6. Neuro p284-299 (Brain - Trauma, Vascular) Flashcards
Parenchymal contusion (4)
Rough part of the skull base can scrape the brain as it slides around in a high speed RTC.
Typical locations include anterior temporal lobes, and inferior frontal lobes.
Coup (site of direct injury) and contre-coup (opposite side of brain along vector of force) injuries can occur.
Contusion can look like blood with associated oedema in the expected regions
Diffuse axonal injury (4)
Multiple theories on why this happens (different density of white and grey matter etc).
Initial CT head is often normal.
Favorite sites of DAI are posterior corpus callosum, grey-white matter junction in the frontal and temporal lobes.
Multiple small T2 bright foci on MRI.
Subarachnoid haemorrhage - trivia (2)
Trauma is commonest cause.
FLAIR is most sensitive sequence.
Epidural vs Subdural (5)
Trauma patient w/skull fracture vs old man or alcoholic with atrophic brain with fall, stretching and tearing the bridging veins.
Biconvex or lenticular vs Biconcave
Can cross the midline vs does not cross midline but may extend into interhemispheric fissure.
Can NOT cross sutures vs can cross sutures.
Usually arterial vs usually venous.
Can rapidly expand and kill you vs can’t
LeFort fracture patterns (6)
LeFort 1: “Palate separated from maxilla” or “floating palate”
LeFort 2: “Maxilla separated from the face” or “pyramidal”
LeFort 3: “Face separated from Cranium”
Essential elements:
LeFort 1: Lateral Nasal Aperture
LeFort 2: Inferior Orbital Rim and Orbital Floor
LeFort 3: Zygomatic Arch and Lateral Orbital Rim/Wall
Facial bones fractures trivia (2)
Nasal bone is most common fracture.
Zygomaticomaxillary complex fracture (tripod) is most common fracture pattern, involving the zygoma, inferior orbit and lateral orbit.
Mucocele (4)
Fracture that disrupts the frontal sinus outflow tract (usually nasal-orbital-ethmoid types) can cause adhesions and obstruction of the sinus, resulting in mucocele development.
“airless expanded sinus” is the buzzword.
Usually T1 bright with thin rim of enhancement (tumours usually have solid enhancement)
The frontal sinus is commonest location - occuring secondary to trauma.
Temporal bone fractures (3)
Traditional way to classify these is longitudinal and transverse.
In reality, most fractures are complex with components of both.
Real predictive finding of value is violation of the otic capsule.
Longitudinal vs transverse temporal bone fractures (5)
Long axis of temporal bone vs short axis.
More common vs less common.
More ossicular dislocation vs more vascular injury (carotid/jugular)
Less facial nerve damage (20%) vs more (>30%)
More conductive hearing loss vs more sensorineural hearing loss
Ageing blood on CT (4)
Hyperacute (<1hr): Hypodense
Acute (1hr - 3 days): Hyperdense
Subacute (4 days to 3 weeks): Progressively less dense, eventually becoming isodense to brain. Peripheral rim enhancement may occur.
Chronic (>3 weeks): Hypodense
Swirl sign (2)
Ominous sign of active bleeding.
Central low attenuation blood represents acute non-clotted blood, with surrounding more acute blood.
MRI ageing of blood (5)
I Bleed, I Die, But Department Boss Bleeds, Department Dies
Hyperacute (<1 day) - T1 Iso T2 Bright (Oxyhaemoglobin, intracellular)
Acute (1-3 days) - T1 iso T2 dark (Deoxyhaeoglobin, intracellular)
Early Subacute (2-7 days) - T1 bright, T2 dark (Methaemoglobin, intracellular)
Late Subacute (7-14 days) - T1 bright T2 bright (Methaemoglobin, extracellular)
Chronic (>14 days) - T1 dark, T2 dark (Ferritin and haemosiderin, extracellular)
Subarachnoid haemorrhage (5)
Most common cause is trauma, and most sensitive sequence on MRI is FLAIR.
Supplemental O2 can give false appearance of SAH on flair.
Non traumatic causes include:
- Aneurysm
- Benign non-aneurysmal perimesencephalic haemorrhage.
- Superficial siderosis
Benign non-aneurysmal perimesencephalic haemorrhage (5)
Not associated with aneurysm, usually a venous bleed.
Pathology not fully understood.
Location of blood, around the midbrain and pons with extension into the lateral sylvian cisterns or interhemispheric fissures is classic.
Anterior to the brainstem.
Rebleeding and ischaemia are rare, outcomes are generally good
Sequella of SAH (3)
Hydrocephalus (early),
Vasospasm (7-10 days)
Superficial siderosis (late)
(4)Superficial siderosis
Side effect of repeated episodes of SAH.
“staining the surface of the brain with haemosiderin”
The classic look is curvilinear low signal on gradient coating the surface of the brain.
Classic Hx of sensorineural hearing loss and ataxia.
Intraparenchymal haemorrhage DDx (4)
Hypertensive haemorrhage,
Amyloid angiopathy,
Septic emboli,
Others (AVMs, vasculitis, brain tumours)
Hypertensive haemorrhage (3)
Common locations are basal ganglia, pons and cerebellum.
Basal ganglia, specificlly putamen, is commonest cause.
Typically get intraventricular extension of blood.
Amyloid angiopathy (2)
Hx of old dialysis patient.
Multiple lobes at different ages with scattered microbleeds on gradient.
Septic emboli (5)
Seen in certain clinical scenarios (IVDU, organ transplant, cyanotic heart disease, AIDS, lung AVMs).
Numerous small foci of diffusion restriction.
Septic emboli to the brain result in abscess, mycotic aneurysms (most commonly distal MCA).
Location favours grey-white matter interface and basal ganglia.
Surrounding oedema around the tiny abscesses.
Classic scenario should be parenchymal bleed in patient with infection.
Intraventricular haemorrhage DDx (5)
Trauma
Tumour
Hypertension
AVMs
Aneurysm
Epidural/subdural haemorrhage DDx (2)
Usually post traumatic.
Dural AVFs and high flow AVMs can bleed, causing subdural/subarachnoid bleeds.
Stroke (2)
Ischaemic (80%) 0r haemorrhagic (20%).
Clinical diagnosis, imaging findings compliment the diagnosis
Watershed zones (3)
Junction between vascular territories.
Prone to ischaemic injury, especially in case of hypotension or low oxygen states (near drowning).
Watershed infarcts in a kid = Moyamoya
Imaging signs of stroke on CT (5)
Dense MCA sign - intraluminal thrombus is dense, usually in M1 or M2 segments.
Insular ribbon sign - loss of normal high density insular cortex from cytotoxic oedema.
Loss of grey-white matter differentiation - Basal ganglia/internal capsular region and subcortical regions.
Mass effect - peaks 3-5 days
Enhancement - Rule of 3s: Starts in 3 days, peaks in 3 weeks, gone in 3 months
Fogging (3)
Phase in evolution of stroke when infarcted brain looks like normal tissue, seen around 2-3 weeks.
Fogging is described on non-contrast CT, but T2 MRI would have a similar effect occuring around day 10.
Could give IV contrast to demarcate the area of infarct.
Imaging signs of stroke on MRI (4)
Restricted diffusion - acute infarcts are usually bright from about 30 mins to about 2 weeks. Restricted diffusion without bright FLAIR signal should make you think hyperacute stroke (<6hrs).
LOTS of other pathologies restrict.
Enhancement - Rule of 3s still applies (starts 3 days, peaks 3 weeks, gone by 3 months)
Aging of stroke on MRI (3)
0-6hrs: Diffusion bright, FLAIR not bright, T1 and T2 iso.
6-24hrs: Diffusion bright, FLAIR bright, T1 dark, T2 bright.
1-7 days: Diffusion bright, FLAIR bright, T1 dark with bright cortical necrosis, T2 bright.
Haemorrhagic transformation. (4)
Occurs in around 50%, typically between 6hrs and 4 days.
Usually within 24hrs if thrombolysis.
Either tiny specs in the grey matter called petechial (90%) or full haematoma (10%).
Risk factors: TPA, anticoagulation, embolic strokes (especially large ones), venous infarcts.
Predictors of haemorrhagic transformation in people getting TPA (2)
Multiple strokes, proximal MCA occlusion, >1/3 MCA territory, >6hrs since onset, absent collateral flow
Venous infarct (8)
Stroke secondary to venous occlusion (usually sequelae of dural venous sinus thrombosis or deep cerebral vein thrombosis).
Venous infarcts are higher risk for haemorrhagic transformation.
In babies, think dehydration, in older kids, mastoiditis, in adults, coagulopathies (protein C and S deficiency) and oral contraceptives.
Most common site of thrombus is sagittal sinus, with associated infarct in 75% of cases.
Venous thrombus presets as dense sinus or empty delta on venogram.
Venous infarcts have heterogenous restricted diffusion.
Can result in vasogenic oedema that eventually progresses to stroke and cytotoxic oedema.
Arterial = cytotoxic oedema, venous = cytotoxic and vasogenic.
Chronic venous thrombosis associated with dural AVF development, or increased CSF pressure from impaired drainage
Aneurysm - risk factors (7)
Smokers,
Polycystic kidneys,
Connective tissue disorders (Marfans, Ehlers-danlos),
Aortic coarctation,
NF,
FMD,
AVMs
Aneurysm - where (3)
Usually at branch points (persistent trigeminals get more aneurysms because they have more branch points).
Favour anterior circulation, with anterior communicating being most common site.
Basilar is the most common posterior circulation location (PICA is second)
Aneurysm - rupture (5)
RIsk is increased with
size,
posterior location,
Hx of prior SAH,
smoking,
female gender
Aneurysm types (6)
Saccular (berry):
Fusiform
Pseudoaneurysm
Pedicle aneurysm
Blister aneurysm
Infundibular widening.
Saccular (berry) aneurysm (5)
Most common type.
Commonly seen at bifurcations.
Underlying pathology may be congenital deficiency of the internal elastic lamina and tunica media at branch points.
Most are idiopathic
Multiple in 15-20% of cases.
Fusiform aneurysm (3)
Associated with: PAN, connective tissue disorders, syphillis
More common in posterior circulation.
May mimic a CPA mass.
Pseudoaneurysm (4)
Irregular, often saccular, arterial outpouching at a strange/atypical location.
May see focal haematoma next to the vessel on non contrast
Traumatic: often distal secondary to penetrating trauma, or adjacent fracture
Mycotic: often distal, most commonly MCA, associated Hx of endocarditis, meningitis or thrombophlebitis.
Pedicle aneurysm (3)
Associated with AVM.
Found on the artery feeding an AVM 75% of the time.
May be higher risk to bleed than the AVM itself because they are higher flow.
Blister aneurysm (2)
Angio often negative.
Broad based at a non-branch point (Supraclinoid ICA is most common site)
Infundibular widening (2)
Not true aneurysm, but funnel shaped enlargement at the origin of the PCOM, at junction with the ICA.
“not greater than 3mm”
Maximal bleeding - aneurysm location (5)
ACOM: interhemispheric fissure
PCOM: Ipsilateral basal cistern
MCA trifurcation: sylvian fissure
Basilar tip: Interpeduncular cistern or intraventricular
PICA: posterior fossa or intraventricular
Vascular malformations - types (6)
High flow AVMs
Dural AVF
DVA
Cavernous malformation
Capilary Telangectasia
Mixed
High flow AVMs (7)
Commonest type of high flow lesion.
Favour supratentoral location, and are due to congenital malformation in the development of the capillary bed.
High flow implies arterial component (arterial component > nidus > draining veins).
Haemorrhage is most common complication, incidence of around 3% per year.
Seizure is second commonest complication.
Adjacent brain may be atrophic and gliotic.
Increased bleeding risk: Small size AVMs (higher pressure), single draining vein, intranidal/perinidal aneurysm, basal ganglia/thalamic/periventricular locations
Dural AVFs (8)
Can be high or low flow.
Less common than high flow AVMs.
Acquired due to dural sinus thrombosis.
No nidus.
Presents in 50s-60s (AVM in 20-30s).
Clasically causes pulsatile tinnitus when it involves sigmoid sinus.
May have vision problems if cavernous sinus is involved.
Increased bleeding risk if direct cortical venous drainage.
Can be occult on MRI/MRA - need catheter angio if suspicion is high.
SPINAL AVFs are most common type, helpful hint is the classic clinical Hx of “gradual onset LE weakness”
DVA (3)
Not actually a vascular malformation, but variation in normal venous drainage.
“Caput medusa” or “large tree with multiple small branches” are buzzwords.
Associated with cavernous sinus malformations.
Cavernous malformations (5)
Also called cavernomas or cavernous angiomas.
Low flow lesions with a dilated capillary bed, without intervening normal brain tissue.
Can be single or multiple, more common in hispanics.
“popcorn like” with “peripheral rim of haemosiderin” - seen on gradient due to haemosiderin.
Can ooze some blood, but rarely have catastrophic bleeds.
May have a nearby DVA
Capillary telangiectasia (5)
another slow flow lesion, unlike the cavernoma, does have intervening normal brain tissue.
Don’t bleed, usually totally incidental.
Commonly a single lesion in the pons.
Best seen on gradient (slow flow and deoxyhaemoglobin).
“Brush like” or “stippled pattern” of enhancement.
Can develop as a complication of radiation therapy.
Mixed
Wastebasket term, most often used for DVA with AV shunting or DVAs with telangiectasias
Vasospasm (5)
Often triggered by vessels bathed in blood (SAH).
Often occurs 4-14 days after SAH.
Smooth, long segments of stenosis, involving multiple vascular territories.
More volume SAH = greater risk.
>1mm thickness or intraventricular/parenchymal extension is higher risk.
Other causes include meningitis, PRES and migraine headaches.
Vascular dissection (3)
Can occur from variety of pathologies, usually penetrating trauma or chiropractors.
Penetrating trauma tends to favour carotids, and blunt trauma tends to favour vertebrals.
T1 bright crescent sign on MRI (intramural haematoma)
vasculitis - causes (5)
Variety of causes of CNS vasculitis.
Primary CNS vasculitis
- Primary angiitis of the CNS (PACNS)
Seconary CNS vasculitis
- Meningitis (bacterial, TB, fungal), septic embolus, sarcoid.
Systemic vasculitis with CNS involvement
- PAN, Temporal arteritis, Wegeners, Takayasu
CNS vasculitis from systemic disease
- Cocaine, RA, SLE, Lyme disease
CNS vasculitis (4)
All causes have similar appearance, with multiple segmental areas of vessel narrowing, with alternating dilatation (beaded appearance).
Can have focal areas of vascular occlusion
PAN is most common systemic vasculitis to involve the CNS.
SLE is most common collagen vascular disease
Moyamoya (8)
Non-atherosclerotic, poorly understood, characterised by progressive stenosis of the supraclinoid ICA eventually leading to occlusion.
Progressive stenosis results in enlargement of basal perforating arteries.
“Puff of smoke” on angiogram.
Watershed distribution
In child, think Sickle cell.
Other notable associations include NF, prior radiation, Downs
Bimodal age distribution (early childhood and middle age)
Children stroke, adult bleed
CADASIL (4)
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
40YO with migraine headaches and eventially dementia.
MRI shows severe white matter disease involving multiple vascular territories, in the frontal and temporal lobe.
Occipital obes often spared.
NASCAT criteria (2)
North Americal Symptomatic Carotid Endarterectomy Trial criteria, used for carotid stenosis.
Degree of stenosis measured, using maximal internal carotid artery stenosis (A) compared to parallel non-curved segment of the distal, cervical internal carotid artery (B).
(1-A/B) x 100%
