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. 2016 Oct 31;10(10):1–6. doi: 10.3941/jrcr.v10i10.2653

Table 2.

Differential diagnosis of Acute-Onset Slurred Speech and Weakness.

Diagnosis Catheter Angiography CT Angiography MR Perfusion + DWI MR Perfusion + DWI + SWI
Occlusive Carotid Artery Dissection Vascular wall abnormality with arterial filling defect, classically flame shaped, and absent distal vessels Filling defect in the affected vessel, classically flame shaped, with distal hypodensity Reversible ischemia: DWI/PWI mismatch; restriction of cerebral blood flow, cerebral blood volume, and increase time to peak flow in the area of reversible ischemia without diffusion restriction
Irreversible ischemia: No DWI/PWI mismatch; restriction of cerebral blood flow, cerebral blood volume, and increase time to peak flow in the area of reversible ischemia with diffusion restriction
Stage I hemodynamic failure: DWI/PWI mismatch without increased prominence of the venous vasculature
Stage II hemodynamic failure (misery perfusion): Increased prominence of the venous vasculature in the area of DWI/PWI mismatch
Irreversible ischemia: Diffusion restriction with decreased blood flow (no DWI/PWI mismatch), and prominence of the venous vasculature on SWI
Non-Hemodynamically Significant (<50–70% Occlusive) Carotid Artery Dissection Vascular wall abnormality with arterial filling defect and normally visualized vessels distally Vascular wall abnormality in the affected vessel with distal contrast opacification Normal cerebral blood flow, cerebral blood volume, and time to peak flow, without diffusion restriction No diffusion restriction or decreased cerebral blood flow
Acute intracranial vasculature thromboembolic occlusion No vascular wall abnormality proximally, with arterial filling defect with absent distal vessels at the site of thromboembolic occlusion. Early (<1hr): normal findings
Late (>1hr):
CT Angiogram: hypodense findings in the distribution of the affected vessel
Noncontrast CT: Hyperdense lesion in affected artery representing acute thrombus
Decreased cerebral blood flow, variable cerebral blood volume, and increased time to peak flow on PWI, with diffusion restriction in the area of the infarct and DWI/PWI mismatch in the at-risk tissue of the penumbra Stage I hemodynamic failure: DWI/PWI mismatch without increased prominence of the venous vasculature
Stage II hemodynamic failure (misery perfusion): Increased prominence of the venous vasculature in the area of DWI/PWI mismatch
Irreversible ischemia: Diffusion restriction with decreased blood flow (no DWI/PWI mismatch), and prominence of the venous vasculature on SWI

This assumes poor collateral flow in the setting of an incomplete circle of Willis. In the setting of adequate collateral flow, no change in perfusion parameters or diffusion characteristics will be seen on MRI.