stroke Flashcards
Define stroke and what is another name for it?
acute onset neurological deficits due to haemorrhagic or ischaemic vascular lesions aka infarction // sudden neuro event of vascular origin
CVA = CEREBROVASCULAR ACCIDENT:
The sudden death of brain cells due to lack of oxygen when the blood flow to the brain is impaired by blockage or rupture of an artery to the brain (stroke).
Symptoms of a stroke depend on the area of the brain affected. With CVA get infarction (death) of brain tissue. Deficit develops over time. Results in either death or some improvement over months
Define infarction
Define ischaemia
- Tissue death/necrosis due to inadequate blood supply to affected area – obstruction to blood flow
- inadequate blood supply to region caused by hypotension, vascular obstruction or both
Define the vascular lesions a/w stroke
Acute ischaemic stroke - due to thrombus/ embolus ;Thrombosis and embolism have similar consequences for the brain: loss of oxygen and metabolic substrates, resulting in infarction or ischemic injury of regions supplied by the affected vessel.
Haemorrhage - arachanoid/intracerebral
due to rupture of blood vessel causing direct injury and secondary ischemic injury
What are subtypes of a stoke?
1) Transient Ischaemic Attack
2) Acute ischaemic stroke
3) Acute haemorrhagic stroke
Define TIA
TIA = TRANSIENT ISCHAEMIC ATTACK:
A neurological event with the signs and symptoms of a stroke, but which go away within a short period of time (mini-stroke, duration<24 hrs). Due to a temporary lack of adequate blood and oxygen (ischemia) to the brain.
How to diagnose TIAs?
Diagnosis is based entirely off of history versus brain imaging
What is the risk of recurrence of TIAs?
highest in the first month
risk 8-10% at 7 days , 11-15% at 30 days
What are the symptoms to be assessed when considering TIAs as diagnosis?
Onset - sudden
Intensity- symptoms max at onset (gradual progression suggests demylelination, migraines or tumour– multiple/intermittent symptoms are atypical)
Focal symptoms-
carotid artery territory symptoms include amarosis fugax(embolic form of TIA in carotid territory which causes painless transient monocular blindness- described as a curtain, shade or mist descending over the eye) , hemianopia, dyshagia, contralateral weakness or numbness
vertebrobasilar territory symptoms - ataxia, vertigo, dysarthria, diplopia, hemianopia, bilateral visual loss (Uzi Ver(Tigo) and Diplo(pia) disguised (dysarthria) in ataxi(a) to prevent people from seeing them (bilateral visual loss)
duration- TIAs last 5-15 mins
Recognisable pattern- symptoms corresponding to a recognised territory of brain are supportive of TIA
headache- severe headache or eye pain is not a feature of TIA
loss of consciousness (syncope) is not a/w TIA
What are the symptoms that are not a/w TIAs?
severe headache eye pain syncope isolated dizziness, lightheadedness or vertigo seizure memory loss acute confusion gradual progression of symptoms multiple recurrent symptoms
Whar are the mimics of TIA
CNS tumours ocular disorders neuropathy and radiculopathy(pinched nerve) partial seizures syncope migraine hypoglycaemia vestibular disorders
How to assess prognosis (aka stroke risk) of TIAs?
ABCDD A-age >60 B-blood pressure >140/80 C-clinical symptoms a/w neuro deficit D-duration D-diabetes max score of 7
only applies for ACUTE TIAs not those which happened weeks/months ago
What is considered low risk, mod risk or high risk?
low risk - 0-3
mod risk - 4-5
high risk- 6-7
What is the consequence of a score greater than five (5) ?
should have immediate intervention and treatment within 24hr if possible
What is the a/ stroke risk with a score of 4-5 for 48hrs, 1 week, 3 months
and likewise for a score of 6-7
48 hrs- 4%
1 week- 6%
3 months- 10%
48 hrs- 8%
1 week- 12%
3 months- 18%
Management and investigations of TIA
Check Pulse, ECG, Neurological Examination
FBC, U&E,Fasting Glucose and Total Cholesterol
Urgent Carotid Doppler-Those with carotid circulation TIA who are fit for surgical intervention
?Prognostic Score-NICE recommends that patients with an ADCD2 score≥4 should be assessed and investigated within 24hrs.
No Driving for 30 days
What are some techniques to aid in secondary prevention?
Antithrombotic therapy
Aspirin+dipyridamole
Clopidogrel if intolerant of aspirin
Anticoagulation (following imaging) in Atrial Fibrillation
Blood Pressure Control (according to National guidelines)
Statin (if total chol>3.5mmol/l or LDL chol>2.5mmol/l)
Other secondary preventive measures-Smoking cessation, exercise, screening for Diabetes
What is TIA considered to be in regard to stroke?
A warning sign for strokes
30-40% of pts with ischaemic strokes have had earlier transient ischaemic attack or minor stroke
90 day risk of subsequent stroke is as high as 10.5%, with almost half occurring within the first 2 days
What are the risk factors for stroke?
Lifestyle- diet-obesity, smoking, Oral contraceptives
Medical- cholesterol-hyperlipidemia/atherosclerosis, atrial fib/CHD/LVH/valvular disease(aka heart diseases/impaired cardiac function due to embolism) ,thrombosis- haematocrit/fibrinogen, BP-hypertension, glucose-diabetes
Non modifiable- gender, age, genetics, race
What is the most common subtype of stroke?
Acute ischaemic stroke -65%
then TIA- 21%
then haemorrhagic stroke-12%
What are classical symptoms of a stroke?
weakness or numbness on one side slurred speech loss of balance blurred vision face drooping syncope headache
Damage to what neurological areas attribute to the classical symptoms of a stroke?
Damage to cerebellar area- unsteadiness and poor coordination
Damage to Wernicke’s area- difficulty in understanding speech, reading and naming objects
Damage to left parietal lobe- loss of coordination in RIGHT arm and leg
Damage to Broca’s area- speech problems
Damage to motor area of right cerebral hemisphere - weakness of left arm, leg and face
Small stroke in brainstem can cause problems as many nerves pass through here to get to spinal cord
Discuss differences between ishaemic and haemorrhagic causes of strokes
Ischemic CVA:
•Cause: Due to occlusion of an artery (within the cerebral circulation or outside the cerebral circulation) by either thrombus/atheromatous plaque or emboli.
•Sources of emboli outside cerebral circulation = Carotid artery thrombi/atheromatous plaques (arterial atherosclerosis) or from mural atheromatous plaques in the heart (which form as a result of a myocardial infarction)or due to valve disease or atrial fibrillation.
•Emboli lodge at a pre-existing stenosis (site of an atheromatous plaque) or at vessel bifurcations.
Haemorrhagic CVA:
Cause = Rupture of a blood vessel within the brain tissue(50% of ruptures due to hypertension; other cause = anti-coagulant therapy, esp. in elderly). Hypertension: Get atherosclerosis of larger arteries; Get hyaline arteriolosclerosis of small arteries (render the vessel wall weaker); Formation of micro-aneurysms (Charcot-Bouchard aneurysms) in chronic hypertension setting which can rupture.
Sites of haemorrhagic CVA with hypertension: Basal ganglia/thalamus; deeper part of brain (rather than cerebral hemispheres) as hypertension affects the deep penetrating arteries of the brain and the arteries that supply the basal ganglia and the white matter of the cerebral hemispheres.
What is the classification of ischaemic strokes?
Arteriothrombosis
Small vessel disease
Cardioembolism
others
Define arteriothrombosis
This is due to insitu thrombotic /atheroscleotic lesions in vertebrobasilar , cerebral and carotids- seen in large vessels
Aortic dissection can occur
Define small artery disease
Small vessel or lacunar strokes are associated with small focal areas of ischemia due to obstruction of single small vessels, typically in deep penetrating arteries, that generate a specific vascular pathology Perforating vessels –End arteries –No collateral –No pressure reduction system –Supply critical areas –Present brain stem –Design fault
Define cardioembolic
Cardiogenic emboli are a common source of recurrent stroke. They may account for up to 20% of acute strokes and have been reported to have the highest 1-month mortality
Sites of emboli Atrial myxoma endocarditis valvular heart disease patent foreamen ovale prosthetic valve mural thrombus left ventricle
What is a special type of small vessel disease?
lacunar infart- small but severe consequences
What is the spectrum of changes in small vessel disease a/w ischaemic strokes?
ischaemic white change
white per vascular changes
old micro haemorrhages
deep white infarcts
What is the cause of intracerebral haemorrhage?
•Hypertension
•Amyloid- most beta!4 derived
•Coagulation deficits
•Aneurysm (berry ; congenital) - AVM - Cavernoma (Raspberry shaped cluster of abnormal blood vessels) -Tumour
•Drugs-therapeutic and recreational eg cocaine/amphetamines which are sympathomimetics (causes increase in bp and pulse) Most patients with drug-related ICH have an associated vascular
lesion such as an aneurysm or an arteriovenous malformation
•Trauma
What is the pathogenesis of intracerebral haemorrhage
Formation of microaneurysm(Charcot Bouchard aneurysm) in parenchymal brain artery as a result of hypertension. Lenticulostriate vessels commonly involved, similar process occurs in thalamus, pons, white matter and cerebellum
Microaneurysm ruptures causing pressure on adjacent (satellite) vessels
Satellite vessels rupture
Amount of blood extravasated into brain tissue depends on tissue turgor as opposed to intravascular blood pressure
1) Expansion of haematoma
2) secondary brain injury - initiation of oedema(first 24-96 hrs) and brain injury
Types of intracranial haemorrhages and their causes?
subarachanoid haemorrhage- due to rupture of aneurysm
subdural/epidural haemorrhage more so a/w trauma
Pathology of intracranial haemorrhage
*hint- a/w causes
Hypertensive haemorrhages typically occur in basal ganglia, thalamus, pons and cerebellum
Eventually haemorrhages are converted to a cavity with a brown, discolored rim. On microscopic examination, early lesions consist of clotted blood surrounded by brain tissue showing anoxic neuronal and glial changes as well as edema. Eventually
the edema resolves, pigment- and lipid-laden macrophages
appear, and proliferation of reactive astrocytes becomes
visible at the periphery of the lesion
Cerebral amyloid angiopathy -The amyloid confers a rigid, pipelike appearance and stains with Congo red. Replacement of smooth muscle with amyloid weakens vessel walls and increases the risk of hemorrhages. Often occur in lobes of cerebral cortex (lobar haemorrhages)
Saccular/berry Aneurysm - beyond the neck of the aneurysm- only lined by thickened hyalinized intima . Adventia covering the sac continues with the parent artery. Rupture usually occurs at the APEX of sac, releasing blood into subarachanoid space
AVM/s - gross inspection - tangled network of wormlike vessels.Microscopic examination
shows enlarged blood vessels separated by gliotic tissue,
often with evidence of previous hemorrhage.
Cavernoma - loosely organized blood vessel channels w./o intervening nervous tissue. Occur in cerebellum, pons and subcortical area
Subarachanoid haemorrhage (SH) is a/w with..? and definition of SH
PCK disease
extravasation of blood in subarachanoid space(between pia mater and arachanoid membrane)
What causes subarachanoid haemorrhage ?
saccular /berry aneurysms
congenital defect
progressive enlargement in life
risk factors- smoking/hypertension
What is the outcome of subarachanoid haemorrhage?
Death
Coma or Alert
Survive- rebleed 4-8 days
What is the presenting complaint of a SH ?
Severely painful headache
How does one manage SH?
Check slide 50
Neuro exam performed
If neck stiffness CT scan performed and assess subarachanoid for blood (hyperdense on CT). Negative CT is followed by a lumbar puncture. however if +ve blood in subarachnoid or if xanthochromia on lumbar puncture – vessel imaging(angiography) performed to locate the cause. This is followed by interventional radiology and or surgery.
If -ve xanthochromia -Admit & observe
Repeat CT
Consider Angio
Or non-invasive
vessel imaging
Causes of increased ICP
Focal/space-occupying lesion = Tumour/haemorrhage/abscess
Diffuse = Inflammation (meningitis)/cerebral oedema/hydrocephalus
Features of increased ICP
Acute ↑ ICP: Headache/nausea & vomiting/dizziness/LOC/coma/brain herniations/death
What are the consequences of increased ICP?
herniation of brain tissue
- Cingulate gyrus herniated under the falx cerebri (subfalcine herniation) 2. Medial part of temporal lobe (uncinate process/uncal herniation) herniates under the tentorium (transtentorial herniation). This type will compress/stretch the third cranial nerve (oculomotor nerve) causing blurred vision/papilloedema (fixed & dilated pupil). 3. Cerebellar tonsils (tonsillar herniation) herniates under/into the foramen magnum- This results in compression of the medulla and it’s respiratory centre which will lead to respiratory arrest & death ( = coning).
•Outcome of ↑ ICP: Brain tissue ischemia & infarction due to reduced cerebral perfusion due to pressure of herniated brain tissue on arterial supply.
define decompressive hemicraniectomy
- Neurosurgical procedure in which part of the skull is removed to allow a swelling brain room to expand.
- Performed on victims of traumatic brain injury and stroke – controversial.
- “Last resort”, some evidence suggests that it does improve outcomes by lowering intracranial pressure (ICP), the pressure within the skull.
- Raised intracranial pressure is very often debilitating or fatal because it causes compression of the brain and restricts cerebral blood flow. The aim of decompressive craniectomy is to reduce this pressure.
- Used to manage major strokes -“malignant” oedema and intracranial hypertension.
- Early (within 48 hours) application of decompressive craniectomy after “malignant” stroke may result in improved survival and functional outcome in patients under the age of 55, compared to conservative management alone.
- Recommended especially for young patients in whom ICP is not controllable by other methods. Age of greater than 50 years is associated with a poorer outcome after the surgery.
Treatment for ischaemic stroke?
Early reperfusion therapy is the most effective therapy for acute ischaemic stroke.
Up to 4.5 hours IV thrombolysis (tpa treatment) , however the benefit declines substantially over time from symptom onset. Dissolves clot.
IV thrombolysis improves the outcome of one in three patients treated between 1 and 3 hours and 1 in 6 patients between hour 3 and hour 4.5 from symptom onset
Another treatment for acute stroke?
Endovascular thrombectomy is a safe, highly effective procedure that saves lives and dramatically reduces disability WHEN:
Patients are carefully selected by imaging to identify proximal occlusions, and exclude large core and exclude patients with absent collaterals
Treatment is extremely fast with target first slice
imaging to groin puncture < 60 min and
imaging to reperfusion < 90 min
Safe effective technology (retrievable stents) is used
What constitutes the stroke rehabilitation team?
Doctor Stroke nurse specalist nursing staff physiotherapist occupational therapist speech and language therapist dietician social worker pharmacist family carers
What are the difficulties experienced after stroke?
- communication- aphasia (inability to understand/produce speech), dysarthria(forming words),
- physical - swallowing difficulties, weakness, impaired balance, coordination and sensation, continence, vision and fatigue
- cognitive and perceptual- attention/concentration, memory, planning and problem solving, perceiving your environment, objects and people, reduced self awareness, apraxia(knowing what to do but unable to do it)
- behavioral and emotional
