BRAIN - Vascular

Question 1

DDx haemorrhagic strokes

Answer 1

• Idiopathic
• Primary causes

1. Arterial hypertension (< 5mm T2*)
2. Cerebral amyloid angiopathy
3. Intracranial neoplasia (Multicentric: hemangiosarc, metastases, histiocytic SK, intravascular lymphoma
   primary: gliomas, meningiomas, choroid plexus t, pituitary, …)

• Secondary causes

1. Coagulopathy (von willebrand factor def, Angiostrongylus vasorum)
2. Parasite migration
3. Bacterial/septicemia
4. Hemorrhagic transformation
5. Vasculopathy
6. Cerebral vascular malformation (Arteriovenous, Venous, Cavernous, Capillary malformations or telangiectases)
7. postprocedural, traumatic

Question 2

Give 3 diagnostic tests in case of CVD

Answer 2

Coagulation panel
Dosage of Von Willebrand factor
Coproscopy in search of Angiostrongylus
Serology for Angiostrongylus

Question 3

What are the 4 lacunar ischemic syndromes?

Answer 3

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

Question 4

Which signs are usually present in T2-FLAIR to evaluate two findings consistent with strokes <24h old?

Answer 4

Hyperintense vessel signs
Hyperintense swollen cortical gyri

Question 5

% of cats with hypertensive encephalopathy presented retinal lesions

Answer 5

93% (28/30)

Question 6

DDx ischemic strokes

Answer 6

• 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

Question 7

Ischemia occurs when the CBF is reduced by more than: 33%, 50%, 60%, 75%, 90%

Answer 7

60%

Question 8

What is the typical histologic manifestation of spontaneous hypertensive encephalopathy in cats?

Answer 8

Bilaterally symmetrical edema of the subcortical cerebral white matter

Question 9

What is the name of the lesion when a main artery is obstructed?

Answer 9

Territorial infarct

For obstruction of the smaller perforating arteries, it is referred as a lacunar infarct.

Question 10

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

Answer 10

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

Question 11

Mannitol is able to pass the BBB: true or false?

Answer 11

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.

Question 12

What are the most common neurological signs in hypertensive cats (vision excluded)? Most common underlying diseases?

Answer 12

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%)

Question 13

canine/feline cerebrovascular blood supply

Answer 13

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

Question 14

supply of rostral cerebellar artery

Answer 14

rostral cerebellar hemisphere and vermis (lateral, intermediate, medial branches)
dorsal medulla

Question 15

supply of caudal cerebellar artery

Answer 15

from basilar artery

caudoventral aspect of cerebelar hemispheres and vermis (including floculus and nodulus)
lateral aspect medulla

Question 16

CBF should be constant at a MAP between..

Answer 16

50 and 150 mmHg

Question 17

major intracranial arterial supply

Answer 17

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

Question 18

patophysiology of ischemic CVD

Answer 18

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)

Question 19

brain region susceptibles to ischemia

Answer 19

cerebral cortex, GM hippocampus, cerebellar cortex, basal and thalamic nuceli

Question 20

physiopathology of intracranial hemorrhage

Answer 20

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

Question 21

vascular malformation causing clinical signs without bleeding

Answer 21

vascular hamartoma, meningiomatosis (mass effect)

Question 22

CT of acute hemmorhage

Answer 22

1. hyperattenuation due to fibrin, globin (40-60 HU acute, 60-80 whithin hours), normal <40)
2. hyperatt increase for 72h than decrease, isoat 1m (beginning at perif)
3. peripheral contrast enhan 6d-6w

Question 23

CSF alteration in hemmoragic stroke

Answer 23

mild increase prot/PNN/mononuclear due to disruption of BBB

xanthochromia, erythrophagocytosis

elevation IL-6

Question 24

prognosis for ischemic/hemorragic stroke

Answer 24

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%

Question 25

sign associated with 1. paramedian thalamic ischemic infarction 2. dorsal midbrain infarction 3. cerebellar interpositus nucleus

Answer 25

1. controlat medial strabismus (esotropia) + vestibular ataxia, head tilted, nystagmus + episodic non intentional tremors 2. convergence retraction nystagmus 3. ispsilateral mydriasis + cerebellar signs

Question 26

maj arteries affected by stroke in dog

Answer 26

rostral cerebellar (47%) > perforating: caudal thalamus + rostral BS (42%) >striate

Question 27

specific localisation of ischemic stroke acording to etiology

Answer 27

hypertensive: deep (thal, basal nuclei) amyloid angiopathy: G/W matter junction

Question 28

In ischemic stroke delay for 1. FLAIR hyper 2. Periferal enhancement 3. T2 hyper 4. DWI hyper

Answer 28

1. 3-8 h 2. 7-10 d 3. 6-12 h 4. minutes, reverse in 24h-5d DWI lesion, normal FLAIR => less than 3h

Question 29

diff for T1 hyperintensity

Answer 29

blood breakdown product fat proteinaceous fluid melanin calcification necrosis paramagnetic sub: iron, manganese, cooper

Question 30

blood breakdown product timing for hemorrhagic strokes

Answer 30

< 24h intrac oxyhb 1-3d intrac desoxyhb 3-7d intrac methb 7-14d extrac methb >14d extrac hemosiderin and ferritin (in macrophages)

Question 31

differential for hypo SWI/T2*

Answer 31

hemosiderin (paramagnetic) mineralisation gaz fibrous tissus iron deposit other causes than hemo are T1/T2 hypo (diamagnetic)

Question 32

ADC difference between glioma and ischemia

Answer 32

glioma has lower ADC than ischemia (ADC inversively proport to cell density)

Question 33

causes of mydriasis

Answer 33

ophtalmologic (increase intraocul pressure...) optic or oculomotor nerve sympathetic innerv eye plant : Datura stramonium phenylephrine (sympatomimetic)

Question 34

most frequent signs and pathology associated with microbleeds

Answer 34

vestibular proteinuria dogs are older and smaller than non affected associated with shorter survival time maj small poodle and shitzu association with cortical atrophy

Question 35

T2 black out effect: definition, exemples

Answer 35

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

Question 36

finding in diffusion/adc sequence to date hemor

Answer 36

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

Question 37

MRI features of intracranial hemorrhage

Answer 37

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

Question 38

Normal D-dimer is an appropriate negative predictor for canine ischemic stroke True or false?

Answer 38

false

Question 39

Is T2star seq affected by gadolinium?

Answer 39

FALSE gadolinium paramagnetic: T2 shortening effect

Question 40

comparison SWI/T2star to detect hemorrhage

Answer 40

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

Question 41

subacute cortical laminar necrosis 1. causes 2. assoc with hyper/hypoperf MRI 3. T1 intensity 4. which lamina more affected

Answer 41

1. hypoxia, hypogly, fluid overload, smoke inhalation, ischemia, encephalitis, prolonged seizure act 2. hyperperfusion 3. T1 hyper 4. lamina 3

Question 42

normal intracranial pressure

Answer 42

7-12 mmHg

Question 43

transcranial doppler US: factor assoc with hypertension

Answer 43

ratio systolic mean velocity / diastolic mean veloc

Question 44

most common signs associated with hypertensive encephalopathy in cat

Answer 44

ataxia seizure altered behaviour

Question 45

fact assoc with brain herniation in cat

Answer 45

age neoplasia low consciousness

Question 46

US optic nerve sheat diameter is larger/smaller in hypertensive brain + related with which other variable

Answer 46

larger related to age in MRI no correlation when age is considered

Question 47

management acute hypertension

Answer 47

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**

Question 48

management hypertension dog

Answer 48

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

Question 49

manifestation of hypertension in cat : % neuro/opthalmo

Answer 49

55% neuro (25% primary complain) ataxia, various manifestations of seizures and altered behaviour

Question 50

TEG, d-dimer in CVA

Answer 50

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%