Headache, the primary symptom of subarachnoid hemorrhage, is a common presenting complaint in office and emergency room settings, but only a small fraction of patients with headache have a subarachnoid hemorrhage, creating a diagnostic challenge. In a multicenter study of 10 university-affiliated emergency departments, among alert and oriented patients with nontraumatic headache peaking in intensity within 1 hour of onset, exclusion of patients with 3 or more similar previous recurrent headaches as well as those with other known causes for headache resulted in a 6.2% rate of confirmed subarachnoid hemorrhage (Perry et al 2013). A selection rule was applied to this population, calling for diagnostic investigation in patients with new severe headache and any of the following high-risk variables:
This rule, termed the “Ottawa subarachnoid hemorrhage rule,” resulted in a very high sensitivity (100%) and modest specificity (15.3%) in this selected population of headache patients (Perry et al 2013). The low specificity points to the common clinical features shared by a number of other conditions that can mimic subarachnoid hemorrhage.
The differential diagnosis of spontaneous subarachnoid hemorrhage can be organized based on the presenting symptoms, the clinical setting, and the appearance of neuroimaging, as outlined below:
Headache, altered mental status, and meningismus.
(2) Noninfectious: chemical, neoplastic
Traumatic subarachnoid hemorrhage. Traumatic subarachnoid hemorrhage is usually recognized with a clear history of trauma. It typically affects the cerebral convexities and is often accompanied by other signs of injury such as orbital frontal contusions, skull fracture, or external scalp trauma.
Pseudo-subarachnoid hemorrhage. Pseudo-subarachnoid hemorrhage is defined as increased density of the basal cisterns and subarachnoid spaces on computed tomography, not due to blood products. This phenomenon has been identified in a number of conditions besides subarachnoid hemorrhage, including pyogenic leptomeningitis, intrathecal administration of contrast material, high-dose intravenous contrast, and diffuse cerebral edema (Spiegel et al 1986; Mendelsohn et al 1994; Eckel et al 1998; Given et al 2003).