Strokes Flashcards
Cerebral circulation:
Blood supplied to brain by -
Internal carotid arteries (run anteriorly)
Vertebral arteries (posteriorly)
2x on R and L of each
Cerebral circulation
What structure supplies blood to cerebral cortex?
Circle of Willis!!!! Really important to learn (should be able to draw and label it)
Cerebral circulation
Anterior circle of Willis -
Internal carotid arteries pass up anterior neck and divide to from anterior cerebral artery (ACA) and middle cerebral artery (MCA)
ACA’s join to form anterior communicating artery
Cerebral circulation
Posterior circle of Willis -
Vertebral arteries pass up through foramina in transverse processes of cervical vertebrae and join in front of brain stem to form basilar artery.
Basilar artery divides at upper brain stem into two posterior cerebral arteries (PCA) and is connected to circle of Willis by the Posterior communicating arteries
Why is the circle of Willis anatomically effective?
It protects the brain via collateral circulation
If Damage/blockage in one supply artery, then the other arteries can compensate for this and ensure appropriate profusion for the brain
Arteries that come off circle of Willis eg ACA,MCA and PCA are terminal arteries, therefore areas of brain they supply are not protected by collateral system
Circle of Willis
Anterior cerebral artery -
Supplies medial/superior parts of frontal lobe and anterior parietal lobe
Includes frontal, pre frontal and supplementary motor cortex and parts of primary motor/sensory cortex eg for lower limb
Circle of Willis
Middle cerebral artery -
Supplies greater part of lateral cerebral surface and supplies deep structures including internal capsule and Basal ganglia
Circle of Willis
Posterior cerebral artery -
Occipital lobe, inferno medial surface, temporal lobe and thalamus
Circle of Willis
Basilar artery -
Supplies blood to all of the brain stem (pons,medulla and midbrain) and cerebellum
Circle of Willis
What can MCA damage potentially lead to?
Upper limb motor deficit, facial drop, sensory symptoms and speech deficits
always think about area of brain it supplies
What is a stroke?
Disruption of blood supply to brain resulting in sudden and lasting neurological deficits
Transient ischaemic attack -
(TIA) ‘mini stroke’
Caused by temporary disruption in blood supply to brain
Causes similar symptoms to stroke, but effects last a few minutes to a few hours and will fully resolve within 24 hours
Stoke types
Ischaemic -
Clot/blockage of blood supply
*more common - 85% of strokes
Atheroma - plaque build up of cerebral A
Thrombosis - blood clot in cerebral A
Embolism - blood clot from somewhere else that has moved and is now blocking cerebral A
Most commonly seen MCA>PCA>ACA
Brain stem strokes are less common and more serious
Stroke types
Haemorrhagic -
A bleed (15% of strokes) rupture of blood vessels in brain
Intracranial or intracerebral haemorrhage (ICH) - bleeding on the brain
Subarachnoid haemorrhage (SAH) - bleeding on surface of brain in subarachnoid space*
*discussion as to whether this is a stroke or brain injury. RN, NOT treated within stroke pathway
Aims within first hours of identifying a stroke:
Stroke = medical emergency
Urgent brain imaging - within 1 hour
Thrombolysis within 4 hours for patients with acute ischaemic stroke
Direct admission of patients with acute stroke to hyper acute stroke unit within 4 hours of hospital arrival
Treatments
Ischaemic - thrombolysis -
Clot busting drug, ONLY ischaemic stroke, with aim of restoring blood flow to area and preventing cell death
Needs to be started within 4 hours, but ideally ASAP
Significant inclusion and exclusion criteria
Can significantly increase stroke recovery
Risks of causing bleeding anywhere in the body
Following it, very closely monitored for 24 hours
Available 24hours 7 days a week in UK
Treatments
Ischaemic - thrombectomy -
Newer
Clot removal with catheter inserted through femoral vein and guided via imaging to side of clot in brain
Strict inclusion and exclusion criteria
Can significantly increase post stroke recovery Risks
Risks associated with procedure
Patients usually admitted to critical care post procedure for a night
London available 24hours a day 7 days a week
Midlands available 8-4 Monday-Friday
Treatments
Ischaemic - carotid endarterectomy -
Treatment of carotid artery stenosis by removing plaque build up in carotid artery
Strict inclusion/exclusion criteria
Risks of bleeding and further strokes associated
Treatments
Haemorrhagic -
If on anticoagulants, they need to be urgently reversed
BP must be lowered
For those who develop hydrocephalus (swelling in brain) should be considered for surgical intervention eg. Insertion of external ventricular drain to reduce swelling
For all strokes, secondary prevention of further strokes:
Review risk factors providing treatment and advice to reverse these if possible
Establish cause of current stroke and treating if possible
**national clinical guidelines for stroke - covers all areas of stroke care and guidelines reviewed every 4 years!
Bamford/oxford stroke classification:
Total anterior circulation stroke (TACS)-
Must have all three of the following
- unilateral weakness (and/or sensory deficit) of ace, arm and leg
-homonymous hemianopia
-higher cerebral dysfunction (dysphasia, visuospatial disorder)
Bamford/oxford stroke classification
Partial anterior circulation stroke (PACS) -
Must have two of the following
- unilateral weakness (and/or sensory deficit) or face arm and leg
- homonymous hemianopia
-higher cerebral dysfunction (dysphasia, visuospatial disorder)
Bamford/oxford stroke classification
Lacunar stroke (LACS) -
Must have one of the following
- pure sensory stroke
-pure motor stroke
- sensory-motor stroke
-ataxic hemiparesis
There is no loss of higher cerebral functions
Bamford/oxford stroke classification
Posterior circulation stroke (POCS) -
Must have one of the following
-cranial nerve palsy and a contralateral motor/sensory deficit
-bilateral motor/sensory deficit
-conjugate eye movement disorder (eg. Horizontal gaze palsy)
-cerebellar dysfunction (eg. Vertigo, nystagmus, ataxia)
- isolated homonymous hemianopia
Signs and symptoms of a stroke -
Hemiplegia (one sided limb weakness)
Sensory deficit
Ataxia (decreased coordination)
Dysarthria (slurred speech)
Dysphasia - expressive and/or receptive
Reduced attention
Homonymous hemianopia (visual deficit)
Dysphagia (impaired swallow)
Dizziness
Reduced memory
Briefly describe the motor pathway:
Motor information originates in the motor cortex in the frontal lobe
It descends via descending spinal tracts (main tract is cortico-spinal tract)
80% of fibres of these tracts cross in the medulla
Within the SC this synapses with the alpha motor neurone
This peripheral motor nerve (lower motor neurone) takes the message to the muscle
Motor pathway
When the tracts cross in the medulla, what does this mean for patient symptoms?
They will appear on the other side
Eg. If someone has an event in the right cerebral cortex, they will present with a left sided weakness
Motor symptoms and what they can lead to:
Lack of muscle innervation
Changes in muscle tone, ataxia, muscle weakness… these can all lead to:
Asymmetry eg. Shortening, loss of normal movement. Loss of postural adjustments and compensations
These all interact so can lead to one an other quite a lot
Muscle tone-
What produces it -
Readiness in a muscle at rest (resting tone)
Normal tone should be high enough to keep you up against gravity, but low enough to allow movement
Neural factors - active contraction and reflex contraction
Mechanical factors - physical inertia of limb, viscoelastic properties of the muscles
Thixotrophy - stickiness of muscle, resistance to movement the longer its at rest
*also think about connecting tissue and surrounding structures within this as well!!!
Muscle tone:
Hypotonicity -
Hypertonicity -
Hypo - diminished residence to passive movement
Can be caused by CNS or PNS lesion (upper and lower motor neurons)
Low tone
Flaccidty and weakness
Hyper - increased resistance to passive movement
Caused by damage to CNS spasticity (local/segemtnal/generalised) - velocity dependant and unidirectional
Rigidity (generalised) - specific to Parkinson’s
Dystonia and dyspraxia
Muscle weakness, when do we see it?
See this due to lack of innervation of muscles straight away post stroke
However, muscle weakness is also a secondary problem as muscles will atrophy very quick due to lack of use post stroke
Eg. Lower limb muscles not used, so will atrophy
Stroke survivors will have primary and secondary muscle weakness problems
Sensory pathway -
Sensory messages are initiated in sensory receptors
They are transferred via sensory peripheral nerves to the spinal cord
Carried up to the cortex via ascending tracts
Synapse at the thalamus
Transferred to sensory cortex (vision to visual cortex)
Sensory impairments
Impaired cutaneous sensation can include -
Problems distinguishing between/ feeling light and deep touch.
Temperature, can’t feel it. Can’t tell difference between sharp and blunt and 2 point discrimination
Sensory impairments
Impaired stereognosis -
Unable to identify object by just tactile feel, in absence of vision
Sensory impairments
Impaired proprioception awareness -
Proprioception is bodies ability to sense movement, action and location
Present in every muscle eg. Allows to walk without consciously thinking where to place foot and touch our nose with our eyes closed
Therefore deficit means they may struggle with these kind of things
Sensory impairments
Visual field deficits -
Homonymous hemianopia - lose visual field in one half of both eyes, therefore can visually only see half of the world around you
Quadrantanopia - lose a quadrant in both eyes, eg. Upper left quadrant (1/4)
What is important to remember about sensory and motor impairments?
Motor and sensory impact each other, our sensory input drives our motor output
Due to this symptoms are not in isolation normally, therefore essential to use clinical reasoning
Speech symptoms
Dysarthria -
Slurred speech.
Related to weakness and changes in tone to muscles related to speech. It is a MOTOR problem NOT a processing problem
Speech symptoms
Expressive dysphasia -
Receptive dysphasia -
Expressive - damage to Broca’s area (on left, frontal lobe)
Difficulty expressing words, can range from being mild to very severe.
When very severe, they believe what they are saying is correct, even when it is very wrong and makes no sense
Receptive - damage to wernikes area (sits on edges of temporal and parietal lobe, mainly temporal)
Difficulty understanding speech - appears to them like we are making no sense
Can range from mild to very severe
Cognitive symptoms examples:
Perceptual problems - struggling to understand world around you
Dyspraxia - problems sequencing and ordering tasks
Memory
Retention - wont retain info you are giving them
Inattention - inattentive to one side of body/one side of the world. Can be very severe eg. Won’t recognise their arm as their own.
It is linked to sensation and visual deficits
Insight -lack of understand of problems
Processing problems
And many more!!!
What factors may affect stroke recovery?
Size and location of stroke
Pre-morbid status - before stroke. Were they fit and active?sedentary?
Patient motivation
Patient insight - do they understand what’s happening to them?
Patient engagement - participating in therapy?
Nutrient and hydration - impacts neuroplasticity
Environment - engaging environment encourages neuroplasticty
Therapy
Age - more neuroplasticty the younger you are. However… not the most important factor here, elderly can still recover really well.
What is neuroplasticty?
Adaptive capacity of CNS and its ability to modify its own structural organisation and functioning
- it is thought to be the underlying principle by which post stroke recovery occurs
What is important to remember about the brain and regeneration?
Neural regeneration does not occur in the CNS!!! - only in PNS
Neuroplasticty only occurs within the brain
Neuroplasticty - changes in synaptic strength
1) ‘unmasking’ of dormant pathways -
Many neural pathways lie dormant naturally - these dormant pathways become more effective once the primal pathways that were previously being used are removed or incapacitated following disease/injury
These pathways will increase in synaptic strength with continued use
Neuroplasticty - changes in synaptic strength
2) formation of new synapses -
Co-lateral sprouting
Occurs at same time as the reorganisation of unmasking pathways
Spouting occurs at uninjured axons to help compensate for the damaged axons
Neuroplasticty - why is important for us as physios?
We want to promote plasticity - using particular neural pathway to make it stronger
Practicing activity will lead to learning
Plasticity occurs in response to demand
Can maximise repetition through:
Interesting and varied activities
Motivation eg. Involve fam and friends
Home programmes
Education and clear communication
Aerobic exercise promotes plasticity!!!
What is the name of the cerebral blood supply?
Circle of Willis
The brain- each areas brief role:
Frontal lobe -
Parietal -
Temporal -
Occipital -
Frontal - cognitive functions and decision making - contains Broca’s area
Parietal - sensation
Temporal - balance and hearing
Occipital - vision
The brain, each areas brief function
Cerebellum -
Brain stem:
- pons -
- medulla -
-mid brain -
Cerebellum - balance and coordination
Pons - links medulla and thalamus
Medulla - respiratory centre
Midbrain - controls movement and sensory information
* most who has a stroke in their brain stem will unfortunately die.
The brain, each areas brief function
Basal ganglia -
Corpus callosum -
Basal - loads of nuclei!! Initiation of movement
Corpus - connects right and left hemisphere together
The brain, each areas brief function
Thalamus -
Hypothalamus -
Relays sensory and motor information between cortex and brain stem
Hypothalamus - homeostasis and autonomic functions
Difference between a stroke and a TIA:
Stroke - rapid loss of brain functions due to disturbance in the blood supply to the brain - can be Ischaemia caused by blockage or a haemorrhage
TIA - sign that part of the brain is not getting enough blood and there is a risk of more serious stroke in the future. Effects last a few minutes to a few hours and fully resolve in 24hour
Ataxia -
Hemiparesis -
Dyspraxia -
Ataxia - impaired coordination of voluntary muscle movement. Cerebella, sensory or vestibular
Hemiparesis - muscle weakness on one side of the body - left/right hemisphere
Dyspraxia - impaired ability to plan and process motor tasks
Spasticity -
Velocity dependant and unidirectional resistance to passive movement. A motor disorder characteristic by velocity dependant increased in tonic stretch reflex’s and muscle tone with exaggerated tendon relflexes, resulting from hyper-excitability of the stretch reflex’s, as one component of the upper motor neurone syndrome
Unilateral neglect/inattention -
Dysarthria -
Unilateral - inability to recognise and/or respond to stimuli on one side of the body - occipital lobe/pareital lobe
Dysarthria - inability to control the muscles used in speech resulting in slurred speech
Agnosia -
Damage to brain results in inability to recognise input from one of your senses, inability to process sensory information such as sight, hearing etc..
often there is a loss of ability to recognise objects
Parietal lobe
Neuroplasticty - prickles of experience dependant plasticity
1) use it or lose it -
2) use it and improve it -
3) specificity -
4) repetition matters -
5) intensity matters -
1) Use it or lose it - failure to drive specific brain functions can to lead functional degradation
2) Use it and improve it - training that drives a specific brain function can lead to an enhancement of that function
3) specificity - nature of training experience dictates the nature of plasticity
4) repetition - induction of plasticity requires sufficient repetition
5) intensity - induction of plasticity requires sufficient training intensity
Neuroplasticty - principles of experience-dependant plasticity
6) time matters -
7)) salience matters -
8) age matters -
9) transference -
10) interference -
6) time - different forms of plasticity occur at different times during training
7) salience - training experience must be sufficiently salient to induce plasticity
8) age matters - training induced plasticity occurs more readily in younger brains
9) transference - plasticity in persons to one training experience can enhance the acquisition of similar behaviours
10) interference - plasticity in response to one experience can interfere with the acquisition of other behaviours
Name some symptoms that may occur with damage to frontal lobe:
Speech deficits
Cognitive issues
Affects decision making eg. Can become impulsive
Personality changes
Loss of Inhibition
Name the two main principles of neuroplasticty and explain how they work:
1) unmasking of Dorman pathways - neural pathways lie dormant naturally, primary pathway becomes blocked, unmasking Dorman ones occurs - synaptic strength increases with repeated repeated/continued use
2) collateral sprouting - injured axons degenerate, uninjured axons sprout new synapses in order to innervate where damage has occurred
How can we promote neurplasticity as a physio?
Interesting and varied activities
Motivation eg. Involving fam and friends, goal orientated working
Home programmes - stimulating environment increases neural plasticity
Education and clear communication
Aerobic exercise promotes plasticity - exercise prescription post stroke must be specific and safely identified to suit individual needs
