Neuroimaging
Alessandro Biffi
Adam B. Cohen
Joshua P. Klein
TIPS FOR REVIEWING SCANS
Review all images & sequences. Reconstructed images screen for abnl findings, but always review raw data. Be systematic: eval gyral-sulcal pattern, gray & white structures, ventricles & CSF spaces, vessels, bones, sinuses, & soft tissues. Look for patterns of abnormalities, asym., mass effect vs. atrophy, shift of midline structures. Note whether lesion involves gray matter, WM, or both.
COMPUTED TOMOGRAPHY (CT)
Signal measured in Hounsfield units (HU). From black (hypodense) to white (hyperdense): air -1,000; fat -30-70; water 0; CSF +15; WM 20-30; GM 35-45; acute hemorrhage/thrombus +60-100; bone +1,000. HU values can complement visual inspection in identifying tissues/lesions. CT w/contrast (iodine based) enhances vessels & areas of BBB breakdown (necrosis, infxn, acute demyelination, many tumors). Delayed postcontrast images to assess temporal dynamics of enhancement (e.g., slow flow, vascular malformations). CT angiography (CTA) uses timed boluses of IV contrast to enhance arteries. CT venography (CTV) uses timed IV contrast to enhance veins. CT perfusion (CTP) measures cerebral blood flow (CBF), cerebral blood volume (CBV), & mean transit time (MTT), used to define an area of tissue w/infarction or ↓ perfusion at risk of infarction (i.e., ischemic penumbra surrounding an infarct). Can also be used to demonstrate ↑ perfusion to a tumor or other highly vascular or hypermetabolic lesion. CBF = CBV/MTT.
MAGNETIC RESONANCE IMAGING (MRI)
Signal from applying magnetic field & measuring relaxation times of hydrogen nuclei.
Gadolinium: MRI paramagnetic contrast, causes “T1 shortening” (hyperintensity). Enhances vessels & areas of BBB breakdown (necrosis, infxn, acute demyelination, many
tumors). Delayed postcontrast images to assess temporal dynamics of enhancement. Lesions that enhance usually neoplastic, pustulent, or bloody.
tumors). Delayed postcontrast images to assess temporal dynamics of enhancement. Lesions that enhance usually neoplastic, pustulent, or bloody.
MRI sequences: T1: GM darker than WM, CSF dark. T2: WM darker than GM, CSF bright. FLAIR (fluid-attenuated inversion recovery); T2-weighted sequence, but CSF signal suppressed (dark). “Fat saturation” or STIR: Helps differentiate diff tissue densities by suppressing bright signal from fat. DWI/ADC (diffusion-weighted imaging/apparent diffusion coefficient): Assesses for acute ischemia or cytotoxic injury (restricted diffusion is DWI bright, ADC dark); several processes besides acute infarction show restricted diffusion (abscess & hypercellular tumors). GRE (gradient echo) & SWI (susceptibility-weighted images): Dark signal corresponds to heavy metals (Fe, Ca, Mn, melanin), including iron-containing blood products; useful for identifying microhemorrhages (hemosiderin). Diffusion tensor imaging (DTI): Useful for WM tractography, emerging clinical applications. MR angiography (MRA): Uses timed boluses of gado to enhance arteries. “Time of flight” (TOF) MR angios are noncontrast-based vessel reconstructions of flow void signal, demonstrate flow rather than vessel structure, & can overestimate stenoses. MR venogram (MRV): Venous study, w/o contrast (TOF). MR perfusion (MRP): Timed contrast bolus to measure perfusion parameters (e.g., for “ischemic penumbra”): CBF, CBV, MTT. MR spectroscopy (MRS): Compares measures of neuronal integrity (N-acetyl aspartate, NAA), cellular metabolism (creatinine, Cr), cell membrane synthesis (choline, Cho) w/in selected foci. In dzs w/↑ cell turnover, Cho is ↑’d. In neurodegenerative dzs, NAA is ↓’d. Functional MRI (fMRI): Blood oxygen level-dependent (BOLD) T2-based measurements of oxy-& deoxy-Hb. OxyHb is hyperintense compared to deoxyHb on T2-weighted images. W/high perfusion to active brain tissue, oxyHb levels rise & deoxyHb fall. Net effect is hyperintense signal in metabolically active tissue. Used in surgical planning to localize eloquent cortex adjacent to infiltrating tumors.
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THINGS THAT ENHANCE
Patent vessels, breakdown of BBB (e.g., w/in cytotoxic processes: infarction, necrosis, infxn, acute demyelination, expanding tumors).
Rim enhance: Fungal or parasitic infxn, abscess, acute demyelinating plaques, granuloma, infarction, lymphoma (in immunocompromised host), radiation necrosis, GBM, subacute ICH. (Mnemonic: “MAGIC DR”: Metastases, Abscess, Glioma (& lymphoma), Infarction, Contusion, Demyelination, Resolving hematoma/Radiation necrosis.)
Pachymeninges (dura & outer arachnoid): CSF leak or intracranial hypotension, SAH, infxn, inflammation, mets.
Leptomeninges (inner arachnoid & pia): Acute stroke, infxn, inflammation, mets.
Cauda equina or roots: GBS, disc herniation, Charcot-Marie-Tooth, mets, neurofibromas, schwannomas, arachnoiditis, granulomatous dz, Lyme, CMV, schistosomiasis.
OTHER IMAGING TECHNIQUES
Conventional angiography: Intra-arterial (IA) contrast to study indiv vessels; allows focal Rx (coiling, embolization, IA tPA). Resolution ˜0.5 mm.
Ultrasound: Helpful to evaluate arterial anatomy, stenosis, & flow (direction & quality). Carotid Doppler: Extracranial carotids & verts; transcranial Doppler: Intracranial vessels.
Positron emission tomography (PET): Indirectly measures metabolism by uptake of a radioactively labeled biologically active compounds, e.g., glucose (tumors & abscesses are hypermetabolic; atrophy & gliosis are hypometabolic). Can be combined w/CT or MRI to improve anatomical localization of lesions.
Single-photon emission computed tomography (SPECT): Eval distribution of a radiologically active compound by emission of gamma rays to study perfusion & metabolism.
Myelography: Intrathecal injection of contrast to assess cord & nerve root anatomy (e.g., protruding discs & other masses).
IMAGING PROTOCOLS, INDICATIONS, & CAUTIONS
Acute focal neurologic deficit: Acute head/neck trauma, concern for stroke/SAH: I-CT.
Hyperacute stroke: ? Thrombolysis/IA intervention: I-CT (w/CTA).
Acute/subacute stroke: MRI w/DWI & GRE/SWI, w/head/neck MRA.
Multiple sclerosis: MRI brain, cervical +/- thoracic spine, w/DWI & gado.
Neoplasm: MRI brain w/DWI, GRE/SWI, gado.
Cranial nerve or brainstem lesion: MRI brain w/SSFP sequence (FIESTA or CISS): thin cuts through brainstem & detailed views of CNs.
Optic nerve lesion: Brain & orbital MRI w/gado coronal slices through orbits.
Aneurysm: CTA if acutely symptomatic, MRA for surveillance.
Dissection: CTA or MRA w/T1 fat-saturated (“fat-sat”) images (to visualize intramural hematoma).
Conventional angiogram: Gold standard for vascular imaging & dissections, residual lumen, vasculitis, vasospasm, moyamoya. Invasive, risk of stroke 0.5%-1%.
NEURORADIOLOGY OF SPECIFIC DISEASES
HEMORRHAGE
CT: Hyperdense (bright) & surrounded by hypodensity (edema, extruded serum).
Note: Hyperacute/chronic subdural hematomas & hygromas can be isodense to CSF.
Blood on MRI: T1/T2 appearance depends on “age” of blood (see table). Blood, hemosiderin, & other substances containing metal (Fe, Ca, Mn, melanin) hypointense on GRE/SWI.
ABC/2 formula for estimating hematoma volume: (A × B × C)/2, where A = max hematoma transverse diameter, B = max hematoma AP diameter, C = no. of axial slices containing hematoma × slice thickness (usually 0.5 cm).
Mnemonic for determining age of intraparenchymal hematoma on MRI: “i be iddy biddy baby doodoo” (or “i bleed, i die, bleed die, bleed bleed, die die”).
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Epidural: Biconvex shape; cannot spread past suture lines (dura adherent to skull).
Subdural: Concave shape; cannot spread past dural reflections (falx, tentorium).
SAH: Aneurysms most often located at branch points around circle of Willis (ICA-PCom, PCA-PCom, ICA-ophth, etc.); depending on artery & extent of bleed, blood can track into parenchyma, ventricles, cisterns, & along tentorium. If SAH seen, CTA indicated.
ICH: HTN: Most commonly basal ganglia, thalamus, pons, & cerebellum. Cerebral amyloid angiopathy (CAA): Typically lobar. Mets that commonly hemorrhage include breast & lung (by incidence) Melanoma, Renal cell ca, Choriocarcinoma, Thyroid papillary ca (“MR/CT”) (by propensity).
Venous infarct: Does not respect arterial territory, extensive edema, hemorrhagic transf.
Intraventricular: Typically seen w/SAH & hypertensive hemorrhage.
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Clues to secondary hemorrhage: Aneurysm rupture: ICH&SAH; Coagulopathy: Fluid-fluid level (=nonclotting blood) w/in hematoma; TBI: Soft-tissue edema of scalp, fractures, or other injury overlying SAH or ICH. Look for coup & contracoup effects.
INFARCTION
CT: Noncontrast: use high-contrast center/window values (30/30) to assess for early infarction: loss of gray-white differentiation, parenchymal hypodensity, sulcal effacement. Hyperdensity w/in a vessel may represent acute thrombus. Soft thrombus appears hypodense compared to calcified atherosclerotic plaque (hyperdense). CTA: Vessel cutoff/stenosis; flame-shaped tapering suggests dissection. CTP: defines ischemic penumbra.
MRI: DWI-bright & ADC-dark acutely. MRA/MRP: Interpreted like corresponding CT studies. Wallerian degeneration can be seen following infarctions involving parent neurons; output tracks appear DWI hyperintense acutely, T2 hyperintense chronically.
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OTHER VASCULAR DISEASES
Microvascular WM disease: Aka leukoaraiosis: 2/2 lipohyalinosis & arteriosclerosis of small vessels. Subcortical sym T2-hyperintense lesions, usu punctate but confluent w/more advanced dz. Binswanger disease: SC WM process a/w HTN & lacunes; spares U-fibers 2/2 to collaterals from cortical arteries.
Developmental venous anomaly (DVA or venous angioma): Dilated veins that converge radially (like a caput medusa) to a draining vein. W/contrast, early venous filling, persistence of venous phase. Low-risk hemorrhage.
Capillary telangiectasias: Capillaries surrounded by nl brain, predilection for pons. Most never hemorrhage. Enhance on CT/MRI, GRE/SWI hypointensity.
Cavernous angiomas/hemangiomas/malformations: Congenital vasc hamartoma of vessels w/o interspersed nl brain parenchyma. Can have assoc DVA. Hyperdense on CT w/calc. T1 hyperdense & T2 heterogeneous “Popcorn” appearance; GRE/SWI: dark rim (hemosiderin). Angiographically occult if no DVA.
Arteriovenous malformation (AVM): Arterialization of veins, large feeding arteries, absent or abnl capillaries, & enlarged draining veins. Often has aneurysms of feeding vessels. CT: Hyperdense, enhances. MR: Irregular serpentine flow voids on T2, enhances. Conventional angiogram: Early venous filling 2/2 absence of capillary phase.
Dural arteriovenous fistula (AVF): Dural-based AVM a/w venous hypertension. Can occur anywhere in CNS. In spine, mostly in thoracolumbar area. Cord infarction w/necrotizing myelopathy can occur causing paraparesis (Foix-Alajouanine syndrome, spinal cord appears T2 hyperintense, tangle of T2 flow voids on surface of spinal cord).
Aneurysms: Focal arterial dilations typically at branch points; fusiform (atherosclerotic dilation), saccular/berry (branch points), mycotic (infectious), neoplastic, pseudoaneurysm (traumatic, dissection).
Dissections: Flame-shaped tapering of vessel lumen, sometimes in corkscrew or spiral orientation on CTA, MRA, or conventional angiography. T1 fat-saturated images may demonstrate thrombus w/in false lumen overall similar sensitivity to
CTA (AJR Am J Roentgenol 2009;193:1167-1174). Note whether dissection extracranial or intracranial, whether there is intradural extension (risk for SAH). Carotid: Tend to occur near C2-C3 vertebral level, 2-3 cm superior to bifurcation. Vertebral: Tend to occur where artery is nearest bone, at C1 & through transverse foramina.
CTA (AJR Am J Roentgenol 2009;193:1167-1174). Note whether dissection extracranial or intracranial, whether there is intradural extension (risk for SAH). Carotid: Tend to occur near C2-C3 vertebral level, 2-3 cm superior to bifurcation. Vertebral: Tend to occur where artery is nearest bone, at C1 & through transverse foramina.
CAA: Lobar ICHs & evidence of prior microhemorrhages in SC WM, T2 hyperintense & GRE/SWI hypointense, superficial siderosis sometimes seen as well.
Moyamoya: Stenosis or occlusion of ICAs → development of abnl network of collateral capillary circulation arising from ACA, MCA, or PCA branches, lenticulostriates, or ECA transdural anastamoses. Angiography: ICA stenosis, proximal ACA/MCA occlusion w/extensive collaterals, & dilation of perforating lenticulostriate arteries (“puff of smoke”).
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