Question 1: Epidural Haematoma (EDH)
Stem: A 19-year-old man is struck in the side of the head with a cricket ball. He briefly loses consciousness but then feels completely normal for two hours (the “lucid interval”). He then develops a rapid decline in GCS and a blown right pupil. An urgent non-contrast CT head is performed.
Question: Which of the following describes the classic CT appearance of this acute injury?
(A) A crescent-shaped, hyperdense collection that crosses cranial sutures. (B) A biconvex (lentiform), hyperdense collection that does not cross cranial sutures. (C) Diffuse sulcal effacement with “star-shaped” hyperdensity in the basal cisterns. (D) Multiple small punctate haemorrhages at the grey-white matter junction. (E) A wedge-shaped area of low attenuation in the temporal lobe.
Correct Answer: (B) A biconvex (lentiform), hyperdense collection that does not cross cranial sutures.
Explanation:
- Why (B) is correct: This is the classic description of an Epidural Haematoma (EDH). It is usually caused by a rupture of the middle meningeal artery associated with a temporal bone fracture. The blood is under high pressure and strips the dura from the bone, but is limited by the cranial sutures where the dura is tightly attached.
- Why (A) is wrong: This describes a Subdural Haematoma (SDH), which is crescent-shaped and crosses sutures because it is in the potential space between the dura and arachnoid.
- Why (C) is wrong: This describes a Subarachnoid Haemorrhage (SAH).
- Why (D) is wrong: This is the pattern of Diffuse Axonal Injury (DAI).
- Why (E) is wrong: This describes an ischaemic infarct.
Key Points: Epidural Haematoma (EDH)
- Vessel: Middle meningeal artery (90%).
- Shape: Biconvex / Lentiform (lemon-shaped).
- Sutures: Does NOT cross sutures; CAN cross venous sinuses.
- Clinical: Classically features a lucid interval.
Question 2: Subacute Subdural Haematoma (SDH)
Stem: An 82-year-old man on warfarin presents with 10 days of progressive confusion and gait instability. A non-contrast CT head shows a crescent-shaped collection over the right hemisphere. The attenuation of the collection is identical to that of the adjacent cerebral cortex (isodense).
Question: The “isodense” appearance of this collection is most characteristic of which stage of a subdural haematoma?
(A) Hyperacute (< 6 hours) (B) Acute (1–3 days) (C) Subacute (3–21 days) (D) Chronic (> 3 weeks) (E) Acute-on-chronic
Correct Answer: (C) Subacute (3–21 days).
Explanation:
- Why (C) is correct: As blood ages, it loses its high protein content and the iron is processed, causing the attenuation to drop. Between 3 and 21 days, the collection often becomes isodense to the brain, making it difficult to spot without looking for secondary signs like sulcal effacement or midline shift.
- Why (A) & (B) are wrong: Acute blood is hyperdense (bright, 60–80 HU).
- Why (D) is wrong: Chronic blood is hypodense (dark, similar to CSF).
- Why (E) is wrong: Acute-on-chronic would show a mixed-density collection (dark fluid with bright, fresh sediment).
Key Points: Evolution of SDH on CT
- Acute: Hyperdense (Bright).
- Subacute: Isodense (Same as brain – “The Great Mimicker”).
- Chronic: Hypodense (Dark/CSF-like).
- Tip: If you suspect an isodense SDH, look for midline shift or use IV contrast/MRI to see the membrane enhancement.
Question 3: Subarachnoid Haemorrhage (SAH)
Stem: A 45-year-old woman presents with the “worst headache of her life” (thunderclap headache). A non-contrast CT head shows hyperdense blood within the Sylvian fissures, interhemispheric fissure, and the suprasellar cistern.
Question: What is the most likely underlying cause of this spontaneous haemorrhage?
(A) Trauma (B) Ruptured berry aneurysm (C) Arteriovenous Malformation (AVM) (D) Hypertensive bleed (E) Amyloid angiopathy
Correct Answer: (B) Ruptured berry aneurysm.
Explanation:
- Why (B) is correct: While trauma is the most common cause of SAH overall, the clinical presentation of a thunderclap headache and a basal cistern distribution on CT is classic for a spontaneous SAH, usually caused by a ruptured saccular (berry) aneurysm (~85% of spontaneous cases).
- Why (A) is wrong: Traumatic SAH is usually found in the sulci over the brain convexities, not primarily in the basal cisterns.
- Why (C) is wrong: AVMs more commonly cause intraparenchymal haemorrhage.
- Why (D) & (E) are wrong: These causes typically lead to bleeds within the brain tissue itself (basal ganglia or lobar), not the subarachnoid space.
Key Points: Aneurysmal SAH
- Locations: Most common at the ACOM (30-35%), followed by PCOM and MCA bifurcation.
- CT Findings: Hyperdensity in basal cisterns, Sylvian fissures, and sulci.
- Complications: Vasospasm (days 4-14), Hydrocephalus, Re-bleeding.
Question 4: Diffuse Axonal Injury (DAI)
Stem: A 22-year-old unrestrained driver is involved in a high-speed rollover accident. His initial CT head is reported as “normal,” but he remains in a deep coma with a low GCS. An MRI of the brain is performed, showing several small areas of restricted diffusion in the corpus callosum and the dorsolateral midbrain.
Question: What is the most likely diagnosis?
(A) Cerebral Contusions (B) Diffuse Axonal Injury (DAI) (C) Hypoxic-Ischaemic Encephalopathy (HIE) (D) Brainstem Infarct (E) Concussion
Correct Answer: (B) Diffuse Axonal Injury (DAI).
Explanation:
- Why (B) is correct: DAI is caused by rotational acceleration/deceleration forces that shear axons. It is classically a “clinical-radiological mismatch”—the patient is in a coma but the CT is often normal. MRI (especially DWI and SWI/GRE) is the gold standard, showing lesions in the grey-white matter junction, corpus callosum, and brainstem.
- Why (A) is wrong: Contusions are visible on CT as “salt and pepper” bleeds in the frontal/temporal poles.
- Why (C) is wrong: HIE shows diffuse cortical and basal ganglia swelling, usually after cardiac arrest.
- Why (D) is wrong: An infarct would follow a vascular territory.
- Why (E) is wrong: Concussion is a clinical diagnosis with no visible imaging findings.
Key Points: Diffuse Axonal Injury (DAI)
- Mechanism: Shearing of axons due to rotation.
- Grading (Adams):
- Grade 1: Grey-white junction.
- Grade 2: Corpus callosum.
- Grade 3: Dorsolateral brainstem.
- Best Sequence: SWI or GRE (to see microhaemorrhages) and DWI (for acute shearing).
Question 5: Hyperacute Ischaemic Stroke (CT Sign)
Stem: A 70-year-old man presents with sudden-onset left-sided weakness and slurred speech (onset 45 minutes ago). The initial non-contrast CT head shows no obvious area of low attenuation. However, there is a focal hyperdensity within the horizontal segment of the right MCA.
Question: This finding is known as the “Dense MCA sign” and represents:
(A) An area of old calcified plaque. (B) Acute thrombus within the artery. (C) Active contrast extravasation. (D) A small subarachnoid haemorrhage in the Sylvian fissure. (E) Hypertensive changes in the vessel wall.
Correct Answer: (B) Acute thrombus within the artery.
Explanation:
- Why (B) is correct: The “Dense MCA sign” is one of the earliest signs of acute ischaemic stroke on CT. It represents the acute thrombus (clot) itself, which is more dense than flowing blood. It indicates a large vessel occlusion (LVO).
- Why (A) is wrong: Calcification would be much brighter (>100 HU) and usually irregular.
- Why (C) is wrong: No contrast was given in a non-contrast CT.
- Why (D) is wrong: Blood in the fissure would be in the CSF space, not outlining the tubular shape of the vessel.
Key Points: Early CT Signs of Stroke
- Dense MCA Sign: Represents acute thrombus.
- Insular Ribbon Sign: Loss of grey-white differentiation at the insular cortex.
- Disappearing Basal Ganglia Sign: Obscuration of the lentiform nucleus.
- Sulcal Effacement: Due to early cytotoxic oedema.
Question 6: Hypertensive Intracranial Haemorrhage
Stem: A 60-year-old man with poorly controlled hypertension presents with acute right-sided hemiplegia. A non-contrast CT head reveals a 4 cm hyperdense haemorrhage centered in the left putamen and internal capsule. There is no associated subarachnoid blood.
Question: What is the most likely etiology of this haemorrhage?
(A) Cerebral Amyloid Angiopathy (CAA) (B) Ruptured Aneurysm (C) Rupture of Charcot-Bouchard aneurysms (D) Venous Sinus Thrombosis (E) Haemorrhagic Transformation of an Infarct
Correct Answer: (C) Rupture of Charcot-Bouchard aneurysms.
Explanation:
- Why (C) is correct: Chronic hypertension leads to the formation of microaneurysms (Charcot-Bouchard) in the small perforating arteries. These classically rupture in the basal ganglia (putamen is most common), thalamus, pons, and cerebellum.
- Why (A) is wrong: CAA typically causes lobar (peripheral) haemorrhages in elderly patients.
- Why (B) is wrong: Ruptured aneurysms primarily cause SAH, though they can sometimes bleed into the brain tissue (e.g., ACOM into the gyrus rectus).
- Why (D) is wrong: Venous infarcts/bleeds are usually parasagittal or in the thalami and associated with dural sinus thrombosis.
Key Points: Hypertensive Bleeds
- Classic Locations: Putamen (35-50%), Subcortical white matter, Thalamus, Pons, Cerebellum.
- Imaging: Acute, homogeneous hyperdensity with surrounding vasogenic oedema.
Question 7: Cerebral Amyloid Angiopathy (CAA)
Stem: An 85-year-old woman with dementia presents with a new onset of right-sided weakness. A CT head shows a haemorrhage in the left parietal lobe. An MRI is performed, and the SWI (Susceptibility Weighted Imaging) sequence shows multiple, tiny “microbleeds” scattered throughout the peripheral cortico-subcortical junctions, sparing the basal ganglia.
Question: What is the most likely diagnosis?
(A) Hypertensive Haemorrhage (B) Cerebral Amyloid Angiopathy (CAA) (C) Diffuse Axonal Injury (DAI) (D) Septic Emboli (E) Cavernous Malformations
Correct Answer: (B) Cerebral Amyloid Angiopathy (CAA).
Explanation:
- Why (B) is correct: CAA is caused by amyloid deposition in the walls of small cortical arteries. This leads to lobar haemorrhages and multiple peripheral microbleeds. The key differentiator from hypertension is the sparing of the basal ganglia and thalami.
- Why (A) is wrong: Hypertension microbleeds are found in the central structures (basal ganglia, pons).
- Why (C) is wrong: DAI microbleeds occur at the grey-white junction and corpus callosum in a traumatic setting.
- Why (E) is wrong: Cavernomas (“popcorn” lesions) are usually larger and don’t typically present with such widespread peripheral microbleeding.
Key Points: Cerebral Amyloid Angiopathy (CAA)
- Demographic: Elderly, often associated with Alzheimer’s.
- Distribution: Peripheral / Lobar.
- Sparing: Classically spares the basal ganglia and thalami.
- Sign: Multiple microbleeds on SWI/GRE.
Question 8: Cerebral Venous Sinus Thrombosis (CVST)
Stem: A 30-year-old woman, 10 days post-partum, presents with a severe headache and a seizure. A contrast-enhanced CT venogram (CTV) is performed. The scan shows a filling defect in the posterior aspect of the superior sagittal sinus, described as the “Empty Delta Sign.”
Question: The “Empty Delta Sign” is a hallmark of:
(A) Arterial Ischaemic Stroke (B) Subdural Haematoma (C) Cerebral Venous Sinus Thrombosis (CVST) (D) Meningitis (E) Normal venous anatomy
Correct Answer: (C) Cerebral Venous Sinus Thrombosis (CVST).
Explanation:
- Why (C) is correct: The “Empty Delta Sign” is seen on contrast-enhanced CT/CTV. It represents the thrombus (which doesn’t enhance) in the centre of the superior sagittal sinus, surrounded by the enhancing collateral veins and dura at the periphery.
- Why (E) is wrong: While there are variants like a “bifid” sinus, a clear central filling defect in this clinical context (post-partum) is pathologic.
Key Points: CVST
- Risk Factors: Pregnancy/Post-partum, OCP use, Dehydration, Hypercoagulable states.
- Imaging:
- Non-contrast: “Dense Triangle Sign” or “Cord Sign” (hyperdense thrombus).
- Contrast-enhanced: “Empty Delta Sign” (filling defect).
- Complication: Venous infarcts, which are often bilateral and haemorrhagic.
Question 9: Uncal Herniation
Stem: A patient with a large right-sided temporal lobe tumour develops a sudden dilated and non-reactive right pupil and left-sided hemiplegia. A CT head shows the medial aspect of the right temporal lobe being displaced over the free edge of the tentorium cerebelli.
Question: This specific type of brain herniation is known as:
(A) Subfalcine Herniation (B) Uncal Herniation (C) Tonsillar Herniation (D) Upward Transtentorial Herniation (E) Extracranial Herniation
Correct Answer: (B) Uncal Herniation.
Explanation:
- Why (B) is correct: Uncal herniation occurs when the uncus (medial temporal lobe) is pushed over the tentorial edge. This compresses the ipsilateral CN III (causing a dilated pupil) and the ipsilateral cerebral peduncle (causing contralateral hemiplegia).
- Why (A) is wrong: Subfalcine herniation is the displacement of the cingulate gyrus under the falx cerebri (causing midline shift).
- Why (C) is wrong: Tonsillar herniation is the displacement of the cerebellar tonsils through the foramen magnum.
Key Points: Herniation Syndromes
- Subfalcine: Cingulate gyrus under the falx.
- Uncal: Medial temporal lobe over the tentorium. Compresses CN III.
- Tonsillar: Cerebellar tonsils through foramen magnum. Life-threatening (brainstem compression).
Question 10: Hypoxic-Ischaemic Encephalopathy (HIE)
Stem: A 10-year-old boy is brought to the ED after a near-drowning episode. He is comatose. A CT head performed 24 hours later shows diffuse loss of grey-white differentiation and oedema of the cerebral cortex and basal ganglia. The cerebellum and thalami, however, appear relatively hyperdense (bright) compared to the dark, oedematous cerebrum.
Question: This CT finding in HIE is known as the:
(A) “White Cerebellum Sign” (B) “Dense MCA Sign” (C) “Mount Fuji Sign” (D) “Panda Sign” (E) “Hummingbird Sign”
Correct Answer: (A) “White Cerebellum Sign”.
Explanation:
- Why (A) is correct: In global HIE (severe brain hypoxia), the cerebrum becomes severely oedematous and hypodense. The cerebellum and brainstem are often relatively spared or less affected, so they appear hyperdense (white) compared to the dark cerebral hemispheres. This is a very poor prognostic sign.
- Why (C) is wrong: The “Mount Fuji sign” is for tension pneumocephalus.
- Why (D) & (E) are wrong: These are signs for Wilson’s disease and Progressive Supranuclear Palsy (PSP), respectively.
Key Points: Hypoxic-Ischaemic Encephalopathy (HIE)
- Cause: Cardiac arrest, drowning, asphyxia.
- CT: Diffuse swelling, loss of grey-white matter distinction, “White Cerebellum Sign.”
- MRI: DWI is the most sensitive, showing restricted diffusion in the cortex and basal ganglia.
Question 11: Watershed Infarcts
Stem: An 80-year-old man experiences a severe episode of hypotension during surgery. Post-operatively, he has “man-in-a-barrel” syndrome (weakness of both arms but preserved leg strength). An MRI shows infarctions in the border zones between the territories of the MCA and ACA, and the MCA and PCA.
Question: This pattern of infarction is termed:
(A) Lacunar Infarcts (B) Malignant MCA Infarct (C) Watershed (Border-zone) Infarcts (D) Venous Infarcts (E) Cardioembolic Stroke
Correct Answer: (C) Watershed (Border-zone) Infarcts.
Explanation:
- Why (C) is correct: Watershed infarcts occur in the distal territories between major cerebral arteries. They are caused by global hypoperfusion (e.g., severe hypotension or carotid stenosis). The “man-in-a-barrel” clinical picture is classic for the ACA-MCA watershed distribution.
Key Points: Watershed Infarcts
- Mechanism: Low-flow / Hypoperfusion.
- External Watershed: Between ACA/MCA and MCA/PCA.
- Internal Watershed: Between deep and superficial perforators (seen as “string of beads” in the centrum semiovale).
Question 12: Basal Skull Fracture (Temporal Bone)
Stem: Following a motor vehicle accident, a patient has blood behind the eardrum (haemotympanum) and a facial nerve palsy. A high-resolution CT of the temporal bone shows a fracture line oriented perpendicular to the long axis of the petrous ridge, extending through the internal auditory canal.
Question: This fracture is classified as a:
(A) Longitudinal Temporal Bone Fracture (B) Transverse Temporal Bone Fracture (C) Diastatic Fracture (D) Depressed Skull Fracture (E) Le Fort Fracture
Correct Answer: (B) Transverse Temporal Bone Fracture.
Explanation:
- Why (B) is correct: Transverse fractures run perpendicular to the petrous ridge. Although less common than longitudinal fractures, they have a much higher risk of facial nerve injury (50%) and sensorineural hearing loss because they often cross the IAC and labyrinth.
- Why (A) is wrong: Longitudinal fractures run parallel to the petrous ridge and are more likely to cause ossicular dislocation and conductive hearing loss.
Key Points: Temporal Bone Fractures
- Longitudinal (Common): Parallel to petrous ridge. Ossicular chain disruption. Conductive hearing loss.
- Transverse (Rare/Severe): Perpendicular to ridge. Facial nerve palsy. Sensorineural hearing loss.
Question 13: ASCORED / ASPECTS Score
Stem: A radiologist is reviewing a CT head for a “code stroke” patient. They are assessing the ASPECTS (Alberta Stroke Program Early CT Score) to determine the extent of early ischaemic changes in the MCA territory.
Question: The ASPECTS score starts at 10 points. For every area of the MCA territory showing early ischaemic changes, how is the score adjusted?
(A) One point is added. (B) One point is subtracted. (C) The score is doubled. (D) The score remains the same; it is only a qualitative assessment. (E) Two points are subtracted.
Correct Answer: (B) One point is subtracted.
Explanation:
- Why (B) is correct: ASPECTS is a 10-point quantitative score. You subtract one point for each of the 10 defined regions (e.g., Caudate, Lentiform, Insula, and M1-M6) that show early ischaemic changes (loss of grey-white distinction). A score of 10 is normal, while a lower score indicates a larger area of stroke. A score < 7 usually indicates a poor prognosis for thrombolysis.
Key Points: ASPECTS Score
- Territory: MCA only.
- Calculation: Start at 10, subtract 1 per area involved.
- Regions: Caudate, Lentiform, Insula, Internal Capsule, and MCA levels M1 through M6.
Question 14: Carotid Artery Dissection
Stem: A 35-year-old man presents with acute neck pain and a partial Horner’s syndrome (miosis and ptosis) after a chiropractic neck manipulation. A CTA of the neck shows a narrow, tapered “string sign” in the left internal carotid artery and a crescent-shaped thickening of the vessel wall.
Question: What is the most likely diagnosis?
(A) Atherosclerotic Stenosis (B) Carotid Artery Dissection (C) Fibromuscular Dysplasia (FMD) (D) Takayasu’s Arteritis (E) Carotid Body Tumour
Correct Answer: (B) Carotid Artery Dissection.
Explanation:
- Why (B) is correct: This is a classic presentation (trauma/manipulation + neck pain + Horner’s). The crescent-shaped wall thickening on CTA/MRI represents the intramural haematoma. The “string sign” is the narrowed true lumen.
- Why (C) is wrong: FMD shows a “string of beads” appearance, not a crescentic wall haematoma.
Key Points: Carotid Dissection
- Clinical: Neck pain + Horner’s Syndrome + Ischaemic symptoms.
- Imaging: Crescent-shaped mural haematoma (T1-bright on MRI), “string sign” of the lumen.
- Location: Usually starts distal to the carotid bulb.
Question 15: Chronic Subdural Haematoma (Evolution)
Stem: A CT head of a 90-year-old patient with a fall 4 weeks ago shows a crescentic collection that is uniformly hypodense (attenuation ~15 HU), similar to CSF. There is mild mass effect on the underlying brain.
Question: The most common surgical complication to look for on a post-operative scan after draining this collection is:
(A) Re-bleeding (Acute-on-chronic) (B) Tension Pneumocephalus (C) Subdural Empyema (D) Normal Pressure Hydrocephalus (E) Cortical Atrophy
Correct Answer: (A) Re-bleeding (Acute-on-chronic).
Explanation:
- Why (A) is correct: Chronic SDHs are prone to re-bleeding from the fragile neo-membranes that form within the collection. This appears as “acute-on-chronic” SDH (bright fresh blood layering within the dark chronic fluid).
- Why (B) is wrong: Pneumocephalus (air) is common after any neurosurgery but is rarely “tension” unless there is a specific valve mechanism.
Key Points: Chronic SDH
- Density: Hypodense (dark).
- Evolution: Occurs > 3 weeks after trauma.
- Appearance: Can have internal membranes or “sepations.”
- Risk: High rate of recurrence or re-bleeding after drainage.
