CT Scan🗸

DWI (Diffusion Weighted Imaging)

• Most sensitive for Acute Stroke.
• Acute infarct shows restricted diffusion.

• ADC (Apparent diffusion coefficient)
• Based on Brownian movement of protons.
• Protons move freely like CSF (Facilitated diffusion).
• Brown (Brownian movement) people diffuse (Diffusion weighted MRI) into other areas very easily

• NOTE: MRI → Gyroscopic movement of protons

Diffusion restriction

• Normal fluid diffuses

• Fluid does not diffuse when Na K pump not working (d/t Ischemia), Eg
• Ischemic Stroke
• Epidermoid cyst (d/t thick secretions)
• CSF-like mass
• Abcess (thick pus)
• Hypercellular tumor

• Note:
• Arachnoid Cyst
• Doesnt show diffusion restriction
• shows FLAIR suppression
• Ara → Arum allathavan → has no flair → but go everywhere (no diffusion restriction)

SWI (Susceptibility Weighted Imaging)

• Identifies MicroHemorrhages and Calcification.

• They appear as black areas of blooming

• IOC: DAI

• Mnemonic: Susceptible people bloom → when beaten down (hemorrhage)

MR Tractography/ DTI (Diffusion Tensor Imaging)

• Done for white matter tracts

• Based on anisotropy of white matter tracts

• Tractor (MR Tractography) operation → Tension (DTI) for white people (white matter)

BOLD MRI / FMRI (Functional MRI)

• Locates functional/eloquent areas of the brain.
• Visual cortex.
• Speech area.
• Auditory cortex.

• Helps in neurosurgery planning.

• Mnemonic: Bold () people are functional () → they can see, hear and speak well () → plan to become Neurosurgeons ()

MR Spectroscopy

• Creates a graph of chemical metabolites.

Condition	Maximum Peak
Normal brain	NAA
Tumor	Choline
Tuberculosis	Single lipid peak + basal exudates
Neurocysticercosis	Multiple amino acid peaks.

Myelography

• Contrast given in subarachnoid space.

• Appears as white contrast surrounding spinal cord.

• Contrast can also appear black.

• CT Myelogram
• Shows white contrast.

• MR Myelogram
• Does not show white bone.
• Is a T2 weighted MRI.
• Useful to see CSF.

STIR

• T2 (-) Fat

• For bone marrow edema

 

• Brain Stem
• Comprises:
• upper midbrain
• middle pons
• lower medulla

• Ventricles and Associated Structures

Structure	Relation / Position
4th ventricle	• Triangular area between pons and cerebellum
Lateral ventricle	• Beneath corpus callosum; • Opens through foramen of Monro into 3rd ventricle
Mamillary body	• In front of midbrain
Colliculi	• Posterior part of midbrain
Pineal gland	• Beneath corpus callosum splenium; • Behind 3rd ventricle; • Posterosuperior to midbrain
Fornix	• White matter tract related to corpus callosum
Pituitary gland	• Adjacent to sphenoid sinus

Brainstem and Vasculature

• Vertebral arteries: Black areas surrounding medulla oblongata.

• Basilar artery: In front of pons.

• Temporal lobe: Inferior most lobe.

• Midbrain: Heart-shaped/mickey mouse-shaped.

• Mammillary body: In front of midbrain, shows hyperintensity.

• Wernicke's encephalopathy affects the mamillary body.

MR Angiography

• Visualizes brain circulation.

• 35-45% die by 1 month due to complications.

• More incidence in Asians and Blacks.

Causes

• Hypertension.

• Coagulopathy.
• Warfarin toxicity:
• Antidote: Prothrombin complex concentrate >> vitamin k.
• Dabigatran toxicity
• Antidote: IDARUCIZUMAB.
• Mnemonic: Dab → Idaru dab cheyyunnnaaaa
• Apixaban toxicity
• Antidote: Andexanet alpha.

• Cocaine and methamphetamine:
• vasoconstriction in cerebral blood vessels
• → increased pressure and rupture.

• Cerebral amyloid angiopathy
• apolipoprotein E gene: E4, E2
• there occurs weakening of blood vessels in the brain.
• Cause of intracerebral hemorrhage in non-diabetic and non-hypertensive patient.

• Head injury IOC: NCCT (Non Contrast CT).
• NCCT looks for:
• Acute hemorrhage.
• Fracture.

• Exception:
• Diffuse Axonal Injury (uses SW-MRI).

• Decompression craniectomy >> Burr hole / craniotomy

Tension pneumocephalus

• Mount Fuji sign is seen.

• Causes
• Head trauma (most common)
• Post-neurosurgery
• Sinus fractures (frontal, ethmoid)
• CSF leak (skull base defects)
• Infections with gas-forming organisms (rare)
• Positive pressure ventilation
• Barotrauma

Diffuse Axonal injury

• Cause: 
• High-velocity impact,
• shearing force (grey/white matter junction)

• Features: 
• History of RTA, GCS worsening, normal CT.
• Persistent coma (GCS not improving)

• Imaging (IOC): 
• MRI
• Multiple petechial hemorrhages at grey/white matter junction
• Corpus callosum, brainstem areas can be involved.

• Worst prognosis

Adam’s classification of DAI

• DAI has low GCS (aDAM aDAI)
• 1 → Grey mater - white mater jn
• 2 → Corpus callosum
• 3 → Brain stem

Concussion

• Mildest primary brain injury

• Management:
• Avoid contact sports briefly
• No surgical intervention

Secondary Injury: 

• Due to ↑↑ intracranial pressure (ICP)

Cerebral Perfusion Pressure (CPP):

• CPP = MAP - ICP

• Normal: >60 mmHg

• Cushing’s Reflex (due to trauma, increased ICP):
• ↑↑ Mean Arterial Pressure (MAP)
• ↓↓ Heart Rate (bradycardia)
• Altered respiration

• Irregularly irregular breathing (Biot's breathing)
• Irregular pattern
• due to raised ICP.

• hyperpnoea interrupted by sudden apnoea.

• indicates a bad prognosis.

• Seen in:
• Damage to medulla
• meningitis

• Mnemonic: Bite (Biots) Me (Meningitis, Medulla)

• 2 changes → Bi Ots

Target: ICP<20mm and CPP >60mm

1. Elevate head end

2. Ventriculostomy

3. Mannitol

4. Steroid
• Use in tumor, abscess
• CI in head trauma / stroke/ hemorrhage

5. Hyperventilation

6. Vasopressors

Management of Increased ICP

• Adequate O2 saturation

• Adequate perfusion (SBP >100 mmHg)

• Avoid hyperglycemia (increases cerebral edema)

• Administer IV mannitol

• Moderate hyperventilation

• Seizure Prophylaxis (Phenytoin/Valproate):
• Useful for early PTS
• Not recommended for late post-traumatic seizures (PTS)

• NOs in Head Trauma
• No steroids in head trauma
• Hypotonic solutions
• Dextrose solutions
• Both promote cerebral edema

Goals of Rx

• ICP: 20–25 mmHg

• CPP: ≥ 60 mmHg

• Na⁺: 135–145

• SBP: ≥ 100 mmHg

• MAP: >90

Glasgow Outcome Score

• Prognostic score after head injury

• Score & Prognosis:
• 1: Death
• 2: Persistent vegetative state
• 3: Severe disability (conscious)
• 4: Moderate disability
• 5: Good recovery + mild disability

Raised ICT

Intraparenchymal Hemorrhage / Contusion:

• Most common type

• Management: Conservative (manage increased ICP)

• Acute hemorrhage is white (Hyperdense).

• Most common cause: HTN.

• Most common site: Putamen (basal ganglia).

• Charcot’s Artery bleed
• Lenticulostriate branches Of MCA rupture first.

Hypertensive Intracerebral Hemorrhage

• M/c site of bleed is putamen

• If cerebellar hamartoma is > 3cm
• obstructive hydrocephalus
• requiring a surgical intervention.

Clinical Features

• Develop over 30-90 minutes after the bleed.

• Contralateral sagging of face.

• Slurring of speech.

• Arm weakness.

• Eye deviation
• In a cortical stroke
• eyes deviate towards the side of the stroke.
• In sub cortical stroke
• eye looks away from the stroke.

• Irregularly irregular breathing (Biot's breathing) due to raised ICP.
• indicates a bad prognosis.

• Decerebrate posturing/Rigidity.

• Coma.

Thalamic Haemorrhage

• Contralateral hemiplegia, hemianesthesia.

• Chronic debilitating contralateral pain (Dejerine Roussy syndrome).
• Severe pain → Acid over half of body → when water falls on body

Pontine Hemorrhage

• Deep coma.

• Quadriplegia.

• Hypertension,

• Pinpoint pupil (~1 mm) + ↑↑ respiratory rate
• Key diff between Pontine hemorrhage and Drug overdose

• Hyperhidrosis

• Hyperthermia

Cerebellar Hematoma

• Occipital headache.

• Vomiting.

• Ataxia.

• Hematoma > 3 cm
• needs a neurosurgical intervention

Posterior Reversible Leukoencephalopathy

• Patient is a known case of hypertension with features of raised ICP.
• Cause of hypertension could be any;
• acute glomerulonephritis,
• CKD,
• toxemia of pregnancy.

Clinical Presentation

• Headache.

• Vomiting.

• Retinal hemorrhage on fundus examination.

• Convulsions

• Stupor and coma.

MRI Head Shows

• Vasogenic cerebral oedema in occipital region.

Treatment

• Reduce blood pressure.

Extradural Hemorrhage (EDH):

• Young patient

• Type of coup injury
• High-velocity impact

• Fracture of temporal bone Pterion
• meeting point of 4 bones:

• Frontal bone

• Parietal bone

• Greater wing of sphenoid

• Squamous part of temporal bone

• Rupture of middle meningeal artery
• Anterior division

• Bleed in the extradural space.

• Brainstem compression.

• Death due to respiratory failure.

• Features: 
• Lucid interval (Period of unconsciousness b/w 2 periods of consciousness)

• Imaging:
• Biconvex opacity
• Restricted by sutures
• Swirl sign:
• Hypodense area + Hyperdense area ⇒ S/O active hemorrhage.
• Needs Decompression
• Acute hemorrhage
• hyperdense on CT.

• Management: Decompressive > Burr hole / craniotomy close to pterion

• Autopsy Findings: Clearing of hemorrhage after pouring water.

Structures Lying Deep to Pterion

• MMA

• Middle cerebral vessels

• Sylvian fissure/ lateral sulcus
  → sulcus between frontal and temporal lobe

• Insula

• Broca’s area

• Lesser wing of sphenoid

Lucid Interval

• Period of consciousness between 2 periods of unconsciousness.

• Seen in EDH > SDH.

• Medicolegal importance:
• Patient can provide valid evidence, will & is criminally liable.
• Death due to failure in diagnosing lucid interval:
• Medical negligence.
• Punishable under 106(1) BNS.
• Mnemonic: Lucy ye 106 idi idich konnu

Subdural Hemorrhage (SDH):

• Trivial injury

• Elderly patient

• Superior cerebral vein (Bridging vein)

Risk factor: Mnemonic ABC.

• Aged person with minor trauma.

• Boxers → c/c sdh

• Child abuse (Shaken baby syndrome).

Features: 

• Gradual altered sensorium after few weeks

Types:

• Acute: Within hours of injury

• Subacute: Hours to days post-injury

• Chronic: Days to weeks post-injury

• Source of Bleed: cortical bridging veins/dural venous sinuses.

• Imaging: Crescentic opacity.
• Not restricted by sutures

Management:

• Decompression craniectomy >> Burr hole / craniotomy

• Indications for Craniotomy (SDH): (any 1)
• Clot size >30 cc
• Midline shift >5 mm
• Clot thickness >1.5 cm

• Autopsy Findings:
• Clearing of hemorrhage after pouring water.

Note

Plaque jaune lesions

• Type of traumatic brain injury

• Due to multiple concussions (Boxing)

• Features
• Depressed
• Retracted
• Yellowish-brown

• Contrecoup areas

Hematoma

Management of Intracerebral Hemorrhage

ICH Score
(Mnemonic: AHIIG)

• A - Age.

• H - Hematoma volume.
• > 3cm

• I -
• Infratentorial location of bleed
• Located in 4th ventricle
• high chances of developing obstructive hydrocephalus
• worse prognosis as compared to supratentorial bleed.

• I -
• Intraventricular hemorrhage
• In Neonates
• common after birth trauma
• e.g. faulty forceps delivery.
• Shrill cry.
• Bulging anterior fontanelle.
• Pallor.
• IOC
• USG done to evaluate, NOT CT
• In adults
• Due to extension from Intracerebral bleed

• G - GCS.

Specific Management of ICH

• Airway protection - with intubation.

• BP control:
• NICARDIPINE >> sodium nitroprusside is used.
• Sometimes nicardipine can cause reflex tachycardia.
• ESMOLOL is used to neutralize in such patients.
• Target blood pressure is < 140 mmHg (page 3349 Harrison).

• Treatment of coagulopathy.

• Midline shift/obtundation in patient
1. osmotic diuretics are used.
• 3% Mannitol
• 5% dextrose is NEVER USED in management.
2. If Mannitol fails, we can perform:
• VENTRICULOSTOMY
• A drain is placed in the lateral horn of the ventricle.
3. If the pressure is still rising,
• then neurosurgical decompression has to be done based on the ICH score.

Subarachnoid Hemorrhage (SAH):

Causes

• Most common cause of subarachnoid hemorrhage is
• Trauma >>
• rupture of berry aneurysm/
• mycotic aneurysm/
• staphylococcus aureus.
• complication of Infective Endocarditis.
• rupture of Charcot Bouchard aneurysm.
• due to Hypertension

Clinical Manifestation

• Thunderclap headache/worst headache of life.

• As blood will spill into meninges it will cause nuchal rigidity.

• Source of Bleed:
• Arteries in Circle of Willis.

• Presents with Thunderclap headache.

• Autopsy Findings: Hemorrhage remains intact after pouring water.

Diagnosis: 

• NCCT
• Spillage of blood in Basal cistern (star appearance).
• Star of Death: whiteness in the sylvian fissure from MCA
• Sylvian fissure → separates temporal and parietal lobes.

• SAH can be seen in interhemispheric fissure.

• Investigation shown is DSA
• Black vessel.

• Tortuous artery seen is Internal carotid artery.
• Divides into middle and anterior cerebral arteries.

• Blob of contrast indicates Aneurysm.
• Rupture leads to SAH.

NOTE

• TB meningitis
• Basal exudates on NCCT
• Cobweb coagulum seen in CSF

• If not available, lower ICP with mannitol and do LP (see bloody CSF).
• LP (avoided if raised ICP)
• Bloody CSF may occur.
• LP after 24–48 hr:
• CSF becomes xanthochromic as RBCs break down.
• Also seen in
• Trauma,
• HSV 1 encephalitis
• subarachnoid hemorrhage

• Elevated BNP
• causes natriuresis → decrease in sodium levels of the body → < 125 meq → seizures

• ECG findings:
• MI due to pain and catecholamines
• ST depression and T wave inversion.

Management: 

• NO SURGERY

• With strict complete bed rest advised.

• Platinum endovascular Coiling > Aneurysmal clip
• Angiography → Intervention (coiling/surgical clipping)

Post-op:

• CCBs (Nimodipine) to prevent vasospasm

Xanthochromic CSF

Causes of Death

• Vasospasm leading to cerebral infarction (most common cause of death).
• When the berry ruptures → the blood vessels in the surrounding area → protective spasm → acts as a double insult → causes cerebral infarction.
• Give Nimodipine to prevent vasospasm

• Rebleeding (rebleeding can occur from the same or different site).

• Hydrocephalus.

• Seizures: when Na <125 meq.

• MI

WFNS and HUNT AND HESS Scale for SAH

• Hunt and Hess
• Mild headache
• Moderate headache
• Confusion
• Stupor
• Coma

MR Angiography

• Visualizes brain circulation.

Pond fracture / Ping-pong fracture:

• Variant of depressed fracture.

• Also known as indented fracture/ping pong fracture.

• Seen in infants (Elastic bones) born out of obstetric delivery.

Cephalhematoma Vs Caput Succedaneum

• Prehospital: Call ahead, activate Code stroke.

Onset <6 h: (“Last seen well” is used for calculation)

• CT: No hemorrhage.

• IV PA eligible?
• If yes: Give IV PA.
• Alteplase → Bolus f/b infusion
• At CT scan: Tenecteplase → Single bolus
• If Not: Perform CT angiography
• Detects Emergent large vessel occlusion (ELVO).
• ICA or M 1-2 of MCA or Basilary Artery occlusion?
• If ELVO present → do CT Perfusion
• checks penumbra vs ischemic core mismatch.
• helps pick up penumbra.
• Viable ischemic areas that can be saved.
• If yes: Consider Mechanical Thrombectomy → MERCI

Onset 6–24 h:

• CT: No hemorrhage.

• CTA/CTP: Favorable perfusion?
• If yes: Thrombectomy → MERCI

Role of MRI (DWI)

• Most sensitive than NCCT for early infarct.

• Not preferred (time, cost, limited availability).

• Non contrast CT head:
• Normal (in majority cases).
• to rule out haemorrhagic stroke

• Thrombolysis can cause increased bleeding risk.

• Hyperdense MCA sign
• Early clot in MCA appears hyperdense
• uncommon
• Later → hypodensity.

• Blackish hypodensity
• which develops over time.
• Ischemic damage

• Acute stroke
1. White → s/o Acute hemorrhage/clot
2. Well-defined hypodense infarct in MCA region.
3. Hypodensity in thalamus: Lacunar infarct
• Charcot's artery/ LS branch of MCA

• White artery (MCA) → Hyperdense artery sign → Acute thrombus

• Loss of insular ribbon:

---

• In MCA stroke → insular cortex becomes oedematous first
• because of its closest proximity to Lateral sulcus





---

• DWI: Restricted diffusion S/O acute infarct.



• Chronic infarct: No restricted diffusion (due to CSF).

Moya Moya disease

 

• On DSA, ICA is shown.

• Due to ICA stenosis and collateral development.
• Black narrowed vessels are seen.
• Contrast appears as a puff of smoke.

Dural Venous Sinus Thrombosis CT/MRI

• Plain CT → Dense clot sign
• Thrombus appears white

• CECT → Delta sign or Empty delta sign.
• In superior sagittal sinus thrombosis
• Accumulation or pooling of blood
• Hemorrhagic infarct
• Triangle (delta) area shows filling defect

• MRI → No Flow Void

Arachnoiditis

• Empty thecal sac sign is seen.
• Normally, thecal sac has black nerve roots.

• Mnemonic:
• Empty thekkan → Aere (Arachnoid) theeykkum ini
• Empty delta sign → D for D → Dural venous sinus → sagittal sinus thrombosis

• In arachnoiditis, inflammation/fibrosis pulls nerve roots to periphery.
• No nerve roots visible in thecal sac.

ICT ↑↑

ICT ↑↑ in children

• Copper beaten / silver beaten appearance

ICT ↑↑ in adults

• Empty sella sign

• Herniation of subarachnoid space into sella
• → Clinoid process erosion / dorsum sella erosion

• Leads to flattened pituitary gland against floor of sella

Subependymal nodules

• Can enlarge to form SEGA (Subependymal Giant Cell Astrocytoma)

• Most common site: foramen of Monro

• Mnemonic: Tube (TS) nte thazhe nodules (Subependymal nodules) vachitt Munroe (Foramen of munro) poi → Giant (SEGA) aale kanan

• B/L ice cream cone appearance in cerebellopontine angle.
• B/L Vestibular schwannoma.

• Chromosome no. 22.

• Mnemonic: Show man () eating Ice cream () with 22 (Chr 22) year old

• Port-wine stain in trigeminal distribution

• Leptomeningeal Angiomatosis (ipsilateral)
• cavernous angioma (vascular malformation).
• Convulsions (Focal)
• behavioural problems,
• Mental retardation

• Choroidal Hemangiomas
• Ocular complications
• ipsilateral glaucoma,
• blindness,
• congestion
• Buphthalmos

• Unilateral weakness
• d/t tumor compressing corticospinal pathway.

CT scan:

• S-shaped intracranial calcifications

• S for Sturge-Weber, S for S shaped





 

• Tram track appearance or rail road calcification
• NOTE: Also seen in
• membranoproliferative glomerulonephritis,
• bronchiectasis.

• Mnemonic: Web of storage (Sturg Weber) of Portwine factories () → connected by rail tram tracks (Tram track apearance)

• Von Hippel-Lindau (VHL) syndrome
• Defect:
• Chromosome 3p deletion (from VHL's three alphabets)
• VHL gene.
• Activate Hypoxemia Inducible Factors (HIF)
• Clear cell RCC
• SmaLL CELL lung cancer (L myc, 3p)
• Pheochromocytoma
• Cerebellar Hemangioblastoma
• Retinal hemangioblastoma
• may bleed causing vision loss
• Spinal cord hemangioblastoma
• Vascular tumour of spinal cord
• Cutaneous: Café-au-lait macules.
• Hemangioendothelioma
• Hemangioendothelioma + RCC ⇒ Paraneoplastic Polycythemia

Huntington's Chorea

• Autosomal Dominant

• 50-60 years of age.

• Genetics: 
• Involves CAG repeats on the exon of chromosome number 4.

• Increased Proteins: 
• Huntington protein and ubiquitin ↑↑ in caudate nucleus

• U quit (ubiquitin) hunting (huntington protein) in kaadu (caudate)

• Atrophy of caudate nucleus.
• Frontal horn of lateral ventricles dilates.
• MRI head: Boxcar ventricle.

Note

• Corpus Callosum Lipoma
• Shows bracket calcification.
• Mnemonic:
1. C C → Brackets
2. Lip → Put brackets

Important Information

• Neurotransmitters affected:
• Dopamine: ↑↑.
• NOTE: In parkinsonism (Typical or atypical variety):
• Dopamine values are less.
• GABA: ↓↓↓
• ↓ inhibitions
• Low inhibitions and high dopamine when hunting

Callosal dysgenesis/agenesis

• Square root wave sign in cardiac catheterization finding with constrictive pericarditis

Neurodegeneration of brain due to Iron accumulation /
Halloverden Spatz disease

• Autosomal recessive neurodegeneration.

• Iron deposition in basal ganglia.
• Basal ganglia: Globus pallidus.

• MRI head: Eye of tiger.

• PKAN: Pantothenate kinase

• Hello Harsha verdan → Tiger eyes → Wear Pants

MRI head:

• KF ring seen in eyes.
• Deposits in Descemet's membrane

• Giant face of Panda
• in midbrain on T2 MRI.

NOTE

• Panda sign is seen in sarcoidosis with Gallium-67 scan.

Treatment: 

• Copper chelators:
• Trientine (Triethylenetetramine)
• D- Penicillamine

• DOC (in maintenance phase):
• Zinc acetate

• DOC For neurological features:
• Tetrathiomolybdate

• Presentation:
• A patient with Parkinsonian features unresponsive to levodopa
• Patient has rigidity or bradykinesia.
• Vertical gaze palsy.
• Difficulty in looking downwards.
• Recurrent falls in backward direction.

• NOTE: In typical parkinsonism:
• Person walks slowly.
• Will not be able to lift foot over obstacle.
• Might hit against stone/brick.
• Topple over and fall forwards.

• EOG:
• Square wave jerks.
• NOTE: Square root wave sign:
• Constrictive pericarditis

• Brain area involved:
• Basal ganglia and superior colliculus.

• MRI head:
• Hummingbird appearance.
• Midbrain atrophy with bulging pons.

• Biopsy:
• Substantia nigra and locus ceruleus show
• neuronal loss,
• ballooned neurons
• tangles.

• No drug of choice for management.

• Poor prognosis.

• Routes: Important
1. Pork
• larvae → intestinal tapeworm.
2. Vegetables on contaminated soil (like cabbage)
• eggs → neurocysticercosis.

• Cysticercosis:
• Rice-grain calcification (dead larvae).
• Alternative: Steroids, Praziquantel.

Neurocysticercosis

• Soli sir affect brain → he is sole cause (sub kuch infective - egg and larvae) → Nakshathram enni (starry sky)
• he was Para (Parenchyma brain)
• solium - systi sercus sellulose → inside the cell

• Cysticercus cellulosae:
• zig-zag tube, hooklets, suckers, convoluted tube-like structure

• Scolex in brain.

• M/C site : Brain parenchyma

• M/C presentation: Seizures

• Imaging: Gadolinium MRI preferred.
• Starry sky appearance

• Drugs: Steroids f/b Albendazole (DOC)
• ↓ inflammation d/t dying larvae

Clinical features

• Low socioeconomic status.

• Multiple focal seizures.
• Vasogenic cerebral oedema can cause focal seizures.

General exam

• Multiple subcutaneous lumps/bumps.

First:

• LP (guarded)
• CSF immunoblot for NCC antigen
• (NOTE: CSF ELISA is for cryptococcus)

NCCT

• Starry sky appearance d/t calcification
• But not early on CT.







• Cyst with a dot inside (scolex).
• End stage: can be calcified.
• Starry sky appearance.
• Can spread to muscles.
• Rice grain calcification.
• Can cause hydrocephalus.

Imaging:

• Gd-MRI.

• Vasogenic cerebral edema

Stages of Lesion in Radiology

Treatment of NCC

1. Start dexamethasone (48h) to control edema.

2. Albendazole
• not started first because
• prevents inflammatory reaction
• ↑ seizures

3. CBZ/Lamotrigine: For seizures.

• Periventricular Calcification.

• Note:
• Zika → White and grey matter calcification
• Toxoplasma → Cerebral calcification

CD4 Count vs Opportunistic Infections

Congenital toxoplasmosis CT

• Eccentric target sign.
• M/c site: basal ganglia

• Gadolinium as there is damage to BBB: FLAIR Sequence
• Plaque lesions
• Dawson finger/Periventricular lesions
• Finger-like projections in calloso-septal interface.

Vein of Galen Malformation (VOGM)

• Suspected in neonate with hydrocephalus and heart failure.

• Is an AV fistula, leading to heart failure.

AV malformation

• Bag of worms appearance.

• On angiography, entanglement of vessels seen (Nidus).

Cavernoma (Cavernous angioma)

• Popcorn appearance on MRI brain.

Popcorn Calcification:

• Seen in pulmonary hamartoma.

• NOTE: Pop corn in brain → Cavernoma

• Mnemonic: Eating Hamara popcorn in a cave

• Mnemonic: Blasted across the midline

• Irregular borders, central necrosis.

Meningioma

• Vividly enhancing, extra-axial lesion.

• Has Dural tail sign.

 

• Most common posterior fossa tumour in a child

• Highly cellular, appears hyperdense

• Medulloblastoma has bad prognosis.

• Can spread from brain to spinal cord (Cranio-spinal axis spread).
• Drop Mets

• Can cause obstructive hydrocephalus.

• Occupies 4th ventricle
• ⇒ 4th ventricle obstruction
• upstream hydrocephalus

Germinoma

• Children are afraid of germs (Children → germinoma)

Meningocele Vs Meningomyelocele

Myelomeningocele: (a type of spina bifida).

• Basic defect:
• Protrusion of neural components
• along with a sac formed by meninges
• through a midline vertebral defect.

• Spinal part and nerve roots present in sac.

• Black nerve roots seen going with the sac.

• Myelomeningocele pull downwards causing:
• Lemon Sign:
• frontal bones become concave.
• Banana sign:
• cerebellum becomes curved.

Meningocele:

• Herniation of meninges +/- brain tissue (meningoencephalocele) into the nasal cavity.

• Improper bone fusion during development creates a gap for herniation.

• Bones of nose roof:

Position	Bone
Anteriorly	Frontal bone
Middle	Cribriform plate
Posteriorly	Sphenoid bone

• Swelling is soft.

• Compressibility test: Positive.

• Reducibility test: Positive.

• Cough impulse test: Positive.
• Furstenberg test + → Cry/cough → ↑ Mass size
• Frustration - cry

• Transillumination test: Positive.

On spine

• On T1, appears dark.

• On T2, appears uniformly white.

• There is a protrusion of a meninges sac
• containing only clear fluid
• no neural components.

• Treatment:
• Excision of herniated mass.
• Reconstruction of defect.

Feature	Meningocele	Glioma	Dermoid
Cause	Improper fusion of bones of base of skull or roof of nasal cavity	No fusion → herniation → delayed fusion	Hamartoma: A congenital anomaly at line of bone fusion.
Consistency of swelling	Soft / Cystic	Firm	Variable
Compressibility test	Positive	Negative	Positive D- Compressible
Reducibility test	Positive	Negative	Negative
Cough impulse test	Positive	Negative	Negative
Transillumination test	Positive	Negative	Negative
Treatment	Excision + Reconstruction	Excision	Excision