Stroke

last authored: April 2010, David LaPierre
last reviewed:

 

 

Introduction

Stroke is a rapidly developing group of clinical signs of focal or gobal disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin. With over 5.5 million deaths yearly, stroke is the second-most common cause of death worldwide, accounting for 9% of mortality (World Health Organization, 2000; Murray and Lopez, 1997). It has a staggering impact on society, and as 40% of stroke survivors are left with some degree of functional impairment, stroke is projected to be the fourth-most important cause of disability in 2030 (Lopez et al, 2006). Perhaps 500 people per 100,000 are living with the effects of stroke, and as care continues to improve survival, demands on health care and social-care systems will likely also continue to increase (Donnan et al, 2008).

 

In Canada, there are 50,000 new patients per year - one every ten minutes. This results in 15,000 stroke deaths/year, and has given Canada 350,000 stroke survivors, at a cost of over $3 billion (Lindsay et al, 2005). Return to work usually not possible; 50% of survivors are dependent and 20% require institutionalization.

75% ofter the age of 65.

 

For every symptomatic stroke, there are 9 'silent' strokes leaving people with some level of cognitive impairment. There are also transient ischemic attacks, which are diagnosed if the symptoms last less than 24 hours, though usually they last 2-15 minutes. A fuller definition: a brief episode of neuro dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without any evidence of acute infarction.

return to top

 

 

return to top

 

 

The Case of...

a simple case introducing clincial presentation and calling for a differential diagnosis. To get students thinking.

return to top

 

 

 

Causes and Risk Factors

There are strong differences in age-standardized death rates of stroke around the world - for Russia, death rates for people age 30-69 is 180 per 100,000, while in Canada, the same meausre is 15 per 100,000 (Strong, Mathers, and Bonita, 2007). These differences suggest not only a difference in management, but also prevalence of risk factors and genetic causes. The continued reduction in death rates in the developed world is most plausibly related to increased living standards, reduced cigarette smoking, and improved blood pressure control, suggesting the importance of the same for people around the world (Donnan et al, 2008).

 

From 15-30% of strokes preceded by TIA, especially those positive on diffusion-weighted MRI scan. The time window for optimal intervention to prevent stroke after TIA is very short.

  • ischemic stroke
  • hemorrhagic
  • stroke risk factors

Ischemic Stroke (80%)

Thrombotic/intrinsic vessel disease originates in the brain's vasculature. Causes include:

  • atherosclerosis
  • small vessel disease
  • vasculitis
  • vasospasm
  • arterial dissection
  • compression
  • fibromuscular
  • hypercoagulable state (oral contracepives, HRT)
  • cerebral venous thrombosis

Embolic disease originates at remote sites. Causes include:

  • cardiac wall thrombi (common): myocardial infarct, valvular disease, and atrial fibrillation important predisposing factors
  • arterial thromboemboli, particulary from atherosclerotic plaques within the carotid arteries
  • septic material
  • air
  • fat
  • tumour
  • paradoxical

 

Lacunar strokes (LACS) are usually due to intracerebral small vessel disease. They are clinically recognizable, with pure motor hemiplegia, pure sensory stroke, or ataxic hemiparesis. They also have the best functional outcomes of all stroke types.

return to top

 

 

 

Pathophysiology

As described, stroke can occur following two separate processes: ischemia or hemorrhage.

  • Ischemic Stroke
  • Hemorrhagic Stroke

Global cerebral ischemia occurs when there is a generalized drop in perfusion such as can occur in cardiac arrest, shock, or severe hypotension. Focal cerebral ischemia follows reduction in blood flow to a given area due to large vessel disease, such as thrombosis or embolus, or due to small vessel disease such as vasculitis.

 

CNS cells show a hierarchy of susceptibility to ischemia, with neurons being the most sensitive. Glial cells are also vulnerable. Differences in blood flow and metabolic needs results in selective vulnerability of different populations following global events.

 

Thrombotic Stroke

The distinction between TIAs and stroke is arbitrary, as permanent tissue damage can be shown on MRI in at least 25% of patients with TIAs (Kidwell et al, 1999).

Large vessel stroke is most commonly due to atherothrombosis. These can be found at the bifurcation or siphon portion of the common carotid artery, middle cerebral artery stem, intracranial vertebral arteries, or origin of vertebral arteries.

Small vessel stroke, aka lacunar stroke, is most commonly due to lipohyalinotic occlusion following hypertension or occasionally atheroma. They occur in the penetrating branches of the anterior, middle, or posterior cerebral/basilar arteries.

 

Cardioaortic Embolic Stroke

Cardiac sources include atrial fibrillation, LV/LA thrombus, rheumatic valve disease, artificial valves, bacterial endocarditis, or atrial myxoma.

 

Ischemic penumbra

The ischemic penumbra is the structurally intact, but functionally impaired, tissue surrounding the area of infarct. It is the target of intervention, as its restoration can aid recovery. Molecular events begin with energy depletion, disruption of ion homeostasis, release of glutamate, calcium channel dysfunction, release of free radicals, membrane disruption, inflammatory changes, and apoptosis and necrosis (Dirnagl, Iadecola, and Moskowitz, 1999).

return to top

 

 

 

Signs and Symptoms

The public should be very aware of the signs and symptoms of stroke, as easrly diagnosis is critical. Most patients present late, beyond the tPA window. This can be due to a lack of knowledge, or due to waking up.

Calling 911 is the best approach, as it saves time and can

 

There are four important questions to answer immediately:

Localization can suggest options for therapy and predicts impairments/disabilities.

Cincinnate prehospital stroke scale and LA prehospital stroke screen are available for EMS.

In hospital assessment scales: NIHSS: 15 item scale

  • history
  • physical exam

History

Assess, as specifically as possible, time of onset of s

Common signs of stroke include:

  • weakness
  • trouble speaking
  • vision problems
  • dizziness
  • headache

It is important to discover how the patient was beforehand, to tease out causes.

What else is wrong? Assess the patient's prior level of function.

 

SAH often presents with the "worst headache ever", neck stiffness, nausea, and vomiting. However, mild SAH is frequently misdiagnosed.

return to top

 

 

 

Investigations

  • lab investigations
  • diagnostic imaging

Lab Investigations

CBC, lytes, ur, sCr

  • blood glucose: Hypoglycemia and hyperglycemia are the most common stroke mimics

return to top

 

 

 

Differential Diagnosis

Differential Diagnosis

With stroke mimics, neurological deficits/symptoms tend to be global rather than focal. Mimics include DIIMMSS:

 

Young people

older patients

any age

return to top

 

 

Prevention

Recommendations Aspirin is not recommended for the prevention of a first stroke in men (Class III, Level of Evidence A). Previous guideline statements have recommended the use of aspirin for cardiovascular (including but not specific to stroke) prophylaxis among persons whose risk is sufficiently high for the benefits to outweigh the risks associated with treatment (a 10-year risk of cardiovascular events of 6% to 10%), and this panel agrees (Class I, Level of Evidence A). Aspirin can be useful for prevention of a first stroke among women whose risk is sufficiently high for the benefits to outweigh the risks associated with treatment (Class IIa, Level of Evidence B). The use of aspirin for other specific situations (eg, atrial fibrillation, carotid artery stenosis) is discussed in the relevant sections of this statement. (Goldstein et al, 2006).

 

 

 

Treatments

The Canadian Stroke Strategy suggests best practices for the following:

  • Health Promotion &
    Primary Prevention
  • Pre-Hosptial &
    Emergency Care
  • Inpatient Stroke Care &
    Early Rehabilitation
  • Long-Term
    Rehabilitation
  • Secondary
    Prevention

Health Promotion and Primary Prevention

Hypertension control is top priority in preventing stroke. Lifestyle modifcation is accordingly very important: quit smoking, eat healthy, exercise, and reduce stress.

Small amounts of alcohol decreases risk.

Medication prevention includes lipid-lowering agents, anti-platelet therapy (81 mg ASA), and antithrombotic therapy (warfarin) for atrial fibrillation. However, warfarin is used in only 54% of patients with AF in Canada due to confusion about benefit and perceived risk of complication (Kapral et al, 2005).

For patients with atrial fibrillation unable or unwilling to take warfarin, both aspirin and clopidogrel appear helpful (ACTIVE investigators, 2009).

return to top

 

 

 

Consequences and Course

  • early events
  • mortality
  • complications
  • recurrence

Early Events

Clinical outcomes depend on disease severity. In mild cases, a transient postischemic confusion state can be followed by complete recovery. In other cases, even with mild global ischemia, severe, irreversible damage can result.

About 1/4 of patients worsen during the first 24-48 hours.

A third of patients with hemorrhagic stroke can have rapid expansion of the hematoma within a few hours.

return to top

 

 

 

Resources and References

http://www.cmaj.ca/cgi/content/full/179/12/S1

Brain Attack Coalition www.stroke-site.org

NHS Health Technology Assessment Study

Am Family Physician, 2009.

ACTIVE investigators. 2009. Effect of Clopidogrel Added to Aspirin in Patients with Atrial Fibrillation. NEJM. April...

Cadilhac DA et al. 2004. Multicenter comparison of processes of care between stroke units and conventional care wards in Australia. Stroke. 35:1035-40.

Donnan GA, Fisher M, Macleod M, and David SM. 2008. Stroke. Lancet.

Goldstein LB et al. 2006. Primary Prevention of Ischemic Stroke. Stroke. 37: 1583-1633.

Gilligan AK et al. 2005. Stroke units, tissue plasminogen activator...

Hankey GJ et al. 2000. Five-year survival....

Johnston SC et al. 2007. Validation and refinement of scores to predict very early stroke risk after transient ischemic attack. Lancet. 369:283-92.

Jorgensen H et al. 1995. Outcome and time course of recovery in stroke. Part II: Time course of recovery. The Copenhagen Stroke Study. Arch Phys Med Rehabil. 76(5):406-12.

Kidwell C et al. 1999. Diffusion MRI in patients with transient ischemic attacks. Stroke. 30:1174-80.

Lopez AD et al. 2006. Global and regional...

Murray CJ, Lopez AD. 1997.

Patel A et al. 2004. Training care givers of stroke patients: economic evaluation. BMJ. 328(7448):1102.

Phillips SJ, Eskes GA, Gubitz GJ. 2002. Description and evaluation of an acute stroke unit. CMAJ. 167(6):655-60.

Pollock A et al. 2007. Physiotherapy treatment approaches for the recovery of postural control and lower limb function following stroke. Cochrane Database Syst Rev. (1):CD001920.

Strong K, Mathers C, Bonita R. 2007.

Thrift AG, Donnan GA, and McNeil JJ. 1995.

Van Peppen RPS et al. 2004. The impact of physical therapy on functional outcomes after stroke: what's the evidence? Clin. Rehabil. 18(8):833-62.

Wardlaw

World Health Organization, 2000. The World Health Report 2000. Geneva, WHO.

Young J, Forster A. 2007. Rehabilitation after stroke. BMJ. 334:86-90.

The Diving Bell and the Butterfly: book and film by Jean-Dominique Bauby, who suffered a stroke leaving him with locked-in syndrome.

return to top

 

 

 

Topic Development

authors:

reviewers:

 

return to top