Investigation Viva Flashcards
Differential of a supratentorial CONVEXITY extra-axial mass lesion?
Meningioma (enhances) Metastasis (enhances) Arachnoid cyst (follows CSF) Epidermoid (restricted diffusion) Porencephalic cyst (WM lined) / Schizencephaly (GM lined)
Differential of a supratentorial intra-axial mass lesion?
Glioma - HGG or LGG Metastasis Abscess Demyelination Lymphoma Pilocytic astrocytoma / ATRT in a child
Differential of a sella / suprasellar mass lesion?
Pituitary adenoma Craniopharyngioma Rathke’s cleft cyst OPG Meningioma Chordoma (Rare: Aneurysm / GCT / metastasis / schwannoma)
Differential of an intraventricular lesion?
Meningoma / metastasis SEGA / Subependymoma Colloid cyst / Craniopharyngioma / Choroid plexus papilloma Ependymoma Neurocytoma / Glioma Teratoma R Abscess / AVM / Aneurysm Lipoma
Differential of an infratentorial extra-axial mass lesion?
Vestibular schwannoma Meningioma Epidermoid AVM
Differential of a infratentorial intra-axial mass lesion?
Metastasis Haemangioblastoma Cavernoma Ependymoma In paeds: Medulloblastoma / pilocytic astrocytoma / brainstem glioma
Differential of a infratentorial intraventricular mass lesion?
Ependymoma Choroid plexus papilloma Metastasis
How does fMRI work?
Based on the differential paramagnetic parameters of oxy- and deoxy-Hb the blood oxygen level-dependent (BOLD) signal can be measured and modelled to calculate changes in blood flow and infer metabolism. This can be performed at rest (Default mode network) or during task-based assessments. Statistical parametric mapping can then be used to identify statistically significant rises in blood flow.
What is the difference between T1 and T2?
T1 is spin-lattice relaxation i.e. the time for protons to realign themselves with the magnetic field. T2 is the spin to spin relaxation i.e. the time for protons to return to their out of phase state.
What types of MR angiography are there?
Contrast-enhanced and non-contrast methods. Non-contrast includes TOF, ASL ad Phase contrast. TOF (velocity dependant) and ASL are for arterial flow. Phase contrast is best for venous.
A 15-year-old girl with headaches and lower limb weakness. What are the important factors in the history?
Site of headaches - frontal / retro-orbital? suggests HCP/raised ICP. Occipital? suggests Chiari. Leg weakness - one or both? distal or proximal? Power? Gait? UL or LL only? Onset - Sudden = vascular / demyelinating, subacute and progressive = neoplastic lesion and chronic stable = congenital lesion. Characteristic - sharp lancinating pain? = TN or chronic burning pain? = dysaesthesia Radiation - Within TN distribution? Associations - UL / gait / falls / dizziness / hearing loss / visual disturbance / diplopia? Timing - Constant headache or comes and goes? Exacerbations - Worse with cough / straining?
A 15-year-old girl with headaches and lower limb weakness has a cerebellar lesion. How do you explain the symptoms?
The headache may be due to raised ICP or dural irritation. The lower limb weakness is difficult to explain from a cerebellar lesion if there is no brainstem compression. There may be other lesions in the supratentorial compartment or in the brainstem (crossed cranial nerve and hemiparesis) or spinal cord.
How would you examine a 15-year-old girl with headaches and lower limb weakness that has a cerebellar lesion?
I would start by an examination of the cranial nerves and cerebellum followed by an UL and LL examination. In the cranial nerves, I would focus on fundoscopy to identify any papilloedema, pupillary response for parinaud’s syndrome, eye movements, nystagmus, and the lower cranial nerves for any bulbar or pseudobulbar palsies. As part of the cerebellar examination, I would assess for Rhomberg’s sign, dysmetria, ataxic gait, intention tremor, hypotonia and slurred speech. In the upper and lower limbs, I would try to identify if there is a pyramidal pattern of weakness and a potential sensory level.
You suspect the patient has a haemangioblastoma. What investigations would you request?
Opthalmology to investigate for retinal angiomas. CT-CAP to identify phaeochromocytomas, renal cell carcinomas, pancreatic cysts. MRI whole neuroaxis for brain or spinal cord haemangioblastomas and endolymphatic sac tumours. BP and urine metanephrines. FBC for polycythaemia.
What is the normal screening for a patient with VHL?
Annually: Opthalmology review, urine and serum metanephrines, MRI abdomen and Brain and whole spine MRI.
What are the implications for children in patients with VHL?
I would refer a geneticist and obstetrician for pre-implantation counselling as this is an autosomal dominant condition meaning there is a 50% chance of the child having the mutation.
What is the natural history of haemangioblastomas in VHL?
Haemangioblastomas exhibit a growth phase and a quiescent phase where they remain static for many years. In asymptomatic patients, it may be reasonable to undertake a period of surveillance imaging and intervene only if the patient becomes symptomatic. In paediatric populations, there is a tendency for the lesion to grow and surgery is recommended even if asymptomatic. The size of the cystic component appears predictive of whether the lesion will become symptomatic and need treatment.
Should you resect the cyst wall with haemangioblastomas?
If it enhances this suggests tumour within the cyst wall.
What is the diagnosis of this 20-year-old patient?
VHL
What is this lesion and what condition is it associated with?
Endolymphatic sac tumour in VHL.
The CT shows a lytic and infiltrative lesion within the posterior petrous bone. The MRI shows that the lesion returns heterogenous T1 signal.
What is this lesion?
There is an infiltrative and exophytic lesion of the posterior petrous temporal bone. There is also abnormal signal intensity within the left vitreous humour. Taken together this would be indicative of a patient with VHL that is exhibiting a left endolymphatic sac tumour and left intravitreal haemorrhage most likely from a retinal angioma. Further screening of the remainder of the neuroaxis, as well as a CT-CAP of the abdomen and serum and urine metanephrines, should be taken. BP and FBC for polycythaemia.
Describe the components of the ICP wave.
P1 = percussion = arterial pulsation
P2 = tidal = intracranial compliance
P3 = dichrotic = aortic valve closure
If the P2>P1 this suggests a loss of intracerebral compliance and raised intracranial pressure.
What type of ICP monitors do you know?
The gold standard is through measurement of CSF pressure int he frontal horn of the lateral ventricle using an EVD.
Other methods include parenchyma, subdural and epidural locations.
How do ICP monitors work?
There are 3 main types:
- Piezoelectric strain gauge devices (Codman)
- Fibreoptic (Camino)
- Pneumatic sensor (Spiegelberg) - does not need zeroing and recalibrates every hour reducing the risk of drift.
How do you measure cerebral oxygenation?
This can be measured directly from the cerebral parenchyma using pBO2 bolts or inferred indirectly from the metabolites using microdialysis catheters via the lactate to pyruvate ratio, which if raised suggests anaerobic respiration.
The partial pressure of the oxygen supplied to the brain can be measured using an arterial line or the saturations.
Central venous saturation from the central line can also be used.
How do you monitor Cerebral Blood Flow?
Clinical status
TCDs
Katy Schmidt method with Xe-133 perfusion CT based on the Fick principle.
A patient with renal failure has a sudden onset of severe headache, how would you investigate them acutely and during follow up?
Acutely they should have a CTA or DSA. In patients with renal dysfunction there is the risk of developing contrast-induced nephropathy. I would discuss this with the renal physicians but the patient’s pre-procedure risk should be stratified (e.g. Mehran classification). If the patient’s risk is low I would encourage oral hydration before the contrast administration. If the risk of moderate or high I would discontinue nephrotoxic drugs, consider high dose statin, provide IV prehydration, N-acetyl cysteine, use the lowest dose of contrast agent and provide IV post-hydration monitoring for any renal dysfunction.
In the longer term, they can have a TOF MRA that does not require contrast and removes the risk of contrast-induced nephropathy. Gadolinium carries the risk of nephrogenic systemic fibrosis.
What are the causes of delayed deterioration following SAH?
Rebleed
Hydrocephalus
Metabolic derangements - hyponatraemia
DNID
Seizure
Other - UTI / chest infection / PE / MI etc
What are the windows for TCD insonation?
Temporal
Orbital
Suboccipital
Through the temporal window, the MCA flows towards the probe and ACA flows away.
The PCA flows towards the probe but is further away and slower than the MCA.
Describe the histological slide
Nuclear atypia with pleomorphism and high nuclear to cytoplasmic ratio.
Increased cell density.
Microvascular proliferation with endothelial hyperplasia forming glomeruloid tufts.
Necrosis with pseudopalisading.
The central necrosis and the high-grade features would be in keeping with a WHO grade 4 IDH-WT GBM.
What is the diagnosis?
A Type 1 split cord malformation - there are two dural sacs with an intervening fibro-osseous intermedian septum. This is due to a failure of gastrulation in which two notochords were present resulting in two distinct spinal cords.
A Type 1 split cord malformation would have two cords within a single dural sac.
What are the histological features of LGG?
Diffuse astrocytoma has a low cell density but there is nuclear atypia.
Oligodendroglioma is characterised by perinuclear halos giving a fried egg appearance. There is also chicken wire vasculature.
The oligoastrocytoma has both astrocytic and oligodendroglial components.
How do you classify CC fistulas?
Barrow classification:
A - Direct high flow shunt between ICA and cavernous sinus
B - Indirect low flow ICA meningeal branches to cavernous sinus
C - Indirect low flow ECA meningeal branches to cavernous sinus
D - Indirect low flow ICA and ECA meningeal branches to cavernous sinus
What factors influence management of a CCF?
- High flow
- Raised IOP
- Symptomatic visual deterioration
- Proptosis
- Cortical venous reflux
What are the different persistent fetal circulations?
PCom is the most common.
Persistant trigeminal = arises proximal to the cavernous sinus, travels lateral to the sella connects to the basiar between the AICA and SCA.
Persistant otic = petrous ICA to Basilar at below AICA. Passes through the IAM.
Persistant hypoglossal = From the cervical ICA to the Basilar.
Persistant proatlantal = From cervial ICA to the VA between the O-C1 or C1-2
What does the histology show?
WHO grade 1 meningioma subtypes
What does the histology show?
WHO grade 2 meningioma subtypes
What does the histology show?
WHO grade 3 meningiomas
