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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To differentiate the functional changes from the organic changes in malignant hypertension, the author studied the changes in the blood vessel of ocular fundus by ophthalmoscopical and histopathological methods using malignant strain of stroke-prone spontaneously hypertensive rat (M-SHRSP; Okamoto, K et al., 1986), an animal model of human juvenile malignant hypertension, in which the systolic blood pressure elevates rapidly with age and death appeared by the 15th month of life, if they are untreated. Fundus changes progressed with age and duration of hypertension and they altered from functional changes to organic ones. In M-SHRSPs with age of 8 weeks, systolic blood pressure was 220mmHg or more and retinal arterioles showed generalised narrowing but no dye leakage was recognized by fluorescein angiography (FAG). Dye leakage was observed on the 9th week of age. Death of M-SHRSP appeared, after the 13th week of age, coincidentally with appearance of wide retinal edema. Papilledema appeared often in this period. Little histological change was found in the retinal arterioles in spite of severe and marked ophthalmoscopic changes. No feature of angionecrosis was observed in the retina while it was recognized in choroidal arteriole with thrombosis. The fundus changes in M-SHRSP were ophthalmoscopically classified by using scores as following. Grade 0: normal fundi, Grade I (score 1): slight generalized narrowing, caliber irregularity and tortuosity of the retinal arterioles, slight retinal edema and choroidal changes. Grade II (score 2): moderate generalised narrowing, caliber irregularity, tortuosity of the retinal arterioles, moderate retinal edema and choroidal ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ophthalmological study on the M-strain of stroke-prone spontaneously hypertensive rat (M-SHRSP) (1). Classification of hypertensive fundus changes in M-SHRSP]. 204 25

The features of hypertensive retinal arterial vessel changes and their sequelae are reviewed. General or focal narrowing, increased reflexes or abnormal arteriovenous crossings, are often associated with, but not specific for, hypertension. They persist, with very rare exceptions, even after long-term successful antihypertensive therapy. Papilledema, cotton-wool spots, hemorrhages, and fatty exudates in malignant hypertension disappear completely within 6 to 12 months if blood pressure is well controlled. Inadequate control of elevated blood pressure delays, but does not prevent, the regression of retinopathy. The reversal into the "benign" phase may continue for years, even if blood pressure control worsens. This may be explained by a regain of autoregulation which allows the arteriolonecrotic lesions to heal. According to their size, retinal arteries are representative of the target organ of hypertensive small vessel disease. They supply a tissue that is highly sensitive to ischemia. However, even long-standing nonmalignant hypertension seems not to damage retinal tissue.
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PMID:Regression of retinal vascular changes by antihypertensive therapy. 651 55

Papilledema is a term generally reserved (at least in the English language use of the term) by neuro-ophthalmologists for optic disc edema due to increased intracranial pressure. The etiology for the intracranial hypertension may be known (e.g., brain tumor, meningitis, cerebral venous sinus thrombosis) or may be idiopathic (idiopathic intracranial hypertension [IIH]). IIH is a disorder that predominantly affects overweight women of childbearing age and these epidemiologic factors should offer clues to pathogenesis. The main morbidity of papilledema is visual loss and the major mechanism for permanent optic nerve damage is axoplasmic flow stasis and resultant intraneuronal ischemia. The current initial management of papilledema in IIH includes weight loss and medical therapy (e.g., acetazolamide or furosemide). Patients who fail, are intolerant to, or noncompliant with maximum tolerated medical therapy might require optic nerve sheath fenestration or cerebrospinal fluid diversion (i.e., shunting) procedures.
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PMID:Papilledema: are we any nearer to a consensus on pathogenesis and treatment? 2235 46

Papilledema is optic disc swelling due to high intracranial pressure. Possible conditions causing high intracranial pressure and papilledema include intracerebral mass lesions, cerebral hemorrhage, head trauma, meningitis, hydrocephalus, spinal cord lesions, impairment of cerebral sinus drainage, anomalies of the cranium, and idiopathic intracranial hypertension (IIH). Irrespective of the cause, visual loss is the feared morbidity of papilledema, and the main mechanism of optic nerve damage is intraneuronal ischemia secondary to axoplasmic flow stasis. Treatment is directed at correcting the underlying cause. In cases where there is no other identifiable cause for intracranial hypertension (ie, IIH) the available options include both medical and surgical modalities. Weight loss and diuretics remain the mainstays for treatment of IIH, and surgery is typically reserved for patients who fail, are intolerant to, or non-compliant with maximum medical therapy.
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PMID:Papilledema: epidemiology, etiology, and clinical management. 2853 94