Stroke disease

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Stroke disease - a neurological deficit of presumed vascular origin lasting more than 24 hrs. In practice, stroke disease is a manifestation of many pathological processes giving a similar clinical picture[1].



Stroke is a major cause of death (about 9% worldwide) and morbidity. Efforts should be focused on stroke prevention through blood pressure control, smoking cessation, reduction of cholesterol, anti-coagulation for atrial fibrillation, anti-platelet agents and surgery for selected patients. To date attributable factors for stroke disease explain only 60% of presentations, a much lower explanation rate than we have for ischaemic heart disease.


There are two main types which can be differentiated by CT scanning. Increasingly urgent CT cranial angiography is being offered to subgroups with ischaemic stroke as part of acute initial treatment determining work up.

  • Infarction 80% (a strong argument has been made that the new gold standard for this is the characteristic changes on diffusion weighted MRI of cerebral ischaemia[2])
  • Haemorrhage 20%

Clinically can present from collapse to clinically silent (a fair proportion of strokes occur when patient is asleep).

  • Hemiparesis
  • Dysphasia
  • Dysarthria
  • Ataxia
  • Nausea
  • Vomiting

Infarction vs Haemorrhage

  • Headache equally likely with both
  • Need CT scan to differentiate
  • Coma and prognosis tend to be worse with haemorrhage
  • Haemorrhage is more common in some Asian populations, in Japan, the ratios are ischaemic stroke 61 %, ICH 25 % and SAH 11 %[3].


For cerebral infarction, the Bamford Classification of infarcts is used, and can be useful for communication of stroke type and in terms of prognosis as below:


Clinical presentation TACS/PACS/TIA in anterior circulation

  • Distal artery – lower limb weakness
  • Proximal artery– more severe hemiplegia & frontal lobe signs
    • Middle cerebral artery
      • Main stem
      • Deep perforators
        • Cortical sparing
        • Contralateral hemimotor loss
      • Superior trunk
        • Contralateral motor and sensory with leg sparring
        • Temporal lobe unaffected
        • Inferior quadrantic hemianopia
        • Visuospatial disorder (non dominant hemisphere)
        • Wernickes type dysphasia (dominant hemisphere)

Total anterior circulation stroke (TACS)

A large stroke anterior/middle cerebral artery

  • New cortical dysfunction eg dysphasia and
  • New sensory/motor deficit 2/3 areas face/hand/leg and
  • Homonymous hemianopia

Could be associated with:

  • Amarosis fugax (blindness in one eye) if embolic/thrombotic

Partial anterior circulation stroke (PACS)

A smaller cortical stroke with either 2 out of 3 components of TACS or

  • New higher cerebral dysfunction or
  • Motor and sensory disturbance less than TACS
LogoKeyPointsBox.pngClinical presentation of POCS/TIA in posterior circulation

Swelling of brainstem can lead to obstructed exit of CSF from IVth ventricle and thus hydrocephalus. Monitor and CT scan/refer if possible

  • Subclavian artery
    • Rarely if severely stenosed or blocked blood may reverse flow down vertebral artery to supply the arm - the subclavian steal syndrome. Seen when arm is exercised. Can be diagnosed radiologically.

Posterior circulation stroke (POCS)

  • Ipsilateral cranial nerve palsies with contralateral motor/sensory deficit or
  • Bilateral motor/sensory deficit
  • Disorder of conjugate eye movements
  • Cerebellar dysfunction without ipsilateral long tract signs
  • Isolated homonymous field defect

Lacunar stroke (LACS)

Small vessel subcortical stroke

  • Pure motor
  • Pure Sensory
  • Sensorimotor
  • Ataxic hemiparsesis

Transient ischaemic attack

- a neurological deficit of presumed vascular origin lasting less than 24 hrs

  • Usually embolic in nature
  • Classically last 20 minutes
  • Is a major risk factor for impending stroke

Pathophysiology of stroke

  • Ischaemic core of dead cells surrounded by penumbra of potentially viable cells.
  • Ischaemia leads to loss of cell membrane function. Glutamate release leads to influx of calcium ions.
  • Local loss of cerebral autoregulation with increased flow around the peripheries of the infarct.
  • Cerebral oedema develops and is manifest by loss of sulci on CT and decreasing GCS. Cheyne stokes respirations. Brainstem herniation and raised ICP.

Global hypoperfusion

with infarction of watershed areas where circulations overlap. Seen in shock/hypotensive states

Vessel occlusion

  • Thrombosis-in-situ
  • Embolism

Thrombus formation in situ

  • Plaque rupture and thrombosis
  • Vasculitis
  • Cervical artery dissection

Embolism from the heart

Embolism from the carotid

  • Ipsilateral carotid - Carotid plaque

Other classifications

Risk Factors for stroke

Population attributable risks for either acute myocardial infarction or stroke internationally



Carotid endarterectomy for those with Carotid territory TIA/Stroke and ipsilateral Carotid stenosis > 70%


Blood tests

  • FBC ? polycythaemia, platelets
  • ESR ? temporal arteritis / vasculitis
  • U&E
  • Glucose and HbA1C including in non diabetics
  • Cholesterol
  • Prothrombin time
  • Partial Thromboplastin time



See main article Imaging in stroke

  • CT scan
  • MRI scan

Additional Investigations



There is good evidence for best supportive care



  • Less than 6 hrs from onset (there is some evidence around the margins for benefit)
  • Stable neurology
  • CT scan excludes bleed
  • Giving t-PA reduces disability but at an increase in bleeds

Relative contraindications

  • Minor neurological deficit
  • NIHSS > 22 National Institute of Health stroke scale
  • Patient comatose
  • Deficit rapidly improving
  • BP > 185/110
  • Seizure at stroke onset
  • Abnormal CT
  • Prolonged PT/PTT
  • Thrombocytopenia
  • Recent surgery/MI/stroke
  • Haemorrhage

Inteventional thrombectomy

This has a place in proven proximal vessel occlusion after alteplase[4]. As of 2014 this is likely to lead to further consolidation of acute stroke treatment centres as happened when acutePCI was developed in myocardial infarction.

Clot busting in perspective

At least one health authority in England had suggested that most strokes can be cured by thrombolysis. This gives a very unrealistic picture to patients.

In all trials 3% to 15% of patients with stroke are eligible for or get thrombolysis. The real life benefit for those presenting early with appropriate acute investigation with first ischaemic stroke are now proven.

A reasonable statement from current evidence is NNT = 8 NNH = 16

The treatment is logical, but is at the stage of enthusiasm - much of the Stroke literature is very positive.

The time-limit on thrombolysis and age for risk benefit have been better defined.

The results of treatment are variable.

An effort to educate or persuade the population to treat stroke as an urgent event needing direct attendance to hospital has been made in England, with some success.


Selected neurosurgical intervention is likely to be beneficial in posterior fossa intracranial haemorrhage. Surgical intervention with intracerebral haemorrhage is unlikely to be benefical[5]

Blood pressure control

This has a very limited role in treating acute stroke. The ENOS trial showed that raised BP (systolic 140-220mmHg) within 48 hours in patients with either haemorrhagic or non-haemorrhagic stroke was not worth treating with either pre-existing oral antihypertensive therapy or GTN infusion in the first 7 days after a stroke[6]. It will still be common to treat BPs above 220mmHg in the first 48 hours with drugs such as labetolol, and indeed the widespread existence of protocols based on evidence before 2014 is problematical.



In ischaemic stroke:

  • Aspirin usually 300 mg/day and then reduced to 75 mg/d is the most resource effective beneficial treatment and despite trends is not statistically inferior to the alternative proven antiplatelet strategies studied in randomised controlled trials with both arms having active therapy published up to 2008[7].
  • Aspirin (50mg) and dipyridamole (200mg MR bd) is slightly superior to aspirin alone but has tendency to induce headache. It appears advantageous in heart failure[8].
  • Clopidogrel may be given in those unable to take aspirin and is as effective as aspirin and dipyridamole and is better tolerated than the combination[9]. It is more costly.
  • The combination of aspirin and clopidrogel is likely to be ineffective or harmful in stroke indications due to (intracranial) haemorrhage[10] .

Blood pressure control

  • Even a minimal reduction (5-6 mmHg) in diastolic blood pressure has been shown in several trials to result in a significant (41%) reduction in subsequent stroke rate
  • However in the acute stroke with loss of cerebral autoregulation BP control is kept to a minimum to maintain perfusion pressures especially in the setting of oedema and raised ICP.
  • It is traditional not to lower the BP aggressively in the first 2 weeks after stroke because of concerns that a high BP may be a beneficial adaptive response for perfusion of the ischaemic penumbra, and also not to lower the BP aggressively before a critical carotid stenosis has been excluded. Clinical evidence exists that hpertensive control early after stroke is of no benefit (see above)


Event comparison of the anticoagulants dabigatran etexilate, rivaroxaban and apixaban in the indication of non-rheumatic atrial fibrillation against warfarin
  • Warfarin for AF significant reduces stroke rate in primary prevention and secondary prevention after an ischaemic cerebrovascular event. Absolute benefit remains even though previous ischaemic stroke is known to increase bleeding risk by about 2.5 times (95% confidence interval: 1.3 to 4.8 times)[11].
  • Dabigatran etexilate, rivaroxaban and apixaban are all clinically superior to warfarin in the populations studied, predominantly because they reduce the rate of haemorrhagic stroke[12]. However, if available, their use is likely to be dictated by both resource effectiveness issues and individual patient, drug and service characteristics. As can be seen from the figure some agents increase the rate of gastro-intestinal haemorrhage or myocardial infarction.

Stroke Units

Organised care by experienced healthcare workers in stroke medicine works

External links


  1. Donnan GA, Fisher M, Macleod M, Davis SM. Stroke. Lancet. 2008 May 10; 371(9624):1612-23.(Link to article – subscription may be required.)
  2. Oppenheim C, Lamy C, Touzé E, Calvet D, Hamon M, Mas JL, Méder JF. Do transient ischemic attacks with diffusion-weighted imaging abnormalities correspond to brain infarctions? AJNR. American journal of neuroradiology. 2006 Sep; 27(8):1782-7.
  3. Yamada Y, Metoki N, Yoshida H, Satoh K, Kato K, Hibino T, Yokoi K, Watanabe S, Ichihara S, Aoyagi Y, Yasunaga A, Park H, Tanaka M, Nozawa Y. Genetic factors for ischemic and hemorrhagic stroke in Japanese individuals. Stroke. 2008 Aug; 39(8):2211-8. Epub 2008 Jun 19.(Link to article)
  4. Berkhemer OA, Fransen PS, Beumer D, van den Berg LA, Lingsma HF, Yoo AJ, Schonewille WJ, Vos JA, Nederkoorn PJ, Wermer MJ, van Walderveen MA, Staals J, Hofmeijer J, van Oostayen JA, Lycklama À Nijeholt GJ, Boiten J, Brouwer PA, Emmer BJ, de Bruijn SF, van Dijk LC, Kappelle LJ, Lo RH, van Dijk EJ, de Vries J, de Kort PL, van Rooij WJ, van den Berg JS, van Hasselt BA, Aerden LA, Dallinga RJ, Visser MC, Bot JC, Vroomen PC, Eshghi O, Schreuder TH, Heijboer RJ, Keizer K, Tielbeek AV, den Hertog HM, Gerrits DG, van den Berg-Vos RM, Karas GB, Steyerberg EW, Flach HZ, Marquering HA, Sprengers ME, Jenniskens SF, Beenen LF, van den Berg R, Koudstaal PJ, van Zwam WH, Roos YB, van der Lugt A, van Oostenbrugge RJ, Majoie CB, Dippel DW. A Randomized Trial of Intraarterial Treatment for Acute Ischemic Stroke. The New England journal of medicine. 2015 Jan; 372(1):11-20.(Link to article – subscription may be required.)
  5. Mendelow AD, Gregson BA, Fernandes HM, Murray GD, Teasdale GM, Hope DT, Karimi A, Shaw MD, Barer DH. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. 2005 Jan 29-Feb 4; 365(9457):387-97.(Link to article – subscription may be required.)
  6. Efficacy of nitric oxide, with or without continuing antihypertensive treatment, for management of high blood pressure in acute stroke (ENOS): a partial-factorial randomised controlled trial. Lancet. 2014 Oct 21.(Epub ahead of print) (Link to article – subscription may be required.)
  7. Kent DM, Thaler DE. Stroke Prevention -- Insights from Incoherence. The New England journal of medicine. 2008 Aug 27.(Epub ahead of print) (Link to article – subscription may be required.)
  8. Sacco RL, Diener HC, Yusuf S, Cotton D, Ounpuu S, Lawton WA, Palesch Y, Martin RH, Albers GW, Bath P, Bornstein N, Chan BP, Chen ST, Cunha L, Dahlöf B, De Keyser J, Donnan GA, Estol C, Gorelick P, Gu V, Hermansson K, Hilbrich L, Kaste M, Lu C, Machnig T, Pais P, Roberts R, Skvortsova V, Teal P, Toni D, Vandermaelen C, Voigt T, Weber M, Yoon BW. Aspirin and Extended-Release Dipyridamole versus Clopidogrel for Recurrent Stroke. The New England journal of medicine. 2008 Aug 27.(Epub ahead of print) (Link to article – subscription may be required.)
  9. Sacco RL, Diener HC, Yusuf S, Cotton D, Ounpuu S, Lawton WA, Palesch Y, Martin RH, Albers GW, Bath P, Bornstein N, Chan BP, Chen ST, Cunha L, Dahlöf B, De Keyser J, Donnan GA, Estol C, Gorelick P, Gu V, Hermansson K, Hilbrich L, Kaste M, Lu C, Machnig T, Pais P, Roberts R, Skvortsova V, Teal P, Toni D, Vandermaelen C, Voigt T, Weber M, Yoon BW. Aspirin and Extended-Release Dipyridamole versus Clopidogrel for Recurrent Stroke. The New England journal of medicine. 2008 Aug 27.(Epub ahead of print) (Link to article – subscription may be required.)
  10. Bhatt DL, Fox KA, Hacke W, Berger PB, Black HR, Boden WE, Cacoub P, Cohen EA, Creager MA, Easton JD, Flather MD, Haffner SM, Hamm CW, Hankey GJ, Johnston SC, Mak KH, Mas JL, Montalescot G, Pearson TA, Steg PG, Steinhubl SR, Weber MA, Brennan DM, Fabry-Ribaudo L, Booth J, Topol EJ. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. The New England journal of medicine. 2006 Apr 20; 354(16):1706-17.(Link to article – subscription may be required.)
  11. Poli D, Antonucci E, Grifoni E, Abbate R, Gensini GF, Prisco D. Bleeding risk during oral anticoagulation in atrial fibrillation patients older than 80 years. Journal of the American College of Cardiology. 2009 Sep 8; 54(11):999-1002.(Link to article – subscription may be required.)
  12. Mega JL. A new era for anticoagulation in atrial fibrillation. The New England journal of medicine. 2011 Sep 15; 365(11):1052-4.(Link to article – subscription may be required.)
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