• MR imaging is based on the behavior of atoms (most often – H, P, and Na) in the magnetic field
  • structures generating low signals are hypointense; structures generating high signals are hyperintense; tissues producing no signal are dark (blood, calcifications)
  • advantages over CT
    • high contrast and resolution, good visualization of pathologies in the posterior fossa
    • possibility of imaging in any plane (coronal, sagittal, oblique) and 3D reconstruction
    • possibility of non-contrast imaging of the cerebral arteries; to depict extracranial arteries, a contrast agent should be used
    • significant improvement in the acute stroke diagnosis using DWI, PWI, SWI, and GRE sequences
  • disadvantages of MRI compared to CT
    • higher costs and longer duration of the examination
    • difficulties with ventilated patients (MRI-compatible respirator must be available)
    • young children and uncooperative patients must be sedated or examined under general anesthesia – the risk of movement artifacts is substantial
    • more MRI contraindications

Magnetic Resonance Imaging modalities



T1C+ (contrast-enhanced)

T1 fat suppressed

T1 fat-supressed sequence showing lipoma

T1C+ fat suppressed



T2 sequence with bright CSF




Cortical cerebral microbleeds and lobar hematomas in patient with cerebral amyloid angiopathy


Cerebral microbleeds on SWI (mixed pattern)


Acute ischema on DWI


ADC map

Diffusion tensor imaging (DTI) tractography

diffusion tensor imaging (DTI tractography
Flow sequences

CSF flow studies

CSF flow study
MR angiography

Bright blood

Non-contrast MRA (TOF)


MR venography (TOF)

MR venography (TOF)

Contrast-enhanced MRA

Contrast-enhanced MR angiography

Dark blood

Fast Spin Echo (FSE) Black Blood MRA

FSE dark blood MRA

Inversion Recovery (IR) Black Blood MRA

Susceptibility-weighted (SW) Black Blood MRI

SWI angiography
Vessel wall imaging

T1C+ black blood

Demonstration of ICA vasculitis using post-contrast high resolution MRI (HRMRI) (Obuses, 2014)


Perfusion weighted images (PWI)


Arterial Spin Labeling (ASL)


MR spectroscopy (MRS)
Basic MRI sequences (T1, T2, PD)
  • the principle of the method is the detection of T1 and T2 relaxation times (resulting in so-called T1 and T2-weighted images)
  • T1 is used for accurate anatomical imaging
    • water signal is low; fat is hyperintense
    • T1 signal is stronger when the relaxation time is shortened (e.g., due to the contrast agent) → T1C+
      • high-resolution MR T1 C+ dark blood sequence (see below) can be used to detect vasculitis  Vasculitis on MR T1C+ black blood sequence
    • fat suppression → see here
      • CHESS (Fat-Sat)
      • STIR
  • T2 – better detection of lesions containing more water
    • FLAIR sequence is used for water suppression (the CSF is dark and periventricular lesions can be better distinguished)
    • CHESS (Fat-Sat) is used to suppress fat
  • PD (proton density) – image quality depends on the density of hydrogen protons in the tissues. Compared to other sequences, it is less useful in CNS diagnostics
Magnetic resonance imaging (MRI)
bone, calcifications
water, CSF
gadolinium bright bright
air dark dark dark
Diffusion-weighted images (DWI)
  • DWI visualizes impaired (restricted) diffusion of water molecules (or protons) caused by the energetic failure of Na+/K+ membrane pumps
  • it is highly sensitive and specific (88-100%) for detecting acute cerebral infarction within minutes of its onset, with a maximum of 4-6 hours
  • acute ischemia appears hyperintense (bright) on DWI (b factor around 1000 s/mm2) and hypointense (dark) on calculated ADC (apparent diffusion coefficient) maps
    • ADC <620×10-3 mm/s is likely to identify ischemia
    • after recanalization, there is often an increase of signal on ADC maps in the ischemic area  (visible on DWI and FLAIR)    After recanalization, there is often an increase in ADC at the site of ischemia (visible on both DWI and FLAIR) [Albers]
  • DWI changes are not specific to ischemia – they can occur in any transport mechanisms impairment (edema). Such changes are often reversible, and lesions are not hypointense in the ADC map)
  • artifacts – DWI depends on the T2 signal
    • increased T2 signal can lead to T2 shine through and T2 washout   
    • reduced T2 signal leads to the T2 blackout phenomenon (hypointense DWI)
MR DWI in stroke
Corpus callosum infarction and intraventricular hemorrhage
Perfusion-weighted images (PWI)
  • PWI provides information about the current blood supply to the brain tissue
  • after bolus administration of gadolinium-based contrast agent (GBCA); the same parameters as for CT perfusion (CBV, CBF, MTT, TTP) can be obtained
  • tissue with impaired perfusion (↑ MTT) comprises infarction (core, approx. corresponding to DWI lesion), penumbra and also the area of benign oligemia. The difference between the area of  impaired perfusion and diffusion  approximately determines the size of the penumbra (PWI/DWI mismatch)
PWI-DWI mismatch
Gradient-echo sequence (GRE)
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Susceptibility-weighted images (SWI)
  • acute thrombus detection Distal MCA thrombus on MR SWI
    • thrombus is hypointense on MR SWI (deoxyhemoglobin)
    • high sensitivity to detect thrombi in distal segments (unlike MRA)
  • detection of venous thrombosis
    • hypointense signal in affected veins and vessels
    • stasis and enlargement of the surrounding veins  Thrombosis of the left transverse sinusu with the dilatation of surrounding the veins (left image). Normalization after successful recanalization (right image)
  • prediction of hemorrhagic transformation
    • detection of cerebral microbleeds – up to 6x more sensitive than conventional gradient sequences (their presence increases the risk of bleeding during thrombolysis or anticoagulation therapy)   Cerebral microbleeds on SWI (mixed pattern)
    • early detection of hemorrhagic transformation (higher sensitivity compared to CT and MR GRE)
Arterial Spin Labeling (ASL)
  • ASL uses water in arterial blood as an endogenous contrast agent
  • enables non-invasive perfusion imaging with the creation of CBF maps
  • ASL seems to overestimate perfusion lesion compared to PWI
  • useful in these indications:
    • acute stroke/TIA
    • chronic cerebrovascular diseases 
    • degenerative diseases (AD, FTD)
    • brain tumors
    • migraine (hyperperfusion) Migraine attack with hyperperfusion on MRI ASL
    • posterior reversible encephalopathy (PRES) Subacute PRES (MR ASL)
Contrast-enhanced MRI
  • contrast agents depict or enhance structures poorly visible in the non-enhanced images Gadolinium-based contrast agents (GBCAs) enhance pathological lesions on MRI
  • contrast agents facilitate proton relaxation, thus shortening the T1 and T2 relaxation times. Shortening the T1 relaxation time leads to enhancement of the T1-weighted image, whereas T2 leads to its attenuation
  • contrast agents can be divided into paramagnetic and super-paramagnetic agents
    • paramagnetic substances amplify the magnetic field, which causes a shortening of the relaxation time. They have a wide range of applications and are often used in CNS examinations because they can penetrate damaged HEB – Magnevist (gadopentetate), Omniscan (gadodiamide), Dotarem (Gd-DOTA, gadoteric acid)
    • super-paramagnetic agents are solid substances that are introduced into the body as suspensions and are highly effective

MRI and acute stroke diagnosis

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MRI angiography (MRA)

MRA techniques

Dark Blood MRA → see here
(vascular imaging strategy where the signal from flowing blood is suppressed – rendering it “black”)

  • Fast Spin Echo (FSE) Black Blood MRA
  • Inversion Recovery (IR) Black Blood MRA
  • Susceptibility-weighted (SW) Black Blood MRI

Bright Blood MRA

  • Contrast-enhanced MRA
  • Non-contrast MRA
    • Time-of-Flight (TOF)
    • Phase-contrast (PC)
    • Steady-state Free Precession (SSFP)
    • Fast Spin Echo (FSE)
    • Arterial Spin Labeling (ASL)

MRA applications

Intracranial arteries

  • TOF (Time Of Flight) method, without contrast agent administration MRA 3D TOF
    • evaluates only flow, false-positive findings are common
    • sufficient to show occlusions/stenoses of major arteries   MCA stenosis on MRA (M1 segment)  TOF showing right PCA occlusion (green arrow) and right MCA stenosis (red arrow)
    • low sensitivity for peripheral occlusions
  • SWI dark blood sequence detects thrombi thanks to blooming artifact MCA thrombus on MR SWI
  • T1C+ dark blood sequence helps to detect inflammatory changes in the vessel wall  Demonstration of ICA vasculitis using post-contrast high resolution MRI (HRMRI) (Obuses, 2014) Vasculitis on T1C+ black blood sequence

Extracranial arteries

  • contrast-enhanced MRA (CE-MRA) for extracerebral vessels  Carotid artery stenoses on MRA
  • the stenosis should be measured according to NASCET criteria
  • MRA may overestimate stenosis compared to DSA (pseudo-occlusion)

MR venography

ICA stenosis on MRA

MCA occlusion

Transverse sinus thrombosis

MRI and dissection diagnosis

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MRI and intracranial hemorrhage

  • the paramagnetic properties of hemoglobin derivatives are responsible for the MRI signal changes
  • imaging depends on the degree and extent of hemoglobin conversion within  the coagulum (see the table)
    • in the acute stage of hemorrhage, the finding in T1,2 is non-specific
    • later, with the transformation of oxy-hemoglobin to deoxy-hemoglobin (max. day 2), a typical decrease in the T2 signal can be seen
    • in the following days, methemoglobin levels increase, and the lesion becomes hyperintense (mainly in T1 and PD)
    • after approx.  2-4 weeks, a rim of low signal in T2 corresponding to hemosiderin in macrophages appears
  • the gradient echo sequence (GRE) can also detect early bleeding with similar sensitivity to CT. Thus, MRI can be used as an initial imaging method in the acute stroke program Acute ICH and SAH on MR GRE  [Lin, 2001]
    • GRE is more sensitive than CT for detecting old bleeding and is equally liable for detecting hemorrhagic infarction [Renou, 2010]
    • does not differentiate between hemorrhagic infarction and ICH
    • hemorrhage is hyperintense in the hyperacute and late subacute stages, hypointense in the acute, early subacute, and chronic stages [Kang, 2001]
    • mean ADC ratio is  0.70-0.73 in early stages and 2.56 in chronic stages [Kang, 2001]
    • in ischemia, the ADC lesion becomes hyperintense around day 30; with hemorrhage, hypointensity persists for > 100 days [Ebisu, 1997]
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Magnetic Resonance Imaging (MRI)
link: https://www.stroke-manual.com/magnetic-resonance-imaging-mri/