Stroke Flashcards
Modified Rankin Score 0
No symptoms
Modified Rankin Score 1
Despite symptoms, able to perform all normal activities of daily living
Modified Rankin Score 2
Slight disability unable to perform all normal activities without assisitance
Modified Rankin Score 3
Moderate disability. Able to walk without assistance - however needs other considerable assistance
Modified Rankin Score 4
Moderately severe disability. Unable to attend to own bodily needs and needs assistance to walk
Modified Rankin Score 5
Severe disability. Bed ridden. Incontinent. Constant care
Modified Rankin Score 6
Death
Velocity criteria for carotid artery stenosis in doppler US
A specificity of 100 percent was found for PSV (peak systolic velocity) >440 cm/sec, EDV (end diastolic velocity) >155 cm/sec, or carotid index >10 (peak internal carotid artery [ICA] velocity ÷ common carotid artery [CCA] velocity). The sensitivity for these measures was 58 percent, 63 percent, and 30 percent, respectively. By combining these criteria, the sensitivity increased to 72 percent.
A sensitivity of 96 percent was found for PSV >200 cm/sec combined with either an EDV >140 cm/sec or a carotid index >4.5. The specificity for these combined measures was 61 percent.
Most sensitive measure on USS of stenosis
Carotid index >4 i.e peak internal carotid velocity/peak common carotid velocity
Two MRIs used for evaluating carotid stenosis
‘time of flight’ MRA (magnetic resonance angiography) or gadolinium enhance MRA/ contrast enhanced MRA (CEMRA)
Five Lacunar syndromes
- Pure motor hemiparesis - equal face, arm, leg - no sensory, visual or language deficit
- Pure sensory - face, arm, leg - sensory loss without weakness, visual or language deficit
- Dysarthria - slurred speech
- Clumsy hand - ataxic hand
- Ataxic hemiparesis - unilateral weakness and clumsiness
Lipohyalinotic occlusion of small penetrating arteries (<200mcm) that branch from larger intracerebral arteries - produce small infarcts call lacunes
TIA: risk of stroke in week
risk of stroke (untreated) is ~10% in first week
TIA therapy
All TIAs must go home in a CAB
o Cholesterol lowering agent - Commence a statin
o Anthithrombotic
• AF absent - antiplatelet
• 1st line – aspirin
• 2nd line – if already on aspirin and had a TIA – clopidogrel
• 3rd line – if on clopidogrel and had TIA - DAPT
• AF present anticoagulate
o Blood pressure lowering meds – commence an oral antihypertensives
• Calcium channel blockers are best, can also use ACE-I/ARB and thiazides
• Beta-blockers – may increase risk of stroke recurrence BUT are indicated with concurrent IHD
Evidence suggests that this approach reduces the RR of stroke by 80%
ABCD3-I score
Utility and meaning
TIA risk stratification score Age >60 BP >140/90 Clinical features - Speech without weakness = 1 - Unilateral weakness = 2 Duration - 10-59 mins = 1 - >1 hour = 2 Diabetes Dual presentatino (2nd pres. in a week) = 2 imaging: ipsilateral carotid stenosis >50% = 2 MRI DWI hyperintensity = 2 Points total 13
0-3 low risk 2-3 %
4-7 Intermediate risk <6%
8-13 High risk >18 %
Antihypertensive therapy for stroke
Labetalol 10mg over 1-2 minutes can use 20 mg
Can use labetalol ongoing to maintain BP <180 with infusion 2-8mg/hr
Or nicardipine 5mg/hr IV titrate up 2.5mg per hour every 5-15 minutes if not down trending. Max 15mg/hr
Hydralazine IV 10mg- direct vasodilator. Can give 20mg. Drop is sudden within 10-30 mins. May need concurrent beta blocker
Lasts 2-4 hours.
BP management of stroke patient NOT receiving thrombolysis
No management unless severe hypertension >220 or 120 diastolic. Or if patient has coronary artery disease, heart failure, dissection or other reason to lower.
Lowering of 15% during first 24 hours after stroke is recommended.
Inclusion and exclusion criteria for thrombolysis
Inclusion criteria
Clinical diagnosis of ischemic stroke causing measurable neurologic deficit
Onset of symptoms <4.5 hours before beginning treatment; if the exact time of stroke onset is not known, it is defined as the last time the patient was known to be normal or at neurologic baseline
Age ≥18 years
Exclusion criteria
–Patient history–
Ischemic stroke or severe head trauma in the previous three months
Previous intracranial hemorrhage
Intra-axial intracranial neoplasm
Gastrointestinal malignancy
Gastrointestinal hemorrhage in the previous 21 days
Intracranial or intraspinal surgery within the prior three months
–Clinical–
Symptoms suggestive of subarachnoid hemorrhage
Persistent blood pressure elevation (systolic ≥185 mmHg or diastolic ≥110 mmHg)
Active internal bleeding
Presentation consistent with infective endocarditis
Stroke known or suspected to be associated with aortic arch dissection
Acute bleeding diathesis, including but not limited to conditions defined under ‘Hematologic’
–Hematologic–
Platelet count <100,000/mm3*
Current anticoagulant use with an INR >1.7 or PT >15 seconds or aPTT >40 seconds or PT >15 seconds*
Therapeutic doses of low molecular weight heparin received within 24 hours (eg, to treat VTE and ACS); this exclusion does not apply to prophylactic doses (eg, to prevent VTE)
Current use (ie, last dose within 48 hours in a patient with normal renal function) of a direct thrombin inhibitor or direct factor Xa inhibitor with evidence of anticoagulant effect by laboratory tests such as aPTT, INR, ECT, TT, or appropriate factor Xa activity assays
–Head CT–
Evidence of hemorrhage
Extensive regions of obvious hypodensity consistent with irreversible injury
Timing for mechanical thombectomy
Thombectomy (clot retrieval) within 6 hours–> indicated in large vessel occlusion
Trial showing extension of time window for stroke management with mechanical thrombectomy
DAWN trial: Endovascular therapy within 24 hours of symptom onset NIHSS >10 ICA or M1 Failed or contraindicated thrombolysis Mismatch age related: mRS at baseline 1 or less Older than 80, NIHSS more than 10 and infarct volume <21 Or Younger than 80 10-19 NIHSS: less than 31 ml 20 or more NIHSS less than 51ml
Hemicraniotomy (When and NNT)
In young patients (younger than 60), before symptoms onset i.e. coma, NNT =2, saves lives but not disability
Define valvular AF
AF caused by low flow states or high thromboembolic risk: mechanical valve or mitral stenosis
When to anticoagulate post stroke?
1,3,6,12 Rule 1 Day post TIA 3 post minor stroke 6 post moderate stroke 12 post large stroke or haemorrhage
Indication for endarterectomy
Greater than 70% stenosis in a patient without already significant morbidity/disability
50-70% may be indicated if good QOL and life expectancy
Below this - Risk of stroke is minimal (0.5%) if medical management is observed (statin, antiplatelet and BP management)
Surgical intervention after TIA or stroke should be within 2 weeks. But greater than 48 hours.
Stenting is not routinely performed except for certain circumstances (radiation induced stenosis, stenosis of prev. endarterectomy)
Single most important risk factor for stroke
HTN
CCB have the best evidence - beta blockers only in the setting of IHD
PROGRESS and PROFESS trials with ACE and ARB
Demonstrated the degree of BP reduction is the key, not necessarily the drug. Telmesartan not shown to have benefit (only reduced BP by 4mmHg vs 2 of placebo
Most common causes of ICH
Hypertension, cerebral amyloid angiopathy, vascular malformations and anneurysms
Most common site of hypertensive bleeds
small penetrator arteries that branch of major intracerebral arteries, often at 90 degree angles – very susceptible to hypertension due to direct pressure of much larger arteries
Supply to :Pons and midbrain, thalamus, putamen, caudate and cerebellum
What is meant by ‘cerebral microbleeds’
Small regions of focal haemosiderin deposition seen on T2-weighted MRI
Marker of bleeding-prone microangiopathy due to hyalinosis (chronic hypertension) or amyloid deposition
Symptoms depending on location of ICH:
Putamen
o Putamen 35%
• Hemiplegia, hemisensory loss, homonymous hemianopsia, gaze palsy, stupor, and coma
Symptoms depending on location of ICH:
Subcortex
Subcortex 30%
• Vary in their neurologic signs depending upon location
• Often parietal and occipital lobes affected
• Seizures
Symptoms depending on location of ICH:
Cerebellum
Cerebellum 16% - often deteriorate quickly
• Ataxia
• Vomiting
• Occipital headache referred to neck/shoulder
• Neck stiffness, gaze palsy, and facial weakness
• Stupor if brain stem compression
• No hemiparesis
Symptoms depending on location of ICH:
Thalamus
Thalamus 15%
• Hemiparesis, hemisensory loss, and occasionally transient homonymous hemianopsia
• May also be an upgaze palsy with miotic pupils that are unreactive, peering at the tip of the nose, skewed, or “wrong way eyes” toward the weak side (in contrast to hemispheric cortical injury in which the eyes are deviated away from the hemiparesis)
• Dominant hemisphere: aphasia
• Non-dominant hemisphere: neglect
Symptoms depending on location of ICH:
Pons
Pons 5-12%
• Deep coma over the first few minutes due to disruption of the reticular activating system
• Total paralysis
• Pinpoint pupils which react to a strong light
• Ocular bobbing, facial palsy, deafness, and dysarthria when the patient is awake
Suspicion of aetiology by location of ICH
Putamen: HTN
Lobar: AV malformations or mets
Basal cisterns: Aneurysm
Cerebellar: Think about hydrocephalus resulting from bleed
Amyloid bleeds - recurrent TIAs
Adjacent to sylvian fissure: MCA anneurysm
Proximity to venous sinus: venous sinus thrombosis
Floor of anterior fossa: aCA aneurysm
Targets of BP, glucose etc. post ICH with catastrophic midline shift
BP: Aim less than 140 systolic:
If SBP >200 or MAP >150 then aggressive therapy with IV Mannitol bolus of 1-1.5g/kg and repeat dose of 0.5mg/kg every 6 to 8 hours.
Caution in patients with renal insufficiency, hypernatraemia or hyperosmolar state
o 2nd line: Frusemide (can be given concurrently with Mannitol),
barbiturates, anaesthesia
o 3rd line: hyperventilation to PaCO2 25-30mmHg (temporary measure)
Barbituates:
Pentobarbital is generally used, with a loading dose of 5 to 20 mg/kg as a bolus, followed by 1 to 4 mg/kg per hour [125,126]. Treatment should be assessed based on ICP, CPP, and the presence of unacceptable side effects. Continuous electroencephalography (EEG) monitoring is generally used
Barbiturate MOA
Barbiturate activates GABA receptors, opening chloride channels. This means the gaba recpetors remain open and hyperpolarise cells. CNS depression results.
Recommencement of antiplatelet and anticoag
1-2 weeks and at lower dose for antiplatelet. 3-4 weeks for anticoag with rigorous INR monitoring.
Secondary management measures post ICH
BP control, <140/90, Stop smoking, alcohol, cocaine etc., manage cerebral salt wasting syndromes and diabetes insipitus. Monitor for DVT, infections etc.
Amyloid definition and common history
Deposition of amyloid beta peptide deposits within small-medium sized blood vessels within the brain
o Can occur sporadically, or in association with Alzheimer’s dementia, two can commonly exist and it is also evident in pts with vascular dementia
Usually manifests with spontaneous lobar hemorrhage
MRI features of amyloid
MRI shows potentially reversible leukoencephalopathy consisting of patchy or confluent white matter hyperintensities on T2 weighted MRI sequences
Post stroke spasticity treatment algorithm
Focal: Botulinum toxin A or Alcohol neurolysis
Nultifocal: Botox, neurolysis and oral centrally acting muscle relaxants (Benzodiazepines, Tizinadine, Gabapentin (high dose), canabinoids.
Regional: Intrathecal therapy
Generalised: Intrathecal therapy or oral therapy
Layers of the scalp
Skin, connective tissue, Galae aponeurotica, loose areolar connective tissue, pericranium
Layers of the meninges
Pad from inside out
Pia mata, arachnoid mata and dura mata
Dura is dual layered periostial and meningeal layer.
Routine management post SAH
(Sit in bed, anticoag, hard poos and hard legs –> SAHH CRAP)
Bedrest at 30 degrees, ceased anticoagulation and antiplatelet, pneumotic stockings, stool softeners
Calcium channel blocker (Nimodipine 60mg Q4h within 4 days), Analgesia, refer for surgery (coil), prevent vasospasm and monitor (transcranial doppler USS)
Extra dural most common cause an history
Dura fractures off of skull and commonly middle meningeal artery causes arterial bleed. Occasional fracture of temporal bone. Lucid period in between trauma.
Lens shaped bi convex
Management of Extra dural
Mannitol, hyperventilate if intubated, fluid restrict and surgical drain
Subdural history
Venous bleed Typically trauma. Colour on CT gives indication to chronicity
Acute: hyperdense
1-2 weeks: Isodense
3-4 weeks: Hypodense
Hydrocephalus: Broadly speaking three causes and three symtpoms
Over production, blockage of outflow or under absorption
Gait disturbance, urinary incontinence and confusion/impaired cognition
Termed communicating or non-communicating depending on ventricular flow i.e. communicating means that the ventricular flow is preserved
Fabry disease
Multisystem lysosomal storage disorder. X linked.
Hypohidrosis (no sweat), acroparaesthesia (small fibre peripheral neuropathy), renal impairment, cardiac conduction abnormalities, cardiomyopathy, corneal dystrophy, early onset ischemic stroke
Alpha galactose a (GAL) gene - leads to Accumulation of glycosphingolipids in the vascular endothelium, smooth muscle cells, and autonomic and DRG
CADASIL
• Cerebral autosomal dominant arteriopathy with subcortical infarcts and leuokoencephalopathy
• Most common cause of inherited stroke and vascular dementia in adults.
o Ischaemic subcortical stroke
o Migraine with aura – avoid vasoactive drugs
o Depression / apathy
o Dementia
• NOTCH3 gene – chromosome 19 mutations
CARASIL
- Similar to CADAIL but onset earlier, without migraine and with the addition of alopecia and low back pain
- Mutations in the HtrA serine peptidase 1 (HTRA1) gene on chromosome 10q
Moya Moya Disease
Progressive occlusive vasculopathy
• Steno‐occlusion of the terminal ICA / proximal ACA / MCA – with development of abnormal vascular networks at the site of the disease that feed the basal ganglia
• Causes both ischaemic and ICH presentations (half of adults have ICH)
F:M 1.8:1
RCVS - Reversible Cerebro Vasoconstriction Syndrome
• Common mimic of cerebral vasculitis
• Presents with: Thunderclap headache, focal neurology, seizures
• Associations
o Post‐partum
o Pregnancy
o Vasoactive medications (SSRIs, TCAs, triptans, cocaine, ecstasy, ergotamine)
o Migraine
• Imaging evidence of spasm – resolves within 3 months
o Infarcts / haemorrhage / convexity SAH
• Normal or near normal CSF
• Most patients have good outcome
• Generally managed with IV / oral nimodipine and removal of inciting agent
PRES
Posterior reversible encephalopathy syndrome
Encephalopathy, seizures, headache, visual disturbances, papilloedema
• Associations: Medications (immunosuppressive, cocaine), organ transplantation, renal failure, eclapmsia, HT, SLE, postpartum haemorrhage, sepsis and multi‐organ failure
• Management
o Removal of inciting agent.
Management of hypertension (some controversy – prompt but gradual reduction likely best) ‐ e.g. by ~25% or to diastolic 110‐120mmHg over 1‐2 hours
Central venous sinus thrombosis
• Spontaneous or secondary to thrombophilia / malignancy / infection
• Presentation can mimic ischaemic stroke / ICH
• Haemorrhagic venous infarction
• Seizures / headaches often prominent
• Management
o Anticoagulation REGARDLESS of the presence of intracerebral haemorrahge (with unfractionated heparin or LMWH)
o Management of mass effect/papilloedema
Intracranial dissection
• Large proportion are spontaneous but Hx may suggest minor trauma
• Common cause of stroke in young adults e.g. 20% of strokes in patient’s below 45yrs
o Incidence peaks ~40yrs
• Individual approach
• Mechanism of stroke with dissection:
o Vessel occlusion > thromboembolism > vessel rupture
• Beware anticoagulation in the setting of
o Intracranial dissection
o Large infarct (risk of haemorrhage)
NIHSS score
1: 3 parts
Consciousness
Month and age
Comprehension|
2:Extraoccular movements
3: Visual fields
4: Facial palsy
5: Motor drift, L&R arms and legs
6: Limb ataxia FNF and heel shin
7: Sensation
8: Aphasia/language
9: Dysarthrita
10: Extinction or inattention
NIHSS Score again
1: 3 parts
Consciousness
Month and age
Comprehension|
2:Extraoccular movements
3: Visual fields
4: Facial palsy
5: Motor drift, L&R arms and legs
6: Limb ataxia FNF and heel shin
7: Sensation
8: Aphasia/language
9: Dysarthrita
10: Extinction or inattention
Common Regional syndromes: Parietal Lobe
SAAGI
sensory inattention apraxias astereognosis (tactile agnosia) inferior homonymous quadrantanopia Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation
Common regional sydromes: occipital lobe
homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia
Common regional syndromes: Temporal lobe lesion
Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)
Common regional syndromes: Frontal lobe lesion
De PAIN expressive (Broca's) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting disinhibition perseveration anosmia inability to generate a list
Common regional syndromes: Cerebellum
midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus
Common regionla brain syndromes: Medial thalamus and mammillary bodies of the hypothalamus
Wernicke and Korsakoff syndrome
Common regionla brain syndromes: Subthalamic nucleus of the basal ganglia
Hemibalism
Common regional brain syndromes: Striatum (caudate nucleus) of the basal ganglia
Huntington chorea
Common regionla brain syndromes: Substantia nigra of the basal ganglia
Parkinsons disease
Common regional brain syndromes: Amygdala
Kluver-Bucy syndrome (hypersexuality, hyperorality, hyperphagia, visual agnosia
