stroke/tia - nebula.wsimg.com
TRANSCRIPT
Definitions
Anatomy Recap
Aetiology
Pathology
Syndromes
Brocas / Wernickes
Investigations
Management
Prevention & Prognosis
TIAs
The Plan
Transient Ischaemia Attack: Clinical syndrome. Neurological dysfunction. Resolves <24hours.
Disruption of blood supply.
Stroke: Clinical syndrome. Neurological Dysfunction. Resolves >24hours or
death. Disruption of blood supply. 85% infarction 15% haemorrhage
10% intracerebral – longstanding hypertension (lenticulostriate arteries) 5% subarachnoid
Complicated stroke: Stroke w/ maximal deficit <6 hours
Minor stroke: Stroke symptoms resolved w/o significant deficit <1 week
Key Definitions
Everyone grab a piece of paper
Arterial Anatomy Recap
Of Ischaemic Strokes:• 5-10% occur in the ACA• 65-75% occur in the MCA• 20-30% in VA/PCA
What do these regions supply?
ACA – medial aspect of cerebral hepsiphereMCA – lateral aspect of cerebral hemisphereVertebral Arteries supply the vetrolateral aspect of the medulla forming the Basillar Artery which supply the cerebellum and brainstem. PCA – occipital lobe of cerebral hemisphere
Risk Factors
↑BP Smoking
Lifestyle
Heart Disease
•Valvular
•Ischaemic
Diabetes
Prev Hx. TIA/Stroke
Carotid BruitOCP↑Lipids
Alcohol
↑Clotting
•↓AT3 or ↑Fibrin
↑Homocysteine
Syphilis
FH CVA <65
AetiologyNB - These are really easy marks for Intermediates. Don’t let Norman down.
Vessel Occlusion
Arterial Atherosclerosis
Cardioembolism
Small-vessel Occlusion (Lacunar Stroke)
Non-AtheromatousDisease
Ischaemic Stroke
Thrombus forms on a pre-
existing plaque or within the ICA or other intracranial vessels
Cardiac thrombus forms due to
AF or recent MI and travels to the cerebral circulation
Thrombus forms in small
penetrating intracerebral arteries that are damaged by longstanding hypertension
Thrombus forms in arteries
damaged by valve defects, vasculitis or arterial dissection
1. Origin of Common Carotid artery
2. Origin of Internal Carotid artery
3. Origin of Vertebral artery
4. Subclavian artery
Stenoses & Plaque Position
Occlusion of the artery
Hypoxic neurons
Disintegration of brain tissue
MØs arrive to phagocytose
debris
Cyst formation
Colliquetive (Liquefactive) Necrosis
Immediate 6 hours 24 hours 3-5 days Days - Years
TACS: Total Anterior Circulation Syndrome
ICA / Large Scale MCA
HemiparesisHomonymous HemianopiaHigher dysfunction
Signs & Symptoms
PACS: Partial Anterior Circulation Syndrome
ACA MCA
Hemiparesis Leg > ArmMutismIncontinenceDisinhibition
Hemiparesis Arm > LegSensory DeficitHemianopiaHigher Dysfunction
2/3 Signs = PACS
LACS: Lacunar Anterior Circulation Syndrome
Occlusion to deep arteries supplying internal capsule
Pure MotorPure SensoryPure Sensorimotor
POCS: Posterior Circulation Syndrome
PCA & PICA
PCA = CN Palsies + VisualPICA = DANISH-PR
Do not forget your anatomy!
Broca’s
Wernicke’s
Broca’s vs Wernicke’s
Three main aims:
(1) confirm the diagnosis
(2) distinguish ischaemia from haemorrhage
(3) identify underlying cause of stroke e.g. AF or atherosclerosis etc.
Blood Tests – FBCs, Renal Function, Lipids, Glucose etc.
ECG – looking for arrhythmias or recent ischaemias
Cardiac Doppler USS – look for Carotid artery stenosis
CT Brain – (Confirm & Distinguish) – URGENT IS PATIENT IS A CANDIDATE FOR THROMBOLYSIS
MRI – occasionally used in diagnostic difficulty – more sensitive than CT for ischaemic strokes but slower and less widely available
Investigations
Differences Between Scans:
1. Resuscitate! ABCDE + OXYGEN
2. Glucose & BP
3. CT/MRI• Urgent: high risk of haemorrhage, thrombolysis is considered or unusual
presentation
• Non-urgent (<24hours)
• Diffusion weighted MRI is most sensitive for an acute infarct but CT will rule out haemorrhage
4. Thrombolysis - Consider if 18-80yrs & Sx onset <4.5hours
5. Assess Swallowing (NBM + Keep Hydrated)
6. Keep Relatives and/or Patient informed
7. Antiplatelets: Aspirin 300mg ONCE HAEMORRHAGE EXCLUDED
8. Admission to Stroke Unit or Haemorrhage = Neurosurgeons
Acute Management
Please note, this is a boring slide, full of boring (but necessary) but still boring information.
Primary Prevention (before a stroke) Control risk factors, e.g. DM, BP, Lipids etc.
Folate supplements etc.
Secondary Prevention (preventing further strokes) Antiplatelet agents after stroke (C/I’d Haemorrhage)
If embolic or AF= Warfarin (INR aim 2-3)
Treat other causes e.g. Carotid Artery Stenosis or Valve replacements etc.
Prognosis Overall 60,000/yr
Survivors require care! BIOPSYCHOSOCIAL!
Rehabilitation
Prevention & Prognosis
Consciousness preserved
Hemiparesis & aphasia commonest
Clinical evidence of embolus
Carotid arterial bruit, AF, difference between L & R brachial BP etc.
Special Syndromes:
Amaurosis Fugax – indicates ICA stenosis
Sudden transient loss of vision in one eye (emboli retinal arteries)
Benign in migraine
Transient global amnesia
Episodes of confusion/amnesia last for several hours
Presumed posterior circulation ischaemia
Prognosis: after 5 years 30% will stroke (1/3 after Y1) and 15% will MI.
Anterior Circulation strokes are often more serious
TIAs
Cheers!