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Patients with imaging findings concerning for subarachnoid hemorrhage, however, with no evidence of hemorrhage following autopsy or cerebrospinal fluid testing are diagnosed with having pseudo-subarachnoid hemorrhage. A 73-year-old female presented to the emergency department with altered mental status one day after undergoing a lumbar epidural steroid injection at an outside hospital; a noncontrast computed tomography scan of the head revealed evidence of diffuse hyperdensity within the subarachnoid space concerning for subarachnoid hemorrhage. The patient underwent magnetic resonance imaging which demonstrated diffuse opacification of the cerebrospinal fluid spaces with gadolinium and the diagnoses of pseudo-subarachnoid hemorrhage and gadolinium encephalopathy were made. The combination of the neurologic symptoms related to gadolinium encephalopathy and the radiographic findings of pseudo-subarachnoid hemorrhage can create a clinical presentation nearly identical to ruptured aneurysmal subarachnoid hemorrhage. Patient history, magnetic resonance imaging findings, and temporal changes in computed tomography provide vital tools in establishing a diagnosis of pseudo-subarachnoid hemorrhage, especially after an iatrogenic intrathecal contrast administration.

Spontaneous intracranial hypotension (SIH) is an important cause of headache mainly associated with spinal cerebrospinal fluid leakage. We herein report the case of a 51-year-old man who developed SIH after swimming. Brain magnetic resonance imaging (MRI) showed a transient high-intensity lesion in the splenium of the corpus callosum (SCC), in addition to bilateral subdural hematomas (SDH) and pseudo-subarachnoid hemorrhage on brain computed tomography. The splenial lesion disappeared and SDH improved after an epidural blood patch. This case emphasizes that transient SCC lesions could coexist with SIH and that SIH should be considered in the differential diagnosis of SCC lesions.

We report the case of an extended pseudo-subarachnoid hemorrhage (PSAH) related to contrast intracerebral diffusion from blood-brain barrier breakdown on periprocedural percutaneous coronary intervention right corticofrontal ischemic stroke. PSAH is a rare and complex phenomenon, and it is important to differentiate PSAH from subarachnoid hemorrhage to avoid inappropriate treatment with potentially severe consequences. (Level of Difficulty: Beginner.), Graphical abstract, We report the case of an extended pseudo-subarachnoid hemorrhage (PSAH) related to contrast intracerebral diffusion from blood-brain barrier…

Background: On rare occasions, cisterns are demonstrated as high-density areas on computed tomography (CT) and misdiagnosed with subarachnoid hemorrhage (SAH). This false-positive finding is called pseudo-SAH. Patients and Methods: From April 2014 to August 2018, a total of 161 patients with chronic subdural hematoma (CSDH) were treated in our hospital. For these cases, the existence of a pseudo-SAH sign on CT was retrospectively examined. Results: One patient with bilateral CSDH showed pseudo-SAH and a further examination to evaluate vascular abnormalities causing true SAH was necessary. In three patients, the Sylvian fissures were demonstrated as high-density areas due to an atherosclerotic middle cerebral artery; however, the condition was not misdiagnosed with SAH. Conclusion: In cases of CSDH, there is a possibility that CT demonstrates a pseudo-SAH sign. In such cases, close examinations to exclude true SAH are mandatory.

Subarachnoid hemorrhage (SAH) usually occurs due to aneurysmal rupture of intracranial arteries and its typical computed tomography (CT) findings are increased attenuation of cisterns and subarachnoid spaces. However, several CT findings mimicking SAH are feasible in diverse conditions. They are so-called as pseudo-SAH, and this report is a case of pseudo-SAH which is misdiagnosed as aneurysm rupture accompanied by bilateral chronic subdural hematoma (cSDH). A 42-year-old male with severe headache visited our institute. Non-contrast brain CT images showed increased attenuation on basal cistern, and cSDH on both fronto-temporo-parietal convexity with midline shifting. Trans-femoral cerebral angiography was done and we confirmed small aneurysm at right M1 portion of middle cerebral artery. Under diagnosis of SAH, we planned an operation in order to clip aneurysmal neck and remove cSDH. cSDH was removed as planned, however, there was no SAH and we also couldn't find the rupture point of aneurysm. Serial follow-up CT showed mild cumulative cSDH recurrence, but the patient was tolerant and had no neurologic deficit during hospitalization. We have checked the patient via out-patient department for 6 months, there are no significant changes in volume and density of cSDH and the patient also have no neurologic complications.