When signs of elevated intracranial pressure, such as dizziness, headache, fundus edema and vision loss, become apparent, this is when some patients are seen, while most patients with milder conditions may remain out of clinical care for a long time until their condition worsens. This is often attributed to “benign cranial hypertension”, “pseudotumor cerebri”, “optic neuritis”, or even “depression The clinical findings are often attributed to “benign cranial hypertension,” “pseudotumor,” “optic neuritis,” or even “depression. The common causes of cerebral venous sinus thrombosis are thought to be abnormal estrogen and progesterone levels in the body, changes in immune factors such as phospholipases, and inflammation and trauma. Thrombosis can develop acutely or insidiously; therefore, it appears clinically with varying degrees and duration of disease. It causes considerable difficulty in clinical diagnosis.
The diseases that need to be differentiated are.
1. cerebral venous malformation, which often has a more typical “scorpion claw”-like image.
2. simple cranial hypertension with prolonged arterial circulation time on DSA images.
3. Proliferative lesions of the skull base (metastatic carcinoma, mycobacterial and tuberculous meningitis), with enhanced MR imaging showing soft meningeal thickening or intracranial metastases.
In most cases, the morphology and filling images of cerebral venous sinuses can be understood by brain CTA and MRV, but for small cerebral venous thrombosis, deep venous thrombosis, and understanding of cerebral arteriovenous circulation time are mainly determined by whole brain angiography (DSA). Clinical measurements at the PLA General Hospital show that the normal cerebral arteriovenous circulation time (the time between the development of the ophthalmic artery and the disappearance of the sinus sink image) in adult subjects is about 11-12 seconds, that is, about 3.5-4 seconds in each of the cerebral arterial, capillary, and venous phases. When the prolonged venous phase leads to an absolute prolongation of the entire cerebral arteriovenous circulation time, accompanied by an intracranial pressure (ICP) greater than 180 mmH2O, it may suggest cerebral venous reflux disorder; if it is accompanied by a significant venous sinus filling defect or contrast retention in the large cerebral venous system, it can be identified as cerebral venous sinus thrombosis or cerebral deep vein thrombosis.
In terms of classification, cerebral venous circulation disorders can be divided into.
1.Small vein thrombosis
2.Deep vein thrombosis
3.Venous sinus thrombosis
4.Venous sinus stenosis
In terms of complexity, there can be two types: simple thrombosis and combined cerebral parenchymal and subarachnoid hemorrhage. Experiments have shown that the degree of clinical symptoms after cerebral venous circulation disorders depends on the presence or absence of reflux channels in the deep and superficial cerebral veins, but not entirely on the patency of the venous sinuses.
In the case of cerebral venous sinus occlusion, the common compensatory pathways for venous return are.
1, reflux to the cavernous sinus via the pterygo-parietal sinus and the lateral fissure vein.
2, return flow via the conduit vein to the extracranial scalp vein
3. return flow via the skull base veins to the paravertebral plexus.
Many times in cases where the venous sinuses are not completely recanalized, the clinical symptoms improve significantly during the same period because of the venous collateral compensatory pathways.
In the course of cerebral venous circulation disorders, anticoagulation is the most basic form of treatment.
Anticoagulation not only reduces the formation of new clots, but also promotes the body’s fibrinolytic system to dissolve the older clots. Although the vast majority of patients with milder disease can be relieved or cured by anticoagulation alone, relying on anticoagulation alone and slow adjustment to treat cases with a longer history, more severe disease, higher intracranial pressure, and difficulty forming collateral pathways for intracranial venous return is far from adequate. Moreover, the etiology of cerebral venous system thrombosis is unknown and the recurrence rate is extremely high, so anticoagulation also needs to be long-term. The experience of PLA General Hospital suggests that anticoagulation of cerebral venous system thrombosis needs at least 2 years to effectively control the trend of thrombosis recurrence.
Therefore, in treatment, emphasis should be placed on individualized treatment options for different conditions of cerebral venous reflux disorders. Anticoagulation can be applied in basic treatment and management of milder cases; venous sinus thrombosis is suitable for selective thrombolysis (fragmentation) within the venous sinus; small and deep venous thrombosis requires thrombolysis via arterial route; and venous sinus stenosis formed after thrombus mechanization is more suitable for balloon dilation and stenting. Hemorrhagic cerebral venous and venous sinus thrombosis can be better treated with sexual anticoagulation and thrombolysis when available.