Stroke Flashcards
What is the difference between a stroke and TIA?
In TIA interrupted blood flow returns to the brain or brainstem WITHIN 24hrs where as a stroke is defined as interrupted blood flow for over 24 hrs
What are the 2 major classifications of stroke and which is most common?
Ischaemic/cerebral infarct= tissue hypoperfusion due to blocked arteries/veins
87% of strokes
Haemorrhagic
Rupturing of vessels which leads to compression damage via ICP
What is the definition of a stroke?
-Sudden onset of neurological deficits lasting >24 hours
-attributable to focal vascular disease rather than global disease= effects ONE vascular territory
where no other cause is apparent
What would you differentiation between an ischaemic and a haemorrhagic CVA on a CT scan? Why is it critical to determine the difference in terms of treatment options?
Ischaemic:
-darker region visible due to ischaemia i.e. can be hard to see early on
-might be able to see white hyperdensity of clot
-develops over period of days becoming very dark and well demarcated
-sulcal effacement i.e. loss of sulcal patter due to
associated oedema
TX
- Anteplase (thrombolytic) w/i 3-4 hrs
- thrombectomy
Haemorrhagic:
-white lesion i.e. high attenuation due to Hb content
-surrounded by dark (low attenuation) i.e. oedema
-present immediately
-changes to isodensity after couple days due to Hb breakdown i.e. might be indistinguishable from ischaemic
TX
-Craniotomy to release pressure and access bleed
-ventricle shunt to treat complication of hydrocephalus
NO THROMBOLYSIS i.e. will exaggerate the problem
What is the acute management process for someone who has suffered a stroke?
Protect the airway to avoid aspiration or hypoxia
Maintain homeostasis:
- blood glucose in 4-11 mmol/L
- only treat blood pressure if hypertensive emergency or patient is being considered for thrombolysis
Screen for swallow
CT or MRI w/i 1 hr essential if:
- thrombolysis considered
- high risk of haemorrhage
- unusual presentation i.e. fluctuation of consciousness
Antiplatelets
-300 mg aspirin given once patient has been confirmed as not having haemorrhagic stroke
Thrombolysis
- w/i 4.5 hrs of onset of symptoms and once haemorrhagic stroke has been excluded
- Anteplase used
Thrombectomy
-catheter with stent used to for patients with occlusion of larger vessels
what are the signs that a stroke patient might be at high risk for haemorrhage?
Drop in GCS Signs of increased ICP Severe headache Meningism= headache, neck stiffness, photophobia and nausea + vomiting Progressive symptoms Bleeding tendency Anticoagulants
What are the treatment options for haemorrhagic stroke?
Craniotomy to remove neurocranium to access to bleed and clip vessels
Ventricle shunt to treat the associated hydrocephalus that can occur as complication due to compression of ventricles preventing CSF from draining
What are the different forms of long term management and secondary prevention used in stroke patients?
Lower BP = Thiazide-duirectics/ ACEi/ CARBs/ beta-blockers
Lower cholesterol= statins
Anti-platelets= aspirin/ clopidogrel/ dipyridamole
Anti-coagulants= warfarin/ apixabran/ dibigatran
- when there is cardiac cause of stroke i.e. AF/DVT
In conjunction with controlling risk factors:
- hypertension
- DM
- smoking
- CVS disease
What is the most common cardiac cause of strokes? How are these patients managed? What are additional cardiac causes of stroke?
Atrial fibrillation= improper emptying of the atria lead to increased risk of clots forming which can then pass into common carotid a and ascending to cerebral circulation
Management:
-commence anti-coagulants 2 weeks after stroke
Eg warfarin or DOACs
Other causes:
- cardio version
- prosthetic valves
- acute MI with large left ventricular wall abnormalities
- infective endocarditis
What is the most common vessels to be involved in stroke? How might a person with a stroke to these vessels present and why?
Middle cerebral artery
Occlusion of cortical branches:
-inferior frontal gyrus= Broca’s area
Eg Expressive dysphasia/aphasia (loss of ability to produce speech)
-superior temporal gyrus= Wenrickes area
Eg Receptive dysphasia/aphasia (loss of ability to understand speech)
-lateral pre and post central gyrus
Eg loss of motor and sensation to upper limb and face
Occlusion of lenticulostriate branches supply internal capsule
- UMN for CNV and CNVII
- Corticospinal tracts = contralateral loss of UL motor interaction i.e. UMN signs
A lady presents with her jaw deviating towards the left side and she has lost facial expressions on the right lower quadrant of her face with preserved wrinkling of the forehead. She has problem moving her hand and wrist and has loss of sensation in these areas. Where is the most likely site of a CVA and why?
Left lenticulostriate artery
Left jaw deviation:
-non-functioning CNV leads to paralysis of masticator muscles and jaw deviates towards the side of paralysis
Loss of facial expression with preserved forehead wrinkle
-indicates stroke on contralateral side rather than Bell’s palsy
Sensory and motor loss in hands and arms
- lateral pre and post central gyrus infarct to problem with corticospinal tract (motor) and thalamic protections (sensory) = infarct is contralateral to side of problems
A CVA involving which artery would lead to right homonymous hemianopia and why?
Posterior cerebral artery due to supplying visual cortex of occipital lobe
Infarct in left posterior cerebral artery leads to hypoperfusion of left occipital lobe which receives the left visual field in both eyes i.e. ipsilateral nasal field and contralateral temporal field due to fibres carrying info from the temporal field decussating in the optic chiasm
How would a patient experiencing a cerebral infarct generally present?
Contralateral sensory loss
- LL= anterior cerebral artery i.e. supplies medial aspect of gyri
- UL= middle cerebral artery i.e. supplies lateral aspect of gyri
Contralateral hemiplegia
- flaccid to begin with and then become spastic i.e. UMN
- dysphasia= broca’s (expressive) + wenrickes (receptive)
Homoymous hemianopia= occipital lobe
Visuospatial deficit
How would a patient with brainstem infarct generally present?
Quadriplegia= ventral pons contains corticospinal and spinothalamic tracts
Disturbances of gaze and vision
Bilateral up-going plantar
Locked in syndrome:
-compromised corticobulbar tracts (V/VII/IX/X/XI/XII) means loss of facial expression, mastication, speech and swallow
-complete muscle paralysis apart from upward gaze
I.e. anarthria, dysphagia
-compromised breathing
-vertigo and dizziness
What occurs in a lacunar stroke?
What are the risk factors?
What key function is preserved compared to cortical stroke?
How would a patient with lacunar infarcts present?
Occlusion of small perforator arteries supplying the deep white matter and brain stem
Risk factors:
- hypertension
- diabetes
- hyperlipidaemia
HMF and visiual problems preserved i.e. speech and no hemianopia
Parts of CNS which can be affected:
- thalamus
- basal ganglia
- internal capsule
- pons
Contralateral UMN hemiplegia
Contralateral hemisensory loss
Contralateral upgoing plantar
How would someone with a thalamic stroke present?
Impaired sensation i.e. numbness or tingling
Sleep disturbances
Amnesia= short or long term memory loss i.e. vascular thalamic amnesia
Speech difficulties = Aphasia
Hemispatial neglect= unaware of environment on the side opposite to the infarct i.e. right thalamic infarct= left neglect
Vision impairments = diplopia or heminopia
Balance problems= due to brainstem possibly being implemented which helps to regulate vertical eye position and head posture
Thalamic/central post-stroke pain
