Pseudo-SAH was first discovered by Spiegel et al., that linear high-density shadows similar to SAH appeared in sulci, cisternae and subarachnoid space on head CT of patients with cerebral edema[4]. However, Avrahami et al. confirmed by lumbar puncture or autopsy that there was no real SAH in these patients and called it pseudo-SAH[5]. The pseudo-SAH reported in the previous literature is based on a large range of diffuse brain edema, and the basal cists, sulci, and fuses in the pseudo-SAH are often similar to SAH. The underlying diseases of these patients are mostly ischemic hypoxic encephalopathy, massive cerebral infarction, venous sinus thrombosis, severe craniocerebral injury, spontaneous intracranial hypotension, acute purulent meningitis, intrathecal or intravascular contrast agent injection, etc[1-5]. The etiologies of the patients with localized pseudo-SAH in this study were ischemic hypoxic encephalopathy, acute cerebral infarction, and viral encephalitis. The basic disease spectrum of pseudo-SAH in this study was basically the same as that reported in previous literature. It has even been reported that the occurrence of pseudo-SAH may be one of the early CT manifestations of acute cerebral infarction[6].
On the basis of localized cerebral parenchyma edema, linear relatively high density shadows appeared in the adjacent sulci and cisternae of all patients, and even the linear high density shadows were significantly enhanced in the contrast-enhanced CT, suggesting that the linear high density shadows may be some vascular structures with relatively high density. As for the mechanism of this illusion, we speculate that this illusion may be caused by the compression of venous sinuses by localized cerebral edema, resulting in blocked venous return and dilation of superficial veins, which is in contrast to the brain parenchyma with reduced density, resulting in an illusion similar to SAH. Or due to the acute cerebral vascular occlusion of the distal side of the affected side, the local leptomeningeal collateral blood flow slowly formed relatively high density shadow of the lumen[6]. Or local lesions may lead to the destruction of the blood-brain barrier and increase the permeability of the meninges, thereby causing the density of the subarachnoid space to increase[7].
Although there are many similarities between localized pseudo-SAH and real SAH CT manifestations, there are some differences between them: ①Density: Most previous studies distinguish real SAH from pseudo-SAH by comparing CT values, and it has certain clinical significance. The relative high density shadow density in pseudo-SAH is lower than that in real bleeding, CT values are 29-33 Hu[8], and 60-70 Hu[9], respectively. ②Enhancement method: high-density images of pseudo-SAH can significantly enhance in contrast-enhanced CT, which is significantly different from SAH[5]. ③Morphology: Patients with pseudo-SAH have relatively narrow or occluded subarachnoid spaces such as adjacent sulci and cisterns due to the cause of cerebral edema, whereas patients with SAH show enlarged subarachnoid spaces such as cisterns at an early stage due to poor cerebrospinal fluid circulation caused by the blockage of hematoma.
The pathologic changes of SAH patients will gradually absorb and decrease over time, and generally disappear completely within 3 weeks, while those of pseudo-SAH are mainly related to the primary underlying disease and its treatment situation, and some patients can even persist[10, 11]. Regarding the prognosis of pseudo-SAH, previous studies have shown that the prognosis is mainly related to the underlying diseases of patients. Some studies also believe that the occurrence of pseudo-SAH means that patients have severe brain edema and poor prognosis[8, 12]. In contrast, all cases of localized pseudo-SAH arose on the basis of localized cerebral edema, generally suggesting localized brain tissue lesions with limited lesion extent, lesser extent, and mostly better prognosis. MRA in the present study revealed one case with localized mild stenosis in the M2 segment of the right middle cerebral artery, which was relatively mild in extent and extent in this patient, which was also consistent with the limited extent of the lesion. After aggressive treatment of the primary underlying disease, 8 of the 9 patients in this paper improved, and only 1 patient died from conversion to multiple organ failure, suggesting that the prognosis of small-scale pseudo-SAH is relatively good.