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Anatomy
The internal carotid artery supplies the anterior part of the brain, the eye and its appendages, and sends branches to the forehead and nose. Its size, in the adult, is equal to that of the external carotid, though, in the child, it is larger than that vessel. It is remarkable for the number of curvatures that it presents in different parts of its course. It occasionally has one or two flexures near the base of the skull, while in its passage through the carotid canal and along the side of the body of the sphenoid bone it describes a double curvature and resembles the italic letter S.
Course and Relations.—In considering the course and relations of this vessel it may be divided into four portions: cervical, petrous, cavernous, and cerebral.
Cervical Portion
This portion of the internal carotid begins at the bifurcation of the common carotid, opposite the upper border of the thyroid cartilage, and runs perpendicularly upward, in front of the transverse processes of the upper three cervical vertebræ, to the carotid canal in the petrous portion of the temporal bone. It is comparatively superficial at its commencement, where it is contained in the carotid triangle, and lies behind and lateral to the external carotid, overlapped by the Sternocleidomastoideus, and covered by the deep fascia, Platysma, and integument: it then passes beneath the parotid gland, being crossed by the hypoglossal nerve, the Digastricus and Stylohyoideus, and the occipital and posterior auricular arteries. Higher up, it is separated from the external carotid by the Styloglossus and Stylopharyngeus, the tip of the styloid process and the stylohyoid ligament, the glossopharyngeal nerve and the pharyngeal branch of the vagus. It is in relation, behind, with the Longus capitis, the superior cervical ganglion of the sympathetic trunk, and the superior laryngeal nerve; laterally, with the internal jugular vein and vagus nerve, the nerve lying on a plane posterior to the artery; medially, with the pharynx, superior laryngeal nerve, and ascending pharyngeal artery. At the base of the skull the glossopharyngeal, vagus, accessory, and hypoglossal nerves lie between the artery and the internal jugular vein.
Petrous Portion
When the internal carotid artery enters the canal in the petrous portion of the temporal bone, it first ascends a short distance, then curves forward and medialward, and again ascends as it leaves the canal to enter the cavity of the skull between the lingula and petrosal process of the sphenoid. The artery lies at first in front of the cochlea and tympanic cavity; from the latter cavity it is separated by a thin, bony lamella, which is cribriform in the young subject, and often partly absorbed in old age. Farther forward it is separated from the semilunar ganglion by a thin plate of bone, which forms the floor of the fossa for the ganglion and the roof of the horizontal portion of the canal. Frequently this bony plate is more or less deficient, and then the ganglion is separated from the artery by fibrous membrane. The artery is separated from the bony wall of the carotid canal by a prolongation of dura mater, and is surrounded by a number of small veins and by filaments of the carotid plexus, derived from the ascending branch of the superior cervical ganglion of the sympathetic trunk.
Cavernous Portion
In this part of its course, the artery is situated between the layers of the dura mater forming the cavernous sinus, but covered by the lining membrane of the sinus. It at first ascends toward the posterior clinoid process, then passes forward by the side of the body of the sphenoid bone, and again curves upward on the medial side of the anterior clinoid process, and perforates the dura mater forming the roof of the sinus. This portion of the artery is surrounded by filaments of the sympathetic nerve, and on its lateral side is the abducent nerve.
Cerebral Portion
Having perforated the dura mater on the medial side of the anterior clinoid process, the internal carotid passes between the optic and oculomotor nerves to the anterior perforated substance at the medial extremity of the lateral cerebral fissure, where it gives off its terminal or cerebral branches
Peculiarities
The length of the internal carotid varies according to the length of the neck, and also according to the point of bifurcation of the common carotid. It arises sometimes from the arch of the aorta; in such rare instances, this vessel has been found to be placed nearer the middle line of the neck than the external carotid, as far upward as the larynx, when the latter vessel crossed the internal carotid. The course of the artery, instead of being straight, may be very tortuous. A few instances are recorded in which this vessel was altogether absent; in one of these the common carotid passed up the neck, and gave off the usual branches of the external carotid; the cranial portion of the internal carotid was replaced by two branches of the internal maxillary, which entered the skull through the foramen rotundum and foramen ovale, and joined to form a single vessel.
Pathophysiology
Transient ischemic attack (TIA) is the result of a brief interruption of blood flow to the brain. In 80% of cases, the interruption occurs as a result of blockage in the arterial circulation to the brain due to an embolus, an obstructing arterial thrombus, or the stenotic effects of atherosclerosis. In the other 20%, the interruption is caused by minor hemorrhage in the brain.
In both types of TIA, the lack of oxygen to the brain produces symptoms similar to those produced during a full stroke. Symptoms can affect vision, behavior, movement, speech, and thought processes. However, the symptoms of a TIA are temporary, generally lasting only 8-14 minutes with most clearing within an hour, although they can continue for as long as 24 hours. Permanent damage is unlikely because the oxygen supply to the brain is restored fairly quickly.
Thrombus causes 25-50% of all TIAs, and embolism causes 11-30%. A lacunar infarction occurs in 11-14% of patients with TIA. Less common causes of a TIA involve minor bleeding or sentinel leaks from a cerebral blood vessel (approximately 10% of cases). Mini strokes caused by bleeding are usually due to high blood pressure (hypertension). Since the underlying cause of this type of TIA is bleeding rather than blockage, the patient must receive an immediate and accurate medical evaluation. Treatment should not include thrombolytic drugs or aspirin because these agents increase bleeding.
Once blockage or bleeding occurs, whether the person is about to have a TIA or a full stroke depends greatly on host factors, eg, the person's age and general health status and the location and size of the blockage or bleed. Other blood vessels in the area may enlarge to improve blood flow to the affected area, thus ending the TIA. Although a TIA is characterized by a brief interruption of blood flow, symptoms of a TIA (eg, weakness on 1 side of the body) may last much longer than the time needed to dissolve the blockage completely or to absorb the bleed. For most people, symptoms last approximately 8-14 minutes and usually clear within an hour, but they can last as long as 24 hours.
Patients with symptoms of a TIA that persist for more than 24 hours usually are treated as though they have had a full stroke. More than 50,000 Americans have TIAs every year. In persons older than 65 years, 8.5% have been diagnosed with at least 1 mini stroke. The risk of stroke is highest soon after a TIA, and the risk continues to be approximately 5% during the first month following the TIA. Of patients with TIAs, 20-25% are estimated to develop a stroke within 2 years.
If the degree of carotid stenosis is severe, in the absence of adequate collateral circulation the ipsilateral cerebral hemisphere may become underperfused. When the arterial circulation falls, there is an increased risk of thrombosis within the middle cerebral artery (MCA), the anterior cerebral artery, and the more peripheral branches of the intracranial arterial circulation. Focal thrombosis may occur in areas of pre-existing atherosclerotic disease.
Other general medical issues which may exacerbate symptoms related to carotid stenosis include chronic lung disease, cardiac disease with restricted cardiac function, and attempts to low systemic hypertension. Any adverse physiological change which further limits oxygenation to the brain may result in cerebral ischemia in patients who otherwise tolerated even high-grade carotid stenosis.
The presence of 2 or more tandem arterial stenoses may result in symptomatic cerebral ischemia, even if any one of the narrowed arterial inflow circulation pathways was not critically narrowed.
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