CAMRT MRI EXAM TEST 2025/2026 QUESTIONS WITH
ANSWERS GRADED A+
✔✔Colloid cyst - ✔✔Typically arise in the anterior aspect of the 3rd ventricle
T1: hyperintense
T2: hypointense most are of low T2/T2* signal (short T2), related to thick "motor oil"
consistency fluid
✔✔Dandy-Walker malformation - ✔✔Non-communicating type of hydrocephalus.
Dandy-Walker malformation (DWM) is the most common posterior fossa malformation,
characterized by the triad of:
hypoplasia of the vermis and cephalad rotation of the vermian remnant
cystic dilatation of the fourth ventricle extending posteriorly
enlarged posterior fossa with torcular-lambdoid inversion (the torcula lying above the
level of the lambdoid due to abnormally high tentorium)
T1 hypointense
T2 hyperintese
✔✔Encephalitis - ✔✔T1: hypointense areas of edema
T2: hyperintense
DWI: restricted diffusion
Herpes virus is the most common cause
✔✔Ependymoma - ✔✔An intracranial glioma. Found in the ventricle system and spinal
cord. Common pediatric tumour. Most common in the 4th ventricle. Hydrocephalus is
common.
T1 Hypointense/isointense
T2 Hyperintese
T1 CE: hyperintense
✔✔Glioblastoma multiforme (GBM) - ✔✔Rapidly growing, highly malignant tumour.
Found usually in the cerebral hemispheres, deep white matter. highly vascular and
central necrosis. Can cross the midline via white matter tracts (butterfly glioma).
T1: mixed signal
T2: Hyperintense/mixed
T1 CE: rim enhancement
,extensive edema and mass effect.
✔✔Hemangioma - ✔✔Cavernous hemangioma, or cerebral cavernoma (CCM) (when
referring to presence in the brain) is a type of benign vascular tumor or hemangioma,
where a collection of dilated blood vessels form a lesion. Because of this, blood flow
through the cavities, or caverns, is slow.
T1: varied signal depending on the age of the blood products, small fluid-fluid levels
may be evident
T2 hypointense rim varied signal internally depending on the age of blood productsif a
recent bleed has occurred, surrounding edema may be present
GRE T2*/SWI prominent blooming useful for detecting smaller lesions otherwise missed
by conventional spin echo sequences, especially in patients with familial or multiple
cavernous malformations
T1 CE (Gd): generally no enhancement
✔✔Brain hemorrhage: What are the time frames and appearance of each of these?
hyperacute
Acute
Subacute
late subacute
chronic - ✔✔Hyperacute:
< 24 hrs oxyhemoglobin
T1 iso/hypo
T2 iso/hypo
Acute
(1-3 days) deoxyhemoglobin:
T1: Isointense/hypointense
T2: Hypointense
Early subacute
(4-7 days) intraacellular methemoglobin
T1: Hyperintense
T2: Hypointense
Late subacute
7-14 days extracellular methemoglobin
T1: Hyperintense
, T2: Hyperintense
dark rim of hemosiderin on both
Chronic (2+ weeks):
T1: Hypointense
T2: Hypointense
dark rim of hemosiderin on both
✔✔Hydrocephalus - ✔✔May result from over production of CSF, under re-absorption, or
obstruction of the ventricles.
T1: enlarged ventricles will be hypointense
T2: enlarged ventricles will be hyperintese
T1 CE: to rule out intracranial mass
✔✔Ischemia (stroke) stages - ✔✔T2 and FLAIR: hyperintense signal within first few
hours
T2* area of abnormal blooming with acute hemorrhage
DWI ischemic tissue is hyperintense, and low signal on ADC map.
Early hyperacute
< 6 hrs
Within minutes of arterial occlusion, diffusion-weighted imaging demonstrates increased
DWI signal and reduced ADC values. Other images may be normal.
Late hyperacute:
6 hrs-4 days
Generally, after 6 hours, high T2 signal will be detected, initially more easily seen on
FLAIR than conventional fast spin echo T2 10. This change continues to increase over
the next day or two.
T1 hypointensity is only seen after 16 hours 10, and persists.
Acute:
During the first week, the infarcted parenchyma continues to demonstrate high DWI
signal and low ADC signal, although by the end of the first week ADC values have
started to increase. The infarct remains hyperintense on T2 and FLAIR, with T2 signal
progressively increasing during the first 4 days. T1 signal remains low, although some
cortical intrinsic high T1 signal may be seen as early as 3 days after infarction 10. After
day 5 the cortex usually demonstrates contrast enhancement on T1 C+
Subacute
ANSWERS GRADED A+
✔✔Colloid cyst - ✔✔Typically arise in the anterior aspect of the 3rd ventricle
T1: hyperintense
T2: hypointense most are of low T2/T2* signal (short T2), related to thick "motor oil"
consistency fluid
✔✔Dandy-Walker malformation - ✔✔Non-communicating type of hydrocephalus.
Dandy-Walker malformation (DWM) is the most common posterior fossa malformation,
characterized by the triad of:
hypoplasia of the vermis and cephalad rotation of the vermian remnant
cystic dilatation of the fourth ventricle extending posteriorly
enlarged posterior fossa with torcular-lambdoid inversion (the torcula lying above the
level of the lambdoid due to abnormally high tentorium)
T1 hypointense
T2 hyperintese
✔✔Encephalitis - ✔✔T1: hypointense areas of edema
T2: hyperintense
DWI: restricted diffusion
Herpes virus is the most common cause
✔✔Ependymoma - ✔✔An intracranial glioma. Found in the ventricle system and spinal
cord. Common pediatric tumour. Most common in the 4th ventricle. Hydrocephalus is
common.
T1 Hypointense/isointense
T2 Hyperintese
T1 CE: hyperintense
✔✔Glioblastoma multiforme (GBM) - ✔✔Rapidly growing, highly malignant tumour.
Found usually in the cerebral hemispheres, deep white matter. highly vascular and
central necrosis. Can cross the midline via white matter tracts (butterfly glioma).
T1: mixed signal
T2: Hyperintense/mixed
T1 CE: rim enhancement
,extensive edema and mass effect.
✔✔Hemangioma - ✔✔Cavernous hemangioma, or cerebral cavernoma (CCM) (when
referring to presence in the brain) is a type of benign vascular tumor or hemangioma,
where a collection of dilated blood vessels form a lesion. Because of this, blood flow
through the cavities, or caverns, is slow.
T1: varied signal depending on the age of the blood products, small fluid-fluid levels
may be evident
T2 hypointense rim varied signal internally depending on the age of blood productsif a
recent bleed has occurred, surrounding edema may be present
GRE T2*/SWI prominent blooming useful for detecting smaller lesions otherwise missed
by conventional spin echo sequences, especially in patients with familial or multiple
cavernous malformations
T1 CE (Gd): generally no enhancement
✔✔Brain hemorrhage: What are the time frames and appearance of each of these?
hyperacute
Acute
Subacute
late subacute
chronic - ✔✔Hyperacute:
< 24 hrs oxyhemoglobin
T1 iso/hypo
T2 iso/hypo
Acute
(1-3 days) deoxyhemoglobin:
T1: Isointense/hypointense
T2: Hypointense
Early subacute
(4-7 days) intraacellular methemoglobin
T1: Hyperintense
T2: Hypointense
Late subacute
7-14 days extracellular methemoglobin
T1: Hyperintense
, T2: Hyperintense
dark rim of hemosiderin on both
Chronic (2+ weeks):
T1: Hypointense
T2: Hypointense
dark rim of hemosiderin on both
✔✔Hydrocephalus - ✔✔May result from over production of CSF, under re-absorption, or
obstruction of the ventricles.
T1: enlarged ventricles will be hypointense
T2: enlarged ventricles will be hyperintese
T1 CE: to rule out intracranial mass
✔✔Ischemia (stroke) stages - ✔✔T2 and FLAIR: hyperintense signal within first few
hours
T2* area of abnormal blooming with acute hemorrhage
DWI ischemic tissue is hyperintense, and low signal on ADC map.
Early hyperacute
< 6 hrs
Within minutes of arterial occlusion, diffusion-weighted imaging demonstrates increased
DWI signal and reduced ADC values. Other images may be normal.
Late hyperacute:
6 hrs-4 days
Generally, after 6 hours, high T2 signal will be detected, initially more easily seen on
FLAIR than conventional fast spin echo T2 10. This change continues to increase over
the next day or two.
T1 hypointensity is only seen after 16 hours 10, and persists.
Acute:
During the first week, the infarcted parenchyma continues to demonstrate high DWI
signal and low ADC signal, although by the end of the first week ADC values have
started to increase. The infarct remains hyperintense on T2 and FLAIR, with T2 signal
progressively increasing during the first 4 days. T1 signal remains low, although some
cortical intrinsic high T1 signal may be seen as early as 3 days after infarction 10. After
day 5 the cortex usually demonstrates contrast enhancement on T1 C+
Subacute
