Cerebral Venous infarcts:

 

Dr. A. Vincent Thamburaj,   

Neurosurgeon, Apollo Hospitals,  Chennai , India.


Venous infarct is an elusive diagnosis because of its nonspecific presentation and its numerous predisposing causes. Cerebral venous infarcts constitute less than 1% of acute strokes. It occurs is in areas atypical for arterial vascular distribution.

The true incidence is not known, but rarer than other types of stroke with a slight female preponderance, accounting up to 50% of strokes during pregnancy and puerperium. It is more common than previously thought. Increased frequency is being reported since advent of DSA (digital subtraction angiography), CT & MRI/V.

Pathophysiology:

Cerebral venous thrombosis results from occlusion of a venous sinus and/or cortical vein and usually is caused by a partial thrombus or an extrinsic compression that subsequently progresses to complete occlusion. Once the vein is occluded, the clot propagates into the cortical veins, leading to the obstruction of cortical venous drainage. Venous pressure increases, and causes breakdown of the brain-blood barrier with vasogenic edema and hemorrhage. Finally, venous infarct with cytotoxic edema ensues. The cerebral cortex is edematous with petechial or gross hemorrhages. Involvement of the deep cerebral veins (eg, basal vein of Rosenthal) can progress to bilateral thrombosis of the internal cerebral veins with thalamic hemorrhagic infarction.

Hemorrhage or infarct (non-arterial distribution) occurs due to elevated venous and capillary pressure.

Usually the onset of symptoms is gradual (weeks).

Acute (days) or insidious (months) onset are not uncommon.

Distribution of venous thrombosis

Multiple vessels                          >70%

Superior sagittal sinus                72%

Transverse sinus                        70%

            Right                             26%

            Left                               26%

            Both                              18%

Straight sinus                             14%

Cavernous sinus                           3%

Cerebral veins                            38%

            Superficial                     27%

            Deep                             8%

Cerebellar veins                         3%

Risk factors:

 

As many as 25% of patients present with no predisposing risk factor.

Multiple pathophysiologic mechanisms and predisposing factors exist, including the following:

 

1) A low-flow state within the venous sinus due hypercoagulable states is the most often detected cause.

 

They include,

Inherited thrombophilias (in 1/3): Protein C / S deficiency, Antithrombin III deficiency, Factov V Leiden mutation (with activated protein C resistance), Prothrombin gene mutation, Hyperhomocysteinemia, Paroxysmal nocturnal hemoglobinuria

 

2)   Acquired causes:

Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies) with or without associated with SLE (lupus) or other connective-tissue disorders.

Dehydration (hyperosmolarity) incl. Burns, diabetic ketoacidosis, Hyperviscosity (incl. Waldenstrom’s Macroglobulinemia), Polycythemia, Sickle cell, Thrombocytosis.

Pregnancy & puerperium

Malignancy

Inflammatory bowel disease

Sarcoidosis

Nephrotic syndrome

Oral contraceptive pill, hormone replacement therapy, heparin-induced thrombocytopenia,

l-asparaginase chemotherapy, corticosteroid therapy.

2) Local or distant infection account for 10% of the patients, and include, mastoiditis, otitis media, paranasal sinus infection, generalized sepsis, and facial or scalp cellulites.

 

3) Extrinsic compression or local invasion of a venous by tumor are other possible causes.

 

4) Iatrogenic causes include, invasive internal jugular venous catheters, post craniotomy (esp. following excision of a convexity meningioma) transvenous pacemaker, Post treatment of AVMs.

 

Clinical features:

The signs and symptoms of cerebral venous thrombosis occasionally are nonspecific and highly variable, making the clinical diagnosis difficult. Patients may have generalized or focal neurologic symptoms and signs with features of raised ICT. Seizures are much more common that with other stroke types.

Focal neurological deficit is seen in up to 2/3 of patients.

They may be bilateral alternating deficits (4%).

Rapidly progressive decreased LOC, headache, nausea, pyramidal signs (rarely), the so-called “Catastrophic presentation” may mimic SAH.

Psychiatric disturbances may be seen.

Headache                                 75%

Papilledema                              49%

Motor or sensory deficit             34%

Seizures                                   37%

Change in LOC                          30%

Dysphasia                                 12%

Multiple cranial nerve palsies      12% Cerebellar incoordination             3%

Nystagmus                                 2%

Hearing loss                               2%

 

Imaging studies:

 

CT reveals hyperdense dural sinuses and rarely cortical veins, related to the presence of clot within the lumen. Hyperdense petechial hemorrhages and hypodense edema may be seen in the cortical grey matter and subcortical white matter. On noncontrast CT scan, the classic finding is the delta sign, which is observed as a dense triangle (from hyperdense thrombus) within the superior sagittal sinus. However, this is not specific, since high attenuation in the healthy nonthrombosed sinus can be observed occasionally and is common in neonates because of an elevated hematocrit.

On contrast-enhanced CT scan, the reverse delta sign (ie, empty triangle sign) can be observed in the superior sagittal sinus from enhancement of the dural leaves surrounding the comparatively less dense thrombosed sinus.

The presence of both the delta and reverse delta signs increases the likelihood of the diagnosis.

 

MRI is more sensitive in the detection of venous sinus occlusion and venous infarcts. Acute clot is usually iso- to mildly hyperintense on T1-weighted and hypointense on T2-weighted images. Venous infarct develops in more than 50% of cases with dural venous sinus thrombosis, characterized by gyral swelling and sulcal effacement. The affected gyri are hypointense on T1-weighted and hyperintense on T2-weighted sequences, however petechial or gross hemorrhages are associated in the cortico-subcortical areas with relevant signal intensity characteristics.

MR venography studies show the occlusion of cortical venous sinuses with abnormal collateral channels.

Rt. parietal venous infarct-MRI

Sagittal sinus thrombosis-MRV

MRI with MRV is preferred for diagnosis. Recently, CT venography can also confirm the diagnosis.

 

Cerebral arteriography and venography may be necessary when MRI scan and MRV are not available. Classic findings are filling defects from thrombus within the venous sinus, and occlusion of a draining sinus. Other findings include decreased focal venous circulation around a thrombosed venous sinus, visualization of collateral circulation, narrowing of arteries in the involved region, prolonged contrast blush in the brain parenchyma, tortuous vessels in the capillary and venous phases, and collateral flow in dilated anastomotic vessels.

 

Management:

 

Supportive management with IV fluids, anticonvulsants, and ICP control, as in acute arterial infarcts, is the mainstay.

The causative factor, such as infection, needs urgent attention.

 

Anticoagulation

Goal is to arrest the thrombotic process. IV heparin is recommended despite some reports to suggest that anticoagulation do not add to recovery. It is generally avoided, in the setting of ICH.

IV thrombolysis (local urokinase) and endovascular thrombectomy may be considered when there is clinical deterioration despite adequate anticoagulation. Oral anticoagulation is continued for 3-6 months or life long if a non-reversible prothrombotic condition identified.

 

Outcome:

 

Despite adequate measures, the reported the mortality rates range from 6 to 20%.

Predictors of death or dependency are: older age, coma or mental state disorder, male sex, hemorrhage on admission CT scan, involvement of deep venous system, presence of CNS infection and malignancy.

In up to 80% of the patients there is no sequelae. 5% of them are severely impaired at follow-up. 10%  of them may recur.

About 15% of them develop venous thrombosis in another location (intra or extracerebral).

Some of the patients may progress to benign intracranial hypertension.  

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


 

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