Brain Flashcards
Pott puffy tumour:
- DDx?
- Complications?
- Treatment?
- DDx of a hypodense expansile process exiting the sinus:
- mucocele
- infection
- lymphoma
- primary sinus neoplasm, e.g., SCC
- mucinous mets
- Complications:
- Dural sinus thrombosis
- Abscess in the frontal lobes
- meningitis
- cerebritis
- subdural empyema
- Tx: surgical drainage w/6 wks IV abx.
- Other points:
- Presents as an abruptly forming forehead mass emanating from the frontal sinus.
- 9:1, M:F
*
In patients over the age of 30, what is the prevalence of pineal calcification on CT scans?
50%
- The prevalences of pineal and choroid plexus calcifications are correlated. Patients with pineal calcification are 4x as likely to have choroid plexus calcifications compared with individuals who demonstrate no pineal calcification.
What do the arrows indicate on this axial T1WI?
Superior cerebellar peduncles.
This image is obtained through the upper pons. The structures indicated by the arrow form the lateral borders of the upper part of the 4th ventricle and are the superior cerebellar peduncles.
Where is choroid plexus located & in what horns is it not?
Lateral ventricles: temporal horns, but NOT occipital.
Roof of 3rd.
Fourth.
Dx?
- Unusual manifestation of these?
Oligodendroglioma: peripherally cortical mass w/heterogeneous enhancement & calcs.
- Intraventricular location-3-8%.
- Calcs in 20-90%.
- Most commonly, heterog enhancement.
- Most commonly peripheral, frontal lobe.
- Vasogenic edema is not as common as with higher glade astros or mets.
- If it has a 1p/19q deletion then it has a better outcome.
List the stages of active neurocysticercosis infection in order (earliest to latest).
VCGC: vesicular, colloidal, granular nodular, calcified nodular
Vesicular: the larva lodges in a capillary & forms a cyst to protect the larva (like the initial, vesicle stage of cold sores, the vesicles form first and are full of the pathogen).
- This form can remain in the brain for years until there is host response and inflammation which can cause seizures.
Colloidal: this is when the scolex dies, it begins to degenerate & leak antigens, then inflammation begins, & edema surrounds the cyst. (Think “collision” with the immune system.)
Granular nodular: as the inflammatory response decreases, there is less edema, but thin rim enhancement persists, surrounding the more proteinaceous cyst.
Calcified nodular: inactive, calcified cyst, like a calcified granuloma.
In neurocysticercosis, which imaging characteristic has been postulated to be helpful for determining the death of a scolex?
Central dot of diffusion restriction, corresponding to the scolex.
What is the most common primary brain tumour in adults?
- Astrocytoma/glial neoplasm.
- These account for 15% of all intracranial primary neoplasms.
Dx? Surveillance MR for a known condition.
vHL: endolymphatic sac tumour & hemangioblastomas.
Most common primary brain tumour of the posterior fossa in adults?
Hemangioblastoma
- 70% of the time you’ll see flow voids in the periphery of the cyst.
- 90% are found in the cerebellum.
- Associated w/polycythemia.
If I say posterior fossa cyst w/a nodule in peds you say…
Juvenile pilocytic astrocytoma
- WHO grade 1, but the nodule will enhance (the exception to the low grade/no enhancement rule).
Dx, DDx?
Vestibular schwannoma: CP angle mass w/o restriction, trumpet-shaped, expanded IAC.
-
DDx:
- Meningioma: 15% of all IAC masses; strongly enhance as it’s extradural; will restrict as it’s highly cellular, w/dural tail & show hyperostosis; more common in women.
- Epidermoid: 5% of all; follows CSF appearance on CT/MR & restricts; peripheral enhancement, if any.
- Neurofibroma: rare as a primary intracranial lesion even in NF-1.
Most common CP angle mass?
Vestibular schwannoma
- 85% of all CP angle masses.
- Most commonly involve inferior division vestibular nerve (CN VIII).
- Most schwannomas occur along sensory nerve fibers, CN8 is the most common, followed by trigeminal nerve.
- <20% are associated w/NF-2.
- Pts commonly present w/hearing loss, but can also have vertigo, imbalance.
Dx?
Ependymoma: 4th vent, heterogeneous, toothpaste-like tumour squeezing through the foramen magnum.
- Originate from ependymal cells of ventricles.
- 70% from 4th vent & often extend into foramen of Luschka & Magendie.
- Bimodal: 6yo & smaller peak at 30yo.
The most common intraventricular mass in an adult?
Central neurocytoma
- 20-40yos
- Swiss cheese appearance, but calcify a lot.
- Most commonly in the lateral ventricle, attached to the septum pellucidum or ventricular wall.
- WHO grade II.
Dx?
Epidermoid cyst: follows CSF, but restricts.
DDx: arachnoid cyst.
- 40-50% occur in the CPA.
- Also seen in 4th vent, sellar region & less commonly intraparenchymal.
- Can be hyperdense on CT due to protein content (white epidermoid).
Primary CNS lymphoma is usually of what cell type?
- Large B-cell.
- Over 50% solitary.
- Solid, uniformly enhancing & restricting lesion.
- Like to abut the CSF surface.
- Periventricular & CC are the most common locations, followed by BG & thalami.
Dx:? 20yo male w/Hx of drug-resistant seizures.
DNET: temporal lobe, bubbly/cheesy, expansile cortical lesion which does not enhance.
Dx? 20yo.
- From where, exactly, is this originating?
- Next step?
- What to look for intracranially, and if seen, what is the association?
Medulloblastoma: homogeneously enhancing, restricting, projecting into 4th vent.
- Roof of 4th ventricle/vermis.
- Image the spine as these love to drop met: Zuckerguss.
- Dural calcs = Gorlin syndrome.
- Gorlin: basal cell cancer after radiation & odontogenic cysts.
Dx: pt w/TS?
- From what structure is this arising?
- What helps to differentiate these from subependymal nodules, also seen w/TS?
SEGA (subependymal giant cell astrocytoma): homogeneously enhancing, >1cm mass.
- Lateral wall of ventricle near the foramen of Munro.
- SEGAs grow.
- These can calcify.
- Occur in 15% of TS pts.
Which segment of the facial nerve most commonly exhibits physiologic enhancement?
The tympanic segment.
Dx?
Bell’s palsy: enhancing meatal & labyrinthine segment of the L facial nerve.
- Acute peripheral nerve paralysis of unknown cause.
- HSV reactivation is the most commonly proposed mechanism.
What is the most commonly involved cranial nerve in CNS Lyme disease?
CN 7, facial. Unilateral involvement is more common.
How common is isolated neurosarcoidosis w/o systemic manifestations of it?
<1%
*
According to the 2010 revised McDonald diagnostic criteria for MS, how is “dissemination in space” & “dissemination in time” defined?
-
Space: more than 1 in at least 2/4 designated areas of the CNS:
- Periventricular
- Juxtacortical
- Infratentorial
- Spinal cord
-
Time: T2 bright lesion that does enhance (active) and a T2 bright lesion that does not enhance (inactive).
- These lesions are in different phases of the disease, therefore, are separated by time.
What is a potentially lethal complication of natalizumab Tx for MS?
- Progressive multifocal leukoencephalopathy (PML), due to JC virus reactivation in the setting of immunosuppression.
Basal meningeal enhancement is most commonly seen with which entity?
TB meningitis.
Which non-infectious etiology has a predilection for basal meningeal involvement?
Neurosarcoidosis.
A 22yo woman presents w/acute-onset painful unilateral visual blurring & and LP was performed. What is the associated CSF abnormality?
- Oligoclonal bands in R optic neuritis w/MS.
Which intracranial mets are known to be hemorrhagic?
- Melanoma
- RCC
- Choriocarcinoma
- Breast
- Lung
- Thyroid
- HCC
- Osteogenic sarcoma
What is the most common developmental malformation of the CNS?
Holoprosencephaly.
Which cranial feature is highly prevalent with this condition?
Dandy-Walker malformation is the Dx: wide opening of the 4th vent w/no vermis.
- Macrocephaly: it’s the most common clinical feature, affecting >90% of infants.
Dx?
- What % of pts can have sarcomatous transformation?
Paget’s of the skull: thickened, enlarged skull w/hetero areas of sclerosis = “cotton wool” appearance.
- <10%
* FD is usually more ground glass & involves the facial bones.
Dx?
- What does this classic imaging finding predictive of?
- Morphologically, what is it?
Joubert syndrome: molar tooth sign on axial imaging; also, batwing 4th vent.
- Hypotonia, ataxia, developmental delay. (Can be seen in other disorders, e.g., COACH & Dekaban-Arima syndromes.)
- Absence of decussation of the superior cerebellar peduncles & hypoplastic vermis.
Dx? 25yo female w/headache & blurred vision.
- Next step?
- How is the clinical Dx made?
Pseudotumour cerebri (idiopathic intracranial hypertension): partially empty sella.
- MR venogram: to look for venous sinus issues.
- Lumbar puncture w/opening pressure ~25mmHg.
- Bilateral transverse sinus stenosis in the outer thirds of the sinuses is present in 90% of cases.
Dx?
- What’s the most common malformation associated w/this?
Septo-optic dysplasia: absent septum pellucidum (could also be absent corpus callosum), prominent lateral vents, small optic nerves, small visual pathways, & low position of the fornix.
- Schizencephaly.
- Dx is made by 2+ of the following:
- Midline brain anomalies: absent septum pellucidum or CC
- Hypoplasia of the optic nerves
- Hypothalamic-pituitary dysfunction
Venous epidural hematomas are commonly associated w/injury to what structure?
Dural venous sinus.
- Although epidural hematomas are most commonly arterial in origin.
Dx?
Subdural empyema w/cerebritis: extra-axial loculated enhancing collection w/associated restricted diffusion & adjacent parenchymal edema/gyral crowding.
Dx? 63yo s/p BMT for plasmacytoma of the skull.
- What is the most likely agent?
multiple abscesses: in an immunocompromised pt, w/enhancing cystic lesions w/restricted diffusion at the brain base = cryptococcomas.
- CNS cryptococcal infection.
- Fungal infection by the bug, Cryptococcus neoformans.
- Commonly seen in pts w/AIDS, cancer or post-BMT.
- Has 3 classic Ix patterns: meningitis, cryptococcoma (as above), or gelatinous pseudocysts.
- Tx: amphotericin B or fluconazole.
- 20% mortality in AIDS pts despite antifungal Tx.
What is the most common location for spinal TB?
Spinal TB = Pott disease
L1
Dx? 40yo immunocompetent, otherwise healthy male.
- What is the mechanism for developing this?
CADASIL (cerebral autosomal dominant arteriopathy w/subcortical infarcts & leukoencephalopathy): multifocal hyperintense FLAIR abnormality w/in the bilateral anterior frontal & anterior temporal lobe subcortical white matter.
- Inherited mutation of the NOTCH3 gene.
- Leads to strokes in young people who are otherwise healthy & w/o stroke RFs.
- Typically presents age 30-50 w/TIA/stroke Sx or migraines w/aura.
- Progressive w/cognitive decline & early death.
Dx? 8yo boy w/hearing loss, decreasing school performance & progressive gain abnormalities.
X-linked adrenoleukodystrophy: symmetric parieto-occipital white matter abnormality w/U-fiber sparing & w/contrast enhancement surrounding it.
- Caused by a variant of the ABCD1 gene.
- Alexander disease is a DDx if this is in the frontal lobes.
Dx? 6mth old w/hypotonia, poor head control, loss of milestones & macrocephaly.
Canavan disease: diffuse T2 hyperintense white matter, globi palladi (putamen spared) & thalami & huge NAA spike.
- Kids are normal for first 1-2 mos of life then develop symptoms.
Dx?
Wilson disease: increased signal in midbrain w/”face of giant panda”, bilateral putamen, caudate & anterior pons.
- Copper metabolism inborn error (mutation of Cu-transporting gene, ATP7B).
- AR inheritance.
- Cu in brain, liver, eyes (Kayser-Fleischer rings along the periphery of the cornea).
Dx? 8yo girl w/progressive dystonia & dysphagia.
Hallervorden-Spatz syndrome: brain iron accumulation causing T2 hypointensity in the GP w/an anteromedial hyperintensity (“eye of the tiger” sign), w/strong susceptibility effect on GRE.
- The degree of Fe deposition does not correlate w/Sx.
Dx? 40yo w/complex partial seizures.
Mesial temporal sclerosis: L hippocampal atrophy w/loss of normal architecture, so becomes hyperintense on FLAIR.
Dx? 45yo male w/increasing musle weakness & cramps.
- Where, exactly, is this abnormality?
- How does death normally occur?
Amyotrophic lateral sclerosis: increased signal in the bilateral corticospinal tracts & precentral/motor cortex.
- Corticospinal tracts, precentral/motor cortex.
- Respiratory failure.
- Most cases are sporadic, there is no FHx.
Re: vascular territories, what supplies:
- Putamen
- GP
- Putamen = lenticulostriates (from ACA & MCA)
- GP = anterior choroidal (part of tetrafurcation of ICA, MCA, PCA)
Dx: if you see this in a kid.
Moyamoya w/watershed infarcts.
The stroke imaging signs on CT re: timing of mass effect & enhancement.
- Mass effect: peaks at 3-5 days.
- Enhancement rule of 3s:
- Enhancement starts in 3 days
- Peaks in 3 weeks
- Gone by 3 months
Dx?
Artery of Percheron stroke: V-shaped bilateral infarct of the paramedian thalami.
- BEWARE! Can also see this w/vein of Galen thrombus!!!!
- This only occurs w/this vascular variant.
- There is a solitary trunk from one of the 2 PCAs to feed both thalami (normally there are several arteries originating from the PCA).
Dx?
- What is the origin of the offending artery?
Recurrent artery of Heubner stroke: unilateral caudate infarct.
- This is a deep branch off the proximal ACA.
Dx?
Fetal PCOM stroke: infarcts in anterior & posterior circulation of the same hemisphere.
- Fetal PCOM: PCOM is larger than the P1 segment of the PCA.
Hemorrhagic xformation of acute stroke:
- In what % of strokes does this happen?
- What is the peak time for hemorrhagic transformation of acute stroke?
- 4 RFs for hem xformation.
- 50%
- 24-48 hrs (really, 6hrs - 4 days).
- RFs:
- multiple strokes
- proximal MCA occlusion
- Greater than 1/3 MCA territory
- Absent collaterals
DDx restricted diffusion in a brain
BEEAACHH:
- Bacterial abscess
- Epidermoid cyst, epilepsy (post-ictal state)
- Acute MS lesions, Acute stroke
- CJD
- HSV, hypercellular tumours (lymphoma)
Restricted diffusion & stroke:
- When does restriction occur, & how long does this last?
- FLAIR signal change?
- What should you think of you see restriction w/o bright FLAIR in a suspected stroke pt?
- W/in 30 mins to 2 wks.
- After 6 hours.
- Hyperacute stroke, i.e., <6hrs.
Aneurysms:
- Which kidney disease is at increased risk?
- Which circulation gets them most?
- Which ones are most common in the posterior circulation?
- RFs for rupture.
- Most common aneurysm type.
- Who gets them?
- Where do they appear most?
- % of the time they’re multiple?
- PCKD
- Anterior–90%
- Basilar >> PICA (basilar has higher hemodynamic stress)
- FEMALE, Hx SAH, larger size, smoking, posterior location.
- Berry.
- CHICKS!
- 90% anterior
- 15-20%
Aneurysm rupture:
- Rupture risk?
- Size for Tx?
- 1% per year when >10mm
- 7mm
Vasospasm:
- Classic timing?
- Classic territories?
- Relationship to blood volume?
- Which score for vasospasm risk?
- 3 non-SAH causes of vasospasm.
- 4-14 days post-SAH.
- Multiple.
- The higher the blood volume, the greater the risk.
- Fisher
- Meningitis, PRES, migraine.
Dx?
- Name 3 associations
- Age of pts?
- Difference in clinical sequelae per age group?
- Tx?
Moyamoya: enlargement of the basal perforating arteries.
- NF, prior radiation, Downs
- Bimodal: kids & middle age
- Kids = stroke; adults = bleed
- ECA to MCA anastomosis surgery.
- 2dry to non-atherosclerotic stenosis of the supraclinoid ICA, leading to occlusion.
- “puff of smoke” angiographic appearance of the enlarged perforators (see below)
- watershed infarcts
- Can show pial vascular congestion = “ivy sign”
Dx?
- Where does the pathology start?
- Which path is involved?
- Which nucs study can show this?
Crossed cerebellar diaschisis: supratentorial insult causing a contralateral cerebellar hemisphere insult
- Supratentorially!!!!
- Corticopontine cerebellar pathway.
- FDG-PET.
- Can be caused by anything: infarct, tumour resection, radiation.
Dx? 67yo male w/chronic HTN presents w/seizures, & visual disturbances.
- What is the underlying path?
- What % will restrict? EXAM QUESTION!!!!
- What other conditions are associated?
- Tx?
PRES: posterior, bilateral, subcortical (U-fibers) & white matter vasogenic edema pattern sparing gray matter.
- The posterior circulation cannot autoregulate in response to the acute BP change.
- 25%.
- Pre-eclampsia, chemo (cyclosporine) use.
- Treat the underlying etiology.
- Can also occur 2dry to sepsis or tacrolimus.
Dx? 60yo female.
- How do they present?
- What are these pts at hugely increased risk for?
Sjogren’s: honeycombed appearance of the parotid glands.
- Dry eyes & mouth.
- 1000x risk for NHL (MALT type).
- Autoimmune-lymphocyte induced destruction of the parotids.
*
Dx?
- Why does this occur?
- How do pts present?
Osmotic demyelination syndrome (central pontine myelinolysis): T2 bright central pons, sparing the periphery.
- Rapid correction of hyponatremia.
- Labile emotional response: slurred speech, sensitive gag reflex.
- Will show early restricted diffusion in the lower pons.
- This can also be seen in post-xplant pts.
Dx?
- How do they present?
- Cause?
Wernicke encephalopathy: high T2/FLAIR in medial thalami & periaqueductal gray matter, but also, mamillary bodies.
- Acute confusion, ataxia, ophthalmoplegia.
- Thiamine (vit B1) deficiency; Tx is to replace this.
Dx?
- Classic presentation?
- Underlying path?
- Order of CC involvement.
Marchiafava-Bignami: swelling/T2 bright signal at the CC body.
- Confusion, gait disturbance, seizure, muscle rigidity.
- Acute demyelination.
- Body, genu, splenium.
Dx?
Methanol toxicity: hemorrhagic putamen
- PUT the methanol away!!!!
- Can also see optic nerve atrophy & white matter necrosis.
Which part of the brain is most affected by direct EtOH injury?
cerebellar vermis
Dx? pt rescued from a fire.
- What is the most classic structure involved in this?
CO poisoning: T2 bright globus pallidus, putamen spared; w/restricted diffusion; (CO causes globus warming!!!)
- Globus pallidus: globus warming!!!!
What is contained in the parotid space?
- Parotid gland, Stensen’s duct.
- CN 7-facial.
- Retromandibular vein: runs just medial to the facial nerve.
When I say adenoid cystic carcinoma, you say…
perineural spread
What structures compose Waldeyer’s ring?
- Palatine tonsils: posterosuperior tongue
- Adenoid tonsils: nasopharyngeal
- Lingual tonsils: base of tongue
What are the contents of the carotid space?
- carotid artery
- jugular vein
- CN 10-vagus
- internal jugular vein nodes: levels 2-4
List the contents of the masticator space, w/muscles in order from lateral to medial.
- masseter
- temporalis
- lateral pterygoid
- medial pterygoid
- Plus the inferior alveolar nerve: branch of V3 (trigeminal mandibular)
- Mandibular ramus
What structure separates the true retropharyngeal space from the danger space?
alar fascia
In a young female, if you see a necrotic level 2 node, what Dx should you consider?
papillary thyroid cancer
Neck LN anatomy:
- Which LN stations are divided into A & B?
- What structures divide:
- 1A/B
- 2A/B
- 1B/2A
- 1, 2, 5.
- Structures:
- anterior belly digastric
- jugular vein
- posterior submandibular gland/sylohyoid muscle
What’s the most common location for nasopharyngeal cancer?
Fossa of Rosenmuller
What should you look for if you see a unilateral mastoid effusion or pathologic retropharyngeal node?
Fossa of Rosenmuller nasopharyngeal SCC.
- These are some early signs.
Nasopharyngeal carcinoma:
- Where to look and why?
- What % have nodal mets?
- Clivus: 30% have skull base erosion.
- 90%: retropharyngeal nodes are usually the first involved.
In vocal cord paralysis, which side has the expanded ventricle.
The involved side!
The abnormality shown is attributable to a defect in which CN?
CN 10-vagus
- recurrent laryngeal branch of the vagus nerve
Most common non-infectious masticator space mass?
mandibular sarcoma
Name the most common congenital neck cyst.
- Where do these most commonly occur?
thyroglossal duct cyst
- Below the level of the hyoid bone.
Dx?
- What is the path behind these?
Ranula: large cystic mass in the sublingual space w/signs of sialadenitis in the R sublingual gland.
- Sublingual gland mucoceles.
- If they extend into the submandibular space then they are plunging.
What is the most common pattern of chronic inflammatory sinonasal disease?
infundibular pattern
- Disease is limited to the maxillary sinus.
- Obstruction at the ostium/infundibulum.
Dx?
- 2 associations?
Sinonasal polyposis: widening of the infundibulum w/bony modeling & erosion.
- CF
- Aspirin sensitivity
Dx?
- Most common location?
- Where will it enhance?
- T1 appearance?
Mucocele: “expanded, airless sinus”; thinned but intact bone.
- Frontal sinus.
- Not centrally, but peripherally it might from the adjacent inflamed mucosa.
- T1 bright as it’s mucus.
Dx?
- What cell type, so where does it originate from?
- Age groups?
- Which nucs agent will be +?
Esthesioneuroblastoma: dumbbell appearance w/growth up and into the skull & down to the sinuses; often marginal cysts in the mass.
- Neural crest, olfactory cells, from cribiform plate.
- Bimodal: 20s/60s
- Neural crest, so octreotide.
- Where does sialolithiasis most commonly occur?
- What can chronic obstruction lead to?
- Submandibular gland/Wharton duct.
- Fatty gland atrophy.
Name the 3 glands & their ducts.
- Submandibular: Wharton; looks like an upside down W in floor of mouth.
- Parotid: Stensen; lateral to mandible.
- Sublingual: Rivinus.
What delineates the sublingual from submandibular spaces?
Which teeth are contained in each space.
Sublingual: above the mylohyoid line. L comes before M, so that’s how you remember that sublingual is above submandibular.
- Anterior mandibular teeth.
Submandibular:
- 2nd, 3rd molars.
Dx?
- How do most of these cases begin?
Ludwig angina:
- Odontogenic infection.
- Aggressive cellulitis in floor of mouth.
- May be gas everywhere.
Dx?
- 2 RFs
Osteonecrosis of the mandible.
- Bisphosphonate use
- Radiation
Dx?
Floor of mouth dermoid: fat-containing.
- Can have a “sack of marbles” appearance.
Dx if you see a young adult with this?
HPV-related SCC: large, necrotic level 2A nodes.
Name the structures:
A: lamina papyracea: (medial orbital wall).
B: uncinate process: bony projection alongside the infundibulum.
C: cribiform plate: roof of the nasal cavity.
D: inferior turbinate: largest of the nasal turbinates.
Dx?
- Which bugs cause this?
Acute, invasive funal sinusitis: hyperattenuating material in the L maxillary sinus w/anterior fat infiltration.
- Aspergillus or Mucor in diabetics/immunocompromised pts.
Which CN supplies this structure & what structure is this?
- Which CNs supply the other ocular muscles?
CN4-trochlear; SO muscle.
- Lateral rectus = CN6-abducens.
- superior rectus, inferior rectus, medial recturs = CN3-oculomotor.
Which syndrome is most closely associated w/the abnormality shown here?
- What is the primary diff b/w NR-related optic gliomas and sporadic?
- What % of pts w/optic nerve gliomas have NF1?
NF-1 & optic nerve glioma: expansion of bilateral optic nerves by gliomas.
- NF-related are more indolent & occur near the globe whereas sporadic are most often at the chiasm.
- 70%
Name the most common primary orbital malignancy in kids.
- What’s their most common location?
rhabdomyosarcoma
- Extraconal.
- Which muscle is most commonly involved in thyroid eye disease?
- What’s the order of involvement?
- Is this usually painful?
- Inferior rectus.
- IMSLO
- NO!
Dx?
- Most common cause?
- Mgt?
- Complications x 3?
Orbital subperiosteal abscess: lenticular, rim-enhancing fluid collection under the periosteum, typically from the ethmoid sinus.
- Acute bacterial rhinosinusitis from the ethmoid sinuses.
- Surgical decompression + IV abx.
- Cavernous sinus thrombosis, abscess, meningitis.
Dx?
- Underlying path?
Tolosa-Hunt syndrome: R lateral rectus swelling & orbital fat enhancement w/enhancing soft tissue in the R cavernous sinus.
- IgG4.
Dx?
- How do these respond to Valsalva manoeuvers?
Orbital lymphangioma: multicystic mass in the R orbit w/fluid-fluid levels.
- They don’t, unlike orbital varices.
Name the most common intraocular lesion in an adult.
- If you see this, what is your next step?
Melanoma
- Liver MR: they have a strong predilection for liver mets.
Dx?
Optic nerve sheath meningioma: “tram track” thickening/calcs; circumferential enhancement around the optic nerve.
Dx?
- Most characteristic location of this?
- Typical age group?
Orbital dermoid: fat/fluid level in characteristic location: superolateral.
- Superolateral.
- First 10 yrs.
Peds orbital masses:
Most common benign & malignant?
- Benign: orbital dermoid.
- Malignant: rhabdomyosarcoma: favours the superior medial orbit (see below).
Orbital lymphoma:
- Assoc w/what bug?
- Usual location?
- 2 Ix chars.
- Chlamydia psittaci.
- Upper outer.
- Restricts & enhances homogeneously.
Dx: kid w/racoon eyes.
Metastatic neuroblastoma: bilateral infiltrative intra-orbital masses.
Dx? Painful unilateral eye.
- Underlying path?
- Most common muscle affected?
- How does this differ from thyroid eye disease?
- T2 appearance?
Orbital pseudotumour:
- IgG4 idiopathic inflammatory condition.
- Lateral rectus, as seen here.
- Does NOT spare the myotendinous junctions.
- T2 dark.
Dx? 3rd trimester/postpartum woman.
- Path?
- With what can these also be related?
Lymphocytic hypophysitis: enlarged pituitary stalk.
- IgG4 disease.
- Rx ipilimumab, an immunotherapy Rx given to pts w/melanoma & RCC.
- Looks like a pituitary adenoma but has a T2 dark rim.
Orbital anatomy:
- Where are the pre- & post-septal spaces?
- On what side of the orbit is the lacrimal sac vs. gland?
- From what origin are post-septal infections usually?
- Pre-septal = outside the orbital septum, so outside the cone/eyeball; post-septal is within the cone.
- Sac = medial; gland = lateral.
- Paranasal sinusitis.
Dx?
- Typical etiology?
Dacryocystitis: inflammation & dilation of the lacrimal sac (not duct–recall, the duct is lateral, the sac is medial).
- Obstruction then staph/strep infection.
Dx?
Optic neuritis: enhancement, but not enlargement, of the optic nerve.
- If the nerve is also enlarged then think ON glioma, then think NF1.
Dx?
- Path?
- Specific Dx if these are bilateral?
Coloboma: focal discontinuity of the globe.
- Failure of the choroidal fissure to close.
- CHARGE syndrome.
Identify the arteries:
A: PCA: the basilar artery bifurcates into these.
B: SCA: the more superior of the 2 basilar artery branches.
C: basilar
D: AICA: the more inferior of the 2 basilar artery branches.
E: PICA: this is the last branch of the vertebral a.
F: vertebral a:
Dural AVFs:
- What is the most important RF for rupture?
- Underlying path?
- Most common sinuses affected?
- Cortical venous reflux.
- Mostly post-traumatic.
- Sigmoid & transverse.
Nasal bone # is the most common facial #, but what is the most common # pattern?
- What bones does this pattern involve?
Zygomaticomaxillary complex # (tripod #).
- Zygoma, inferior orbit, lateral orbig.
Dx?
Labyrinthitis: cochlea & semicircular canal enhancement on post-con T1 images.
Dx?
- Presentation?
Superior semicircular canal dehiscence: absent osseous roof.
- Noise-induced vertigo (aka Tullio’s phenomenon).
Dx?
- Classic presentation?
- Path?
- Is this usually bilateral or unilateral?
- What should it normally look like?
- What is this associated w/?
Large vestibular aqueduct syndrome: >1.5mm enlargement.
- Progressive sensorineural hearing loss–they are NOT born deaf.
- Failure of the endolymphatic sac to resorb endolymph, leading to dilation.
- BILATERAL, like the pic.
- The normal VA is never larger than the adjacent posterior semicircular cana.
- 100% w/cochlear deformity–absence of bony modiolus in 90%.
Most common cause of congenital sensorineural hearing loss?
Large vestibular aqueduct syndrome.
Dx?
- What drug is assoc w/this?
- How to differentiate from labyrinthitis ossificans?
Michel deformity/aplasia: complete absence of the cochlea, vestibule & VA.
- Thalidomide.
- Look for the missing vestibular aqueduct. It will be present in LO.
Dx?
- Syndromic association?
- MR appearance?
Endolymphatic sac tumour: crumbled up/missing vestibular aqueduct w/amorphous internal calcs.
- vHL
- T2 bright w/intense enhancement (see below).
- Hypervascular w/flow voids & tumour blush on angio.
Where is Dorello’s canal?
Most medial point of the petrous ridge–between the pontine cistern & cavernous sinus.
- This is where CN6-abducens runs.
Dx?
- What syndrome does this cause?
- What is the classic triad?
- Underlying path?
- What is this a complication of?
Petrous apicitis: enhancement of the petrous apex; erosion on CT.
- Gradenigo.
- Otomastoiditis, LR palsy, face pain (trigeminal neuropathy).
- Dorello’s canal runs through the petrous apex, where CN6-abducens, runs.
- Infectious otomastoiditis.
Identify the structures:
A: pterygopalatine fossa.
B: foramen ovale.
C: foramen spinosum.
D: carotid canal.
Identify the structures:
- What travels through the superior orbital fissure?
A: optic canal.
B: SOF
C: foramen rotundum: comes out at you like a gun; transmits the V2 (maxillary); “R2V2”.
D: vidian canal
- Oculomotor (CN3), trochlear (CN4), ophthalmic (V1) & abducens (CN6) nerves, & superior/inferior orbital veins.
Which syndrome is associated w/polyostotic fibrous dysplasia?
- When the skull base is involved, which bones are most commonly involved?
- What are some other features of this syndrome?
McCune Albright.
- Ethmoid & sphenoid.
- Precocious puberty, endocrine dysfunction, abnormal pigmentation (cafe au lait spots).
Dx: 74yo male w/DM & pus from the R ear.
- What’s the causative agent?
- What % of these pts have DM?
Malignant/necrotizing otitis externa: more aggressive version of OE w/swolled EAC soft tissues, w/abscesses & adjacent bony destruction.
- Pseudomonas.
- 95%.
Identify the stuctures:
A: superior semicircular canal.
B: lateral SCC.
C: tympanic segment of facial nerve canal.
D: vestibule.
Name the structures:
A: CN7-facial
B: CN8-VC, superior vestibular
C: CN8-VC inferior vestibular
D: CN8-VC, cochlear
Dx?
- When does this occur in gestation vs. Michel’s aplasia?
- What kinds of sounds are preserved & why?
Mondini malformation (aka incomplete partition 2): modiolus deficiency w/only 1.5 turns of the cochlea & a cystic cavity instead of the middle & apical turns; additionally, an enlarged vestibular aqueduct.
- 7th week.
- High frequency, since the basal turn is normal.
Dx: hearing loss.
- T2 signal?
- How does this differ from its main DDx?
Cholesterol granuloma: T1W image showing bright material = fat at the petrous apex.
- Also bright on T2.
- This doesn’t restrict; cholesteatoma will be T1 dark (epidermoid) and will restrict)
- This is the most common petrous apex lesion.
Dx?
- Which is the first bone usually eroded by this?
- What is the most common ossicle eroded?
- Typical MR signal?
Pars flaccida cholesteatoma: it’s in Prussak’s space, blunting the scutum.
- Scutum.
- Incus.
- No enhancement & restricts.
Glomus jugulare is supplied by which artery?
Ascending pharyngeal a.
What other vascular anomaly is most commonly associated w/an aberrant ICA?
- Which bony foramen will be missing w/it?
Persistent stapedial artery.
- F. spinosum.
