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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The causes of visual loss in benign intracranial hypertension are related to long standing papilloedema, ischaemic optic neuropathy or haemorrhage into a subretinal neovascular membrane. Decompression procedures generally preserve or improve visual acuity but surgical treatment with subtemporal decompression may lead to visual impairment. Such a deficit has been recorded in the past as occurring with ventriculography. Postulated mechanisms have included brain herniation, spasm of vessels supplying the visual cortices or retinal vascular disturbance. To our knowledge treatment with lumboperitoneal shunting has not previously been reported as leading to further significant visual loss in this condition. This report describes such an occurrence in a patient. Retinal vascular disturbance is postulated on the basis of several normal CT scans, normal CSF pressure measured after surgery and visual evoked responses suggesting retinal or optic nerve damage.
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PMID:Lumboperitoneal shunting as a cause of visual loss in benign intracranial hypertension. 366 76

Cafergot is a combination of ergotamine tartrate and caffeine and may cause symptoms of peripheral vascular insufficiency. Iatrogenic ergotism should be suspected in any patient exhibiting ischemic symptoms while receiving this medication. Progression to fulminant necrosis and gangrene can occur. Two cases are presented and the management reviewed. This effect of ergotamine tartrate and caffeine may be an idiosyncratic hypersensitivity reaction with therapeutic doses or may result from excessive medication. Iatrogenic ergotism occurs most often in women in their mid-thirties with migraine syndrome. By alpha-adrenergic agonism, as well as by possible interactions with prostaglandins, calcium, and serotonin, ergotamine causes vasoconstriction of both arteries and veins. The angiographic pattern of spasm, collateral formation, and intravascular thrombi is typical. Treatment of ergotism depends on the severity of the symptoms and the possibility of gangrene. Discontinuation of ergotamine, cigarette smoking, and caffeine may be all that is necessary in most patients. Nitroprusside is the drug of choice in the treatment of acute vascular insufficiency from ergotism, but in a less urgent situation, prazosin has also been effective. Intra-arterial balloon dilatation has also been helpful. Other forms of therapy have been supportive and the results inconsistent. Cafergot should be used with extreme caution in patients with renal or hepatic failure, peripheral vascular disease, or pregnancy. Relative contraindications include hypertension, ischemic heart disease, and Raynaud's phenomenon.
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PMID:Recognition and treatment of arterial insufficiency from cafergot. 372 91

Delayed ischemic deficits from vasospasm after subarachnoid hemorrhage remain a major source of death and disability to patients surviving subarachnoid hemorrhage. Ideal treatment for this condition would prevent or reverse spasm in major subarachnoid vessels. This goal remains elusive. Considerable success has been obtained with augmentation of flow in ischemic regions by induced hypertension and hypervolemia. Some patients are not good candidates for this therapy because of underlying cardiovascular disease or the presence of unsecured aneurysms. A total of 11 patients have recently undergone extracranial-intracranial bypass for the treatment of symptomatic vasospasm. Bypass was performed in 4 patients due to failure of medical management and in 7 patients due to our reluctance to induce hypertension in the setting of unsecured aneurysms. Eight of the 11 patients responded neurologically to the bypass procedure within 24 hours. In 6 cases, neurological deficits either improved or resolved. After operation, all 8 patients maintained their preoperative neurological status with lower mean arterial blood pressures than before bypass. Noncomatose patients with focal middle cerebral ischemic deficits and secured aneurysms in whom medical management has failed or in whom these measures are contraindicated may indeed benefit from extracranial-intracranial bypass. Patients with unsecured aneurysms remote from an ischemic middle cerebral territory should probably be revascularized if cautious hypertension fails to improve their conditions.
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PMID:Use of extracranial-intracranial bypass in the management of symptomatic vasospasm. 374 51

The goal of pharyngeal reconstruction after laryngectomy is to prevent fistulization and to permit rapid resumption of satisfactory deglutition. Alaryngeal speech acquisition by the traditional method of esophageal speech is effective if insufflation is rapidly learned and tolerated by the pharyngoesophageal segment. Experience with tracheoesophageal phonation revealed an incidence of pharyngoesophageal spasm in 40% of an esophageal speech failure population which prevented useful air flow for speech production. This is related to esophageal distention and reflexive upper esophageal sphincter hypertension. It is suggested that pharyngeal reconstruction after total laryngectomy may permit higher wall tension than is desirable for speech acquisition. The problem of post laryngectomy pharyngoesophageal spasm may be reduced by myotomy of the pharyngeal constrictors with resultant higher air flows in the residual vocal tract for speech. Alterations in the pharyngeal wall tonicity will affect the pitch of the speech and listener acceptability. Recently identification and division of the pharyngeal plexus has produced a similar result in improved phonatory air flows with subjective vocal pitch approximating more normal voices. The above mentioned techniques are readily applied to the laryngectomy procedure and enhance the likelihood of alaryngeal speech acquisition.
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PMID:Pharyngeal reconstruction after total laryngectomy with preservation of phonation. 383 43

As I have indicated in the foregoing discussion, there are several syndromes that with various degrees of proof seem to be caused by unilateral vascular compression of a cranial nerve at the brain stem. Jannetta has summarized this concept as follows: "As we age, our arteries elongate and our brains 'sag'. As a consequence of these processes, redundant arterial loops and bridging or intrinsic hindbrain veins may cause cross-compression of cranial nerve root entry zones in the cerebellopontine angle. This pulsatile compression can be seen to produce hyperactive dysfunction of the cranial nerve. Symptoms of trigeminal or glossopharyngeal neuralgia (somatic sensory), hemifacial spasm (somatic motor), tinnitus and vertigo (special sensory), and some cases of 'essential' hypertension are caused by these vessels compressing cranial nerves V, IX-X, VII, VIII, and left X and medulla oblongata. Using microsurgical techniques, the symptoms may be relieved by vascular decompression. . .".
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PMID:Neurovascular compression syndromes. 389 20

From among 899 consecutive patients who underwent their first coronary arteriography, we selected 147 pts with vasospastic angina (VA) and 356 pts with classic angina (CA) and divided them into three different age groups: -49 years old, 50 to 59, and 60-. In these 899 pts, incidences of VA showed no increase with aging. Prevalence of coronary risk factors in CA, such as diabetes, hypercholesterolemia, hypertension, and obesity, was higher than in VA, although prevalence of smoking in CA was lower than in VA. In VA, we found an age-related increase in the incidence of smoking only, in contrast to the other four risk factors. The VA showed no age-related increase in the incidence of complication of fixed coronary stenosis. These findings suggest that aging and atherosclerosis might not play a major role in pathogenesis of VA, although the mere presence of atherosclerosis irrespective of its severity could interact with local susceptibility to spasm, leading to coronary vasospasm.
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PMID:Age-related changes of clinical features and prevalences of coronary risk factors in Japanese patients with vasospastic angina. 394 Jul 72

One hundred and forty consecutive patients who sustained proven spontaneous subarachnoid hemorrhage (SAH) with negative cerebral panangiography were studied retrospectively. Attention was directed to the presence, amount, and distribution of subarachnoid blood on computerized tomography (CT) scans. It was determined that the finding of blood on CT had a significant association with clinical grade, loss of consciousness, ventricular ratio, fixed ischemic deficit, and total of all complications, but not with epilepsy, hypertension (previously known or detected on admission), treated hydrocephalus, rebleeding, angiographic spasm, and eventual outcome (which was generally excellent on follow-up examination). The distribution of blood, predominantly around the basal cisterns, suggests leakage from ventriculostriate and thalamoperforating vessels as the cause of SAH, and closer study of these vessels is suggested.
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PMID:Spontaneous subarachnoid hemorrhage and negative cerebral panangiography. Review of 140 cases. 395 Jul 37

Regional cerebral blood flow (rCBF), cerebral metabolic rate of oxygen (CMRO2), intraventricular pressure, and lactate/pH levels in the cerebrospinal fluid (CSF) were measured in 38 patients with ruptured intracranial aneurysms between the 3rd and 13th day after subarachnoid hemorrhage (SAH). Angiography was performed following the rCBF study and the degree of vasospasm was measured on the angiograms. The patients were graded clinically according to the system of Hunt and Hess. Cerebral vasospasm significantly influenced rCBF: global reductions and focal changes (ischemia, hyperemia, and tissue peaks) were commonly associated with vasospasm. Patients with severe diffuse spasm always had global ischemia (21 +/- 5 ml/100 gm/min), and cerebral infarctions were demonstrated subsequently, The CMRO2 was more reduced than rCBF, indicating an uncoupling between flow and metabolism. This relative luxury perfusion was associated with CSF lactic acidosis and intracranial hypertension. The arteriovenous difference of oxygen was equally reduced in all categories of patients, probably due to the primary insult of SAH. The CMRO2 decreased concomitantly with arterial caliber, indicating a secondary impairment of cerebral metabolism due to vasospasm.
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PMID:Regional CBF, intraventricular pressure, and cerebral metabolism in patients with ruptured intracranial aneurysms. 396 55

Vascular smooth muscle is activated through 2 major systems. One, which can be inhibited by calcium-entry blocking agents, involves the influx of calcium through potential-sensitive channels. The other, which can be inhibited by sodium nitroprusside, involves the entry of calcium through agonist-controlled channels and probably its mobilization from within the cell as well. Human veins, muscular arteries and resistance vessels show differing patterns of response to agents that selectively inhibit the 2 activation systems. The responses indicate that physiologic contractions of cutaneous veins and muscular arteries depend on the agonist-controlled system; contractions of veins induced by high concentrations of potassium depend on the potential-sensitive system as, probably, does local spasm in arteries. The tone of resistance vessels depends on a balance between the potential-sensitive and agonist-controlled systems. The forearm resistance vessels of men with primary hypertension respond to verapamil with larger-than-normal dilatation compared with that induced by nitroprusside. This is interpreted as showing an increased contribution to resistance vessel tone from the potential-sensitive system. This functional abnormality does not depend on the inhibition of sodium pump activity that is known to occur in hypertension, because it cannot be reproduced by local infusion of ouabain. It probably results from a primary disorder of calcium handling by the cell membrane.
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PMID:Functional differences in blood vessels determined from studies with calcium-channel blockers. Functional changes in forearm resistance vessels of men with primary hypertension. 396 57

A 23-year-old man developed lethal cerebral hypoperfusion associated with angiographically demonstrable cerebral arterial spasm while being treated for acute angiotensinogenic hypertension due to a traumatic coarctation of the aorta. This complication occurred even though the treatment maintained his blood pressure at normotensive to mildly hypertensive levels, without producing more than rare and fleeting periods of hypotension. To explain this enigmatic development, we propose that the high concentration of angiotensin II in the blood constricted the cerebral arteries and thus prevented adequate cerebral autoregulation when his blood pressure was lowered by drug therapy.
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PMID:Role of angiotensin in lethal cerebral hypoperfusion during treatment of acute hypertension. 403 55


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