• a. CT brain plain (Bone window): Left occipital bone fracture line with slight diastasis and overlying extracranial scalp soft tissue swelling.

• b. Primary survey in trauma resuscitation: Order of priority in initial assessment and resuscitation:
  • A: Airway maintenance with cervical spine stabilization/protection
  • B: Breathing and ventilation
  • C: Circulation with bleeding/hemorrhage control
  • D: Disability — neurologic status evaluation (GCS, pupils)
  • E: Exposure (complete visualization) and Environmental control (hypothermia prevention)
• c. PECARN rule: Pediatric Emergency Care Applied Research Network rule clinically predicts/identifies children at very low risk of clinically important traumatic brain injury (ciTBI) to avoid unnecessary CT head scans.
• d. PECARN Clinical Prediction Rule:

For age < 2 years:

CT Recommendation	Clinical Conditions
CT Recommended	GCS < 15, Altered mental status, or Palpable skull fracture
Observation vs CT (CT if multiple findings, worsening signs, age < 3 months, or parental preference)	Non-frontal scalp hematoma, Loss of consciousness (LOC) > 5 seconds, Severe mechanism of injury, or Not acting normally per parent

For age ≥ 2 years:

CT Recommendation	Clinical Conditions
CT Recommended	GCS < 15, Altered mental status, or Signs of basilar skull fracture (hemotympanum, CSF otorrhea/rhinorrhea, raccoon eyes, Battle sign)
Observation vs CT (CT if multiple findings, worsening signs, or parental preference)	History of LOC, History of vomiting, Severe mechanism of injury, or Severe headache

• a. CT brain plain (Brain window): Soft tissue swelling in left temporal region, biconvex / lenticular hyperdense extra-axial lesion in left temporoparietal region — suggestive of extradural hemorrhage (EDH).
  • Mnemonic (BCCT for hyperdense lesion on CT brain): Blood, Calcification, Contrast-enhanced ring lesion, Tuber.
  • Mnemonic for EDH: Biconvex / lens-shaped (side view of idli).
• b. Tearing of branches of the middle meningeal artery (less commonly middle meningeal vein or dural venous sinus) between the dura mater and inner table of the skull.
• c. Uncal/transtentorial herniation, raised intracranial pressure, seizures, and respiratory arrest.
• d. Lucid interval: Transient initial loss of consciousness after trauma followed by temporary recovery of normal consciousness, and subsequent rapid neurological deterioration as the arterial hematoma expands.
• e. Management:
  • Airway, breathing, and circulation stabilization.
  • Neuroprotective measures: 30° head-end elevation, maintain normothermia, normoglycemia, normal electrolytes, and avoid hypovolemia/hypotension.
  • Urgent neurosurgical consultation for craniotomy and surgical evacuation of hematoma if volume > 30 mL, thickness > 15 mm, midline shift > 5 mm, or GCS < 9 / neurological deterioration.

• a. CT brain plain: Extra-axial hyperdense crescent-shaped (concavo-convex) collection along the left cerebral hemisphere with compression of left lateral ventricle and significant midline shift — Acute Subdural Hemorrhage (SDH).
• b. Tearing of bridging cortical veins traversing the subdural space between arachnoid and dural venous sinuses.
• c.
  • Acute SDH: Hyperdense (bright white, 0–3 days).
  • Subacute SDH: Isodense (3 days – 3 weeks).
  • Chronic SDH: Hypodense (dark, > 3 weeks).
• d. ABC stabilization, emergency seizure termination (IV benzodiazepine followed by Levetiracetam/Fosphenytoin loading), hyperosmolar therapy (3% NaCl / Mannitol) for raised ICP, and urgent neurosurgical craniotomy/burr hole evacuation.

• a. Cutaneous ecchymosis and bruising on the left arm and forearm with acute neurological deterioration, indicating a systemic bleeding diathesis with intracranial hemorrhage.
• b. CT brain plain: Hyperdense intraparenchymal hemorrhage in the left temporal lobe with surrounding hypodense perilesional edema.
• c. Late Vitamin K Deficiency Bleeding (VKDB), inherited bleeding disorders (Hemophilia A/B, Factor VII deficiency), severe immune thrombocytopenia, child abuse / non-accidental trauma, and vascular malformations (AVM).
• d. Late-onset Vitamin K Deficiency Bleeding (VKDB) in an exclusively breastfed, home-delivered infant who missed neonatal prophylactic vitamin K.
• e. Routine administration of intramuscular Vitamin K1 (1 mg IM) at birth to all neonates.
• f. PIVKA-II (Proteins Induced by Vitamin K Absence or Antagonist-II) / undercarboxylated prothrombin.

• a.
  • CT brain plain (Image A): Bilateral scalp hematomas with punctate microhemorrhages at the grey-white matter junction without focal mass lesion or midline shift.
  • MRI brain (Images B & C): Multiple punctate hyperintense foci on T2/FLAIR in the subcortical white matter of the right frontal lobe and the splenium of the corpus callosum.
• b. Diffuse Axonal Injury (DAI).
• c. Shearing and rotational acceleration-deceleration forces that stretch and tear axonal cytoskeleton and microvasculature across grey-white matter boundaries, corpus callosum, and upper brainstem.

• a. CT brain plain: Prominent periventricular punctate and linear calcifications outlining the anterior horns of the lateral ventricles, along with cerebral volume loss (widened interhemispheric and Sylvian fissures).
• b. Congenital Cytomegalovirus (CMV) infection.
• c. Chorioretinitis (and optic atrophy).

• a.
  • Plain CT (Image A): Well-defined hypodense lesion in the right parietal cortex.
  • CECT (Image B): Thick-walled, conglomerate ring-enhancing lesion with extensive surrounding hypodense vasogenic edema.
• b. Differential diagnosis: Intracranial Tuberculoma vs. Neurocysticercosis (NCC).

Feature	Neurocysticercosis (NCC)	Tuberculoma
Size	Usually < 20 mm	Often > 20 mm
Wall	Thin, smooth, regular ring	Thick, irregular, nodular ring
Scolex	Often visible as eccentric bright nodule	Absent
Edema	Mild to moderate perifocal edema	Severe, extensive vasogenic edema
Location	Corticomedullary junction	Supratentorial or infratentorial

• c. Treatment plan for CNS Tuberculoma:
  • Standard Antitubercular Therapy (ATT): 2 months intensive HRZE followed by 7–10 months continuation HRE.
  • Adjuvant systemic corticosteroids (prednisolone 1–2 mg/kg/day or dexamethasone 0.6 mg/kg/day for 4 weeks, then tapered over 4 weeks) to reduce cerebral edema and prevent paradoxical expansion.
  • Antiseizure medication (e.g., Levetiracetam, Carbamazepine).

• a. Diagnosis: Neurocysticercosis (NCC) illustrating different evolutionary stages of parenchymal larval infection.
• b.
  • Image A (CECT): Thin-walled cyst with central non-enhancing fluid and hyperdense eccentric scolex without surrounding edema — Vesicular stage (viable, quiescent).
  • Image B (MRI T2/FLAIR): Thick enhancing cyst wall with turbid fluid content and extensive perilesional vasogenic edema — Colloidal vesicular stage (degenerating parasite, highly symptomatic).
  • Image C (MRI / CT): Small, punctate, calcified nodule without perilesional edema — Nodular calcified stage (healed, inactive scar).
• c. Taenia solium (larval stage of pork tapeworm / Cysticercus cellulosae).
• d. False. Humans acquire cysticercosis by ingesting Taenia solium eggs via contaminated water, vegetables, or fecal-oral contamination from a human tapeworm carrier (not by eating pork itself, which causes intestinal taeniasis).

• a. Prominent gyriform / serpentine cortical calcifications ("tram-track" sign) along the right cerebral cortex with ipsilateral cerebral hemiatrophy.
• b. Leptomeningeal capillary-venous angiomatosis causing chronic venous stasis, cortical hypoperfusion, ischemia, and subsequent cortical calcification and laminar necrosis.
• c. Sturge-Weber syndrome (Encephalotrigeminal angiomatosis).
• d. Glaucoma, buphthalmos, choroidal hemangioma, and episcleral hemangioma.
• e. No. It is caused by a non-hereditary, postzygotic somatic activating mutation in the GNAQ gene.

• a.
  • Image A: Multiple hyperdense calcified cortical and subcortical tubers.
  • Image B: Dense calcified subependymal nodules (SENs) projecting into the lateral ventricles ("candle-guttering" appearance).
• b. Tuberous Sclerosis Complex (Bourneville disease).
• c. Cutaneous manifestations: Hypomelanotic macules (ash-leaf spots), facial angiofibromas (adenoma sebaceum), shagreen patches (connective tissue nevi), ungual/periungual fibromas (Koenen tumors), and confetti skin lesions.
• d. Systemic manifestations:
  • CNS: Subependymal giant cell astrocytoma (SEGA), epilepsy, intellectual disability, autism spectrum disorder.
  • Cardiac: Cardiac rhabdomyomas.
  • Renal: Renal angiomyolipomas, renal cysts, renal cell carcinoma.
  • Pulmonary: Lymphangioleiomyomatosis (LAM), multifocal micronodular pneumocyte hyperplasia.
  • Ocular: Retinal astrocytic hamartomas.

• a. Marked symmetric dilatation of both lateral ventricles and the third ventricle with a normal-sized, non-dilated fourth ventricle.

• b. Obstructive (non-communicating) hydrocephalus.
• c. Congenital aqueductal stenosis (Sylvian aqueduct narrowing).
• d. Normal CSF Pathway:
  • Choroid plexuses of lateral ventricles $\to$ Foramen of Monro $\to$ Third ventricle $\to$ Aqueduct of Sylvius $\to$ Fourth ventricle $\to$ Foramina of Luschka & Magendie $\to$ Subarachnoid space & basal cisterns $\to$ Absorption through arachnoid villi/granulations into superior sagittal sinus.

• a. Generalized dilatation involving all ventricles (lateral, third, and fourth ventricles) with effacement of cortical sulci — Communicating hydrocephalus.

• b. Impaired CSF resorption at the arachnoid villi/granulations into dural venous sinuses (e.g., following pyogenic/tuberculous meningitis, intraventricular hemorrhage).
• c. Surgical diversion of CSF: Ventriculoperitoneal (VP) shunt placement or Endoscopic Third Ventriculostomy (ETV) with choroid plexus cauterization.

• a. Well-defined, rounded hypodense lesion in the right occipital lobe with thin surrounding ring and perilesional vasogenic edema.
• b. Brain Abscess in the right occipital lobe.
• c. Cyanotic congenital heart disease with right-to-left shunt (bypass of pulmonary capillary phagocytic filtration), chronic suppurative otitis media (CSOM), mastoiditis, paranasal sinusitis, dental infections, and meningitis.
• d. Streptococcus viridans, Streptococcus pneumoniae, Staphylococcus aureus, Enterococcus, Citrobacter koseri (neonates), and anaerobes (Bacteroides, Peptostreptococcus).
• e. Indications for surgical aspiration / excision:
  • Abscess size $>2.5\text{ cm}$ in diameter.
  • Significant mass effect, midline shift, or raised ICP.
  • Location in posterior fossa / proximity to ventricular system (risk of intraventricular rupture).
  • Presence of gas within the abscess cavity.
  • Fungal or multiloculated abscess.
  • Failure to improve after 2–3 weeks of targeted IV antimicrobial therapy.

• a. Craniopharyngioma (suprasellar/sellar calcified mass compressing the optic chiasm and pituitary stalk).
• b. Endocrinological manifestations:
  • Growth hormone (GH) deficiency $\to$ Short stature / growth failure
  • Gonadotropin (LH/FSH) deficiency $\to$ Delayed / absent puberty
  • TSH deficiency $\to$ Central hypothyroidism
  • ACTH deficiency $\to$ Secondary adrenal insufficiency (lethargy, hypoglycemia, hypotension)
  • ADH / Vasopressin deficiency $\to$ Central diabetes insipidus (polyuria, polydipsia)

• a. CT brain plain: Symmetrical, patchy, subcortical hypodense lesions predominantly affecting the parieto-occipital white matter bilaterally.
• b. Posterior Reversible Encephalopathy Syndrome (PRES).
• c. Severe acute hypertension secondary to Acute Post-Streptococcal Glomerulonephritis (APSGN).

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Basics of MRI Brain Interpretation

• Common Sequences:
  • T1W (Plain): Best for anatomical detail (CSF is dark/hypointense, white matter is hyperintense).
  • T1W + Contrast: Identifies breakdown of blood-brain barrier (infections, tumors).
  • T2W: Best for visualizing pathology, edema, and demyelination (CSF is bright/hyperintense).
  • FLAIR: T2 with CSF suppression (CSF is dark; periventricular lesions and edema stand out brightly).
  • DWI: Restricts water movement; acute ischemic stroke/infarct appears bright.
  • SWI / GRE: Identifies paramagnetic substances; microhemorrhages and calcifications appear black (signal drop-out).

Magnetic Resonance Spectroscopy (MRS):

Spectroscopy measures relative metabolite concentrations across chemical shifts (ppm):

Metabolite	Chemical Shift (ppm)	Clinical Significance
Lipid	1.3	Elevated in necrosis, tuberculoma, high-grade tumors
Lactate	1.33 (inverted doublet)	Elevated in mitochondrial disorders, hypoxia/ischemia
N-acetylaspartate (NAA)	2.02	Neuronal integrity marker (decreased in brain injury; markedly elevated in Canavan disease)
Creatine	3.03 & 3.93	Energy metabolism reference peak
Choline	3.22	Cell membrane turnover (elevated in malignancies and active demyelination)