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S t rok e I m a g i n g

Shahmir Kamalian, MD*, Michael H. Lev, MD

KEYWORDS
 Stroke  CT  CT angiography  MR imaging  MR angiography  Intravenous thrombolysis
 Intra-arterial thrombectomy  Endovascular thrombectomy

KEY POINTS
 Abrupt onset of a focal neurologic deficit typically defines the clinical syndrome of stroke.
 Neuroimaging has an essential role in differentiating ischemic from hemorrhagic stroke and guiding
patient selection for intravenous thrombolysis (IVT) and intra-arterial thrombectomy (IAT).
 Obtaining advanced imaging (CTA, DWI) for patient selection for IAT should never delay the admin-
istration of IVT when the patient is otherwise eligible, up to 4.5 hours post ictus.
 The recent DAWN and DEFUSE 3 trial results showed a strong benefit of IAT when performed within
24 hours post ictus, in appropriately selected patients using advanced imaging.

INTRODUCTION embolus (approximately 85%) and with only a


small percentage attributable to global cerebral
It is estimated that 795,000 persons have a stroke hypoperfusion (so-called low-flow or border-zone
each year in the United States, causing 140,000 strokes); global anoxic injury from near-drowning,
deaths.1,2 That said, stroke has moved from the carbon monoxide poisoning, or other causes of
third leading cause of death in 2007 to the fifth in suffocation are also less common. Approximately
2017.1–3 Although major recent advances in neu- 10% of strokes are hemorrhagic resulting from
roimaging and stroke treatment have contributed intracerebral hemorrhage, with 3% being due to
to a decrease in mortality, stroke remains the lead- subarachnoid hemorrhage.1,2
ing cause of serious long-term disability in the Neuroimaging has a central role in the differen-
United States and costs the health care system tial diagnosis of patients with suspected stroke,
an estimated $34 billion each year.1 by differentiating ischemic from hemorrhagic
Abrupt onset of a focal neurologic deficit stroke, identifying other causes of acute neuro-
typically defines the clinical syndrome of stroke, logic deficit (ie, stroke mimics), and helping in
although stroke mimics—which include but are patient selection for intra-arterial thrombectomy
not limited to seizure (20%), syncope (10%– (IAT). An estimated 9% to 30% of patients with
20%), sepsis or hypo-/hyperglycemia (14%), suspected stroke—and 3% to 17% of patients
subdural hematoma or tumor (10%–12%), soma- treated with intravenous tissue plasminogen acti-
tization/anxiety and hyperventilation (5%–10%), vator (IV-tPA)—have stroke mimics.5–14 Current
transient global amnesia, and complex migraine treatment options for acute embolic stroke include
(30%–35%)—have been estimated to occur as IV-tPA, IAT, or a combination of both. Therapeutic
often as 10-fold more frequently as ischemic or options for intracerebral hemorrhage, subarach-
hemorrhagic stroke.4 noid hemorrhage, and stroke mimics vary accord-
Most “true” stroke syndromes are ischemic, ing to the etiology.
with a majority caused by an intracranial, circle Ischemic stroke reflects neuronal dysfunc-
of Willis large vessel occlusion (LVO) from an tion secondary to hypo-oxygenation and can be
radiologic.theclinics.com

Conflicts of Interest: S. Kamalian: None. M.H. Lev: Consultant for Takeda Pharm, GE Healthcare; institutional
support for Siemens postprocessing software license.
Department of Radiology, Division of Emergency Radiology, Massachusetts General Hospital, Harvard Medical
School, 55 Fruit Street, Blake SB Room 29A, Boston, MA 02114, USA
* Corresponding author.
E-mail address: skamalian@mgh.harvard.edu

Radiol Clin N Am 57 (2019) 717–732


https://doi.org/10.1016/j.rcl.2019.02.001
0033-8389/19/Ó 2019 Elsevier Inc. All rights reserved.

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