create barcode c# .net Ophthalmic A Ant cerebral artery Middle cerebral stem Int carotid A in Microsoft Office

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Post communicating A 3rd cranial nerve Sup cerebellar A Post cerebral A
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Post inf cerebellar A Vertebral A Figure 34-22 Diagram of the circle of Willis showing the principal sites of saccular aneurysms Approximately 90 percent of aneurysms are on the anterior half of the circle The sizes of the aneurysms depicted correspond roughly to the frequency of occurrence at those sites
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There is an increased incidence of congenital polycystic kidneys, bromuscular dysplasia of the extracranial arteries, moyamoya, and coarctation of the aorta among persons with saccular aneurysms A saccular aneurysm occurs in approximately 5 percent of cases of arteriovenous malformation, usually on the main feeding artery of the malformation Numerous reports have documented a familial occurrence of saccular aneurysms, lending support to the idea that genetic factors play a role in their development The number of rst-degree relatives found to harbor an unsuspected aneurysm has been about 4 percent in most series This low rate, the nding that half of the discovered aneurysms are small, and the complications of surgery make routine screening of siblings, children, and parents of patients with ruptured aneurysms impractical, according to the Magnetic Resonance Angiography in Relatives of Patients with Subarachnoid Hemorrhage Study Group However, since aneurysms of the familial variety tend to be larger at the time of rupture and more numerous than in patients who have sporadic ones, there are exceptions to this statement (Ruigrok et al) While hypertension is more frequently present than in the general population, nevertheless aneurysms most often occur in persons with normal blood pressure Pregnancy does not appear to be associated with an increased incidence of aneurysmal rupture, although there is always concern about the possibility of rupture during the straining of natural delivery Atherosclerosis, though present in the walls of some saccular aneurysms, probably plays no part in their formation or enlargement Approximately 90 to 95 percent of saccular aneurysms lie on the anterior part of the circle of Willis (Fig 34-22) The four most common sites are (1) the proximal portions of the anterior communicating artery, (2) at the origin of the posterior communicating artery from the stem of the internal carotid, (3) at the rst major bifurcation of the middle cerebral artery, and (4) at the bifurcation of the internal carotid into middle and anterior cerebral arteries Other sites include the internal carotid artery in the cavernous sinus, at the origin of the ophthalmic artery, the junction of the posterior communicating and posterior cerebral arteries, the bifurcation of the basilar artery, and the origins of the three cerebellar arteries Aneurysms that rupture in the cavernous sinus may give rise to an arteriovenous stula (page 749) There are several types of aneurysm other than saccular, eg, mycotic, fusiform, diffuse, and globular The mycotic aneurysm is caused by a septic embolus that weakens the wall of the vessel in which it lodges (page 727) The others are named for their predominant morphologic characteristics and consist of enlargement or dilatation of the entire circumference of the involved vessels, usually the internal carotid, vertebral, or basilar arteries The latter are also referred to as arteriosclerotic aneurysms, since they frequently show atheromatous deposition in their walls, but it is likely that they are at least partly developmental in nature Some are gigantic and press on neighboring structures or become occluded by thrombus; they rupture only infrequently (see further on) Clinical Syndrome With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space (usually in relation to the circle of Willis), and the resulting clinical events assume one of three patterns: (1) the patient is stricken with an excruciating generalized headache and vomiting and falls unconscious almost immediately; (2) headache develops in the same manner but the patient remains relatively lucid the most common syndrome; (3) rarely, consciousness is lost quickly with-
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out any preceding complaint Decerebrate rigidity and brief clonic jerking of the limbs may occur at the onset of the hemorrhage, in association with unconsciousness If the hemorrhage is massive, death may ensue in a matter of minutes or hours, so that ruptured aneurysm must be considered in the differential diagnosis of sudden death A considerable proportion of such patients probably never reach a hospital Persistent deep coma is accompanied by irregular respirations, attacks of extensor rigidity, and nally respiratory arrest and circulatory collapse In these rapidly fatal cases, the subarachnoid blood has greatly increased the intracranial pressure to a level that approaches arterial pressure and caused a marked reduction in cerebral perfusion In some instances the hemorrhage has dissected intracerebrally and entered the ventricular system Rupture of the aneurysm usually occurs while the patient is active rather than during sleep, and in a few instances during sexual intercourse, straining at stool, lifting heavy objects, or other sustained exertion (see page 160) Momentary Valsalva maneuvers, as in coughing or sneezing, have generally not caused aneurysmal rupture (they may cause arterial dissection) In patients who survive the initial rupture, the most feared complication is rerupture, an event that may occur at any time from minutes up to 2 or 3 weeks In less severe cases, consciousness, if lost, may be regained within a few minutes or hours, but a residuum of drowsiness, confusion, and amnesia accompanied by severe headache and stiff neck persists for several days It is not uncommon for the drowsiness and confusion to last 10 days or longer Since the hemorrhage is con ned to the subarachnoid space, there are few if any focal neurologic signs That is to say, gross lateralizing signs in the form of hemiplegia, hemiparesis, homonymous hemianopia, or aphasia are absent in the majority of cases On occasion, a jet of blood emanating from an aneurysm may rupture into the adjacent brain or clot in the insular cistern and produce a hemiparesis or other focal syndrome There may also be a focal syndrome from acute or delayed ischemia in the territory of the aneurysm-bearing artery Usually this occurs several days after a large subarachnoid hemorrhage The pathogenesis of such manifestations is not fully understood, but a transitory fall in pressure in the circulation distal to the aneurysm is postulated in early cases and vasospasm is responsible for the later focal signs Transient de cits are not common, but they do constitute reliable indicators of the site of the ruptured aneurysm (see below) Convulsive seizures, usually brief and generalized, occur in 10 to 25 percent of cases according to Hart et al (but far less often in our experience) in relation to acute bleeding or rebleeding These early seizures do not correlate with the location of the aneurysm and do not appear to alter the prognosis Prior to rupture, saccular aneurysms are usually asymptomatic Exceptionally, if large enough to compress pain-sensitive structures, they may cause localized cranial pain With a cavernous or anterolaterally situated aneurysm on the rst part of the middle cerebral artery, the pain may be projected to the orbit An aneurysm on the posteroinferior or anteroinferior cerebellar artery may cause unilateral occipital or cervical pain The presence of a partial oculomotor palsy with dilated pupil may be indicative of an aneurysm of the posterior communicating internal carotid junction (less often posterior communicating posterior cerebral junction) Occasionally, large aneurysms just anterior to the cavernous sinus may compress the optic nerves or chiasm, third nerve, hypothalamus, or pituitary gland In the cavernous sinus they may compress the third, fourth, or sixth nerve or the ophthalmic division of the fth nerve A monocular visual eld defect may also develop with a
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