficult with anticoagulation
If effective → consider lumbar drain
4️⃣ Focal Cerebral Edema
=>Spectrum:
* Mild → improves with anticoagulation
* Severe → herniation risk
=>Supportive measures
* Head elevation
* Osmotherapy
=>Decompressive craniectomy
* Strongly recommended in European guidelines
* No RCT-level evidence
Young CVST patients may be excellent candidates.
Radiologic indications:
* Uncal herniation
* PCA territory ischemia due to herniation
* Midline shift >5 mm
* Persistent severe ICP elevation
=>Steroids: Not useful
5️⃣ Treat Underlying Cause
=>Infection
* Cultures
* Broad-spectrum antibiotics
* Imaging for focus
* Surgical drainage if needed
=>Autoimmune / Vasculitis
* Steroid therapy if indicated
=>Prothrombotic drugs
* Stop hormonal therapy if possible
Role of Catheter-Directed Endovascular Therapy
May include:
* Local thrombolysis
* Mechanical clot disruption
RCT evidence:
* No demonstrated benefit
=>Role:
* Rescue therapy only
* When deterioration despite optimal anticoagulation
If Neurologic deterioration despite Tt
=>Neurologic Deterioration Despite Treatment, Consider:
* Thrombus extension
* Worsening edema
* New hemorrhage
* Deep venous involvement
* Refractory ICP
* Missed underlying infection
=>Escalation pathway:
1. Repeat imaging
2. Optimize anticoagulation
3. Manage ICP aggressively
4. Consider decompressive craniectomy
5. Rescue endovascular therapy
Prognosis
=>In general better than arterial stroke- Younger pt group, better neuroplasticity
* Mortality ~5%
=>Worst predictors:
* Coma
* Deep venous thrombosis
* Intracerebral hemorrhage