The pathophysiology of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is complex and is not entirely understood. Mechanistic insights have been gained through advances in the capabilities of diagnostic imaging. Core techniques have focused on the assessment of vessel caliber, tissue metabolism, and/or regional perfusion parameters. Advances in imaging have provided clinicians with a multifaceted approach to assist in the detection of cerebral vasospasm and the diagnosis of delayed ischemic neurologic deficits (DIND). However, a single test or algorithm with broad efficacy remains elusive. This paper examines both anatomical and physiological imaging modalities applicable to post-SAH vasospasm and offers a historical background. We consider cerebral blood flow velocities measured by Transcranial Doppler Ultrasonography (TCD). Structural imaging techniques, including catheter-based Digital Subtraction Angiography (DSA), CT Angiography (CTA), and MR Angiography (MRA), are reviewed. We examine physiologic assessment by PET, HMPAO SPECT, 133Xe Clearance, Xenon-Enhanced CT (Xe/CT), Perfusion CT (PCT), and Diffusion-Weighted/MR Perfusion Imaging. Comparative advantages and limitations are discussed.

A 15-year-old male high school football player presented with episodes of headache and complete body stiffness, especially in the arms, lower back, and thighs, immediately following a football game. This was accompanied by severe nausea and vomiting for several days. Viral meningitis was suspected by the primary clinician, and treatment with corticosteroids was initiated. Over the next several weeks, there was gradual symptom improvement and the patient returned to his baseline clinical status. The patient experienced a severe recurrence of the previous myriad of symptoms following a subsequent football game, without an obvious isolated traumatic episode. In addition, he experienced a new left sided headache, fatigue, and difficulty ambulating. He was admitted and an extensive workup was performed. CT and MRI of the head revealed concurrent intracranial and spinal subdural hematomas (SDH). Clinical workup did not reveal any evidence of coagulopathy or predisposing vascular lesions. Spinal SDH is an uncommon condition whose concurrence with intracranial SDH is an even greater clinical rarity. We suggest that our case represents an acute on chronic intracranial SDH with rebleeding, membrane rupture, and symptomatic redistribution of hematoma to the spinal subdural space.

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