= DURAL SINUS THROMBOSIS = VENOUS SINUS /SUPERIOR SAGITTAL SINUS THROMBOSIS

◊The radiologist may be the first to suggest the diagnosis!

Annual Incidence: 2–7÷1,000,000

Cause:>100 causes suggested

1. IDIOPATHIC = spontaneous (10–30%)
2. LOCAL CAUSE (= intrinsic / mechanical conditions of veins / dural sinuses)
   • Septic causes (esp. in childhood): sinusitis, otitis, mastoiditis, sub- / epidural empyema, meningitis, encephalitis, brain abscess, face + scalp cellulitis
   • Aseptic causes:
     1. Tumor compressing sinus: meningioma
     2. Trauma: fracture through sinus wall, brain damage, cranial surgery, jugular vein catheterization
3. SYSTEMIC CAUSE (= conditions that promote thrombosis)
   • Septic causes: septicemia
   • Aseptic causes:
     1. Low-flow state: CHF, CHD, dehydration, shock, surgery, immobilization
     2. Hypercoagulability: antithrombin III deficiency, antiphospholipid syndrome, protein S + C deficiency, pregnancy, peripartum state, oral contraceptives, malignancy, polycythemia vera, idiopathic thrombocytosis, thrombocytopenia, sickle cell disease, cryofibrinogenemia, disseminated intravascular coagulopathy
     3. Chemotherapy: eg, ARA-C, L-asparaginase
   • Unusual causes: Behçet disease, AIDS, ulcerative colitis, SLE, nephrotic syndrome, sarcoidosis

Pathophysiology:

dural sinus thrombosis → thrombus propagation into cortical veins → venous congestion → cerebral venous infarction (in 50%) → vasogenic / cytotoxic edema → intracranial hemorrhage; occasionally hydrocephalus (→ decreased CSF absorption ← impaired function of arachnoid granulations)

Onset: acute = <2 days (in 30%), subacute = 2–30 days (in 50%), chronic = >30 days (20%)

• symptoms of intracranial hypertension (20–40%): headaches (75–95%), nausea, vomiting, visual blurring, papilledema
  often confused with: tension headaches, migraine
• drowsiness, confusion, coma, decreased mentation, lethargy, obtundation, seizures, fever
• focal neurologic deficits = stroke symptomatology (dysphasia, cranial nerve palsy, cerebellar incoordination) ← frequently parenchymal changes

Location: superior sagittal sinus (62%) >L transverse sinus (45%) >R transverse sinus (41%) >sigmoid sinus (15%) >straight sinus (18%) >cortical veins (17%) >deep venous system (11%) >jugular bulb (8%) >vein of Galen (7%) >cavernous sinus (1%) >cerebellar veins (0.3%)

• bilateral parasagittal hemispheric lesions ← superior sagittal sinus thrombosis
• ipsilateral temporo-occipital + cerebellar lobe lesions ← transverse sinus thrombosis
• bilateral thalamic lesions ← deep cerebral venous thrombosis

NECT (usually subtle findings):

• hyperattenuating intravascular material (← acute blood clot) in sagittal sinus = “dense triangle” sign / straight sinus / cerebral cortical vein = “cord” sign lasting for 1–2 weeks (seen in only 20% ← variability in degree of thrombus attenuation)
  DDx to hyperattenuated thrombus:
  dehydrated patient, elevated hematocrit level, polycythemia, nonmyelinated brain in neonates, subjacent subarachnoid / subdural hemorrhage
• subdural collection
• stroke (often hemorrhagic)
  • Thrombosis of intracranial dural sinuses, cortical / deep cerebral veins, cavernous sinus is an easily recognizable condition that accounts for 1% of acute cerebral infarcts.
• dense transcortical medullary vein ← collateral drainage

CECT venography (30–40 sec delay):

1. direct
   • “empty delta” sign / “empty triangle” = filling defect in straight sinus / superior sagittal sinus surrounded by a triangular area of enhancing collateral dural venous channels + cavernous spaces (in 25–35–75%)
     False positive: subdural hematoma / empyema, arachnoid granulations
     False negative: partial volume averaging, small / recanalized organized thrombus
   • enlargement of thrombosed vein near obstruction
   • shaggy irregular contour of veins (= small collateral veins enhance near the obstructed vein)
2. indirect (subtle early changes)
   • brain edema + swelling of gyri
   • low attenuation lesion of venous infarction
   • ± subcortical hemorrhage in venous distribution

Advantage over MR: shorter exam time, NO contraindication to pacemaker, fewer equivocal findings, NO flow-related artifacts

Disadvantage over MR: difficult MIP reconstruction (due to adjacent bone), adverse reaction to contrast material, ionizing radiation

NEMR:

• replacement of flow void by abnormal signal intensity
  1. acute thrombosis (first 5 days)
     • clot isointense to gray matter on T1WI (and therefore easily missed) + hypointense on T2WI (← deoxyhemoglobin in RBCs trapped in thrombus)
     • low SI rather than normal flow void on T1WI
     • blooming artifacts on GRE in thrombosed segment
     • hyperintense thrombosed sinus on DWI with diminished mean ADC value (in 41%)
  2. subacute thrombosis (6–15 days = in 55% of patients)
     • most frequent stage at clinical presentation (55%) + easiest stage for thrombus detection
     • hyperintense thrombus within sinus on T1WI (← intra- and extracellular methemoglobin)
     • iso- / hyperintense thrombus on T2WI (← extracellular methemoglobin)
       N.B.: hypointense thrombus on T2WI ← intracellular methemoglobin may mimic flow void of a patent dural sinus
  3. chronic thrombosis (>15 days = 15% of patients) with incomplete recanalization
     • Most difficult stage to diagnose!
     • isointense on T1WI + iso- / hyperintense T2WI

MR venography (TOF, CEMR):

• excellent sensitivity to slow flow perpendicular to plane of acquisition for 2D-TOF
  Pitfalls: nulling of venous signal in plane of acquisition; hyperintense thrombus on T1WI time-of-flight venography can simulate flow-related enhancement
• filling defect in sinus on CEMR
  Pitfall: marked contrast enhancement of organized revascularized thrombus in chronic thrombosis
  • Sinus contrast enhancement does NOT DEFINITELY indicate patency!
• wall-enhancement of thrombosed dural sinus

Angio (DSA):

• nonfilling of thrombosed sinus
• filling of collateral cortical veins, deep venous system, cavernous sinus

Prognosis: high mortality

Bad outcome: hemorrhage on admission CT, thrombosis of deep cerebral veins, CNS infection

Rx: heparin (full recovery in 70%), local thrombolysis (worsening in spite of adequate anticoagulation), reduction of intracranial pressure