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14.2 MRI and CT/MR Perfusion

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ABIM Neurocritical Care Subspecialty Certification Exam

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1 Introduction & Exam Overview

1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide

2 ICU Neurologic Exam, Cerebral Physiology, and CSF

2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology

3 Core Neuropharmacology

3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes

4 Reperfusion Drugs, Airway, and Ventilation

4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation

5 Hemodynamics and Shock

5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock

6 Nutrition, Temperature, and ICU Prophylaxis

6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)

7 General Trauma

7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation

8 Pulmonary Critical Care

8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)

9 Cardiovascular Critical Care

9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound

10 Renal and Infectious Disease

10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed

11 Endocrine and Salt-Water Disorders

11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)

12 Gastrointestinal Critical Care

12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)

13 Hematologic Disorders

13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)

14 Neuroimaging

14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography

15 EEG, EMG, and CSF Analysis

15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)

16 ICP, TCD, and Multimodality Monitoring

16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)

17 Brain Death and Bedside Procedures

17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)

18 Coma, Anoxia, and Intracranial Hypertension

18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)

19 Acute Ischemic Stroke

19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)

20 Intraparenchymal Hemorrhage

20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)

21 SAH, CVST, and Spinal Cord Infarction

21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)

22 Vascular Anomalies and Traumatic Brain Injury

22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)

23 Spine, Hydrocephalus, and CNS Infection

23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)

24 Seizures and Neuromuscular Emergencies

24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)

25 Inflammatory Disease, Neuro-Oncology, and Special Populations

25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)

26 Neurosurgical and Perioperative Complications

26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)

27 Ethics, Prognostication, and Organ Donation

27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)

14.2 MRI and CT/MR Perfusion

Key Takeaways Explain This Topic AI

Hyperacute infarct is DWI hyperintense and ADC hypointense; T2 shine-through is bright on both DWI and ADC and is not true restriction.

GRE/SWI (T2*) blooms blood products and is the MRI screen for hemorrhage and microbleeds; T2 and FLAIR show vasogenic and established cytotoxic edema later than DWI.

CT and MR perfusion separate core (very low CBF and CBV) from penumbra (Tmax delay with relatively preserved CBV).

DEFUSE-3 style imaging mismatch is core volume ≤70 mL, mismatch ratio ≥1.8, and mismatch volume ≥15 mL; this section teaches the maps, not the full thrombectomy protocol.

MRI is superior to CT in the posterior fossa; unsafe ferromagnetic devices, an unstable patient who cannot lie flat, and time-critical NCCT/CTA/CTP protocols are the usual reasons MRI is not first.

Last updated: September 2026

MRI and CT/MR Perfusion

Quick Answer: DWI bright plus ADC dark = cytotoxic restriction (hyperacute infarct). FLAIR and T2 show edema later. GRE/SWI bloom blood. CTP/MRP split core (collapsed CBF/CBV) from penumbra ( Tmax delay). DEFUSE-3 style mismatch is core ≤70 mL and ratio ≥1.8 —an imaging concept, not this guide’s stroke-treatment chapter. MRI beats CT in the posterior fossa . Skip the magnet if the device is unsafe, the patient is crashing, or a faster CT stroke protocol is the clock you have.

Independent ExamFinch teaching in this section covers MRI and CT/MR perfusion listed under Diagnostic studies and procedural skills in the ABPN Content Specifications (02.A.2–3). This guide is not an ABIM or ABPN product.

Sequence toolkit in the neuro ICU

You do not order a generic MRI. You order a question . Each contrast mechanism answers a different one.

  • Sequence What is bright / dark ICU job
  • T1 Fat and subacute methemoglobin bright; CSF dark Anatomy, subacute blood, contrast post-gadolinium
  • T2 Water/CSF and established edema bright Vasogenic edema, chronic infarct, cysts
  • FLAIR T2 contrast with CSF suppressed Cortical/subarachnoid signal, gliosis, DWI–FLAIR mismatch
  • DWI Restricted water bright Hyperacute ischemia, pus, some highly cellular tumors
  • ADC map True restriction dark Confirms that DWI brightness is not T2 shine-through
  • GRE / T2 * Blood, calcium, air bloom dark Hemorrhage, microbleeds, DAI shear
  • SWI Even more bloom than GRE Microbleeds, cortical veins, CVST susceptibility

Bold the ADC. A stroke stem that says DWI bright without ADC is incomplete. True restriction is DWI hyperintense and ADC hypointense. T2 shine-through (chronic infarct, some vasogenic edema) is bright on DWI and bright or normal on ADC. Treat shine-through as old water, not as a new core.

DWI/ADC in hyperacute ischemia

Cytotoxic edema slows water diffusion within minutes . DWI can be positive by about 30 minutes from onset, far earlier than NCCT hypodensity or T2 change. That is why the previous section said a normal 90-minute CT does not exclude infarct.

Worked example: last seen well 70 minutes ago, NIHSS 14, NCCT ASPECTS 10. DWI shows a bright left insula and ADC is dark in the same pixels. That is hyperacute MCA ischemia , not a chronic leukoaraiosis patch (chronic patches are T2/FLAIR bright with high ADC).

FLAIR often remains nearly normal in the first ~4.5 hours . A DWI-positive, FLAIR-negative pattern is the imaging idea behind unknown-onset / wake-up protocols (WAKE-UP used DWI–FLAIR mismatch). FLAIR-positive cortex in the same territory means the infarct is old enough to have accumulated T2 water—useful chronology, still not a full treatment algorithm.

DWI is not exclusive to arterial infarct. Abscess , Creutzfeldt–Jakob , seizure-related cortical change, hypoglycemia , and highly cellular tumor can restrict. Clinical context and ADC extent keep you from calling every bright DWI a candidate for lytics.

T2 edema versus GRE/SWI blood

T2 (and FLAIR) show edema : vasogenic (tumor, abscess, PRES—bright T2, facilitated ADC) versus cytotoxic (infarct—bright T2 later, restricted ADC early). Mass effect from T2-bright swelling in a malignant MCA infarct is how you anticipate herniation, but the earliest infarct signature remains DWI, not T2.

Gradient recalled echo (GRE) and susceptibility-weighted imaging (SWI) are the MRI blood sequences. Paramagnetic blood products distort the local field and bloom . SWI is more sensitive than GRE for microbleeds , diffuse axonal injury shear hemorrhages at the gray–white junction and corpus callosum, and the susceptibility vessel sign of thrombus. A CT-negative, MRI-positive convexity SAH or a field of amyloid microbleeds is an SWI diagnosis.

Blood on conventional T1/T2 follows hemoglobin state (oxy → deoxy → intra- then extracellular methemoglobin → hemosiderin). For ICU decision-making, remember the practical ends: GRE/SWI dark bloom for acute and chronic blood products, T1 bright for subacute methemoglobin, T2 dark rim for chronic hemosiderin. Do not use a non-contrast T1-only survey as your hemorrhage screen.

Posterior fossa: MRI’s home field

CT beam-hardening through the petrous bones hides the brainstem, middle cerebellar peduncles, and fourth ventricle. A lateral medullary or small pontine infarct that will declare itself as an NIHSS of 3 and an aspiration risk can be CT-negative and DWI-positive . Cerebellar infarct that will swell at 48–72 hours is likewise more honest on MRI. If the stem is vertigo, crossed findings, or a “normal CT, still can’t walk,” the imaging answer is MRI with DWI, not a third NCCT.

Contraindications: device, instability, time

MRI is the wrong first test when any of the following dominate:

Barrier Why it matters What you do instead

Unsafe ferromagnetic device Torque, heating, or malfunction (older pacemakers, some aneurysm clips, orbital metal, certain pumps) NCCT ± CTA/CTP; involve MRI safety for labeled MRI-conditional hardware

Physiologic instability Long acquisition, limited pumps, difficult airway access, ICP crisis Resuscitate and use CT; do not park a herniating patient in the magnet

Time Door-to-image in code stroke is measured in minutes Many centers run NCCT/CTA/CTP as the primary hyperacute pathway

  • Agitation without a safe anesthetic plan Motion ruins DWI and perfusion CT, or MRI only after airway control
  • Programmable shunt Magnet may change the setting Recheck and reprogram after MRI

Gadolinium is unnecessary for DWI diagnosis of infarct. If contrast MRI is required in advanced CKD, prefer group II agents; NSF is the group I / very low GFR story. Pregnancy is a “need-to-know” conversation, not a default contrast MRI.

CT and MR perfusion: core versus penumbra

CT perfusion (CTP) tracks an iodinated bolus with repeated cine CT and builds time–density curves. MR perfusion (MRP) most often uses dynamic susceptibility contrast after gadolinium; arterial spin labeling (ASL) can estimate CBF without contrast. Both try to separate tissue that is already dead from tissue that is ischemic but still salvageable.

  • Parameter Abbreviation Penumbra-style pattern Core-style pattern
  • Cerebral blood flow CBF Reduced but not collapsed Severely reduced
  • Cerebral blood volume CBV Relatively preserved (vasodilation) Collapsed
  • Mean transit time MTT Prolonged Prolonged

Time to maximum of the residue function Tmax Tmax >6 s is the usual at-risk threshold on RAPID-type maps Delay plus dead tissue on CBF

Time to peak TTP Delayed Delayed

Operational definitions used on automated CTP maps (RAPID and similar) commonly call core the volume with relative CBF <30% of contralateral brain, and hypoperfusion / penumbra the volume with Tmax >6 seconds . Mismatch volume is hypoperfusion minus core. Mismatch ratio is hypoperfusion volume divided by core volume.

Pitfalls: very early CTP can overestimate core (ghost core). Seizure, chronic stenosis, and poor cardiac output scramble maps. Tiny cores with huge delays still need a vessel occlusion on CTA/MRA to make physiologic sense. Perfusion is a selection tool , not a stand-alone diagnosis of stroke.

Loading diagram... Perfusion core, penumbra, and DEFUSE-3 style mismatch

Example CTP volumes that meet DEFUSE-3 style mismatch (mL)

DEFUSE-3 style mismatch, conceptually

DEFUSE-3 (Albers et al., NEJM 2018) tested endovascular therapy 6–16 hours after last known well in anterior-circulation large-vessel occlusion using perfusion imaging. The imaging profile that defined a favorable mismatch was:

  • Ischemic core ≤70 mL
  • Mismatch ratio ≥1.8 (Tmax >6 s volume / core)
  • Mismatch volume ≥15 mL

Worked example: core 22 mL, Tmax >6 s volume 95 mL. Mismatch volume = 95 − 22 = 73 mL . Ratio = 95 / 22 ≈ 4.3 . That is a favorable imaging mismatch on DEFUSE-3 rules. A core of 95 mL with Tmax volume 110 mL (ratio 1.16) is not.

DAWN used a different idea: clinical–core mismatch (NIHSS versus core volume, with age bands) out to 24 hours . You will meet both trials in the acute ischemic stroke chapter. This section’s job is to read the maps: small core, large Tmax lesion, ratio at least 1.8. Do not turn this chapter into a thrombectomy consent lecture, and do not quote DEFUSE-3 thresholds for a cerebellar perforator with no vessel imaging.

Malignant profile teaching: a huge core with little penumbra means little to salvage and more reperfusion hemorrhage risk. Large-core thrombectomy trials exist and are a treatment-chapter nuance; they do not erase the need to measure core and penumbra honestly.

Putting MRI and perfusion next to CT

  • Question Faster CT pathway MRI pathway
  • Is there blood or herniation right now? NCCT GRE/SWI if CT is equivocal and the patient is stable
  • Is there hyperacute ischemia? Often still occult on NCCT; CTP core as a surrogate DWI/ADC
  • Is there salvageable tissue? CTP (Tmax, rCBF) MRP or DWI versus perfusion
  • Brainstem / cerebellum? CT often inadequate MRI with DWI
  • Microbleeds, DAI? CT insensitive SWI

If GFR is low, DWI and TOF MRA still work without iodine or gadolinium. CTP is an iodine bolus; MRP is usually a gadolinium bolus. Choose the contrast that the kidneys and the clock can tolerate.

  • Exam-style traps
  • Calling DWI-bright, ADC-bright tissue an acute core (that is shine-through)
  • Using T2 without DWI as the hyperacute stroke sequence
  • Sending an MRI-unsafe pacemaker or an actively herniating patient to the magnet as first imaging
  • Equating any Tmax delay with core

Treating DEFUSE-3 numbers as if this were the mechanical thrombectomy chapter rather than an imaging-selection concept

Trusting CT over MRI for a crossed brainstem syndrome

Independent practice items at /practice/abim-neurocritical-care are a study bank for this reasoning, not the computer-based examination administered by ABPN.