The clinical manifestations of these patients are often variable, and patients may show a range of symptoms depending on the location and extent of thrombosis, the patient's age, and the underlying factors. (11) The most common symptoms include increased intracranial pressure such as headache, blurred vision, papillae edema, focal neurologic defects, seizures, and diffuse encephalopathy. Other unusual manifestations include subarachnoid hemorrhage, a thunderclap headache, recurrent transient ischemic attacks, tinnitus, and multiple cranial nerve palsy. (10) Strong and clinically appropriate suspicion is vital for diagnosing affected individuals. Early diagnosis is essential because prompt treatment of cerebral venous thrombosis significantly impacts clinical outcomes. Based on these non-specific clinical features and complications, NCCT plays a vital role in the first-line diagnostic workup, localization, and prognosis. The diagnosis of venous sinuses in the brain has increased over the past few years due to advances in imaging techniques. (12) This increase is more prominently seen in children, young adults, women of childbearing age, and low-income countries. (13) The estimated male-female ratio is 3: 1 and accounts for 0.5-1% of all stroke cases. (14) The most common venous sinus thrombosis is the subacute type, accounting for almost half of the patients.(13) It must be noticed that this stage of disease is the most challenging phase on both radiological and clinical work-up.
Acute thrombosis within the lumen is usually seen as a dense substance on an NCCT scan in the acute phase of the disease. (15) The increase in density is generally attributed to a decrease in the amount of water accumulated in the clot and an increase in red blood cells and hemoglobin concentration. The sensitivity of this finding has been reported in 63–73% in various studies. (11) It is believed that quantitative density measurement is more accurate than qualitative assessment because it can understand the average increase in sinus density. The rate of venous recanalization in follow-up imaging has been reported to be about 85%, leading to density changes during subsequent phases of clot development. (16)
In our study, during the acute phase, the density of the thrombosis was statistically different compared to non-thrombotic counterparts. These findings indicate the diagnostic value of acute venous sinus hyperdensity in NCCT scan, which is in line with the results of previous studies. Previous studies have reported a sensitivity of about 64% for this symptom. (6–8, 11, 16, 17) In the subacute phase, the density of thrombosis did not differ significantly from a normal sinus. As mentioned in previous studies, the equalization of involved sinus density is the main reason for the delayed diagnosis(16–19). In a study by Buyck.F et al., the theory of a gradual decrease in the density of venous sinuses during 14–17 days after thrombosis was proposed, which caused the similarity of the involved sinus density with the density of blood in the subacute phase and its hypodensity in the chronic stage. (8) The results of our study confirmed this hypothesis. Figure 3 shows the temporal changes of sinus density in patients with acute cerebral sinus vein thrombosis.
Furthermore, the density of involved sinuses was significantly lower than uninvolved cases in the chronic stage. Hypodensity of sinuses was not noticed as much as required in the previous investigations. We believe these patients are easily missed. So far, no study has directly examined the evolution of cerebral venous thrombosis, and the reduction in the density of thrombotic sinuses has not been objectively proven in any single study. The above findings are not yet recognized as a diagnostic finding. This potentially fatal condition can be easily missed in patients presenting more than two weeks after the onset of the event. By teaching and applying this simple but critical point by radiologists, a significant reduction in the complications of dural sinus thrombosis is predicted. Figure 4 represents a hemorrhagic infarct in a patient with a hypodense thrombosis on the NCCT.
In our study, a good agreement (0.7) for the hypodense sinus sign in the non-acute phase was seen among radiologists. Therefore, this subjective sign can be used as an alarm to diagnose non-acute thrombosis of the dural sinuses. The differential diagnosis for hypodensity within the dural sinus on NCCT, including arachnoid granulation, dural sinus cyst, and dural sinus adipose tissue, should be considered. (20)
Ideally, our findings should be confirmed by further prospective studies with large sample sizes. However, given the low incidence of patients with CVST, it seems challenging to conduct a study with a larger sample size. Furthermore, due to the horizontal path of transverse sinuses, which are essential locations for thrombosis, their examination with an NCCT scan is too tricky. These structures were not evaluated in our study.