Intracranial venous sinus stenosis is a relatively rare obstructive cerebrovascular disease in clinical practice. It can cause intracranial venous return obstruction, resulting in intracranial hypertension (IH), which often manifests clinically as headache, vision loss and optic papilledema caused by intracranial hypertension. Sometimes the disease progresses rapidly, or long-term IH can damage the optic nerve and cause permanent blindness, or it may be followed by thrombosis of the intracranial venous system, which can lead to hemorrhagic infarction and even endanger the life of the patient. In addition to high cranial pressure can also cause a range of symptoms such as pulsatile tinnitus, dizziness, and sleep disturbances, all associated with impaired intracranial venous hemodynamics. For those with cranial hypertension secondary to thrombosis of the intracranial venous system caused by a hypercoagulable state, anticoagulation therapy has been clinically proven to be an effective treatment. However, for anatomical structural lesions such as cerebral venous sinus stenosis, anticoagulation is usually not effective and does not effectively address the problem of impaired intracranial venous return, while the application of dehydration and diuretics can only temporarily reduce IH or is ineffective. In addition to VSS, the promotion of cerebral venous return is the key treatment to reduce intracranial pressure and improve long-term prognosis from the pathogenesis. In recent years, MRV or DSA examinations have allowed to understand the presence of abnormal changes in intracranial venous sinuses and structures, allowing a significant improvement in diagnostic accuracy, thus revealing that venous sinus stenosis is severely underestimated as a cause of IIH and its true incidence is high. Epidemiological and morphological studies have found transverse and sigmoid sinus stenosis in about 90% of patients with IIH and have shown two different types, one with narrowing of the transverse sinus collapse secondary to an unexplained increase in intracranial pressure, resulting in external pressure stenosis, and the other with partial obstruction of the sinus lumen due to filling lesions in the venous sinus lumen, such as enlarged arachnoid granules or thrombotic fibrotic changes in the venous sinus Although the pathological mechanisms of these conditions are different, regardless of whether venous sinus stenosis is a cause or a consequence of increased intracranial pressure, venous sinus hypertension is an important factor that exacerbates cerebral circulation disorders and needs to be promptly relieved. Based on existing theories, another mechanism has been hypothesized to be a positive feedback loop system with self-limiting characteristics between intracranial hypertension and CVSS, in which changes in either of the two factors would cause the same or similar changes in the other factor. The presence of venous sinus stenosis can lead to obstructed hemodynamics in the cerebral veins, resulting in increased venous pressure, which leads to impaired absorption of cerebrospinal fluid and consequently to increased intracranial pressure until the venous sinus wall is compressed, which is another explanation for cerebral venous sinus stenosis. However, in recent years, there has been a gradual increase in reports related to increased intracranial pressure due to cerebral venous return obstruction caused by transverse sinus stenosis, which has raised the attention of neurologists and researchers. It is now known that previous anatomical studies have explained that bilateral transverse sinus asymmetry is generally due to congenital development, and this explanation that transverse sinus development can be asymmetrical initially identifies that this condition does not cause specific pathological changes. Only transverse sinus stenosis, which can cause pathological changes, is a possible cause of cranial hypertension and its associated symptoms. The role of arachnoid granules in intracranial venous sinus stenosis and high cranial pressure has been of increasing interest, as it has been found that stenosis of the main transverse sinus tract is often the location of arachnoid granules. The presence of large arachnoid granules in the wall of the venous sinus makes it more likely that arachnoiditis will occur and complicate local venous sinus stenosis. The presence of a significant stenosis of the transverse or sigmoid sinus with a clearly large pressure gradient difference between the anterior and posterior ends of the stenosis, and the contralateral venous sinus can often be normal, unremarkable, or absent, is now tentatively considered as a possible association of venous sinus stenosis with IIH and can be a cause of refractory cranial hypertension.