BRAIN - Vascular Flashcards
DDx haemorrhagic strokes
- Idiopathic
- Primary causes
- Arterial hypertension (< 5mm T2*)
- Cerebral amyloid angiopathy
- Intracranial neoplasia (Multicentric: hemangiosarc, metastases, histiocytic SK, intravascular lymphoma
primary: gliomas, meningiomas, choroid plexus t, pituitary, …)
- Secondary causes
- Coagulopathy (von willebrand factor def, Angiostrongylus vasorum)
- Parasite migration
- Bacterial/septicemia
- Hemorrhagic transformation
- Vasculopathy
- Cerebral vascular malformation (Arteriovenous, Venous, Cavernous, Capillary malformations or telangiectases)
- postprocedural, traumatic
Give 3 diagnostic tests in case of CVD
Coagulation panel
Dosage of Von Willebrand factor
Coproscopy in search of Angiostrongylus
Serology for Angiostrongylus
What are the 4 lacunar ischemic syndromes?
Striates arteries: ipsilateral circling, ipsilateral head turn, contralateral menace deficit, contralateral PR deficit
Paramedian: vestibular
Extensive dorsal: vestibular, contralateral menace deficit
Ventrolateral: circling, contralateral PR deficit
Which signs are usually present in T2-FLAIR to evaluate two findings consistent with strokes <24h old?
Hyperintense vessel signs
Hyperintense swollen cortical gyri
% of cats with hypertensive encephalopathy presented retinal lesions
93% (28/30)
DDx ischemic strokes
- Atherosclerosis: hypothyroidism, diabetes, hyperlipemia
- Emboli: metastatic tumor cells, septic thromboemboli, migrating parasite or parasitic emboli (Dirofilaria immit), leishmania, intravascular lymphoma, fibrocartilaginous embolism
- Hypertension: CKD, hyperthyroidism, pheochromocytoma, hyperadrenocorticism, primary hyperaldosteronism
- Vasospam (Cuterebra migrans)
- Hypercoagulable state: hyperadrenocorticism, protein losing nephropathy/enteropathy, systemic neoplasia (including splenic HSK), immune mediated haemolytic anaemia, sepsis, infective endocarditis
- Cardiomyopathy
- Hemodynamic (anaesthetic)
- Idiopathic (~50%): CKC & Greyhound are predisposed
Ischemia occurs when the CBF is reduced by more than: 33%, 50%, 60%, 75%, 90%
60%
What is the typical histologic manifestation of spontaneous hypertensive encephalopathy in cats?
Bilaterally symmetrical edema of the subcortical cerebral white matter
What is the name of the lesion when a main artery is obstructed?
Territorial infarct
For obstruction of the smaller perforating arteries, it is referred as a lacunar infarct.
Which of the followings cross the BBB?
Amlodipine
Penicillin
Carbamazepine
Morphine
Cytosine arabinoside
Doxorubicin
Glucose
Neutral amino acids
Glutamate
Glycine
Potassium
Chloramphenicol
Sulfonamides
Vincristine
Gabapentin
Ampicillin
Amlodipine: not
Penicillin: not
Carbamazepine: cross
Morphine: cross
Cytosine arabinoside: cross
Doxorubicin: not
Glucose: cross
Neutral amino acids: cross
Glutamate: cross
Glycine: cross
Potassium: cross
Chloramphenicol: cross
Sulfonamides: cross
Vincristine: not
Gabapentin: cross
Ampicillin: cross
Cross: carbamezepine, morphine, cytosine arabinoside, glucose, neutral amino acids, glutamate, glycine, potassium, chloramphenicol, gabapentin, sulfonamides, ampicillin
Do not cross: amlodipine, penicillin, doxorubicin, vincristine
Mannitol is able to pass the BBB: true or false?
False
But, with prolonged use, mannitol can also disrupt the blood–brain barrier, and it may pass into the brain parenchyma and cause a rebound effect, with subsequent increases in ICP.
What are the most common neurological signs in hypertensive cats (vision excluded)? Most common underlying diseases?
Most common neurological signs
Ataxia
Various manifestations of seizures
Altered behaviour
Retinal lesions found in 28/30 cats
Most common underlying diseases
CKD (34%)
Hyperthyroidism (21%)
Primary hyperaldosteronism (2%)
Idiopathic (34%)
canine/feline cerebrovascular blood supply
from basilar and internal carotid arteries
in cat craniocaudal blood flow through basilar artery + external carotid artery (via maxillary art) supply most of the blood to arterial circle
+rete mirabile in max art
supply of rostral cerebellar artery
rostral cerebellar hemisphere and vermis (lateral, intermediate, medial branches)
dorsal medulla
supply of caudal cerebellar artery
from basilar artery
caudoventral aspect of cerebelar hemispheres and vermis (including floculus and nodulus)
lateral aspect medulla
CBF should be constant at a MAP between..
50 and 150 mmHg
major intracranial arterial supply
rostral cerebral: rostral/rostromedial cerebrum
middle cerebral: lateral cerebrum
caudal cerebral: caudo-dorsal and caudo-medial cerebrum
medial striate: glob pallidus, putamen, medial int capsule, head caudale
lat striate: doral caudate, lat int caps, claustrum
rostral choroidal: caudate caudal, int capsule, thalamus lat, optic tract
proximal perforating: rostromedial/ventromedial thalamus
distal perforating: caudolat thalamus, subthalamic nuclei
caudal perforating: caudal/medial/paramedian thalamus, ventromed midbrain, median/paramedian pons
patophysiology of ischemic CVD
primary injury: due to energy failure
failure na+/k+ ->cytotoxic odema
failure aerobic metab ->lactic acidosis -> cytotox
loss ionic gradient ->increase Ca2+ release-> activ protease/lipases-> mb damage and free radical fomation
secondary injury: due to compromise of vascular endoth and suporting cells (4/6h-24/48h)
damage to BBB -> vasogenic edema and inflam cells infiltrate
hemoragic conversion (extravation blood product)
brain region susceptibles to ischemia
cerebral cortex, GM hippocampus, cerebellar cortex, basal and thalamic nuceli
physiopathology of intracranial hemorrhage
primary injury: direct damage to growing hematoma
compression tissue (6h)
increasing ICP
breakdown blood product -> proinflam and prooxidant, stim glutamate release
secondary: peaks 3-5d, may persist up to 7d
perihemoragic edema due to thrombin-induced activ inflam cascade, overexp matrix metalloprotease; cause increase ICP
ischemia secondary to increase ICP or ruptured vessel
vascular malformation causing clinical signs without bleeding
vascular hamartoma, meningiomatosis (mass effect)
CT of acute hemmorhage
- hyperattenuation due to fibrin, globin (40-60 HU acute, 60-80 whithin hours), normal <40)
- hyperatt increase for 72h than decrease, isoat 1m (beginning at perif)
- peripheral contrast enhan 6d-6w
CSF alteration in hemmoragic stroke
mild increase prot/PNN/mononuclear due to disruption of BBB
xanthochromia, erythrophagocytosis
elevation IL-6
prognosis for ischemic/hemorragic stroke
ischemic: 23% died within first 30d
concurrent condition assoc with shorter survival and more recurr
hemorr: single non trauma >5 mm long term good in 60%, multiple non trauma > 5 mm poor outcome in 70%
sign associated with
1. paramedian thalamic ischemic infarction
2. dorsal midbrain infarction
3. cerebellar interpositus nucleus
- controlat medial strabismus (esotropia) + vestibular ataxia, head tilted, nystagmus + episodic non intentional tremors
- convergence retraction nystagmus
- ispsilateral mydriasis + cerebellar signs
maj arteries affected by stroke in dog
rostral cerebellar (47%) > perforating: caudal thalamus + rostral BS (42%) >striate
specific localisation of ischemic stroke acording to etiology
hypertensive: deep (thal, basal nuclei)
amyloid angiopathy: G/W matter junction
In ischemic stroke delay for
1. FLAIR hyper
2. Periferal enhancement
3. T2 hyper
4. DWI hyper
- 3-8 h
- 7-10 d
- 6-12 h
- minutes, reverse in 24h-5d
DWI lesion, normal FLAIR => less than 3h
diff for T1 hyperintensity
blood breakdown product
fat
proteinaceous fluid
melanin
calcification
necrosis
paramagnetic sub: iron, manganese, cooper
blood breakdown product timing for hemorrhagic strokes
< 24h intrac oxyhb
1-3d intrac desoxyhb
3-7d intrac methb
7-14d extrac methb
>14d extrac hemosiderin and ferritin (in macrophages)
differential for hypo SWI/T2*
hemosiderin (paramagnetic)
mineralisation
gaz
fibrous tissus
iron deposit
other causes than hemo are T1/T2 hypo (diamagnetic)
ADC difference between glioma and ischemia
glioma has lower ADC than ischemia (ADC inversively proport to cell density)
causes of mydriasis
ophtalmologic (increase intraocul pressure…)
optic or oculomotor nerve
sympathetic innerv eye
plant : Datura stramonium
phenylephrine (sympatomimetic)
most frequent signs and pathology associated with microbleeds
vestibular
proteinuria
dogs are older and smaller than non affected
associated with shorter survival time
maj small poodle and shitzu
association with cortical atrophy
T2 black out effect: definition, exemples
low signal in T2 due paramagnetic substance reduced signal in DWI (inverse of T2 black out effect)
hemorrhage, brain abcess, toxoplasmose, aspergilose, metastatic lesion, blastomycose
finding in diffusion/adc sequence to date hemor
in stratified intracereb hemorrhage
ADC apparence of peripheral hypo in hyperacute and iso/hypo in acute
T2 hypointense rim in hemo: conversion of oxyhemog to desoxyhem
MRI features of intracranial hemorrhage
complet T1/T2 hypointense peripheral rim, periferal enhancement pattern
<2d T1 hypo, T2 hypo and hyper, GRE hypo
2-14d T1 hyper, T2 hyper, GRE hyper
>14d T1 iso to hypo, T2 hypo to hyper GRE hypo
Normal D-dimer is an appropriate negative predictor for canine ischemic stroke
True or false?
false
Is T2star seq affected by gadolinium?
FALSE
gadolinium paramagnetic: T2 shortening effect
comparison SWI/T2star to detect hemorrhage
SWI more artefact in frotal sinus
better detection microbleed with SWI
SWI: differenciate dia and paramagnetic with phase images (right handed para hypo and dia hyper)
19% presumed hemor in T2star diagnosed as vessel in SWI
paramagnetic subst increase local magnetic field stength, diamagnetic decrease
subacute cortical laminar necrosis
1. causes
2. assoc with hyper/hypoperf MRI
3. T1 intensity
4. which lamina more affected
- hypoxia, hypogly, fluid overload, smoke inhalation, ischemia, encephalitis, prolonged seizure act
- hyperperfusion
- T1 hyper
- lamina 3
normal intracranial pressure
7-12 mmHg
transcranial doppler US: factor assoc with hypertension
ratio systolic mean velocity / diastolic mean veloc
most common signs associated with hypertensive encephalopathy in cat
ataxia
seizure
altered behaviour
fact assoc with brain herniation in cat
age
neoplasia
low consciousness
US optic nerve sheat diameter is larger/smaller in hypertensive brain + related with which other variable
larger
related to age
in MRI no correlation when age is considered
management acute hypertension
diagnosis of SBP ≥ 180 mm Hg with signs of intracranial TOD
decreased by approximately 10% over the first hour and another approximately 15% over the next few hours
parent: fenoldopam (dopamine-1-receptor agonist = arterial vasodilation, natriuresis, and increased GFR)
labetolol, hydralazine, nitroprussine (none of these medications has the advantage of renal vasodilatation)
without evidence of acute TOD may be treated with PO medication: hyralazine, amlodipine
management hypertension dog
0.5-2.0 mg enalapril or benazepril/kg PO q12h
1.1.0 mg telmisartan/kg PO q24h
severely hypertensive
dogs (SBP > 200 mm Hg) initial coadministration of a
RAAS inhibitor and a CCB (eg, 0.1-0.5 mg/kg amlodipine PO q24h)
use of CCB as monotherapy in dogs should be avoided because CCB preferentially dilate the renal afferent arteriole potentially exposing the glomerulus to damaging increases in glomerular capillary hydrostatic pressure
in cat first choice CCB
manifestation of hypertension in cat : % neuro/opthalmo
55% neuro (25% primary complain)
ataxia, various manifestations of seizures and altered behaviour
TEG, d-dimer in CVA
D DIMER
low-risk population (CVA prevalence, 37%), abnormal blood D-dimer concentration was not significantly associated with CVA. The sensitivity of D-dimer concentration for CVA diagnosis was 31.1% and specificity was 86.4%
TEG
In this high-risk population (prevalence of CVA, 82%), abnormal TEG was not significantly associated with CVA. The sensitivity of TEG for CVA diagnosis was 64.3%, and the specificity was 67.7%
