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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

Two patients are presented in whom cerebral angiography was complicated by bioccipital infarcts resulting in cortical blindness with persisting severe restriction of the visual field (case 1) and persisting cortical blindness (case 2). One patient (case 1) demonstrated a compensated, protracted disseminated intravascular coagulation (Table 1), which disappeared after treatment with phenprocoumon (Marcoumar). The other patient (case 2) demonstrated increasee spontaneous platelet aggregability (Table 2), which was treated sucessfully with acetylsalicylic acid (Magnyl) and dipyridamole (Persantine). We presume that the coagulation disturbances demonstrated after the angiography may be pathogenetic to the complications. We propose that patients with transient cerebral ischemia and apoplexy who are undergoing cerebral angiography should be studied with regard to coagulation before and after the cerebral angiography so that coagulation disturbances demonstrated may be treated before, or corrected after the angiography.
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PMID:Possible increased tendency to thrombosis after cerebral angiography. 45 38

The results of 72 carotid endarterectomy operations carried out by three consultant surgeons were analysed. Thirty-eight operations (32.8 per cent) were performed in patients with mild or resolving stroke and 33 operations (45.9 per cent) in patients with transient ischaemic attacks and/or amaurosis fugax. Five patients (7 per cent) died in the early postoperative period, 2 as a result of strokes and the others from cardiac causes. Seventy-six per cent of patients had a satisfactory long term result, remaining free from storke, blindness or recurrent transient ischaemic attacks over the follow-up period of 1--7 years. There were 10 patients (13.8 per cent), including 2 who died, who developed early postoperative neurological deficits; 4 (5.5 per cent) had transient defects and 6 (8.3 per cent) had permanent deficits. Of these patients, 4 had proved occlusions of the reconstructed artery. In 3 patients, cerebral embolization during operation was suspected as the cause. There were, in addition, 2 asymptomatic patients whose reconstruction was shown to be occluded on follow-up postoperative angiography. The continued absence of symptoms, therefore, is no guarantee that the reconstruction is patent and some more objective method of assessment is necessary if the results of carotid endarterectomy are to be critically analysed. The incidence of neurological deficits could, it is believed, be reduced by greater experience with the operation, the routine use of peroperative intra-arterial shunting and peroperative angiography to confirm the patency of the reconstruction.
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PMID:The morbidity of carotid endarterectomy. 46 30

Unilateral cerebrovascular occlusion was produced in heparinized rats within seconds after injection of microgram quantities of sodium arachidonate into the internal carotid artery. Electroencephalographic activity over the affected cerebral hemisphere became attenuated, and cerebral blood flow decreased by half. A neurologic syndrome, including ipsilateral blindness and contralateral sensorimotor deficits, resulted from occlusion of the microvasculature by platelet thrombi. Although aspirin strongly inhibited arachidonate-induced platelet aggregation in vitro, the drug offered little protection against arachidonate-induced stroke.
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PMID:Arachidonate-induced cerebrovascular occlusion in the rat. The role of platelets and aspirin in stroke. 94 86

Amaurosis fugax (transient monocular blindness) is a symptom of retinal ischemia just as contralateral hemiparesis and sensory loss are symptoms of cerebral ischemia. These symptoms are produced by atherosclerotic stenosis of the carotid vessels at the ipsilateral carotid bifurcation and emboli from these areas causing focal, repetitive, retinal ischemia. A study of 31 endarterectomy patients was undertaken to see if eight patients with amaurosis fugax (25%) could be differentiated from 22 patients with transient cerebral ischemia. The patients with amaurosis fugax were found to be younger. They all had 75% or greater stenosis of the internal carotid artery at the bifurcation on the symptomatic side. They all had unilateral visual symptoms and these symptoms were relieved by surgery. The patients with amaurosis fugax were devoid of cardiac disease, while 45% of the cerebral ischemic patients had documented myocardial disease. Amaurosis fugax (transient monocular blindness) in the setting of clinically significant atheroslerosis of the carotid vessels is an indication for carotid endarterectomy.
Stroke
PMID:Amaurosis fugax: a clinical comparison. 117 55

The CHAT classification separates various current and historical presentations of cerebrovascular disease in an effort to determine important prognostic clues for management and prognosis. To evaluate known risk factors for late stroke and death, we followed up for an average of 44 months 633 patients who had undergone 714 carotid operations. We analyzed the indication for surgery (by CHAT) and the effect of preoperative risk factors (age, hypertension, cardiac disease, tobacco use, diabetes, hyperlipidemia, renal disease, pulmonary disease, and total risk factor score) on the end points of late stroke and death. Ipsilateral stroke was uncommon after carotid endarterectomy: with life-table analysis, the probability of late stroke at 5 years after carotid endarterectomy was 3%. Among the 127 patients with amaurosis fugax, the incidence of late stroke and of mortality was a combined total of 1% per year, and the 17 patients who had been first seen with permanent ocular stroke (blindness) fared equally well. The 28 patients who were first seen with vertebrobasilar symptoms and were treated by carotid endarterectomy also fared particularly well, with no late strokes or deaths within the first 5 years. Logistic regression analyses revealed that the various indications for carotid endarterectomy were associated with differing patterns of risk factors as significant predictors of late stroke or death. For patients first seen with asymptomatic lesions, only diabetes was an important predictor for late stroke (p = 0.05) and renal disease was the only marker for early death (p = 0.05). On the other hand, those factors were not significant risk factors for patients first seen with amaurosis fugax, for whom tobacco use was a negative predictor for stroke (p = 0.06) and male gender a negative predictor for early death (p = 0.03). After cortical transient ischemic attacks and carotid endarterectomy, there were no risk factors predictive of late stroke or of death. For patients with prior stroke, age was a very strong predictor of stroke (p = 0.01) and both age and a history of cardiac disease were significant risk factors for early death (p = 0.007). In contrast to the results in reports of patients treated medically for transient ischemic attacks and stroke, we found that several risk factors appeared to play relatively minor roles. In conclusion, stroke after carotid endarterectomy was uncommon, least common after ocular symptoms, and most likely after permanent cortical stroke. Specific risk factors were less important for patients after carotid endarterectomy than for the medically treated stroke patient.
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PMID:CHAT analysis of the influence of specific risk factors on late results after carotid endarterectomy. 140 78

One to ten years after laser coagulation for diabetic retinopathy, 229 type I diabetics (mean age 44.3 years) and 157 type II diabetics (mean age 65 years) were re-studied for morbidity and mortality (progression of late damage, duration of survival, cause of death). The duration of diabetes at the first laser coagulation averaged 23.1 years for type I diabetics (15.9 years for type II). Average period from the first laser coagulation to the re-examination was 6.5 years for type I, 5.1 for type II diabetics. Of those patients still alive 6.7% had gone blind (type II: 7.3%). 2.1% and 4.6%, respectively, were receiving dialysis treatment, while renal transplantation had been performed in 3.1 and 1.8%, respectively. Stroke was the most frequent macrovascular complications (8.4 and 16.5%), followed by leg amputation (3.6 and 14.7%) and myocardial infarction (3.7 and 18.3%). 83 patients had died: 35 (15.3%) type I and 48 (30.6%) type II diabetics. Causes of death were septicaemia 14.3% (0%), uraemia 11.4% (8.3%), myocardial infarction 14.3% (33.3%), heart failure 8.6% (29.2%) and stroke 5.7% (6.3%). 10.7% (24.2%) had died within the first 5 years after laser coagulation. Despite a lower incidence of blindness in patients with diabetic retinopathy, the vascular disease progresses in other vascular regions so that a large proportion of diabetics will develop renal failure or die early from macrovascular complications.
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PMID:[Morbidity and mortality in type 1 and type 2 diabetes mellitus after the diagnosis of diabetic retinopathy]. 142 83

A 37-year-old man experienced cortical blindness following a bilateral stroke in the territory of the posterior cerebral arteries. Four years later, the measurement of visual field defects (Goldmann perimeter) showed persistence of bilateral blindness with a 2-degree preservation of macular vision and a perifoveal sparing between 10 to 30 degrees of eccentricity in the left inferior quadrant. Despite this visual impairment, the subject was able to perform visually-guided locomotion. Moreover he consciously perceived visual motion in the blind parts of his visual field. CT and MRI showed a lesion involving most of the striated cortex. The visual cortex located in the internal occipito-parital regions was relatively spared. The contribution of this structure to extra-striated vision of motion is discussed.
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PMID:[Ambulatory autonomy and visual motion perception in a case of almost total cortical blindness]. 144 48

The purpose of this study was to review data from published cerebrovascular studies to determine if it is possible to predict, based on clinical manifestations (eg, cervical bruit, transient ischemic attack, or stroke) of cerebrovascular atherosclerosis, the annual probability of having a stroke, as well as to determine and discuss the methods used in calculating and reporting vascular event rates. This overview analysis reveals that the annual stroke rates are as follows: for asymptomatic carotid stenosis, 1.3% (95% confidence interval [CI], 1.0 to 1.6); for transient monocular blindness, 2.2% (95% CI, 1.3 to 3.0); for transient ischemic attack, 3.7% (95% CI, 3.1 to 4.3); for minor stroke, 6.1% (95% CI, 5.7 to 6.6); and for major stroke, 9.0% (95% CI, 8.0 to 9.9). The data analyzed here suggest that a hierarchical profile of worsening clinical characteristics mirrors a hierarchical progression of increasing risk of stroke. These data support the idea that there is a clinical risk profile, in addition to the conventional atherosclerosis risk factor profile, for predicting subsequent stroke.
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PMID:Vascular event rates in patients with atherosclerotic cerebrovascular disease. 152 19

Point mutation of mitochondrial DNA has been described in the blood from a MELAS patient. The 39-year-old patient developed progressive dementia, stroke-like episodes, heart conduction defect (Lown-Ganong-Levin syndrome) and cortical blindness. CT scan revealed brain atrophy and low density areas in the bilateral occipital lobes. Laboratory tests showed hyperglycemia and lactic acidosis. Muscle biopsy showed ragged red fibers on Gomori trichrome staining. He was clinically diagnosed as having MELAS and insulin-dependent diabetes mellitus. Onset of diabetes mellitus and MELAS was almost same. Family history showed his mother's brother and sisters had also insulin-dependent diabetes mellitus. We amplified the leucine (UUR) tRNA gene from the patient's blood with polymerase chain reaction (PCR) and analysed it by restriction enzyme analysis and sequencing. Genetic analysis showed A-to-G substitution at the nucleotide position 3243 in the leucine (UUR) tRNA gene. This substitution made a new restriction site Apa I. Mutant DNA coexisted with wild type DNA (heteroplasmy). It is shown that in some types of mitochondrial encephalomyopathies, especially patients of Kearns-Sayre syndrome (KSS), diabetes mellitus is often complicated. And in KSS patients insulin receptor in normal, but insulin secretion from beta cells of pancreas is decreased. In MELAS patients, however, has diabetes mellitus been reported to be rarely complicated and relationship between MELAS and diabetes mellitus is not done. As far as we know, two cases, including ours, with genetically diagnosed MELAS have been reported to have diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[MELAS associated with diabetes mellitus and point mutation in mitochondrial DNA]. 159 Nov 3


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