Core Neuroimaging: Brain Flashcards
1
Q
CSF spaces (4)
A
- Sulci.
- Fissures.
- Basal cisterns.
- Ventricles.
2
Q
Most important Sulcal/fissural elements (3)
A
- Central sulcus: Divides the primary motor cortex (Precentral gyrus of the frontal lobe) and primary somatosensory cortex (postcentral gyrus of the parietal lobe).
- Sylvian fissure: Divides frontal/parietal lobes from the temporal lobe below.
- Parieto-occipital sulcus: Divides the parietal lobe from the occipital lobe.
3
Q
CSF and ventricular volumes
A
- CSF: 125 ml.
- Ventricular volume: 25 ml.
- CSF production: 500 ml/day.
- Total rechange: 3-4 times per day.
4
Q
Communicating hydrocephalus
A
- Ventricular enlargement due to an increase in CSF volume without an obstructing lesion.
- Obstruction of arachnoid reabsorption (HSA, meningitis, leptomeningeal metastases).
- Normal pressure hydrocephalus.
5
Q
Normal pressure hydrocephalus
A
- Form of communicating hydrocephalus.
- Normal CSF pressure and clinical triad of ataxia, urinary incontinence and dementia.
- Imaging: Ventriculomegaly, acute callosal angle, widened sylvian fissures and tight high convexity.
6
Q
Non-communicating hydrocephalus
A
- Hydrocephalus secondary to an obstructing lesion within the ventricular system.
- Ex: Ventricular colloid cyst, aqueductal stenosis, posterior fossa mass, etc.
7
Q
Obstructive hydrocephalus
A
- Non-communicating hydrocephalus + communicating hydrocephalus due to obstruction at the level of the subarachnoid spaces or arachnoid granulations.
8
Q
Hydrocephalus ex vacuo
A
- Ventricular enlargement due to brain parenchymal volume loss.
9
Q
Edema appearance on CT and MRI
A
- Compared with normal brain parenchyma, edematous brain appears hypoattenuating on CT and FLAIR hyperintense on MRI.
10
Q
Cytotoxic edema
A
- Cell swelling due to damaged NaK Atpase ion pumps.
- Mostly because of ischemia.
- Generates true cytotoxic edema (Fluid moves from the extra to intracellular space).
- Followed by ionic edema (fluid moves from intravascular space to extracelular space across an intact blood-brain barrier).|
11
Q
Vasogenic edema
A
- Blood-brain barrier breakdones generates it.
- Protein rich fluid moves from the intravascular to the extracelular space.
- Causes: Neoplasm, infection, inflammation, hemorrage, subacute arterial infarct and venous infarcts.
- White matter is primarily affected.
- MRI: Increased diffusión. CT shows accentuated gray-white differentiation.
12
Q
Insterstitial edema
A
- Increased ventricular pressure generates transependymal flow.
- CSF moves from the intraventricular space into the brain extracecular space.
- Mostly due to acute obstructive hydrocephalus.
- Periventricular white matter is primarily affected.
13
Q
Types of brain herniations
A
- Subfalcine.
- Downward uncal.
- Upward uncal.
- ## Cerebellar tonsillar.
14
Q
Subfalcine herniation
A
- Cingulate gyrus slides underneath the falx cerebri.
- Rarely: compression of ACA.
- Contralateral ventricular entrapment (focal hydrocephalus) from foramen of monro obstruction.
15
Q
Downward transtentorial herniation
A
- Uncal or central herniation.
- The ipsilateral cranial nerve III may be compressed.
- Compressión of ipsilateral PCA.
- Duret hemorrages: Shearing of perforating basilar branches on the brainstem.
- Kernohan notch phenomenon (paralisis ipsilateral to the herniated site).
- Central herniation: Impairment of the brainstem (coma, breathing abnormality, posturing).
16
Q
Upward transtentorial herniation
A
- Superior displacement of the upper parts of the cerebellum due to posterior fossa mass effect.
- Main complitacion: obstructive hydrocephalus from aqueductal compresion.
17
Q
Cerebellar tonsil herniation
A
- Displacement of the cerebellar tonsils through foramen magnum.
- Compresion of medullary respiratory centers is often fatal.
18
Q
Transcalvarial herniation
A
- Shift of brain outside the brain case.
- Mushroom-like apprearance of craniectomy may suggest it is too small and potentially constrict vessels and brain tissue at the margins.
19
Q
Paradoxical herniation
A
- Sunken/sinking skin flap syndrome.
- Complication of large craneoctomy where ICP falls below the atmosferic pressure, resulting in concave deformity and displacement of the brain from the calvarial defect.
20
Q
T1-weighted spin echo imaging
A
- Most brain lesions are hypointense in T1.
- Hyperintensity in T1: fat, proteinaceous material, methemoglobin, melanin and minerals (gadolinium copper, manganese, iron and calcium).
- Slow-flowing blood also apprears as T1 hiperintense.
21
Q
T2-weighted spin echo imaging
A
- Most brain lesions are T2 hyperintense due to water content or edema.
- Hypointensity in T2: Most stages of blood, calcifications, highly celullar tumors, desiccated secretions in the paranasal sinuses).
- Fast moving blood also appears hypointense in T2 (Flow-void).
22
Q
T2 Fluid attenuated inversion recovery (FLAIR)
A
- Addition of inversion pulse which nulls fluid signal.
- T1 vs T2 FLAIR: look at the relative intensity of white and grey matter (White matter is T1 hyperintense and FLAIR hypointense)
23
Q
Spin echo proton density (PD)- weighted imaging
A
- Not used in may neuroradiology protocols.
- Used in multiple sclerosis.
24
Q
Diffusion-weighted imaging (DWI)
A
- Depicts brownian movement of protons.
- Free water experiences the most signal attenuation (CSF).
- Inherently T2-weighted sequense with diffusion-sensitive pulsed gradients.
- b-value determines the degree of difussion weighting (higher = more sensitive).
- Trace images: Reduced diffusivity will be hyperintense.
- ADC map: Reduced diffusivity will be hypointense.
25
T2 shine-through of DWI
- DWI images are T2-weighted.
- Lesions with long T2 relaxation times will also be hyperintense on DWI (specially on low b-values).
- **True restricted diffusion will correlate with the ADC map**.
26
Gradiend recalled echo (GRE) and susceptibility-weighted imaging (SWI)
- T2-weighted GRe sequences are suceptible to signal loss from field inhomogeneities.
- SWI is similar to GRE, but with higher spatial resolution and other features to reduce artifacts.
- Blooming artifact of signal dropout with materials like hemosidering and calcium.
- Multiple dark spots on GRE/SWI may have different causes (other card).
27
Causes of multiple dark spots on GRE/SWI (8)
- Hypertensive microangiopathy.
- Cereberal amyloid angiopathy.
- Familial cerebral cavernous malformation syndrome.
- Radiation induced cerebral vasculopathy.
- Diffuse axonal injury.
- Hemorragic metastases.
- Fat embolism.
- Complication of cardiac sugery (microbleeds).
28
Magnetic resonance spectroscopy (MRS)
- Various types: Single-voxel spectroscopy and multiple voxel chemical shift imaging.
29
Hunter's angle
- Quick way to see if a spectrum is normal.
- Line connecting the highest peaks shoud **point like a plane taking off**.
- Most tumors disrupt this angle.
30
Peaks of compounds on MRS
- Peaks of compounds are analysed from left to right:
- Choline 3.2 ppm: marker of cell membrane turnover
- Creatinine 3.0 ppm: cellular energy stores
- N-acetylaspartate NAA 2,0 ppm: marker of neuronal viability.
- Lipids and lactate 1,3 ppm: abnormal tissue damage and anaerobic glycolisis.
31
MR perfusion-weighted imaging types (3)
- Dynamic susceptility contrast (DSC).
- Dynamic contrast enhanced (DCE).
- Arterial spin labeling (ASL).
32
Dynamic susceptility contrast (DSC)
MR perfusion, injection of a bolus of gadolinium causes a magnetic field disturbance, which transiently decreases the signal intensity on T2-weighted images.
33
Dynamic contrast enhanced (DCE)
MR perfusion, injection of a bolus of gadolinium causes T1 shortening, which increases the signal intensity on T1-weighted images.
34
Arterial spin labeling (ASL).
MR perfusion, a non contrast technique, radiofrequency pulses at the neck magnetically label photons, which then travel to the brain where they are imaged.
35
MR perfusion caculated parameters (5)
- Cerebral blood flow (CBF).
- Cerebral blood volume (CBV).
- Mean transit time (MTT=CBV/CBF).
- Time to maximum (Tmax).
- Time to peak concentration (TTP).
