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- 1. Stroke in Adults <45 Years of Age A brief summary for Translators in the medical field Lifelong Learning Provided by Medical Translator
- 2. Stroke • 3rd most common cause of mortality in UK • Leading cause of adult disability • Incidence increases with age • Also occurs in young adults – Up to 12% of first strokes occur in patients <45 years of age
- 3. “Young stroke” • Under age of 45 • Reported incidence variable – Annual incidence of 10 per 100000 in UK • 50% are ischaemic (compared with 85% in older patients)
- 4. Causes of ischaemic stroke • Older adults – Atherosclerosis – Small vessel disease – Cardioembolism – Risk factors: Hypertension, smoking, cholesterol, atrial fibrillation, diabetes • Young adults – Atherosclerosis and small vessel disease less common • 2% 15-30 year olds; 30-35% 30-45 year olds – Causes of stroke more diverse
- 6. Carotid and Vertebral Artery Dissection • 2% of all ischaemic strokes • BUT – up to 10% of young adult stroke <45 yrs – up to 20-25% < 30 yrs – (compared to ~ 2.5% in older people)
- 7. What is arterial dissection? • Tear in the intima or media • Bleeding within the arterial wall • Bleeding tracks/dissects ciurcumferentially and longitudinally • Ischaemic stroke due to – Embolisation of thrombus formed at the site of the tear into an intracranial artery – Occlusion of the dissected artery
- 8. What causes arterial dissection? Spontaneous • Genetic connective tissues disorders (1-5%) – Ehlers-Danlos, Marfan’s, osteogenesis imperfecta, polycystic kidney disease, psuedoxanthoma elasticum • Fibromuscular dysplasia • Cystic medial necrosis • Possibly atheromatous risk factors (?) -BP, DM, Smoking, cholesterol Traumatic • Sports • RTA • Whiplash injury • Neck manipulation chiropractor • Minor precipitating events - painting ceiling, reversing car, yoga, coughing, vomiting
- 9. Clinical features • Carotid artery dissection – Headache/neck pain – Horner’s syndrome – TIA and stroke in carotid territory – Cranial nerve palsies • Vertebral artery dissection – Neck pain, pain in occipital region, ears – TIA and stroke in vertebrobasilar territory Symptoms usually within hours/ days of dissection but there may be delay of weeks or even months
- 10. When should the diagnosis be suspected? • Clinical features as described on previous slide – Head or neck pain in a (young?) patient with neurological deficit – High index of suspicion even in the absence of obvious trauma
- 11. Treatment • No consensus: variation in treatment regimes used • Current treatment is with warfarin (INR 2-3 for 3-6 mths) or antiplatelets • CADISS (Cervical Artery Dissection in Stroke Study) – antiplatelets vs warfarin
- 13. Cardioembolism • 20-30% of young stroke patients • Most common cardiac lesions – Prosthetic heart valves – Infective endocarditis – Dilated cardiomyopathy – Atrial septal aneurysm (ASA) – Patent foramen ovale (PFO) • Diagnosed on transthoracic echo or transoesophageal echo
- 14. Patent foramen ovale (PFO) •
- 15. How might PFO cause stroke?
- 16. Atrial septal aneurysm (ASA) • Bulging of the inter- atrial septum into the right or left atrium or both • Can be present in healthy people • Associated with increased risk of stroke especially with a co- existing PFO
- 17. PFO and ASA • Uncertain importance as cause of stroke • PFO prevalence higher in young stroke pts compared with controls • However other studies suggest risk of recurrent stroke in pts is low • Management unclear – Percutaneous closure vs anticoagulation vs antiplatelets
- 19. Thrombophilia in stroke • Rare, usually familial conditions in which spontaneous and recurrent thromboses occur – usually venous • Protein C and S deficiency, activated protein C resistance • Lupus anticoagulant and anticardiolipin antibodies • Weak evidence in sporadic arterial stroke • Small studies in young stroke have suggested an association
- 22. Cerebral venous thrombosis • Headache • Raised intracranial pressure with papilloedema • Focal neurological deficit • Seizures • Cranial nerve palsies Especially in a young patient who is or has recently been pregnant, has a past history of, or risk factors for venous thrombosis e.g. thrombophilia, oral contraceptive pill
- 23. Treatment • Limited evidence from randomised trials • Usually treated with anticoagulation (heparin followed by warfarin), even in the presence of haemorrhage • Prognosis often good with aggressive treatment – International Study on Cerebral Vein and Dural Sinus Thrombosis – 624 pts: • 79% complete recovery • 13.4% dead or dependent
- 24. Day 2: Post op scan Day 8: 5 days after starting heparin
- 25. Differential diagnosis of ischaemic stroke in young adults • Arterial dissection • Haematological – thrombophilia, polycythaemia, thrombocythaemia, antiphospholipid antibody, thrombotic thrombcytopaenic purpura, cancer • Rheumatic and inflammatory – SLE, rhematoid arthritis, sarcoid, Sjogren’s, PAN, primary CNS angiitis • Cardiac – PFO, myocardiomyopathy, arrhythmias, endocarditis, atrial myxoma, prosthetic heart valves, • Female hormone related – oral contraceptive pill, pregnancy, dural sinus occlusion • Premature atherosclerosis – hypertension, diabetes, smoking, homocysteinuria, hyperlipidaemia • Others: moyamoya, Behcets syndrome, Takayasu’s syndrome, Sneddon’s syndrome, fibromuscular dysplasia, Fabry’s disease • Drugs – cocaine, heroin, amphetamines • Genetic - CADASIL • Venous stroke
- 26. Prognosis in young stroke • Initial mortality: 2-7% • 1-3% risk of recurrent stroke per year • No underlying cause found in up to 40% • Low risk of recurrence if no underlying cause found: 0.5-1% per year • Greater potential for recovery compared with older adults
- 27. Malignant MCA infarction in young stroke Decompressive hemicraniectomy
- 28. Malignant MCA infarction • Gaze deviation, hemiplegia, visual field defect, aphasia or neglect • Early/rapid neurological deterioration • Headache • Vomiting • Poor prognosis – 80% mortality – Transtentorial herniation – Brainstem compression
- 29. Decompressive hemicraniectomy • Removal of a large bone flap on the side of the stroke and dura opened to relieve pressure • Life saving operation • Early identification of at risk patients; operated on by a maximum of 48 hours • Results less good with older patients – Current NICE guidelines <60 years
- 30. Day 4: post hemicraniectomy
- 31. Summary • Large differential diagnosis in ischaemic stroke in young adults • Arterial dissection and cardioembolism are important causes • Arterial and venous strokes
Editor's Notes
- Hemicraniectomy PFO, cardiac causes Thrombophilia prengancy 50/50 young stroke, 85/15 old stroke
- Doubling of stroke risk for every decade above 55
- How young is young? Different case series have used different definitions. Less than 30? Less than 50? Most studies and reports of young stroke refer to adults under the age of 45 Reported incidence varies according to definition of “ young”, study design and population structure Often defined as those under the age of 45 Other countries in Western Europe have reported incidence rates of up to 3 times higher
- The range of causes is similar compared to older people, but the probabilities differ
- Dissection arises from intimal tear Tear allows blood to enter the wall of the artery and form an intramural haematoma
- Can be spontaneous – Those with spontaneous dissection are thought to have an underlying structual defect of the arterial wall for example, due to a connnective tissue disorder Trauma is the other major cause – other cases – skiing, RTA, Sometimes the trauma can be minor – e.g. coughing Often no cause identified Other precipating events associated with hyperextension or rotation of the neck such as yoga, painting a ceiling, coughing, vomiting - ? Recall bias Only strong association was with genetic factors 1-5% have a connective tissue disorder
- Local features such has headache or neck pain on the same side as the dissection Carotid territory – hemiparesis, dysphasia, amaurosis fugax Vertebrobasilar territory – posterior circulation I.e. cerebellum, occipital lobes Head or neck pain can be mistaken for musculoskeletal pain Stroke/Tia usually occurs within a month of the dissection, the majority within a week
- CADISS – multicentre, radomised study comparing antiplatelets with warfarin in extracranial carotid and vertebral artery dissection 80 patients randomised so far as of August 2010
- Cardiac origin embolism is a very impt cause of ischaemic stroke in young adults Cardiac source of embolic found in 20-30% PFO/ASD – unclear/uncertain association with stroke Found in 20-30% of healthy people
- PFO is a communication between the right and the left atrium of the heart Foramen ovale – in a fetus is a tunnel/flap in the wall dividing the 2 atria of the heart which allows blood to flow from the right side of the heart, to the left bypassing the lungs in the fetus as oxgenated blood derived from placenta The foramen ovale usually closes shortly after birth However in up to 20% of people, they have a patent foramen ovale I.e. doesn’t close
- Paradoxical embolus from venous thrombosis (most likely) Or due to associated cardiac arrrthmia However investigations rarely show a co-exisitng DVT Pressure in left heart greater than in right side of heart – would require a right to left shunt in order for the thrombus to cross over the PFO into the arterial circulation
- The presence of PFO and ASA is increased in younger adults with stroke, especially in those with otherwise unexplained stroke Lechat – 40% of young stroke pts had PFO compared with 10% of controls of the same age without stroke Optimal management remains uncertain Some recommend closure, others suggest anticoagulation with warfarin or treatment with antiplatelets
- Increased tendency to clotting/thrombosis in association with laboratory evidence of an abnormality in the clotting pathway Causes of thrombophilia include deficiencies of protein C, proten S and antithrombin III, activated protein C resistance, lupus anticoagulant and antiphospholipid syndrome Lupus anticoagulant and anticardiolipin antibodies – most often in assocation with SLE but can also occur alone Larger studies in sporadic stroke – no association Smaller studies have suggested an association with young stroke Often tested for in young stroke Treatment with anticoagulation if confirmed
- Most brain ischaemia is caused by thromboemboism and atherosclerosis affecting the arterial system However infarcts of the brain and haemorrhage can also be caused by thrombosis of the venous system in the brain which consists of the dural sinuses, cerebral and cerebellar veins.
- Venous sinuses drain blood from the brain and the bones of the skull Eventualy drain into jugular vein into superior vena cava
- A number of clinical features that can come on abruptly or subacutely Headache, focal neurological deficits, seizures, impairment of consiousness
- Now generally accepted that treatment is with anticoagulation even with haemorrhagic transformation. In contrast to arterial infarcts with haemorrhagic transformation when anticoagulation if indicated is delayed by up to 2 weeks or more Small studies have shown that anticoagulated pts do better; no significant worsening of the haemorrhage In contrast to arterial strokes, patients with venous infarcts can often make surprising recoveries even with widespread haemorrhagic infarcts
- No underlying thrombophilia found on blood tests Started on heparin 2 days post hemicraniectomy then warfarin Extubated on a few days later Dysphasic, right sided weakness
- Stroke in younger people can be a presenting feature of a range of local and sytemic illnesses
- Prognosis depends on the underlying cause and extent of neurological damange Greater collateral reserve in the young adult brain may limit the initial size of the stroke Greater potential for recovery compared with the elderly brain With the majority of strokes occuring in those over the age of 65, unsurprising that many community services concentrate on the older stroke survivor
- Large Mca infarction = devastating stroke Brain oedema with swelling of the infarcted hemisphere causing midline shift and brain hernation is an important complication in large MCA territory strokes Particularly likely to occur in young patients with large Mca infarcts
- Occlusion of one of the large arteries such as the Ica or proximal part of the MCa Rapid neurological deterioation following due to the space occupying effects of cerebral odema after large MCA infarct Even with the best medical management – mortality of 80%
- Allow brain to herniate through the bone flap rather than downwards causing brainstem compression Life saving operation rather than disaiblity reducing Patients with early signs of large MCA infarcts should be identified early NICE guidelines state age under 60
- Metanalysis of data from 129 patients from 3 small RCTs show a reudction in mortality from 71% to 22% Cerebral venous thrombosis patient also had a hemicraniectomy - survived