stroke management

Question 1

initial evaluation of sstroke presentation

Answer 1

ABCDE
clinical assessment: risk factors, last known normal, time of onset of symptoms

Question 2

imaging

Answer 2

non contrast CT to evaluate for acute haemorrhage
diffusion weighted MRi to detect acute ischaemia
consider further neurovascular imaging depending on the type of stroke: Can be noninvasive (e.g., duplex sonography of the carotid arteries, magnetic resonance angiography) or invasive (e.g., conventional angiography).

Question 3

non-contrast head CT

Answer 3

first line
CT allows for the detection of ischemic changes within 6–24 hours after stroke onset. Remember to compare to previous CT results when possible.
allows for detection of acute haemorrhage

Question 4

non-contrast head CT cannot be used to identify

Answer 4

ischaemic changes prior to 6 hours after onset

Question 5

non contrast head CT is indicated for

Answer 5

Indicated in all patients suspected of having an acute stroke to rule out intracranial hemorrhage before administering thrombolytic therapy

Question 6

diffusion weighted MRI

Answer 6

Allows identification of ischemia earlier than a CT (within 3–30 minutes after onset) [29]
Allows detection of hyperacute hemorrhage
Evaluates reversibility of ischemic injury

Question 7

how does diffucion weighted MRI evaluate reversibility of ischaemic injury

Answer 7

Perfusion-weighted imaging (PWI): visualizes areas of decreased perfusion and allows quantification of perfusion parameters, e.g., mean transit time (MTT), cerebral blood flow (CBF) and cerebral blood volume (CBV)
Perfusion-diffusion mismatch MRI: allows identification of the penumbra (or “tissue-at-risk”)

Question 8

laboritory investigations

Answer 8

should not delay imaging for acute stroke
serum glucose
FBC, electrolytes, coagulation parameters, urine drug screen for recreational substances eg. cocaine
blood alcohol level
serum troponin

Question 9

why do serum glucose

Answer 9

For most patients with acute ischemic stroke, only serum glucose is required prior to administration of tPA. Symptoms of hyper- and hypoglycemia can resemble a stroke.

Question 10

postictal paralysis

Answer 10

The development of focal weakness after a seizure, which typically resolves within 48 hours. Thought to result from exhaustion of the primary motor cortex.

Question 11

vestibular neuritis

Answer 11

An idiopathic inflammation of the vestibular nerve. Typically manifests with acute-onset vertigo, nausea, vomiting, and gait instability with increased risk of falling to the affected side. Prognosis is good with vestibular rehabilitation therapy.

Question 12

stabilization and monitoring

Answer 12

maintain euvolaemia with fluid replacement as needed: Avoid free water, which may exacerbate cerebral edema in patients with acute stroke.
maintain oxygen and consider intubation if the patient shows signs of increase ICP
maintain euglycaemia
maintain normothermia
cardiac monitoring
maintain normal acid base status
electrolyte repletion as needed
analgesia as needed
monitor for sign of elevated intracranial pressure
seizures should be treated pharamcologically
evaluate for dysphagia

Question 13

blood pressure managemnt

Answer 13

always treat hypotension: with fluid replacement, vasopressors
ischaemic stroke: permissive hypertension
only treat if >220 systolic or 120 diastolic
hemorrhagic: reduce systolic to 140-160

Question 14

permissive hypertension

Answer 14

Hypertension is treated less aggressively in ischemic stroke than in hemorrhagic stroke; in ischemic stroke, the perfusion of the penumbra depends on the mean arterial pressure.

Question 15

nitrates

Answer 15

should be avoided because they increase ICP

Question 16

cushing reflex

Answer 16

A hypothalamic response to maintain cerebral perfusion in patients with elevated ICP. Results in the Cushing triad, which consists of increased systolic blood pressure, bradycardia, and irregular breathing

Question 17

neurological complications of all strokes

Answer 17

elevated ICP and brain herniation (cushing triad)
seizures
syndrome of innappropriate secretion of antidiuretic hormone
persistant neurological deficits
central post stroke pain
neuropathic pain

Question 18

central post stroke pain

Answer 18

Affects < 10% of all stroke patients
Can occur with thalamic lesions
Unilateral facial pain and/or extremity pain associated with previous stroke
Contralateral or ipsilateral initial paresthesia followed by neuropathic pain (e.g., allodynia, dysesthesia)

Question 19

ischaemic stroke neurological complications

Answer 19

haemorrhagic transformation
vascular dementia

Question 20

risk factors for haemorrhagic transformation

Answer 20

onset: usually 1–2 days after the inciting ischemic event
Risk factors: thrombolytic medications (e.g., alteplase), antiplatelet therapy (e.g., aspirin, clopidogrel), and/or thrombosis prophylaxis (e.g., heparin, enoxaparin) within 24 hours of ischemic injury
Management: discontinuation of anticoagulation and/or antiplatelet therapy, admission to a neurointensive care unit, and neuroprotective measures

Question 21

neuroprotective measures

Answer 21

tight blood pressure and glycemic control, targeted temperature management, electrolyte repletion

Question 22

haemorrhagic stroke neurological complications

Answer 22

Vasospasm (typically occurs 5–7 days after SAH) → ischemic stroke
Recurrent hemorrhage
Intraventricular hemorrhage
Hydrocephalus

Question 23

carotid artery stenosis management

Answer 23

ultrasonography of the neck
symptomatic CAS may include TIA, ameurosis fugax or ischameic stroke
in patients with CAS, US shows a focally increased velocity of blood flow
it can quantify the degree of stenosis
antiplatelet therapy is used for prevention of stroke

Question 24

bell palsy

Answer 24

unilateral facial paralysis
recovery over weeks
sensation not affected

Question 25

anterior cerebral artery stroke

Answer 25

upper motor neuron weakness resulting in contralateral positive babinski sign, incontinence, and sensory deficits in the contralateral lower limb

Question 26

pure motor stroke of the posterior limb of the internal capsule presents with

Answer 26

contralateral hemiparesis without sensory loss or cortical signs (e.g., aphasia).
usually caused by occlusion of the lanticulostriate artery

Question 27

MCA stroke manifestations

Answer 27

contralateral facial droop
contralateral muscle weakness
contralateral pronator drift downward

Question 28

do ischeamic strokes typically cause headaches?

Answer 28

nah

Question 29

thalamus stroke manifestations

Answer 29

hemiparesis, hemisensory deficits, miotic and nonreactive pupils, gaze deviation downward and toward the affected side of the body (ie. away from the side of the brain lesion)

Question 30

wrong way eyes

Answer 30

characteristic of thalamic haemorrhage
eyes deviate downward and away from affected brain side

Question 31

ballismus

Answer 31

A condition of uncontrolled, large amplitude movements of the arms (and sometimes legs) that can have a flailing quality. Unilateral ballismus (hemiballismus) occurs following contralateral subthalamic nucleus damage, usually from ischemia.

Question 32

broca aphasia

Answer 32

preserved comprehension
nonfluent telegraphic speech
A form of aphasia caused by lesions in the inferior frontal gyrus of the dominant hemisphere.

Question 33

how does alteplase work

Answer 33

it converts plasminogen to plasmin which degrades fibrin and lyses formed clots
effective when administered within 4.5 hours of onset

Question 34

wernecke’s aphasia

Answer 34

Wernicke aphasia is caused by lesions in the superior temporal gyrus of the dominant (usually left) hemisphere, usually along the left middle cerebral artery (MCA) distribution. Patients with Wernicke aphasia typically present with impaired repetition and language comprehension; although they can speak fluently, they produce nonsensical phrases. Furthermore, these patients lack awareness of their impairment

Question 35

gaze deviation in MCA stroke is

Answer 35

towards the side of the deviation

Question 36

reactive gliosis

Answer 36

Following CNS damage (e.g., stroke, traumatic brain injury), astrocytes at the margin of the damaged region proliferate and enlarge (reactive gliosis) to form a permanent glial scar. The process of reactive gliosis usually begins 1–2 weeks after the injury.

Question 37

horner syndrome

Answer 37

symptom triad of miosis (an abnormally small pupil)
partial ptosis (drooping of the upper eyelid)
facial anhydrosis (absense of sweating)
lesions that interupt the ipsilateral symapthetic nervous supply to the head, eye and neck