Blood supply and stroke Flashcards
What is the general blood supply to the brain?
The circle of Willis supplies the internal carotid artery and basilar artery with blood which go on to supply the Forebrain (cerebrum and diencephalon)
The basilar artery supplies the vertebral arteries with some blood and these go on to supply the Hindbrain (Brain stem and cerebellum)
What are some features of the internal carotid artery ?
Internal carotid;
- Has several segments
- Originates at C3-4 at bifurcation of common carotid
- Travels in carotid sheath
- Enters base of skull via carotid canal
- Passes through petrous temporal bone emerges from internal opening of carotid canal
- Passes over foramen lacerum
- Passes through the cavernous sinus, piercing its roof at the anterior clinoid process, enters sub arachnoid space
- Gives off the ophthalmic artery first, followed by the posterior communicating and anterior choroidal artery
- Then bifurcates into the middle and anterior choroidal artery
- The bifurcates into middle and anterior cerebral arteries
- Then branches of the ICA thus make up the anterior circulation
What are some features of the vertebral arteries ?
- Vertebral’s are branches of the subclavian arteries
- Cours posterior-superiorly from the subclavian
- Enter deep to transverse process of C6/7, running in the transverse foramina of cervical vertebrae
- Pass across the posterior arch of C1 before entering the skull at the foramen magnum
- These give rise to anterior spinal arteries
What are the different parts of the vertebral artery (bits it can be split up into) ?
Vertebral artery;
- Suboccipital part
- Vertebral part
- Cervical part
What are some features of the basilar artery ?
Basilar Artery;
- Result of the union of vertebral arteries at the transition between the medulla and pons at the level of abducens nerve root
- Gives off branches to the pons, cerebellum, labyrinth and ultimately produce the posterior cerebral arteries
What arteries help to supply the hindbrain?
Vertebral supply from;
- Anterior spinal
- Posterior inferior Cerebellar (gives posterior spinal)
Basilar supply from;
- Pontine Arteries
- Superior cerebellar artery
- Anterior inferior cerebellar artery
- Labyrinthine artery
- Quadrigeminal artery
What are some features of the circle of Willis ?
The circle of Willis is an anastomotic network made from the meeting of the supply to the hindbrain and the forebrain
Anterior circulation - ICA
Posterior circulation - Basilar/vertebrals
Much variation exists however, which can -present with clinical implications
- Thought to be at increased risk of ischaemic stroke in variant anatomy of the Circle of Willis
What are some variants you can get in the Circle of Willis ?
Variants are most common in the posterior communicating and anterior cerebral arteries.
- Hypoplasia of one or both Posterior Communicating arteries about 30%
- Hypoplastic/absent A1 segment 15%
- Absent/fenestrated ACOM 12.5%
- Origin of Posterior Cerebral Artery (PCA) from Internal carotid artery (ICA) with absent/hypoplastic P1 segment 20%
- Infundibular dilation of PCOM - 10% (Posterior communicating artery)
What are the relations of the Circle of Willis?
The Circle of Willis forms around the optic chiasma and the vertebrals to the brain stem
What are features of the anterior cerebral supply?
The Anterior cerebral artery supplies the medial frontal and parietal lobes
Passes over corpus callosum and terminates close to the Pareto-occipital sulcus where it overlaps with branches of the posterior cerebral artery
Key structures, medial part of primary motor and somatosensory cortices, supplementary motor cortex, corpus callosum
What are features of the middle cerebral supply?
After giving off important cerebral branches to diencephalon passes along depth of lateral fissure of syvius
Lateral striate arteries are branches of the MCA, supply Corpus striatum, internal capsule and thalamus.
Supplies most of the frontal, parietal and temporal lobes and small part of occipital, supplying 2/3rds of lateral surface of brain
Key structures include most pre and post-central gym (primary motor and primary somatosensory cortices) pre frontal cortex, Wernicke’s area, Broca’s area, primary auditory cortex, insular cortex
What are features of the posterior cerebral supply?
Courses around midbrain with optic tract
Gives medial and lateral branches
Medially supplies the calcimine cortex (location of primary and visual cortex), cuneus and precious (basic visual processing/integration) and selenium of the corpus callosum (interloper somatosensory communication between parietal and occipital lobes)
Laterally - anterior/posterior temporal and occipital cortex
- Doesn’t supply motor function in cortex
What 4 things should you start to think about when asked about deficits?
Where is the deficit - arm, leg, face?
What type of deficit (sensory, motor, cognitive, integrative)?
Where does it lateralise to (left or right)?
Is it in ascending tract;
Spinothalamic (pain/temp, dorsal columns (fine/proprio)
or descending tracts;
Corticospinal (vol movement), rubrospinal (flexor tone) ?
What is the motor homunculus?
Graphical representation of the localisation of cortical motor control
Note that from lateral to medial the body is descended
Note that much space is given to movemens of face and hand but relative to lower limb
What artery supplies the territory responsible for the lower limbs?
The anterior cerebral artery ! (does medial 1/3d - lateral 2/3rd would be medial cerebral artery)
ACA strokes are more likely to affect the leg than the arm !
A patient is expriencing sudden onset right leg weakness and loss of sensation in the same leg, where is the lesion likely to be?
Since the patient has right leg weakness and right hemisensory loss the lesion is on the left hemisphere as the pathways (spinothalamic, dorsal columns and portico spinal) decussate and therefore the lesion is on the contralateral side.
We should consider that the primary motor and primary somatosensory cortices have been affected
The deficits are local to legs, no involvement of upper limb
- Medial aspect these cortices therefore we have medial aspect of primary motor and somatosensory cortices affected which are supplied by the anterior cerebral artery which means its likely he is having an ACA thrombotic event
A 62 year old woman with right arm and leg weakness, right arm sensory deficit with a slight facial droop, is found to have a problem with her speech. She speaks in short responses and her speech is slurred. Where is this ladies lesion?
Lady has dysarthria - due to disruption in the motor nerve supply to the face via the corticobulbar tracts/motor cortices
Expressive dysphasia - Broca’s area - inferior fontal gyrus
MCA and ACA territory to primary motor/somatosensory cortices
Where is language most commonly found?
Most people are LEFT hemisphere dominant and language is therefore localised to the left hemisphere
Where is language most commonly found?
Most people are LEFT hemisphere dominant and language is therefore localised to the left hemisphere
What are the 3 components of speech?
1). Generation;
- Non-fluent aphasia (inability to produce words and sentences mentality)
2). Articulation;
- Dysarthria (Speech sounds are slurred due to facial paresis)
3). Reception;
- Fluent aphasia (inability to understand the meaning of speech leads to inappropriate speech production - “word salad”
What is Broca’s Expressive Aphasia?
Th pattern of speech is clipped, one to two words but patient clearly understood words spoken to them. There is an inability t generate words and sentences but no issue with speech articulation, speech is also not inappropriate.
Where is Broca’s area found ?
Broca’s area is located in the inferior frontal gyrus (pars op and pars try) MCA supplies this
What is Wernicke’s Receptive Aphasia?
WORD SALAD - inappropriate speech that makes little sense
Locates at dorsal/caudal end off superior temporal gyrus
Primary auditory cortex is located ventrally in the gyrus
MCA supplies this
A patient presents with left leg and arm weakness, he arrives into the department and when you go too see him you call his name, he jumps, and acts surprised as he did not see you, despite being a meter away to his left hand side. What is going on?
- Right MCA stroke
- Left sensory and motor deficit with left hemispatial neglect
- Right hemisphere is affected/lesioned
- Lesions are of structures covered by MCA territories
What is hemispheric neglect ?
Same as before but these people don’t believe the other side is real, in body, on plate
Get these people to draw a clock!
What is hemispheric neglect ?
Same as before but these people don’t believe the other side is real, in body, on plate
Get these people to draw a clock!
How is the visual system supplied by brain?
Remember PITS;
- Parietal Inferior
- Temporal Superior
Mnemonic to remember where a lesion here would cause
What is homonymous hemianopia and quadrantopias ?
Homonymous hemianopia is a notable feature of post-chiasma lesions of visual pathways.
Quadrantopias occur when parts pathway are lesioned (PITS)
Thrombosis of the PCA can produce cortical homonymous hemianopia. By infarction of tissue in the V1/primary visual cortex (numbers 7,8) and macular cortex (number 8)
What is prosopagnosia?
Prosopagnosia - face blindness
Thought to be due to right fusiform gyrus dysfunction in the temporal lobe
What is Anton’s syndrome ?
Cortical blindness (bilateral infarction of V1) with no insight (anosognosia) and confabulation
Confabulation refers to the production or creation of false or erroneous memories without the intent to deceive
What is the definition of a stroke and the modifiable and non-modifiable factors associated with it?
Stroke originates from 1599 in the idea that such sudden symptoms were a result of ‘stroke of God’s handle’
Known in some places as cerebrovascular accident (CVA)
Clinical syndrome characterised by sudden onset of rapidly developing focal or global neurological disturbance persistent for greater than 24 hours or leads to death
Modifiable;
- Hypertension
- Type 2 Diabetes
- Hyperlipidemia
- Smoking
- Heart disease
- Excessive alcohol intake
- Oestrogen containing drugs
- Polycythaemia
Non-modifiable;
- Age
- Gender (Male > female)
- Race (Black > Asian > White)
- Previous vascular event
- Heredity
- High fibrinogen
What are TIA’s?
Transint ischaemic attack
Last less than 24 hours for 60% and 2/3rds less than 10 mins, neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without evidence of acute infarction
Most episodes lass less than an hour and some still result in infarction
May be a sign of further stroke events “crescendo TIA”
How common are Ischaemic strokes and how do they happen?
Make up 85% of cases
Common sites of atherosclerotic disease !
Mechanism can be via;
- Large vessel thrombosis with/out embolism
- Cardiac emboli - AF, endocarditis, replacement valve thrombus
- “Lacunes”/ small vessel degeneration - particularly in diencephalon
- Arterial dissection
Rarer causes;
- Vasculitis
- Illicit drug - cocaine/amphetamine
- Haematological cause
- sickle cell, hyper coagulation syndromes
How might an atherosclerotic plaque cause a thrombus to form?
Atherosclerotic plaques in large vessels may cause either thrombus formation (e.g MCA thrombosis) which may embolise downstream (such as in carotid artery disease) or may themselves cause hypo perfusion of so called “boarder territories” - causing watershed infarcts (drop in BP due to blockage or restriction)
What is the Bamford stroke classification /
Total anterior circulation stroke;
- Hemiparesis / hemisensory loss
- Higher cerebral dysfunction
- Homonymous hemianopia (optic radiation damage)
(ALL 3 NEED TO BE PRESENT!)
= Middle cerebral artery occlusion
Partial anterior circulation stroke (PACS);
- Isolated higher cerebral dysfunction
OR ANY 2;
- Hemiparesis / sensory loss, higher cerebral dysfunction, hemianopia
Posterior circulation stroke (POCS);
- Isolated homonymous hemianopia
- Brainstem or cerebellar syndromes
= occlusion in vertebral, basilar or posterior cerebral artery
Lacunar stroke;
- PURE motor or PURE sensory or sensorimotor stroke or cerebellar dysfunction
No higher cerebral dysfunction/visual signs (language and memory preserved)
= Thrombotic occlusion of small perforating arteries typically in thalamus and/or basal ganglia
A 72 year old female presents with right and and leg weakness and hr speech is nonsensical, you are unable to test sensation due to this.
What type of Bamford classification is her stroke?
Total anterior circulation stroke - likely large ACA and MCA infarct;
- Higher cerebral dysfunction (speech)
- Hemiparesis
- Visual field deficit
Note - VF could be difficult to test if someone doesn’t understand speech
What issues would you see in cerebral artery strokes?
Anterior cerebral artery (rarer as if proximal A1 is occluded there is good collateral from contralateral ACA)
- Contralateral hemiparesis and hemisensory loss of lower limb
- Incontinence
Middle cerebral artery (most common)
- contralateral hemiplegia (if pure MCA then upper limb > lower limb)
- Contralateral hemisensory loss
- Conjugate eye deviation (looking to the side of the lesion) contralateral homonymous hemianopia
- Language defects if dominant hemisphere, neglect if non-dominant
Posterior cerebral artery;
- Homonymous hemianopia - if there is no macular cortex involvement then ocular sparing hemianopia
- Dominant hemisphere; Alexia without agraphia - write but can’t read, visual agnosia - inability to recognise objects
- Bilateral - cortical blindness without insight and confabulation - Anton’s syndrome
What are the features off Lacunar Strokes?
These refer to small infarctions of the internal capsule, thalamus, striatum and brainstem
Occlusion of perforating arteries such as the lenticulostriate of MCA and thalamic branches of the PCA
They lack higher cortical signs
Specific modality of lesion - Think Lacunar!
Pure motor? - think internal capsule, corona radiate
Pure sensory? think Thalamus
What would Basilar artery occlusion show?
Brain stem lesions present with cranial nerve signs (of particular note being gazed palsies)
- Cerebellar signs
- Deficits in concord level
- In some cases quadriplegia
- Bulbar symptoms including facial weakness, dysarthria, dysphasia, dysphonia
- Wide variety of brain stem syndromes
What would you expect to see if the lesion was in the lateral medulla ?
Wallenberg’s syndrome! - Lateral medullary syndrome
Wobbly Wallenberg!
Ataxia, abnormal eye movements
Occluded posterior inferior cerebellar or vertebral artery.
What would you expect to see if the lesion was in the pons ?
Foville syndrome - medial inferior pontine syndrome
What would you expect to see if the lesion was in the midbrain ?
Weber’s syndrome - ventromedial brain
What artery occlusions in the hindbrain give what deficits?
Vertebral or PICA penetrator arteries - Deficits; ipsilateral limb ataxia, horners syndrome, crossed sensory loss, vertigo, dysphagia, hoarseness
Anterior inferior cerebellar artery - Gait and limb ataxia, dysfunction of ipsilateral trigeminal, facial, vestibulocochlear nerve
Superior cerebellar - Dysarthria and limb ataxia
Right posterior cerebral - Contralateral visual field defect, visual neglect, prosopagnosia
Left posterior cerebral - Contralateral visual field defect, Alexia without agraphia, impaired memory, visual agnosia
Top of basilar artery - Somnolence, vivid hallucinations, dreamlike behaviour, oculomotor dysfunction (rostral brainstem)
What is the stroke patient pathway?
Examination ->
ROSIER or NHSS score ->
Imaging if stroke possible ->
Immediate management ->
Thrombolysis or thromboectomy ->
Rehab (speech and language therapy, clinical psychology, PT/OT, dedicated stroke unit)
What types of imaging can you use for strokes?
CT with no contrast
- Requires no vascular access
- Fast compared to MRI
- Able to clearly show haemorrhage
- Able to clearly show mass effect, infarction, herniation and hydrocephalus
CT head with contrast (CT cerebral angiogram)
- Enables better resolution of BBB permeability altering proceess
- Breakdown of BBB causes leakage of contrast into parenchyma
- Enables clear inflammation, ischia, angiogenesis, increased pressure identification
- Ideal for occlusion identification, brain tumour/mets, abscesses, MS and various infection pathology
Magnetic resonance angiogram
- Validated but not favoured in acute setting due to time to get images
- Higher sensitivity/specificity than CT
What radiographic features can we see on stroke scans?
Hyperacute: 0 - 24 hours - Hyperdense sign, loss of grey-white matter differentiation, cortical hypodensity, parenchymal swelling and gyros effacement (loss of clear sulk and gyro second to swelling of brain tissue)
Acute: 24 hrs to 1 week - infarct with lower attenuation tissue visible, mass effect due to swelling
Subacute: 1 to 3 weeks - CT fogging - cortical petechial haemorrhages - the hypo attenuation reverses as the oedema settles resulting in an almost normal appearance
Chronic: more than 3 weeks - Gliosis - low density with negative mass effect
What are the 2 ways to asses strokes?
ROSIER; recognition of stroke in the emergency room, validated ED scale
NIHSS - National Institute of health stroke scale - research tool but validated for stroke assessment in NICE guidance in certain. scenarios - 11 point
What would the treatment for ischaemic stroke be?
- Use validated tool such as ROSIER
- EXCLUDE hypoglycaemia with sudden onset neurological symptoms
If normal glucose;
- Offer 300mg aspirin once daily for all suspects TIA stroke (if no oral route - enteral/rectal)
- Give PPI with aspirin
- If allergic then consider clopidogrel or dipyridamole
- Continue aspirin for 2 weeks at 300mg before changing to long term anti-thrombotics
How should you assess and treat acute stroke?
- Non-enhanced CT immediately to run out intracranial haemorrhage especially if patient is on anticoagulant, has papilloedema, neck stiffness or fever, has depressed level of consciousness (GCS < 13)
Oxygen therapy and blood sugar control if
- Oxygen saturation is <95%
- Maintain a blood glucose level between 4 - 11 mol/litre
Blood tests, including coagulation screen, FBC and U&E
If confirmed ischaemic then;
- Thrombolysis with Altepase (haemorrhage excluded) or Thromboectomy
- Aspirin 300 mg as soon as possible but certainly within 24 hours (haemorrhage excluded)
- Avoid antihypertensive medications unless mean arterial pressure > 130 mmHg or hypertensive encephalopathy/nephropathy
Why do we reperfuse in ischaemic stroke?
As there are areas that are potentially salvageable called the penumbra and has a functioning electrophysiological activity, and reperfusion aims to restore supply to the penumbra, preventing extension of core
When do you give thromboylsis?
Thrombolysis - tissue plasminogen activator drugs, such as atlas and Tenecteplase. These convert plasminogen to plasma which breaks down fibrin and fibrinogen, the constituents of thombuses.
Criteria;
- Must be started as soon as possible within 4.5 hours of symptom onset
- Intracranial haemorrhage has been ruled out
- Immediate reimagine is accessible (in case of hemorrhagic transformation)
When do you give thromboectomy?
Criteria;
- Offer as soon as possible and within 6 hours of onset of symptoms, together with thrombolysis if within 4.5 hours to acute ischaemic stroke with confirm occlusion of proximal antieorr circulation demonstrated on CT cerebral angio or MRA.
Can be offered within 24 hours provided prove made findings and salvageable tissue defined by CT.
People should previously have good functional status and NIHSS >5
What is don in secondary prevention and post-stroke care?
Treat hypertension with normal targets of < 130/80 mmHg
Antithrombotics;
- Either clopidogrel monotherapy or Aspirin + Dipyridamole
- In AF - direct oral anticoagulation (Apixaban, rivaroxaban) or Warfarin
- Statins on discharge if total cholesterol >4mmol/L
Whats the Treatment for a TIA?
- Offer aspirin (300mg daily) unless contraindicated
- TIA clinic review 24 hours of onset of symptoms
- Do not use scoring systems such as ABCD2 to assess risk
- No routine CT
- Consider MRI (including diffusion-weighted and blood-sensitive sequences)
- NICE do not recommend Extracranial to intracranial bypass
- Modified-release dipyridamole in combination with aspirin is recommended
What are the features of Subarachnoid haemorrhage ?
- Form of Hemorrhagic stroke
- Haemorrhage into the subarachnoid space between arachnoid and Pia mater
- Classical presentation of thunderclap occipital headache
- Rule of thirds - 1/3rd die, 1/3rd severely disabled, 1/3rd recover well
Investigations:
- Xanthochromia > 12 hours post op onset on Lumbar puncture
- CT cerebral angiogram - shows haemorrhage
What are the 5’s that mimic strokes?
5’s that mimic strokes:
- Seizure
- Sepsis
- Syncope
- Space occupying lesions
- Somatisation
