Introduction

The earliest link reported between carotid disease and stroke was credited to Savory in 1856. In 1954 Eastcott reported the first carotid artery reconstruction to prevent stroke at St. Mary's Hospital in London. Main diseases affecting carotid artery are occlusive, dissection, aneurysms, trauma and inflammatory.

Definition

There are three clinical presentations of carotid occlusive disease.

1. Asymptomatic: patients with no history of cerebral symptoms

2. Transient ischaemic attacks (TIA): temporary neurological deficits >24 hours with complete recovery. Crescendo TIA suggests repeated frequent embolization with complete recovery in between. The average reported rate of risk of stroke ranges from 5% within the first 2 days and 20% within the first month to 10.5% within 90 days. The benefit from intervention is greatest for patients undergoing surgery within two weeks of their last ischaemic event.

3. Stroke: permanent neurological deficit – defect ranging fromminimal with good recovery to massive causing death.

Pathogenesis

Up to 30% of cerebral events are caused by embolization from atherosclerotic lesions at the carotid bifurcation, or low-flow related ischaemic events. Other causes include embolization from the aortic arch, intracerebral bleeds and tumours.

Symptoms and signs

Presentation is usually in the form of discrete motor or sensory dysfunction contralateral to the side of the ischaemic event. Since the left hemisphere is dominant in 95% of the population, an ischaemic event affecting the left hemisphere may also cause receptive or expressive aphasia. It can also present as transient visual loss (amaurosis fugax) in the ipsilateral eye. Patients typically describe a curtain drawn over the eye, or field defect.