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

The methods used presently for abortion of the attacks of migraine and cluster headache are not fully satisfactory which causes that the search for new therapies is continuing. Although the mechanism of migraine attacks remains unexplained, it is thought that an important role in it is played by serotonin receptors, vasodilation in certain regions and opening of arteriovenous communications in the head. Sumatriptan is an agonist of 5-HT1 -like receptors and exerts a selective vasoconstricting effect on the arteries of the head, particularly in the rami of the carotid artery. In 1988 the first reports appeared on the effectiveness of the drug in migraine attacks. In the following years extensive, multicentre and international studies of the drug were carried out on over 600 healthy volunteers and nearly 6000 patients with migraine. The studies demonstrated that Sumatriptan was effective in abortion of migraine attacks. After oral administration of 100 mg or subcutaneous injection of 6 mg in nearly 70% of cases the attack regressed or was greatly alleviated, similarly as other symptoms accompanying the headache such as photophobia, nausea, vomiting. Studies were undertaken also on the effectiveness of Sumatriptan in emergency treatment of cluster headache, and good results were again achieved. The tolerance of the drug is good, although in some cases side effects develop, usually transient and mild, among them tingling, feeling of pressure, heat or heaviness of the head or chest, taste change and burning sensation at the site of injection. Sumatriptan, similarly as all novel drugs, requires caution in its use, particularly in patients with coronary heart disease and hypertension, and also in old patients. As yet, the use of the drug in paediatric migraine or in pregnancy is not recommended.
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PMID:[Sumatriptan and its use in treatment of migraine and cluster headaches]. 133 66

Topical and systemic steroids have proven to be invaluable agents in the treatment of a wide range of disorders, but their use is not without potential complications. Before initiation of therapy with systemic steroids, a personal or family history of cataracts, glaucoma, hypertension, diabetes, hyperlipidemia, renal stones, peptic ulceration, and current infection or pregnancy should be ascertained, because these patients have an increased risk of complications. Prior to long-term therapy with systemic steroids, blood pressure measurement, tuberculin skin test, and anergy panel are recommended. Monthly follow-up may include measurements of weight, blood pressure, electrolytes, and blood sugar and guaiac testing of the stool. To prevent the ocular complications of steroid therapy, routine screening is indicated (Table 1). Screening for cataracts, which occur most commonly as a sequela of continuous systemic steroid use, may be performed by slit-lamp examinations conducted three or four times a year for patients on long-term therapy and twice a year for patients taking intermittent topical ocular or systemic steroids. Glaucoma is more often associated with topical ocular or periocular steroids than with systemic steroids; recommended screening includes a baseline intraocular pressure measurement, then routine pressure measurements taken every few weeks initially, then every few months. Ocular rebound inflammation may develop secondary to rapid tapering or abrupt discontinuation of topical ocular steroid use and is best prevented with gradual tapering. Opportunistic infections of the eye include bacterial, viral, and fungal infections and are most often associated with the use of topical ocular steroids. Ophthalmologic evaluation is indicated promptly if patients treated with ocular steroids develop ocular discharge, pain, photophobia, or redness.
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PMID:Ocular effects of topical and systemic steroids. 161 9

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

3 case studies of migrainous patients taking oral contraceptives (OCs) are presented in this report. The role of OCs in triggering a migraine attack and possibly elevating the risk of a stroke in a patient with migraines is examined. In the 1st case, a 27-year old white female accountant complained of temporal throbbing headaches associated with nausea, vomiting, hazy vision, small scotomas, and photophobia. The patient had been having the headaches twice a month since 1978 and she took Fiorinal to relieve them. Her physician diagnosed the headaches as migraine. The patient acknowledged that she started getting these headaches after beginning to use OCs 3 years earlier. Her family history revealed that her mother had severe migraine headaches which sometimes were accompanied by unilaterial paresthesia, as well as high blood pressure. Ophthalmoscopy, slitlamp, accommodation, and intraocular pressure findings were unremarkable. The patient was counseled about the factors which can trigger a migraine attack and was advised that eliminating these factors may reduce the frequency and intensity of the headaches. The patient was advised that OCs could increase her risk of having a stroke, especially with her family history. Her family physician subsequently reduced the dosage of her OCs. 5 months later the patient reported that she was trying to avoid the migraine triggering factors (e.g., she was wearing her sunglasses). Her headaches had become less frequent and less severe. The 2nd patient also began to have migraine attacks after beginning to use OCs. The 3rd patient's headaches became so severe after taking the pill that she consulted a neurologist. The 2nd and 3rd patients complained that the headaches were most severe at the time each month when they resumed OC use. None of the 3 patients discontinued OC use. The 2nd and 3rd patients were using a low estrogen OC, and the 1st patient was put on a low estrogen dosage after this optometrist's recommendation to her physician. Encouraging the patients to discuss the dosage of OCs with their family physician may be one of the ways to reduce the unwanted effect of the pill. The effect of OCs goes beyond triggering a headache. They may trigger a stroke particularly if the patient has a family history of high blood pressure as did the patients in this study. Differential diagnosis of migraine headaches includes muscle contraction, tension, sinus, and allergic headaches. Optometrists can be most helpful to the patients by counseling them to avoid the triggering factors. Glare, a triggering factor, could be reduced by tinted spectacles.
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PMID:Migraine and oral contraceptives. 714 75

Orthoclone OKT3 (Ortho Biotech Inc, Raritan, NJ) is a potent immunosuppressive agent effective in the therapy of acute renal allograft rejection. Following the first one or two doses, patients often exhibit a "flu-like" illness ascribed to OKT3-induced release of cytokines. Systemic reactions resulting from the cytokines include pyrexia, pulmonary edema, bronchospasm, photophobia, headache, hypotension, rigors, hypertension, gastrointestinal disturbances, and arthralgias/myalgias. The cyclooxygenase inhibitor indomethacin has been shown to ameliorate the pyrexia associated with OKT3 administration. We conducted a retrospective analysis with the purposes of (1) confirming that indomethacin reduces pyrexia and (2) determining the effect of indomethacin on the other aforementioned adverse side effects. Group 1 patients (n = 28) received indomethacin during the initial 48 hours of OKT3 antirejection therapy. Group 2 patients (n = 28) received OKT3 without indomethacin. The incidence of fever (P < 0.0001), headache (P < 0.030), and gastrointestinal disturbances (P < 0.030), and the number of adverse effects (P < 0.0001) were significantly less in the indomethacin-treated group. There were no differences between the groups in pre- and post-OKT3 serum creatinine levels. The indomethacin was well tolerated. We conclude that the widely available and relatively inexpensive cyclooxygenase inhibitor indomethacin safely and significantly reduces adverse effects associated with OKT3 therapy of acute renal allograft rejection.
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PMID:A retrospective analysis of the effect of indomethacin on adverse reactions to orthoclone OKT3 in the therapy of acute renal allograft rejection. 807 74

A 7-year-old boy presented with a 4-week history of daily headache. His parents reported that he was unable to attend school the week prior to presentation. Intermittent nausea without vomiting was reported, but no blurred vision, photophobia, or diplopia were described. There was no history of trauma or recent systemic illness. The physical examination showed mild neck discomfort, no papilledema, and normal cranial nerve, motor and sensory functioning. Both a CT scan of the sinuses and an MRI of the brain were normal. Although the opening pressure was elevated, the cerebrospinal fluid was also normal. In previous accounts of idiopathic intracranial hypertension in children, concomitant papilledema, visual symptoms and/or palsy of the sixth cranial nerve are described. This case demonstrates that idiopathic intracranial hypertension in a young child can present as a daily headache without any visual symptoms or signs.
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PMID:Idiopathic intracranial hypertension in a young child without visual symptoms or signs. 891 68

The authors report on female homozygous twins with idiopathic intracranial hypertension. At the age of 12 years, both twins simultaneously developed visual disturbances with photophobia. At the age of 19 years, an ophthalmological examination disclosed papilloedema in both their eyes. At the age of 22 years, a lumbar puncture showed raised CSF pressure over (200 mm H2O) in both twins. Their neurological and radiological examinations were extremely similar; both of them had severely impaired visual acuity and impaired visual field, bilateral optic nerve atrophy, intracranial hypertension, an enlarged and partial empty sella turcica, digital markings of the calvalium, and an enlarged frontal subarachnoid space. This is the first case report describing idiopathic intracranial hypertension occurring in homozygous twins.
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PMID:Idiopathic intracranial hypertension in female homozygous twins. 921 59

We conducted a population-based headache questionnaire survey including questions on physician consultation for headache in Taipei, Taiwan from August 1997 to June 1998. The participants comprised 3377 subjects aged > or = 15 years, of whom 328 (9.7%) had a diagnosis of migraine and 1754 (52%) had a diagnosis of non-migraine headache. Migraineurs had a higher physician consultation rate (once or more in the past year) than the subjects with non-migraine headache (54% vs. 31%, P < 0.0001). When frequency > or = 10 times was taken as 10 times, the analysis showed that migraineurs consulted physicians more often than non-migraine headache subjects (2.36 vs. 0.96, P = 0.04). A small proportion of the subjects with either migraine (12%) or non-migraine headache (6%) accounted for 50% of total consultations within their groups. In addition to old age, low education levels, living in a rural area, migrainous features (nausea and photophobia), and work day loss, predictors of physician consultations also included 'having been troubled with headache' (odds ratio (OR) = 1.7) and co-morbidity with hypertension (OR = 1.8) or heart disease (OR = 2.2). Low copayment and unrestricted access to medical care, as well as cultural factors played an important role in the high consultation rates in our headache subjects. Moreover, this study found self-perception of headache impact and co-morbid illnesses were important factors affecting the decision to consult physicians about headache.
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PMID:Frequency and predictors of physician consultations for headache. 1129 60

The most common adverse events reported with the use of leflunomide are hypertension, infections, alopecia, and various gastrointestinal complaints. No fatal adverse hematologic events have been reported in humans, although anemia and leukopenia have been described in animals receiving 20 mg/kg/day. We describe a patient with relapsing polychondritis, in whom treatment failure with glucocorticoids, methotrexate, hydroxychloroquine, and azathioprine led to the institution of therapy with leflunomide at a maintenance dose of 20 mg/day. Two months after the dose of leflunomide had been increased to 30 mg daily, the patient developed high fevers, photophobia, thrombocytosis, and leukocytosis that returned to normal following treatment with cholestyramine and discontinuation of leflunomide. Rechallenge with leflunomide was not attempted and the syndrome did not recur during 14 month followup.
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PMID:Leflunomide induced fevers, thrombocytosis, and leukocytosis in a patient with relapsing polychondritis. 1696 Sep 61

A case is presented in which a woman diagnosed with a longstanding history of idiopathic intracranial hypertension reported improvement of frontal headaches, photophobia, transient blindness, enlarged blind spots, and tinnitus after smoking marijuana. All these symptoms and signs were associated with increased intracranial pressure (220-425 mm of water). Treatment with dronabinol at a dose of 10 mg twice a day, then reduced to 5 mg twice a day, relieved all of her symptoms. Previously noted papilledema and enlargement of blind spots also resolved, and this, in the absence of psychoactive effect or weight gain.
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PMID:Dronabinol reduces signs and symptoms of idiopathic intracranial hypertension: a case report. 1650 78


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