Neuroimagem Flashcards
Qual a sistematica para revisão de neuroimagem?
Review all images & sequences.
# Be systematic:
- Eval gyral-sulcal pattern and Gray & white structures
- Ventricles & CSF spaces
- Vessels
- Bones, sinuses & soft tissues.
# Look for patterns of abnormalities: asym., mass effect, shift of midline structures. Note whether lesion involves gray matter, WM, or both.
Como diferenciar as sequencias na ressonancia magnética?
MRI sequences: T1: Gray matter darker than WM, CSF dark. T2: WM darker than gray, CSF bright. FLAIR (fl uid-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 coeffi cient): Assesses for acute ischemia or cytotoxic injury (restricted diffusion is DWI bright, ADC dark); many processes besides acute infarction show restricted diffusion. GRE (gradient echo, aka “susceptibility”): Dark signal corresponds to heavy metals (Fe, Ca, Mn, melanin), including iron-containing blood products; useful for chronic hemorrhage (hemosiderin). Diffusion tensor imaging (DTI): Useful for WM tracts. MR angiography (MRA): Uses timed-boluses of gado to enhance arteries. “Time of fl ight” angios are non–contrast-based vessel reconstructions of fl ow void signal, more subject to artifact. MR venograms (MRV): Venous study, without contrast. MR perfusion (MRP): Times 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 diseases w/ ↑ cell turnover, Cho is ↑’d. In neurodegenerative diseases, 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 infi ltrating tumors.
O que realça ao contraste na RM?
Patent vessels, breakdown of BBB (e.g., w/ in cytotoxic processes: infarction, necrosis, infxn, acute demyelination, expanding tumors). # Ring-enhance: Fungal or parasitic infxn, abscess, 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, infl ammation, mets. Leptomeninges (inner arachnoid & pia): Acute stroke, infxn, infl ammation, mets. # Cauda equina or roots: GBS, disc herniation, Charcot-Marie-Tooth, mets, neurofi bromas, Schwannomas, arachnoiditis, granulomatous disease, Lyme, CMV, schistosomiasis.
Quais os protocolos de neuroimagem usados na neurologia?
IMAGING PROTOCOLS, INDICATIONS, & CAUTIONS # Acute focal neurologic deficit: Acute head/neck trauma, concern for stroke/ SAH: I-CT. # Acute stroke: I-CT (w/ CTA & CTP if available). # Subacute stroke: MRI w/ DWI & GRE, & head/neck MRA. # Multiple sclerosis: MRI brain, cervical, & thoracic spine w/ DWI & gado. # Neoplasm: MRI w/ DWI, GRE, gado. # Cranial nerve or brainstem lesion: FIESTA or CISS sequence, w/ thin cuts through brainstem & detailed views of CNs. # Optic nerve lesion: Brain & orbital MRI w/ gado. # Aneurysm: CTA (MRA has slightly lower resolution). # Dissection: CTA or MRA w/ T1 fat-saturated images (to visualize intramural hematoma). # Conventional angiogram: Gold standard for vascular imaging & dissections, residual lumen, vasculitis, vasospasm, Moya Moya. Invasive, risk of stroke ∼1%.
Como ver sangue na neuroimagem?
HEMORRHAGE CT: Hyperdense (bright) & surrounded by hypodensity (edema, extruded serum). Note: Hyperacute/chronic subdural hematomas & hygromas can be isodense. 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. 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 x slice thickness (usually 1/2 cm).
Como classificar os diferentes sangramentos?
# Epidural: Biconvex shape; cannot spread past suture lines (dura adherent to skull). # Subdural: Concave shape; cannot spread past dural refl ections (falx, tentorium). # SAH: Aneurysms most often located at branch points around circle of Willis (ICAPCom, 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 & cerebellum. Cerebral amyloid angiopathy (CAA): Typically lobar. Mets that commonly hemorrhage include breast and lung (by Greerincidence) Melanoma, Renal cell ca, Choriocarcinoma, Thyroid papillary ca (“MR/ CT”) (by propensity). # Venous infarct: Does not respect arterial territory, extensive edema, var hemorrhage. # Intraventricular: Typically seen w/ SAH and hypertensive hemorrhage. # Clues to secondary hemorrhage: Aneurysm rupture: ICH&SAH; Coagulopathy: Fluid-fl uid level (=nonclotting blood) w/in hematoma; TBI: Soft-tissue edema of scalp, fractures, or other injury overlying SAH or ICH. Look for coup & contra-coup effects.
Qual a classificação de transformação hemorragica do AVE?
HI-1 Small petechiae w/in or along margins of infarct w/o mass effect
HI-2 Confl uent petechiae w/in infarct w/o signifi cant mass effect
PH-1 Hematoma <30% of infarct w/ some mass effect PH-2 Hematoma >30% infarct w/ mass effect or any hemorrhage outside infarct
Quais os achados de infarto na neuroimagem?
Noncontrast CT: Can use high contrast windowing (30/30) to assess for early infarction—loss of grey-white differentiation, parenchymal hypodensity. Hyperdensity w/in a vessel may represent a thrombus. Soft thrombus appears hypodense compared to calcifi ed atherosclerotic plaque (hyperdense). CTA: Vessel cutoff/stenosis; fl ame-like tapering suggests dissection. CTP defi nes 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.
Quais as doenças vasculares que devemos identificar na neuroimagem?
# Microvascular disease: Aka leukoaraiosis: 2/2 lipohyalinosis & arteriosclerosis of small vessels. Subcortical sym T2-hyperintense lesions, usu. punctate but confl uent w/ more advanced dz. Binswanger disease: SC WM process a/w HTN & lacunes; spares U-fi bers 2/2 to collaterals from cortical arteries. # Developmental venous anomaly (DVA or venous angioma): Dilated veins which converge radially (like a caput medusa) to a draining vein. W/ contrast, early venous fi lling, 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 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 hypodense; GRE: Dark ring (hemosiderin). “Popcorn” appearance. # 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 fl ow voids on T2, enhances. Conventional angiogram: Early venous phase 2/2 absence of capillary phase. # Dural arteriovenous fi stula (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 fl ow voids posterior to 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, but CTA is superior (AJNR 2008;29:1753– 1760). Note whether dissection extracranial or intracranial, whether there is intradural extension (risk for SAH). Carotid: Tend to occur near C2–3 vertebral level, 2–3 cm superior to bifurcation. Vertebral: Tend to occur where artery is nearest bone, at C1. # CAA: Lobar ICHs & evidence of prior microhemorrhages in SC WM, T2 hyperintense & GRE hypointense. # Moya moya: 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”). # CADASIL (cerebral autosomal dominant arteriopathy w/ subcortical infarcts & leukoencephalopathy): Sym T1 hypointense & T2 hyperintense lesions in anterior temporal lobes, external capsules, & widespread subcortical WM. # Fibromuscular dysplasia (FMD): Large vessel (ICA & renal artery) “string of beads” appearance; diameter of beading greater than diameter of artery; commonly spares fi rst few cm of ICA (unlike atherosclerosis). # Vasculitis: Segments of circumferential vessel narrowing (atherosclerotic lesions usu. more eccentric & focal c/w vasculitic lesions); multiple areas of cortical & subcortical infarction, hemorrhage, & nonspecifi c WM T2-hyperintensities. Differentiate from reversible cerebral vasoconstriction syndrome and vasospasm via clinical presentation. # Migraine: Nonspecifi c SC T2 hyperintensities, “UBOs” (“unidentifi ed bright objects”). Transient global amnesia (TGA): Punctate foci of restricted diffusion within limbic structures, typically reversible. # Susac syndrome (retinocochleocerebral vasculopathy): “Punched out” punctate T1 hypointense and T2 hyperintense lesions in the corpus callosum and deep gray nuclei.
Quais as principais doenças da substancia branca?
# Multiple sclerosis: Focal, ovoid WM lesions of PV>SC (perpendicular “Dawson’s fingers”) hemispheric WM, corpus callosum, optic nerves, brainstem (esp medial longitudinal fasciculus), cerebellum (esp middle cerebellar peduncle), optic nerves, spinal cord (<2 spinal segments); old lesions T1 dark; acute lesions enhance w/ gado (ring, incomplete ring, or diffuse), may be DWI bright. Rare cortical & deep gray matter lesions. # ADEM: Multiple lesions of same age; round, enhancing SC T2 bright lesions in hemispheric WM (& brainstem & cerebellum). # Acute MS or ADEM variants: Acute hemorrhagic leukoencephalitis (Weston Hurst disease): confl uent T2 bright WM signal w/ mass effect & minimal enhance; hemorrhage on GRE (or CT). Marburg variant of MS: Large region of T2 bright signal in hemispheric WM w/ mass effect & periph enhancement. Balo concentric sclerosis: Alternating concentric rings of T2 bright & dark signal (& alternating rings of enhancement) in hemispheric WM w/ var mass effect. NMO (Devic disease): Longitudinal cord T2 bright lesion (>3 spinal seg, central or occupying entire cross section) w/ optic nerves & chiasm T2 bright lesions; all lesions expansile with var enhance; var PV WM T2 bright lesions.
Quais as doenças desmielinizantes incomuns?
# SLE/APLA: SC WM (posterior predilection) T2 bright lesions; may be in vascular distribution & true infarct may occur (DWI bright); relative PV sparing; cortical lesions & diffuse atrophy also seen; T2 bright signal in cord (transverse myopathy). # Sjögren: SC & PV WM T2 bright lesions; also w/ basal ganglia T2 bright lesions; corpus callosum involvement less common. # Behcet: Multifocal or confl uent hemispheric WM T2 bright lesions w/ var enhancement; usually w/ concurrent diencephalon & upper brainstem lesions (often edema & enhancement); occassional cortical vein thrombosis/infarctions (var hemorrhage). # Sarcoidosis: Focal, multifocal, or confl uent T2 bright lesions of WM w/ var enhancement; also enhancement and thickening of pachymeninges w/ parenchymal infi ltration (pituitary- hypothalamus, optic nerve, optic chiasm). # Primary CNS vasculitis: Acute lesions DWI bright in hemispheric white (& gray) matter (may follow clear vascular territory), a/w stenoses & aneurysms; var lesional, meningeal & perivascular enhancement; chronic lesions w/ T2 bright hemispheric WM. Immune reconstitution infl ammatory syndrome (IRIS): Confl uent, multifocal T2 bright diffuse WM lesions w/ areas of focal enhancement & mass effect. # Infl ammatory CAA: Predominantly cortical & SC microhemorrhages (on GRE) w/ extensive asym & confl uent ↑ T2 & ↓ T1 signal of SC WM w/ minimal enhancement (Neurology 2007;68(17):1411–1416). # Tolosa Hunt: Idiopathic granulomatous dz typically involving cavernous sinus, orbital apex & adjacent structures, lesions are T1/T2 isointense & strongly enhance. # Paraneoplastic disease: a/w multiple systemic ca’s incl SCLC, testicular germ cell, ovarian, etc. Sym T2 hyperintensity w/ edema. PRES & hypertensive encephalopathy: b/l, sym T2 bright WM lesions in posterior hemispheres at MCA-PCA border zones; other regions may be affected (frontal & temporal, brainstem, cerebellum, gray structures); var restricted diffusion & peripheral enhancement.
Quais os achados de neuroimagem das doenças metabolicas do SNC?
# Metabolic diseases: # B12 deficiency: Scattered PV T2 bright WM lesions; ↑ T2 signal in posterior cord. # Marchiafava-Bignami syndrome: Acutely, central T2 & DWI bright lesions of corpus callosum; chronically, central cavitation; var mass effect & enhancement. # Osmotic demyelination: b/l, sym T2 bright lesions of central pontine WM (var sparing of corticospinal tracts), & var SC WM, midbrain, & deep gray lesions w/o enhance or mass effect. # Hypoxia-ischemia: b/l, sym diffuse DWI & T2 bright confl uent lesions after resp or cardiac arrest; predilection for SC WM (involves U-fi bers), corpus callosum, capsules (internal & external), globus pallidi hippocampus, cerebellum. # High altitude encephalopathy: b/l, sym posterior deep WM > SC WM & corpus callosum T2 bright lesions; var DWI bright lesions. # Acute intermittent porphyria (AIP): Similar to PRES (above).
Quais os achados de neuroimagem de encefalopatia toxica?
# Chemotherapy (cyclosporine, tacrolimus, methotrexate): (1) Acutely, PRES (see above); (2) chronically, b/l, sym, confl uent, diffuse, deep T2 bright WM lesions (spares U-fi bers) # Radiation: (1) w/ focal exposure, T2 bright WM lesion (often spares corpus callosum) w/ var mass effect & ring enhancement. Ddx: Tumor recurrence (choline peak on MRS, may involve corpus callosum); (2) w/ diffuse exposure, b/l, sym, confl uent T2 bright deep & PV lesions w/o enhancement or mass effect. # Illicits: b/l, sym lesions; (1) IV or inhaled heroin: diffuse WM high T2 signal (sparing U-fi bers), high convexities; (2) cocaine: scattered T2 bright WM lesions; stroke; ICH; vasculitis; (3) MDMA: globus pallidi & diffuse WM high T2 signal. # Organic solvents: b/l, sym, confl uent, diffuse T2 bright lesions; (1) toluene: corpus callosum & cerebellum; (2) methanol: SC WM, putamen, & optic nerve; (3) ethylene glycol: thalamus & pons. Mercury: b/l, sym, postcentral gyrus, occipital lobe & cerebellar T2 bright WM lesions w/ cortical atrophy in chronic phase. Carbon monoxide (CO) poisoning: Similar to hypoxic-ischemic injury (above), but sparing SC region & T2 bright globus pallidi lesions typical.
Quais os achados de neuroimagem das principais doenças infecciosas?
# PML/JC virus: Often begins asym, usually evolves into b/l sym dz; parietal & occip (but may occur anywhere) SC (involves U-fi bers) T2 bright confl uent nonenhancing WM dz w/ var pontocerebellar WM lesions; no mass effect. # HIV/ AIDS: b/l, sym PV T2 bright lesions, nonenhancing; diff atrophy. # CMV: (1) AIDS-related: Ventriculitis w/ PV T2 bright lesions & subependymal enhance; assoc lumbosacral meningeal & nerve root thickening & enhancement, (2) Congenital CMV: Temporal SC & PV T2 bright lesions w/ cystic regions. # VZV: (1) Immunocompromised pts (small vessel vasculitis): Diffuse, patchy T2 bright multifocal WM lesions; angiographic abnormalities (proximal MCA-ACA); (2) Immunocompetent pts (large vessel vasculitis): Acute stroke from VZV-vasculitis w/ DWI bright lesions in deep WM & cortex; var enhancement. # HTLV-1 & 2: Small, multifocal T2 bright SC WM lesions; in early stages of spinal disease, multifocal enhancing T2 bright thoracic lesions w/ var mass effect. # Lyme: Scant T2 bright PV WM lesions; meningitis, polyradiculitis & cranial neuritis (with enhancement of corresp structures). # SSPE (rubeola/measles): Early stages, posterior SC (spares U-fi bers) T2 patchy bright lesions w/ adjacent gray matter involvement; var enhancement & mass effect; mid-stages w/ PV & putamen and pontocerebellar T2 bright lesions w/ regression of SC lesions; late stages w/ atrophy & worsening PV T2 bright lesions.
Quais os principais achados de neuroimagem das doenças hereditarias?
# Metachromic leukodystrophy: Diffuse, sym T2 bright signal of cerebral (+corpus callosum, −U-fi bers) & cerebellar WM; tigroid WM pattern; predom frontal involvement in adult-onset forms. # Pelizaeus-Merzbacher: Diffuse, sym T2 bright signal of WM w/ var T2 dark signal in deep gray nuclei, midbrain, & cerebellum; “eye of the tiger” sign. # X-linked ALD: Sym SC & deep WM T2 bright signal (U-fi ber sparing); begins parietal & occip w/ enhancement at leading edge & var mass effect; involves corpus callosum; progresses anteriorly & posteriorly. # Krabbe (globoid cell): Parietal & cerebellar WM T2 bright signal; var bright lesions in deep gray (thalami), WM & cortex. # Alexander disease: (1) Childhood forms: begins w/ T2 bright signal in frontal lobes w/ enhancing edge, followed by cystic changes; macrocephaly; var bright lesions in caudate on CT; (2) adult form—var PV T2 bright lesions; upper cervical cord & medulla atrophy. # Canavan dz: SC (involves U-fi bers) & deep gray T2 bright signal; macrocephaly; ↑ NAA peak on MRS. # Vanishing WM (VWM) disease: Sym, diffuse T2 bright signal in cerebral & cerebellar hemispheres (loss of WM; rel temporal lobe & U-fi ber sparing); nl head size. # Megaloencephalitic leukoencephalopathy: Temporal T2 bright signal w/ cysts; macrocephaly. # Aicardi-Goutiere’s: Diffuse, T2 bright signal in hemispheric WM; basal ganglia calc on CT. Tuberous sclerosis: # Cortical tubers & areas of dysmyelination: T2 bright SC lesions (in adults); subependymal enhancing lesions (small hamartomas, large giant cell astrocytomas [SEGA]).
