Imaging in Stroke: A comprehensive review

Introduction

There are two categories of stroke:

1. Ischemic

   1. Thrombotic

   2. Embolic

2. Hemorrhagic

   
   

Each type of stroke presents with different patterns on imaging.

Risk factors for ischemic stroke	Risk factors for hemorrhagic stroke
Atherosclerosis Hypertension High cholesterol Smoking DM	Hypertension Aneurysm rupture Anticoagulants Trauma

“Time is brain” - emphasizes the importance of providing immediate medical treatment to stroke patients (González, 2012), which is mainly informed by neuroimaging.

The ‘Four P's’ - parenchyma, pipes, perfusion and penumbra – describes the aim of stroke imaging (Rudkin et al., 2018; Rowley, 2001).

Role of imaging in stroke

In most clinical settings, CT is the first line of imaging. However Diffusion weighted MR imaging (DWI) is vastly superior in early ischemic stroke.

In early onset of symptoms, the role of CT is to rule out hemorrhagic stroke, so that prompt thrombolytic therapy can be provided.

The main purpose of these neuroimaging is to locate the affected vascular region of a stroke patient's brain, the infarct core and the penumbra, as it is very important to know an infarct's location to minimize the severity of a stroke by using the most appropriate treatment.

Role of CT in stroke

Primary role of CT in hyperacute stroke is to rule out hemorrhage.

Many times early ischemic stroke is not visible or CT, or the findings can be so subtle that is easily missed on CT.

Hence, a normal CT does not rule out early ischemic stroke.

Imaging features of Ischemic stroke on CT:

Hyperacute phase (0-24 hrs):

• Hyperdense vessel sign: one of the earliest signs that can be visible on non contrast CT.

  
  

• 0-3 hrs: usually thr infarct is not visible on CT in early hyperacute phase.

  
  

• <6 hrs: Loss of grey-white junction.

  • This phenomenon occurs due to cytotoxic edema in the grey matter - leading to its hypo attenuation.

    
    

Acute phase (24 hrs to 1 week):

Hypo attenuation and swelling become more pronounced

↓

Edema may produce significant mass effect

↓

Seen in the form of effaced sulci, cisterns or the ventricles

• Edema peaks around 4-7 days from the onset.

Subacute phase (1 week to 3 weeks):

• Edema begins to subside.

  
  

• The ‘Fogging effect’:

  There comes a phase during the evolution of infarct, where the hypodense infarcted cortex becomes normal or near normal in attenuation - causing the lesion to temporarily disappear.

  1. It is believed to result from several histopathological changes, including decreased bulk edema fluid, proliferation of capillaries in the infarcted area, and infiltration by lipid-laden macrophages which clean up the necrotic tissue

  2. The decrease in bulk water due to resolving edema combined with increased cellular and capillary density leads to the temporary normalization of density.

  3. Eventually, the infarct area becomes hypodense again with the development of encephalomalacia and volume loss in the chronic stage.

     (reference)

Chronic phase (>3 weeks):

• Gliosis and encephalomalacia develop → appear as low density areas

  1. Negative mass effect → cause ex vacuo dilatation of ventricles.

References:

1. Rudkin, Scott & Cerejo, Russell & Tayal, Ashis & Goldberg, Michael. (2018). Imaging of acute ischemic stroke. Emergency Radiology. 25. 10.1007/s10140-018-1623-x.

2. https://doi.org/10.1212/WNL.55.2.315