neuroradiology

Question 1

investigating methods

Answer 1

• x-ray
• fluoroscopy
• pneumoencephalography
• ventriculography
• myelography
• US: neonatal, intraoperative
• CT
• MRI (H. MRA, MRS, fMR): multiplanar, tissue contrast, bone-artefact, white matter
• angiography: mass effect, vascularity, preoperative, intervention -> catheter. – not diagnostic, just for intervention!
• nuclear medicine: circulation, metabolism (SPECT, PET)

Question 2

white matter - symmetric lesion

Answer 2

a. confluens: leukodystrophia metachromatica, adrenoleucodystrophia, necrosis (post-radiation, chemotherapy)
b. no confluens: ALS (amyotrophic lateral sclerosis), Binswanger (subcortical leucoencephalopathy)

Question 3

white matter - asymmetric lesion

Answer 3

a. confluens: PML (progressive multifocal leukoencephalopathy), MS
b. no confluens: tumors/metastases, pons myelinolysis, MS

Question 4

white matter - investigating methods

Answer 4

• angiography (DSA): aneurysm (basilar artery)
• MRA-3D TOF (time-of-flight): sensitivity > 90%, specificity > 90%: for stenosis / carotid bifurcation angiography (intervention)
• 3D rotational angiography: pre- and post- intervention (coil)

Question 5

acute neurological deficit: stroke – pathology

Answer 5

• cerebral ischemia: territorial, microangiopathy, watershed/border, global hypoxia
• -> the effect depends on the flow reduction, the location, the duration of cause
• haemorrhage: intreacerebral haemorrhage (15%), apoplexia (mass haemorrhage), lobar haemorrhage (amyloid angiopathy), tumorous origin, coagulopathy, venous occlusion, vascular malformation, aneurysm
• extracerebral haemorrhage: Willis circle, berry aneurysm
• Traumatic haemorrhage: subdural, epidural
• Contusion: parenchymal

Question 6

acute neurological deficit: stroke – investigation

Answer 6

CT Vs MRI [angiography (DSA)]

Question 7

critical regional CBF values

Answer 7

• normal rCBF = 54 +/- 12 ml/100g/min
• ischemia threshold = 23 ml/100g/min
• neurological function loss = 10-23 ml/100g/min
• if rCBF recovers >23 ml –> the neurological deficit is reversible
• ischemic infract:
  a. in medulla < 10 ml/100g/min
  b. in cortex < 17 ml/100g/min

Question 8

developing edemas in stoke

Answer 8

• ATP pump and ion transport impairment -> water accumulation within the cells -> cytotoxic edema –> Diffusion Weighted Imaging (DWI)
• anaerob metabolism -> intracellular lactate acidosis -> blood-brain-barrier impairment -> vasogenic edema –> CT, MRI
• capillary dilation / proliferation -> luxury perfusion –> CT, MTI angiography

Question 9

penumbra (notion)

Answer 9

tissu at risk! Occluded artery in the peripheral zone -> vulnerable, but potentially reversible: if perfusion pressure and collateral flow together > 23 ml/100g/min –> maintains rCBF.
THIS IS THE AIM OF EARLY STROKE THERAPY

Question 10

the role of imaging in acute stroke

Answer 10

exclude haemorrhage!
-> differentiate between irreversible and reversible damaged brain tissue (dead Vs tissue at risk)

• suprantetorial infarcts: ant. cerebral A., medial cerebral A., post. cerebral A.
• infratentorial infarcts: sup. cerebellar A., ant. cerebellar A., post-inf. cerebellar A.

Question 11

CT image of hyperacute stroke:

Answer 11

early cytotoxic edema, neutrophil infiltration -> loss of differentiation btw grey-white matter, insular ribbon loss, hyperdense artery (GACS sign), sulcal effacement, gyral swelling, lentiform nucleus obscured (within 1 hour)

Question 12

CT radiology of cerebral infarcts (4-7 days, 1-8 weeks, months-years)

Answer 12

a. 4-7 days: gyri -> enhancement, space occupying effect, oedema presents
b. 1-8 weeks: persistent enhancement, space occupying effect, transient calcification (infants)
c. months-years: encephalomalacia (cyst), volume decreases

Question 13

stokre: MRI

Answer 13

Earliest: loss of “ flow void”, vessel vascular enhancement (slow flow) -> from the first min, till 2 weeks

• T1: cerebral swelling (sulci decrease), 2h: intracellular cytotoxic edema
• T2: signal intensity (SI) may grow in 2-4 hours, definitely increases within 24h hours -> extracellular (vasogenic) oedema.
• diffusion MRI: Brownian motion is free (water, liquor), diffusion quick, SI low. in the brain diffusion is directed, hampered (fibres, membranes), 2-10x slower that water.
  Infarct -> cytotoxic oedema -> diffusion is restricted -> SI high
• DWI: because of vasogenic oedema, diffusion increases again (- SI low), reaches the normal brain tissue.
• encephalomalacia: diffusion is not restricted anymore , same as in CSF
• DWI with perfusion mismatch -> penumbra: rescue the brain!