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].

Contents

Introduction

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.

Details

There are two main types which can be differentiated by CT scanning.

  • 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].

Classification

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:

LogoKeyPointsBox.png

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

Prevention

Surgery

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

Investigations

Blood tests

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

ECG

Radiology

See main article Imaging in stroke

  • CT scan
  • MRI scan

Additional Investigations

Treatment

Thrombolysis

Prerequisites

  • Less than 3 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


In perspective

At least one health authority in England has 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. Some of these people may have had very mild symptoms that didn't warrant thrombolysis.

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 may be extended, to perhaps 4.5 hours, which increases the chance of patients attending within the specified time.

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, the results remain to be seen.

Prevention

Antiplatelets

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[4].
  • 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[5].
  • 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[6]. It is more costly.
  • The combination of aspirin and clopidrogel is likely to be ineffective or harmful in stroke indications due to (intracranial) haemorrhage[7] .

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.

Anticoagulation

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)[8].
  • Dabigatran etexilate, rivaroxaban and apixaban are all clinically superior to warfarin in the populations studied, predominantly because they reduce the rate of haemorrhagic stroke[9]. 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

Surgery

Selected neurosurgical intervention is likely to be beneficial in posterior fossa intracranial haemorrhage. Surgical intervention with intracerebral haemorrhage is unlikely to be benefical[10]

External links

References

  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. 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.)
  5. 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.)
  6. 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.)
  7. 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.)
  8. 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.)
  9. 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.)
  10. 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.)
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