Neuroradiology — MCQs

Neuroradiology Indian Medical PG Practice Questions and MCQs

Question 21: Which of the following is NOT a radiological feature of meningioma?

A. Lamellar calcification
B. Enlarged foramen spinosum
C. Increased meningeal vascular markings
D. Decalcification of the inner table (Correct Answer)

Explanation: ### Explanation **Meningiomas** are the most common benign intracranial tumors, arising from the arachnoid cap cells. Their radiological features are primarily driven by their slow growth and high vascularity derived from the meningeal vessels. **Why "Decalcification of the inner table" is the correct answer:** Meningiomas typically cause **hyperostosis** (thickening and increased density) of the overlying bone, rather than decalcification or erosion. This reactive bone formation occurs due to tumor invasion of the haversian canals or as a response to chronic irritation. Therefore, decalcification (thinning/destruction) of the inner table is not a characteristic feature. **Analysis of Incorrect Options:** * **A. Lamellar calcification:** Meningiomas frequently contain **Psammoma bodies**, which are microscopic, laminated (lamellar) calcifications. On CT, roughly 20–25% of meningiomas show visible calcification. * **B. Enlarged foramen spinosum:** Meningiomas are highly vascular and often receive their blood supply from the **middle meningeal artery**. Chronic increased blood flow through this artery leads to the compensatory enlargement of the foramen spinosum. * **C. Increased meningeal vascular markings:** Due to the recruitment of dural vessels (external carotid artery branches), X-rays often show prominent, tortuous vascular grooves on the inner table of the skull leading toward the tumor site. **NEET-PG High-Yield Pearls:** * **Gold Standard Imaging:** Contrast-enhanced MRI (shows the characteristic **"Dural Tail Sign"**). * **Angiography:** Shows a **"Sunburst"** or **"Mother-in-law"** appearance (tumor flushes early and stays late). * **Histology:** Look for **Psammoma bodies** and **whorled patterns** of cells. * **Location:** Most common at the parasagittal region/convexities.

Question 22: What is true about the MRI/CT appearance of a lateral meningocele?

A. Solid dural masses
B. Usually outside the spinal canal
C. Widened neural foramen (Correct Answer)
D. Generally, there is no spinal cord compression and deformity

Explanation: **Explanation:** A **Lateral Meningocele** is a protrusion of the arachnoid and dura mater through an enlarged intervertebral foramen. It is most commonly associated with **Neurofibromatosis Type 1 (NF-1)**. **1. Why "Widened neural foramen" is correct:** The hallmark of a lateral meningocele is the herniation of the thecal sac through the neural foramen. Over time, the CSF pressure within the meningocele causes **pressure erosion** of the surrounding bone. This leads to the characteristic imaging finding of a **widened neural foramen**, often accompanied by scalloping of the posterior vertebral bodies and thinning of the pedicles. **2. Analysis of Incorrect Options:** * **A. Solid dural masses:** This is incorrect because a meningocele is a **cystic** lesion. On MRI, it follows CSF signal intensity (hypointense on T1, hyperintense on T2) and does not show internal solid enhancement. * **B. Usually outside the spinal canal:** While the "sac" protrudes outward, the condition is defined by its communication with the spinal subarachnoid space. It is an extension of the spinal canal contents, not a separate entity outside it. * **D. Generally, there is no spinal cord compression and deformity:** This is incorrect. Large meningoceles can cause significant **mass effect**, leading to spinal cord compression, displacement, and progressive kyphoscoliosis. **High-Yield Facts for NEET-PG:** * **Association:** Strongly associated with **NF-1** (found in ~70-85% of cases). * **Location:** Most common in the **thoracic spine** (apex of the convex side of a scoliosis curve). * **Differential Diagnosis:** Must be distinguished from a **Schwannoma** (which is solid and enhances) and a **Paravertebral Abscess**. * **Imaging Gold Standard:** **MRI** is the investigation of choice to demonstrate the communication with the subarachnoid space.

Question 23: 'Tiger eye' appearance on MRI brain is a characteristic feature of which of the following conditions?

A. Refsum's disease
B. Hallervorden Spatz disease (Correct Answer)
C. NARP mitochondrial disease
D. Abetalipoproteinemia

Explanation: ### Explanation **Correct Answer: B. Hallervorden Spatz disease** **Understanding the 'Eye of the Tiger' Sign:** The 'Eye of the Tiger' appearance is a pathognomonic MRI finding seen on **T2-weighted images** of the brain. It is characteristic of **Hallervorden-Spatz disease**, now more commonly known as **Pantothenate Kinase-Associated Neurodegeneration (PKAN)**, a type of Neurodegeneration with Brain Iron Accumulation (NBIA). * **Pathophysiology:** The appearance is caused by excessive iron deposition in the **globus pallidus**. * **Imaging Anatomy:** It consists of a central area of **hyperintensity** (representing gliosis and vacuolization) surrounded by a rim of **hypointensity** (representing iron/hemosiderin deposition). This contrast mimics the appearance of a tiger's eye. **Analysis of Incorrect Options:** * **A. Refsum’s Disease:** A peroxisomal disorder (phytanic acid storage) characterized by retinitis pigmentosa, ataxia, and neuropathy. MRI typically shows non-specific white matter changes or cerebellar atrophy, not the tiger eye sign. * **C. NARP (Neuropathy, Ataxia, and Retinitis Pigmentosa):** A mitochondrial DNA disorder. MRI usually shows symmetrical lesions in the basal ganglia similar to Leigh syndrome, but lacks the specific central hyperintensity of PKAN. * **D. Abetalipoproteinemia:** A fat malabsorption syndrome leading to Vitamin E deficiency. It primarily affects the posterior columns of the spinal cord (similar to Subacute Combined Degeneration) rather than the globus pallidus. **High-Yield Clinical Pearls for NEET-PG:** * **Gene Mutation:** PKAN is caused by a mutation in the **PANK2 gene** (Chromosome 20p). * **Clinical Triad:** Extrapyramidal symptoms (dystonia, rigidity), pigmentary retinopathy, and cognitive decline. * **Differential for Basal Ganglia Hypointensity:** Always consider iron deposition (NBIA), Wilson’s disease (though Wilson's usually shows the "Face of the Giant Panda" sign in the midbrain), and Carbon Monoxide poisoning.

Question 24: Which peak on MR spectroscopy is seen in tuberculoma?

A. Lipid lactate (Correct Answer)
B. N-acetyl aspartate
C. Creatinine
D. Choline

Explanation: **Explanation:** In Magnetic Resonance Spectroscopy (MRS), the presence of a **Lipid-Lactate peak** is a hallmark finding for **CNS Tuberculosis (Tuberculoma)**. 1. **Why Lipid-Lactate is correct:** Tuberculomas are characterized by solid caseous necrosis. The cell walls of *Mycobacterium tuberculosis* are exceptionally rich in lipids (mycolic acids). During the necrotic process, these lipids are released, resulting in a prominent **lipid peak** (at 0.9 and 1.3 ppm). Additionally, the anaerobic metabolism within the granuloma leads to the accumulation of **lactate** (at 1.33 ppm), which typically appears as a doublet. 2. **Why other options are incorrect:** * **N-acetyl aspartate (NAA):** This is a marker of neuronal integrity. It is **decreased** in almost all pathological lesions (tumors, infections, infarcts) because of the displacement or destruction of healthy neurons. * **Creatine:** This represents energy metabolism. It is usually stable or decreased in lesions; it is not a specific marker for infection. * **Choline:** This is a marker of cell membrane turnover. While it may be mildly elevated in inflammatory processes, a significantly high Choline peak is more characteristic of **malignant tumors** (like high-grade gliomas) rather than tuberculomas. **High-Yield Clinical Pearls for NEET-PG:** * **Tuberculoma vs. Neurocysticercosis (NCC):** On MRS, Tuberculomas show a high lipid peak, whereas NCC typically shows peaks of succinate, acetate, and amino acids (like leucine). * **The "Target Sign":** On MRI, a central calcification or enhancement surrounded by a hypointense rim is classic for tuberculoma. * **MRS Peaks Summary:** * **NAA (2.0 ppm):** Neuronal marker. * **Choline (3.2 ppm):** Membrane turnover (Tumors). * **Creatine (3.0 ppm):** Energy stores. * **Lipid/Lactate (1.3 ppm):** Necrosis/Infection.

Question 25: The "Rail Road pattern" in neuroimaging is typically seen in which of the following conditions?

A. Tuberous sclerosis
B. Sturge weber syndrome (Correct Answer)
C. Ataxia telengiectasia
D. Neurofibromatosis

Explanation: ### Explanation **Sturge-Weber Syndrome (SWS)**, also known as encephalotrigeminal angiomatosis, is the correct answer. The "Rail Road pattern" (or "Tram-track" appearance) refers to the characteristic **gyriform intracranial calcifications** seen on a CT scan or skull X-ray. 1. **Why it occurs:** SWS is characterized by a leptomeningeal angioma (usually ipsilateral to a facial Port-wine stain). This vascular malformation leads to chronic venous stasis and localized hypoxia in the underlying cerebral cortex. This results in cortical atrophy and the deposition of calcium in the second and third layers of the cerebral cortex, following the contours of the gyri and sulci, thus creating the "Rail Road" or "Tram-track" appearance. 2. **Analysis of Incorrect Options:** * **Tuberous Sclerosis:** Characterized by "Candle guttering" appearance (subependymal nodules) and cortical tubers, but not gyriform calcification. * **Ataxia Telangiectasia:** Primarily involves cerebellar atrophy; it does not typically present with specific intracranial calcification patterns. * **Neurofibromatosis (NF-1):** Associated with sphenoid wing dysplasia, optic nerve gliomas, and "unidentified bright objects" (UBOs) on MRI, but not the Rail Road pattern. ### High-Yield Clinical Pearls for NEET-PG: * **Imaging Gold Standard:** While CT shows calcification best, **Contrast-enhanced MRI** is the most sensitive investigation to detect the leptomeningeal angioma (seen as pial enhancement). * **Clinical Triad:** 1. Facial Port-wine stain (Nevus flammeus, usually in $V_1/V_2$ distribution); 2. Leptomeningeal angioma (causing seizures/hemiparesis); 3. Glaucoma. * **Genetics:** Caused by a somatic mutation in the **GNAQ gene**. It is *not* inherited (sporadic). * **Skull X-ray:** The calcifications are usually not visible until after 2 years of age.

Question 26: In children, increased intracranial pressure is manifested by which of the following?

A. Lytic lesions in the skull wall
B. Rarification of the dorsum of the sella
C. Sutural diastasis (Correct Answer)
D. None of the above

Explanation: **Explanation:** In children, the skull is a dynamic structure where the cranial bones are not yet fused, being held together by fibrous joints called sutures. When intracranial pressure (ICP) increases, the expanding brain or cerebrospinal fluid exerts outward pressure. In pediatric patients (typically up to age 10–12), this results in **Sutural Diastasis**—the widening of the cranial sutures (usually >2mm). This is the most sensitive and earliest radiological sign of increased ICP in children, as the skull expands to accommodate the pressure. **Analysis of Options:** * **Sutural Diastasis (Correct):** As explained, the unfused sutures in children act as a "pressure release valve," making this the hallmark sign. * **Rarification of the dorsum sellae (Incorrect):** While this is a classic sign of chronic increased ICP, it is primarily seen in **adults** or older children whose sutures have already fused. In these cases, the pressure is transmitted to the bony sella turcica, leading to erosion. * **Lytic lesions (Incorrect):** Lytic lesions represent focal bone destruction (e.g., Multiple Myeloma, Metastasis, or Langerhans Cell Histiocytosis) and are not a physiological response to generalized intracranial pressure. **High-Yield Clinical Pearls for NEET-PG:** * **Copper Beaten Skull (Silver Beaten):** Gyral impressions on the inner table of the skull due to chronic increased ICP. While suggestive, it can be a normal finding in growing children (ages 4–10). * **Macewen’s Sign:** A "cracked pot" sound heard on percussion of the skull, clinically correlating with sutural diastasis. * **Adult Signs of Increased ICP:** Erosion of the dorsum sellae, thinning of the floor of the sella, and enlargement of the internal auditory canal (if associated with specific tumors).

Question 27: An extra-axial enhancing lesion is seen on MRI. What is the most likely diagnosis?

A. Meningioma (Correct Answer)
B. Ependymoma
C. Arachnoid cyst
D. Lipoma

Explanation: **Explanation:** The diagnosis of an extra-axial lesion is based on specific imaging features: displacement of the subarachnoid space, widening of the bony margins, and the "CSF cleft sign." **1. Why Meningioma is correct:** Meningiomas are the most common **extra-axial** intracranial tumors. On MRI, they typically appear as well-circumscribed, dural-based masses that are isointense to gray matter on T1 and T2 sequences. Crucially, they show **intense, homogenous enhancement** after gadolinium administration and often exhibit a **"Dural Tail Sign"** (thickening of the adjacent dura), which is a classic NEET-PG high-yield finding. **2. Why the other options are incorrect:** * **Ependymoma:** These are typically **intra-axial** (specifically intraventricular) tumors. In children, they commonly arise from the floor of the 4th ventricle and may extend through the foramina of Luschka and Magendie ("plastic ependymoma"). * **Arachnoid Cyst:** While extra-axial, these are CSF-filled sacs. They follow CSF signal intensity on all sequences (dark on T1, bright on T2) and **do not enhance** with contrast. * **Lipoma:** These are composed of fat. They appear hyperintense (bright) on T1 and show a characteristic **drop in signal on fat-suppression sequences**. They do not show typical solid enhancement. **High-Yield Clinical Pearls for NEET-PG:** * **Meningioma Association:** Often associated with **NF-2** (especially if bilateral or multiple). * **Histology:** Look for **Psammoma bodies** (concentric calcifications) and whorled patterns. * **Imaging Sign:** The **"Sunburst" or "Spoke-wheel" appearance** on angiography due to supply from the middle meningeal artery. * **Location:** Most common at the parasagittal/falcine region.

Question 28: What is the investigation of choice for cystic lesions in the brain?

A. Ultrasound
B. Angiography
C. CT Scan (Correct Answer)
D. MRI scan

Explanation: **Explanation:** The investigation of choice for identifying and characterizing **cystic lesions in the brain** is a **CT Scan**. **Why CT Scan is the Correct Choice:** In the context of neuroimaging, a CT scan is highly sensitive at detecting fluid-filled spaces (cysts) because fluid has a characteristic low attenuation (0–20 Hounsfield Units). CT is particularly superior for identifying **calcification** within the cyst wall or internal components (e.g., the scolex in Neurocysticercosis), which is a critical diagnostic feature. Furthermore, contrast-enhanced CT (CECT) effectively demonstrates ring enhancement, helping differentiate between simple cysts, abscesses, and cystic tumors. **Analysis of Incorrect Options:** * **Ultrasound (A):** Limited by the adult skull; it is only useful in neonates through the open anterior fontanelle. * **Angiography (B):** This is an invasive procedure used to visualize vascular structures (aneurysms, AVMs) and does not provide detail on the internal morphology of cystic lesions. * **MRI Scan (D):** While MRI offers superior soft-tissue contrast and is excellent for evaluating the brain parenchyma, CT remains the preferred initial "investigation of choice" for cystic lesions due to its ability to detect calcification and its widespread availability in emergency settings. **High-Yield Clinical Pearls for NEET-PG:** * **Neurocysticercosis (NCC):** The most common cause of seizures worldwide; CT shows the "hole-with-a-dot" appearance (scolex). * **Hydatid Cyst:** Appears as a large, unilocular cyst with a "water lily sign" or "double-line sign" on imaging. * **Arachnoid Cysts:** Follow CSF density on all sequences and do not show contrast enhancement. * **Gold Standard for Calcification:** Always choose **CT** over MRI for any lesion where calcification is a diagnostic hallmark.

Question 29: Extradural hemorrhage is seen as:

A. Hyperdense biconvex (Correct Answer)
B. Hypodense biconcave
C. Hyperdense biconcave
D. Hypodense biconvex

Explanation: ### Explanation **Extradural Hemorrhage (EDH)** occurs when blood collects between the inner table of the skull and the dura mater, most commonly due to a rupture of the **middle meningeal artery** following a temporal bone fracture. **1. Why "Hyperdense Biconvex" is correct:** * **Hyperdense:** On a non-contrast CT (NCCT) scan, acute blood appears white (hyperdense) because of the high hemoglobin concentration. * **Biconvex (Lentiform):** The dura mater is firmly attached to the skull at the cranial sutures. As the arterial bleed expands under high pressure, it cannot easily cross these suture lines. This forces the hematoma to bulge inward toward the brain, creating a characteristic **lemon-shaped** or biconvex appearance. **2. Why the other options are incorrect:** * **B & D (Hypodense):** Hypodensity (dark appearance) on CT typically indicates old blood (chronic stage), CSF, or edema. Acute EDH is almost always hyperdense. * **B & C (Biconcave):** A biconcave (crescent-shaped) appearance is the hallmark of a **Subdural Hemorrhage (SDH)**. SDH occurs in the potential space between the dura and arachnoid mater; since this space is not limited by sutures, the blood spreads thinly along the brain's curvature. ### NEET-PG High-Yield Pearls * **Classic Clinical Presentation:** A "Lucid Interval" (initial loss of consciousness → temporary recovery → rapid deterioration). * **Source of Bleed:** Arterial (90%), specifically the **Middle Meningeal Artery** (branch of the maxillary artery). * **Anatomical Landmark:** Often associated with a fracture at the **Pterion**. * **Key Constraint:** EDH **does not cross suture lines** but can cross the midline (dural folds like the falx). In contrast, SDH can cross suture lines but does not cross the midline.

Question 30: Subependymal calcified nodules are seen in which of the following conditions?

A. Sturge Weber syndrome
B. Tuberous sclerosis (Correct Answer)
C. Neurofibromatosis type 2
D. Von Hippel Lindau syndrome

Explanation: **Explanation:** **Tuberous Sclerosis Complex (TSC)** is the correct answer. It is a neurocutaneous syndrome (phakomatosis) characterized by the classic **Vogt’s triad** of seizures, intellectual disability, and adenoma sebaceum. The hallmark neuroimaging findings include: 1. **Subependymal Nodules (SENs):** These are small hamartomas located along the walls of the lateral ventricles. They frequently undergo **calcification** (best seen on CT) and have a "candle-guttering" appearance. 2. **Subependymal Giant Cell Astrocytoma (SEGA):** A benign tumor typically located near the Foramen of Monro. 3. **Cortical Tubers:** Areas of cortical dysplasia. **Why the other options are incorrect:** * **Sturge-Weber Syndrome:** Characterized by **"tram-track" cortical calcifications** (gyriform) and leptomeningeal angiomatosis, usually in the occipital/parietal regions, not subependymal nodules. * **Neurofibromatosis Type 2 (NF2):** Associated with the **MISME** mnemonic (Multiple Inherited Schwannomas, Meningiomas, and Ependymomas). Bilateral vestibular schwannomas are the pathognomonic feature. * **Von Hippel-Lindau (VHL):** Characterized by **hemangioblastomas** of the cerebellum and retina, along with renal cell carcinoma and pheochromocytoma. **High-Yield Clinical Pearls for NEET-PG:** * **Ash-leaf spots** (hypopigmented macules) are the earliest cutaneous sign of TSC. * **Shagreen patches** (connective tissue nevi) are commonly found on the lower back. * **Cardiac Rhabdomyomas** are the most common fetal/neonatal cardiac tumors associated with TSC (often regress spontaneously). * **Renal Angiomyolipomas (AMLs)** are the most common renal manifestation.

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