MRI

Question 1

T1 shortening and prolongation

T2 shortening and prolongation

Answer 1

T1: Hyperintense and hypointense
T2: Hypointense and hyperintense

Question 2

Spin-echo conventional

Answer 2

T1 and T2

Question 3

T1 shortening causes

Answer 3

Gad, fat, protein

• Paramagnetic blood stage (intra/extra methemglobin)
• Melanin
• Mineralization
• SLOW flowing blood
• Calcium, when not in bone

Question 4

T2 shortening

Answer 4

Paramagnetic blood stage (except hyper acute and extracellar methemoglobin
-Calcification
-Fibrous
-High cellularity (lymph, Medulloblastoma)
Vascular flow void
Mucin (dessicated sinus mucin is hypointense and muscinous lesions which are hydrated are hyper)

Question 5

FLAIR

Answer 5

Water suppressed T2

Question 6

White/grey on T1

Answer 6

T1: White matter BRIGHT DUE TO FAT

Question 7

Diffusion MRI

Answer 7

DWI and ADC. Principle that with ncrease Brownian motion, signal is lost. Pathology reduces diffusion and hence less signal loss
-DWI is a T2 weighted sequence and reduced diffusion is HYPER, and hypo on ADC.

Question 8

T2 shine through

Answer 8

Anything bright on T2 is bright on DWI hence look at ADC to confirm for restricted diffusion

Question 9

B value

Answer 9

Higher the b value, the higher the contrast provided for determining reduced diffisivity.

Question 10

Downside to increasing the B value

Answer 10

Decrease in signal to noise ratio meaning scan time should be proportionally increased

Question 11

How to calculate ADC

Answer 11

Need at least two different B value images

Question 12

Restricted diffusion differential

Answer 12

Acute stroke
Bacterial abscess
Lymphoma, mdulloblastoma
epidermoid cyst
herpes encephalitis
Creutzfieldt-Jakob

Question 13

GRE

Answer 13

T2* signal. Omits 180 degree rephasing pulse. Susceptible to signal loss

Question 14

Causes of dark spots on GRE

Answer 14

Hemosiderin and calcium

Question 15

Differential for dark spots on GRE

Answer 15

• Hypertensive microbleedss
• Cerebral amyloid angiopathy
• Familial cerebral cavernous malformation
• Axonal shear injury
• Multiple hemorrhagic mets

Question 16

Difference b/w hypertensive microbleeds and cerebral amyloid angiopathy

Answer 16

Location!

• Cerebral amyloid spots= subcortical white matter (parietal and occipital lobes)
• Hypertensive= Basal ganglia thalami, cerebellum, pons

Question 17

Blood products components over time (hyperacute, acute, early and late subacute, chronic)

Answer 17

Hyperacute: Intracellular oxy-Hb
Acute: intracellular deoxy-hb
Early subacute: Intracellular methe-Hb
Late subacute: Extracellular methe-Hb
Chronic: Extracellular hemosiderin/ferritin

Question 18

T1/T2 for the following:

Hyperacute: Intracellular oxy-Hb
Acute: intracellular deoxy-hb
Early subacute: Intracellular methe-Hb
Late subacute: Extracellular methe-Hb
Chronic: Extracellular hemosiderin/ferritin

Answer 18

Hyperacute: Iso to low/High
Acute: Iso to low/Low
Early subacute: High/Low
Late subacute: High/High
Chronic: Low/Low