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CT Head: Principles, Basics, Evaluation & Clinical Correlation

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1. Historical Background & Introduction

• Low cost relative to MRI
• Rapidly acquired (5–10 seconds for a basic scan)
• Relatively low radiation dose
• Capable of rapid identification of haemorrhage, hydrocephalus, and herniation — all potentially treatable neurosurgical emergencies
• The key technique for differentiating ischaemic stroke from haemorrhage
• Feasible in medically unstable patients receiving active resuscitation

• Slip-ring technology (1980s): Continuous tube rotation; 1 second/image; enabled helical CTA
• Multidetector CT (MDCT, late 1990s): 64–320 detector rows; sub-0.3 second rotation; truly isometric voxels; high-quality multiplanar reconstructions

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2. Basic Principles of CT

Detector System

• A scintillator absorbs x-rays → converts to visible light → photodiode → electrical signal → image
• Modern MDCTs use 64, 128, or 320 parallel detector rows simultaneously

Scanning Parameters

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3. Hounsfield Units (HU) — The Language of CT

HU Reference Values for Neuroimaging

Hyperdense = higher HU than brain (bright) — e.g. acute blood, calcification, contrast
Isodense = same HU as brain (may be hard to see)
Hypodense = lower HU than brain (dark) — e.g. oedema, infarct, CSF

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4. Window Settings — How to Customise the Image

• Window Width (WW): The range of HUs displayed — wide = less contrast; narrow = more contrast
• Window Level (WL): The centre of the displayed range

Standard Window Presets

Tip: Small extra-axial haemorrhages — especially in the posterior fossa — can be occult on standard brain windows but visible on subdural/blood window settings (Fig. 54.2 in Grainger & Allison).

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5. Indications for CT Head

Emergency / Acute Indications

• Head trauma — most frequent indication; replaced skull X-ray
• Acute stroke — differentiates ischaemia from haemorrhage; combined with CTA (aortic arch to skull vertex)
• Suspected subarachnoid haemorrhage (SAH) — thunderclap headache
• New-onset seizure / altered consciousness
• Acute headache — rule out haemorrhage, raised ICP
• Suspected meningitis/encephalitis — pre-lumbar puncture screening
• Hydrocephalus — shunt assessment

Elective Indications

• Known or suspected intracranial tumour / metastases
• Pre-surgical planning (complex fractures, vascular malformations)
• Follow-up of known pathology
• Dementia workup (structural causes)

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6. Intravenous Contrast

• Characterise known pathology with blood-brain barrier breakdown (tumour, abscess, inflammation)
• CTA for vascular assessment (aneurysm, stenosis, AVM)

Contrast Precautions

• eGFR < 30 mL/min/1.73 m²: Avoid if possible (risk of contrast-induced nephropathy); prehydration if essential
• Known contrast allergy: Premedicate with antihistamines/corticosteroids (though no definite reduction in severe reactions)
• Mild reactions (1 in 10): Flushing, nausea, vomiting, urticaria
• Severe anaphylaxis: ~1 in 100,000
• Hyperthyroidism: Risk of delayed thyrotoxicosis (up to 8 weeks post-contrast)
• Breastfeeding: Can continue after iodinated contrast per most guidelines

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7. Multiplanar Reconstructions

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8. Systematic Approach to Reading a CT Head

Step 1 — Technical Adequacy

• Patient positioning, rotation, motion artefact?
• Correct windows applied?

Step 2 — Skull & Scalp (Bone Window)

• Fractures (linear, depressed, comminuted)
• Scalp swelling/haematoma localises point of impact
• Sutural diastasis
• Intracranial calcifications (pineal, choroid plexus — normal landmarks for midline)

Step 3 — Extra-Axial Spaces

• Epidural space: Biconvex (lenticular) hyperdense collection — bounded by sutures
• Subdural space: Crescent-shaped collection — crosses sutures, conforms to brain surface
• Subarachnoid space: Basal cisterns (suprasellar, perimesencephalic, Sylvian), interhemispheric fissure
• Subgaleal / subperiosteal collections

Step 4 — Brain Parenchyma (Brain Window)

• Grey-white matter differentiation preserved?
• Any focal hypodensity (oedema, infarct) or hyperdensity (haemorrhage, calcification)?
• Basal ganglia, thalami, internal capsule, brainstem

Step 5 — Ventricles and Cisterns

• Size and symmetry of lateral ventricles (temporal horns should be <2 mm normally)
• Third and fourth ventricle
• Hydrocephalus? (obstructive vs. communicating)
• Cisternal effacement = raised ICP

Step 6 — Midline

• Falx cerebri — midline shift? (>5 mm is significant)
• Pineal gland displacement

Step 7 — Posterior Fossa

• Cerebellum, brainstem
• Beam-hardening artefact at petrous apices is a major limitation here — use thin slices

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9. Normal CT Head Anatomy

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10. Artefacts & Limitations

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11. Clinical Correlations with Images

11.1 Acute Ischaemic Stroke

• Loss of grey-white differentiation in MCA territory
• Sulcal effacement
• Hyperdense MCA sign (clot in artery ~70–80 HU)
• "Insular ribbon" sign — loss of normal insular cortex definition

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11.2 Subarachnoid Haemorrhage (SAH)

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11.3 Epidural Haematoma (EDH)

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11.4 Subdural Haematoma (SDH)

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11.5 Intracerebral/Hypertensive Haemorrhage

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11.6 Cerebral Venous Sinus Thrombosis (CVST)

• Hyperdense sinus sign (dense transverse/superior sagittal sinus ~60–70 HU)
• Cord sign — hyperdense cortical vein

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11.7 Haemorrhagic Transformation of Ischaemic Stroke

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11.8 Normal CT vs. Pathology — Quick Reference

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12. Summary: Key Teaching Points

1. HU scale underpins everything — acute blood is hyperdense (50–80 HU); oedema/infarct is hypodense; CSF is ~0 HU
2. Window settings must be adjusted for each clinical question — always apply both brain and bone windows
3. EDH = biconvex, bounded by sutures; SDH = crescent, crosses sutures
4. SAH = blood in basal cisterns — check Sylvian fissures, interhemispheric fissure
5. Early ischaemic stroke may be very subtle — look for loss of grey-white differentiation and sulcal effacement
6. Posterior fossa is a blind spot on CT — use thin slices and multiplanar reformats
7. Coronal reformats are essential for vertex/tentorial haemorrhage and herniation syndromes
8. Always review bone windows for fractures, even if clinical question is vascular

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MRI Head — Complete PG Resident Notes

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SECTION 1 — BASICS & PHYSICS

1.1 What is MRI?

• Noninvasive diagnostic technique using nonionising electromagnetic radiation — NO X-ray, NO radiation dose
• Uses a powerful superconducting magnet + radiofrequency (RF) pulses + magnetic field gradients
• Images the distribution of hydrogen nuclei (protons) in water and lipids
• Superior soft-tissue contrast compared to CT
• Scan time: 10 min (simple brain) to >60 min (complex protocol with contrast)
• Disadvantages: longer scan time, higher cost, limited availability, multiple contraindications

1.2 Historical Landmarks

1.3 How MRI Works — Step by Step

• Patient placed in static magnetic field (B₀)
• Proton spins align parallel or antiparallel to B₀ (slight excess parallel → net magnetisation M in z-direction)

• RF pulse flips M into the transverse (x/y) plane
• Protons precess in phase → generate a Free Induction Decay (FID) signal

• After RF pulse OFF → protons relax back to equilibrium
• Two independent relaxation processes:
  • T1 relaxation (longitudinal): Recovery of Mz — "spin-lattice relaxation"
  • T2 relaxation (transverse): Decay of Mxy — "spin-spin relaxation"

• Three gradient coils encode frequency, phase, and slice location
• Data fills k-space → Fourier transform → recognisable image

• Spin Echo (SE): 90° + 180° RF pulses → reliable T1/T2 weighting
• Gradient Echo (GRE): Shorter TR, faster, T2* weighted — sensitive to susceptibility effects (blood, calcium)
• Inversion Recovery (IR): Preparatory 180° pulse → FLAIR, STIR

1.4 Key Timing Parameters

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SECTION 2 — MRI SEQUENCES & THEIR CLINICAL MEANING

2.1 Core Sequences — The Fundamental Five

PG Memory Aid:

• T1 = "Tissue" — anatomy, bright fat, subacute blood (methemoglobin)
• T2 = "water (Two)" — water is bright, pathology lights up
• FLAIR = "Fluid Attenuated" — CSF goes dark, lesions near ventricles become obvious
• DWI = "Diffusion" — acute stroke lights up in minutes

2.2 Advanced/Specialised Sequences

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SECTION 3 — SIGNAL INTENSITY — WHAT IS BRIGHT/DARK?

3.1 T1 Signal — Bright (Hyperintense) Structures

Mnemonic: "FATMID"

3.2 T2 Signal — Bright (Hyperintense) Structures

Mnemonic: "VESSEL"

3.3 DWI Interpretation — Critical for PG Residents

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SECTION 4 — INDICATIONS FOR MRI BRAIN

Primary Indications

• Seizures / epilepsy
• Cranial nerve dysfunction
• Diplopia / visual disturbance
• Ataxia
• Acute and chronic neurological deficits
• Suspicion of neurodegenerative disease (dementia, Parkinson's)
• Primary and secondary neoplasm
• Intracranial aneurysm
• Cortical dysplasia / morphological brain abnormalities
• Vasculitis
• Encephalitis / meningitis and complications
• Brain maturation assessment (paediatric)
• Headache (complex/red-flag)
• Mental status change
• Hydrocephalus
• Ischaemic disease / infarction
• Suspected pituitary dysfunction
• Demyelination / dysmyelination
• Vascular malformations

Extended/Specialised Indications

• Functional imaging / brain mapping (pre-surgical)
• Blood flow and brain perfusion
• MR Spectroscopy (tumour, infection, epilepsy)
• Volumetry and morphometry (dementia research)
• Tractography (DTI — surgical planning)
• Post-traumatic assessment
• Haemorrhage characterisation / follow-up

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SECTION 5 — CONTRAINDICATIONS

Absolute Contraindications

• Ferromagnetic cerebral aneurysm clips (older generation)
• Cochlear implants (older non-MR-conditional)
• Certain cardiac devices: Older pacemakers, ICDs, neurostimulators without MR-conditional certification
• Metallic intraocular foreign bodies (e.g., metal workers — screening mandatory)
• Ferromagnetic intracranial hardware

Relative Contraindications (needs risk-benefit assessment)

• Modern MR-conditional pacemakers/ICDs — permissible at 1.5 T with strict protocols
• Claustrophobia — requires sedation/anaesthesia; open MRI as alternative
• First trimester of pregnancy — generally safe after 1st trimester; MRI preferred over ionising radiation when clinical necessity justifies; contrast (Gd) generally avoided throughout pregnancy
• Cochlear implants — some are MR-conditional (1.5 T or 3 T); verify manufacturer data
• Severe renal impairment (eGFR <30) — gadolinium contraindicated due to risk of Nephrogenic Systemic Fibrosis (NSF) — avoid older linear Gd agents; macrocyclic agents have lower risk

Key Safety Points for PG Residents

• MRI magnetic field is ALWAYS ON (even when not scanning)
• Field strength may exceed 60,000× Earth's magnetic field
• All patients, staff, and equipment must be safety-screened before entering the scan room
• Heating of metallic implants is a risk
• Website: www.mrisafety.com (check device compatibility before scanning)
• Breastfeeding: continue normally after gadolinium (very minimal excretion)
• Hearing protection mandatory for patient (gradient coil noise)

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SECTION 6 — GADOLINIUM CONTRAST

When to Use

• Blood-brain barrier (BBB) breakdown: tumour, abscess, encephalitis, active MS, meningitis
• Characterise lesion after non-contrast abnormality found
• Pituitary, cranial nerve, meningeal disease
• Post-operative assessment (residual tumour vs. surgical change)
• Active inflammation vs. chronic scar

How It Works

• Gadolinium is paramagnetic → causes T1 shortening → bright signal on T1W post-contrast
• Normally excluded from brain by intact BBB
• Enhances where BBB is disrupted

Enhancement Patterns — Key Clinical Correlations

Gadolinium Safety

• Nephrogenic systemic fibrosis (NSF): Rare, severe; avoid in eGFR <30 (especially older linear agents like gadodiamide, gadopentetate)
• Brain deposition: Gadolinium accumulates in dentate nuclei and globus pallidus with repeated dosing — significance uncertain; macrocyclic agents (gadobutrol, gadoterate) have significantly lower deposition
• Recent guidance: use lowest effective dose; prefer macrocyclic agents for repeated scans
• Allergic reactions: Rare (<1%); urticaria most common; true anaphylaxis extremely rare

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SECTION 7 — HOW TO READ AN MRI BRAIN — SYSTEMATIC APPROACH

Step 1 — Check Technical Quality

• Correct sequences acquired?
• Motion artefact? (ghosting, blurring)
• Field of view adequate?
• Pre- AND post-contrast if requested?

Step 2 — T1W First (Anatomy)

• Overall brain volume (atrophy?)
• Sulcal effacement or enlargement?
• Midline shift?
• T1 bright lesions: fat, blood, Gd contrast, calcification (rare on T1)
• Pituitary fossa, brainstem, cerebellum (no beam hardening artefact unlike CT)

Step 3 — T2W (Pathology Detection)

• Any focal hyperintensity?
• Distribution: cortical, subcortical, periventricular, deep white matter, basal ganglia, thalamus, brainstem, cerebellum
• CSF space enlargement — hydrocephalus?
• Posterior fossa: cerebellar/brainstem lesions (MRI superior to CT here)

Step 4 — FLAIR (Periventricular & Cortical Lesions)

• CSF suppressed → periventricular lesions become obvious
• MS plaques: ovoid, periventricular, perpendicular to ventricles ("Dawson's fingers")
• Cortical lesions, leptomeningeal spread
• SAH: blood in CSF sulci → bright on FLAIR

Step 5 — DWI + ADC (Acute Pathology)

• Acute ischaemia: DWI ↑, ADC ↓ → detectable within minutes to hours (MRI advantage over CT)
• Abscess: DWI ↑ (restricted pus)
• Epidermoid cyst: DWI ↑ (restricted diffusion, cholesterol)
• Confirm with ADC map to exclude T2 shine-through

Step 6 — GRE/SWI (Blood & Susceptibility)

• Haemorrhage (any age), microbleeds, cavernoma, calcification
• "Blooming artefact" — lesion appears larger on GRE/SWI than on other sequences → characteristic of blood products

Step 7 — Post-Contrast T1W (Enhancement)

• BBB breakdown sites?
• Enhancement pattern (see Section 6)
• New enhancing lesions (MS activity, new metastases)

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SECTION 8 — MRI SIGNAL OF HAEMORRHAGE OVER TIME

Evolution of Intracranial Haemorrhage on MRI

PG Tip: "Bright on T1 = subacute bleed (methemoglobin)." Chronic blood leaves a permanent dark hemosiderin rim on T2/GRE.

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SECTION 9 — CLINICAL CORRELATIONS WITH IMAGES

9.1 Acute Ischaemic Stroke

• DWI: ↑ (bright) — detectable within minutes (vs. CT negative for 6–24 h)
• ADC: ↓ (dark) — confirms true cytotoxic oedema
• FLAIR: may be normal <4.5 h — DWI+/FLAIR− mismatch = golden window for thrombolysis
• MRA: vessel occlusion

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9.2 Multiple Sclerosis (MS)

• FLAIR/T2: Multiple ovoid periventricular hyperintense plaques
• Dawson's Fingers: Lesions perpendicular to lateral ventricles (along medullary veins) on sagittal FLAIR — pathognomonic
• T1 "Black holes": Chronic plaques appear hypointense on T1 = irreversible axonal loss
• Post-Gd: Active plaques enhance (ring or nodular) = BBB breakdown during relapse
• Spinal cord: T2 hyperintense intramedullary lesion (usually <2 vertebral segments)
• McDonald Criteria 2017: Dissemination in space (DIS) + dissemination in time (DIT) on MRI

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9.3 Glioblastoma (GBM) / High-Grade Glioma

• T2/FLAIR: Heterogeneous hyperintense mass + extensive surrounding vasogenic oedema
• T1 + Gd: Ring enhancement (irregular, thick rim) — active tumour margin; central necrotic dark core
• DWI: Restricted diffusion in solid components (high cellularity)
• MRS: ↑ Choline (cell membrane turnover), ↓ NAA (neuronal loss), lipid/lactate peaks (necrosis)
• Perfusion (DSC): Elevated rCBV in tumour (hyperperfusion)
• DTI: Corticospinal tract displacement — surgical planning

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9.4 Brain Abscess

• T2/FLAIR: Hypointense rim (free radical-rich capsule) surrounded by hyperintense oedema
• T1 + Gd: Thin, smooth, regular ring enhancement — smooth inner wall (vs. GBM: thick, irregular)
• DWI: ↑ BRIGHT — restricted diffusion of pus (viscous fluid with restricted Brownian motion) — key differentiator from tumour
• ADC: ↓ dark — confirms true restriction
• MRS: Lactate, alanine, acetate, succinate, cytosolic amino acids — suggests pyogenic organisms

PG Exam Tip: Ring-enhancing lesion on MRI — if DWI bright = abscess; if DWI variable = tumour

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9.5 Meningioma

• T1: Isointense to grey matter
• T2: Variable (iso- to hyperintense)
• Gd T1: Intense homogeneous enhancement + dural tail sign (enhancing dura extending from lesion)
• Extra-axial location (displaces brain, does not invade)
• Calcification: Hypointense on T2/SWI; may be visible as psammoma bodies
• Associated hyperostosis of adjacent bone

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9.6 Pre-Surgical Brain Mapping (Advanced — Neurosurgery/Neurology PG)

• Maps eloquent cortex (motor, language — Broca's/Wernicke's, visual)
• Identifies critical white matter tracts (corticospinal tract, arcuate fasciculus)
• Allows safe surgical margins to minimise postoperative deficits
• Combined with MEG and intraoperative neuronavigation

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SECTION 10 — MRI vs. CT — WHEN TO USE WHICH

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SECTION 11 — MRI ARTEFACTS

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SECTION 12 — RECENT UPDATES (2023–2025)

12.1 7 Tesla (7T) MRI — Clinical Approval

• FDA/CE approved for clinical neuroimaging (2017 FDA, expanding clinical use 2023–2025)
• Advantages: Ultra-high spatial resolution, improved cortical architecture, small lesion detection (hippocampal sclerosis, small MS lesions, cortical dysplasia)
• Limitations: Susceptibility artefacts, RF non-uniformity, limited body applications, higher cost, fewer contraindicated implants cleared
• Key use: Drug-resistant epilepsy, MS, dementia research, neurosurgical planning

12.2 AI-Accelerated MRI (Deep Learning Reconstruction)

• Compressed sensing + deep learning reduces scan time by 60–80% with maintained image quality
• FDA-cleared tools: Vendor-specific (e.g., GE AIR Recon DL, Siemens Deep Resolve, Philips SmartSpeed)
• Clinical impact: Paediatric brain MRI in <5 minutes; feasible in agitated patients
• Synthetic MRI: Single acquisition generates multiple contrast weightings simultaneously (T1, T2, PD, FLAIR, Myelin maps)

12.3 DWI-FLAIR Mismatch — Clinical Practice Update

• WAKE-UP Trial (NEJM 2018): Gd thrombolysis guided by DWI+/FLAIR− in unknown onset stroke → significantly better outcomes vs. placebo
• Now incorporated into 2023 ESO/AHA stroke guidelines for unknown-onset stroke

12.4 Gadolinium Deposition — Current Guidance

• Linear Gd agents (gadodiamide, gadopentetate) → higher brain deposition → several withdrawn/restricted in EU
• Macrocyclic agents (gadobutrol, gadoterate, gadoteridol) → significantly lower deposition → preferred for all repeated-dose applications
• 2023 ACR/ESR guidance: Use macrocyclic agents; record cumulative lifetime Gd dose; document clinical indication

12.5 Quantitative MRI (qMRI) — Emerging Standard

• T1/T2 mapping, myelin water imaging: Quantitative biomarkers replacing subjective visual assessment
• qMRI in MS: Myelin content tracking over time; treatment response monitoring
• Body/brain MRI vendors: Increasing integration of qMRI into clinical workflows

12.6 MR-guided Focused Ultrasound (MRgFUS)

• Combines MRI guidance with high-intensity focused ultrasound
• FDA-approved: Essential tremor, Parkinson's tremor (thalamotomy without surgery)
• Real-time thermal monitoring via MRI thermometry during treatment

12.7 Neuroradiological Updates — Brain Tumour (WHO 2021 Classification)

• Integrated molecular-MRI diagnosis: WHO 5th ed. (2021) requires IDH mutation status, MGMT methylation, 1p/19q codeletion for glioma grading
• MRI implications: Ring-enhancing T1 lesion alone is insufficient — biopsy/molecular profile mandatory for WHO grade
• Radiomics & AI: Machine-learning models can predict IDH status, MGMT methylation from standard MRI features with ~85% accuracy (research, not yet standard clinical practice)

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SECTION 13 — QUICK REFERENCE — DIAGNOSIS AT A GLANCE

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SECTION 14 — PG EXAM HIGH-YIELD POINTS

1. MRI uses NO ionising radiation — can be used in pregnancy (avoid Gd in 1st trimester)
2. T1W: anatomy, anatomy, anatomy — bright fat/blood/Gd; T2W: pathology lights up
3. FLAIR suppresses CSF → periventricular lesions (MS Dawson's fingers) become obvious
4. DWI + ADC: Acute stroke detectable in minutes — DWI↑ + ADC↓ = true restriction
5. DWI-FLAIR mismatch (DWI+ / FLAIR−) = stroke onset <4.5 h → thrombolysis window
6. Abscess = DWI↑ (restricted pus); Tumour = variable DWI — key ED differentiator
7. MS: Dawson's fingers (sagittal FLAIR) + black holes (T1) + Gd-enhancing = active disease
8. Haemorrhage: Subacute = T1 bright (methemoglobin); Chronic = T2 black rim (haemosiderin)
9. Gadolinium deposition → prefer macrocyclic agents; avoid in eGFR <30 (NSF risk)
10. Posterior fossa: MRI is always preferred over CT (no beam-hardening artefact)
11. 7T MRI now clinically approved — best for epilepsy, cortical dysplasia, small MS lesions
12. WHO 2021 glioma classification requires molecular profile — MRI alone is insufficient for final grade
13. MR-conditional devices — check www.mrisafety.com; never assume safety from appearance alone
14. Macrocyclic Gd agents (gadobutrol, gadoterate) = safer for repeated exposure; preferred currently

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