Subarachnoid hemorrhage

Differential diagnosis
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By Alejandro Hornik MD and James R Brorson MD

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:

  • Age of 40 years or more
  • Neck pain or stiffness
  • Witnessed loss of consciousness
  • Onset during exertion
  • Thunderclap headache (defined as instantly peaking pain)
  • Limited neck flexion on examination

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:

Thunderclap headache.

  • Cerebral venous sinus thrombosis: associated with focal deficits and seizures. Neuroimaging often shows characteristic features. MR and/or CT venography can confirm the diagnosis.
  • Benign coital headache: diagnosis of exclusion is based on history and physical exam.
  • Idiopathic thunderclap headache: diagnosis of exclusion is based on history and physical exam.
  • Reversible cerebral vasoconstriction: associated with focal deficits. Vascular imaging shows vasoconstriction on large- to mid-size cerebral arteries.
  • Sentinel headache: associated with expanding and possibly leaking saccular aneurysms.
  • Craniocervical arterial dissection: characteristic headache location and focal deficits depending on vascular territory.
  • Pituitary apoplexy: visual field abnormalities and possible panhypopituitarism.
  • Trigeminal cephalalgias: characteristic syndromic presentation.
  • Worsening migraine: diagnosis of exclusion based on history and physical exam.

Headache, altered mental status, and meningismus.

  • Meningitis: look for fever and other signs of infection. Lumbar puncture results can verify the diagnosis.

(1) Infectious
(2) Noninfectious: chemical, neoplastic

  • Parenchymal hematoma: focal deficits and signs of intracranial hypertension.
  • Extra-axial hematomas: focal deficits, seizures, and signs of intracranial hypertension.
  • Vasculitis: angiographic changes leading to leptomeningeal biopsy, most often subacute course.
  • Basilar migraine: posterior circulation deficits, normal angiogram and neuroimaging.
  • Idiopathic intracranial hypertension: transient visual obscurations, postural variability of deficits, progressive visual loss.

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).

In This Article

Historical note and nomenclature
Clinical manifestations
Clinical vignette
Pathogenesis and pathophysiology
Differential diagnosis
Diagnostic workup
References cited