Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diseases that cause malfunction of the sympathetic nervous system provide insight into how the sympathetic nerves normally modulate responses to stress. This paper discusses insight from a number of such diseases. Transection of the cervical spinal cord leads to autonomic dysreflexia. This syndrome causes episodic hypertension in quadriplegic patients from excess sympathetic activity reflexly activated by bowel or bladder distention. These patients lack cerebral control of spinal sympathetic reflexes. Radiotherapy to the neck can destroy the arterial baroreceptors that monitor blood pressure fluctuations. Patients who lack baroreceptors have exaggerated blood pressure responses to stress. They have episodes of hypertension and hypotension that cause headaches and dizziness. Diabetics and uremics often develop a peripheral sympathetic neuropathy. They have postural hypotension and diminished blood pressure responses to stress. They are often unable to tolerate heat, exercise, or fluid deprivation. Patients with heart failure deplete sympathetic neuronal norepinephrine stores. The continual stress of heart failure diminishes their ability to respond to further stresses such as standing upright or exercising. Patients with diseases of the sympathetic nervous system illustrate that everyday occurrences such as a change in posture or ambient temperature are stresses requiring a marked change in sympathetic nervous activity. Both physical and psychological stresses elicit large initial sympathetic neuronal responses that are subsequently damped by feedback inhibition from structures such as the baroreceptors. Damage to part of these feedback loops leads to exaggerated pressor responses to stress.
 ...
PMID:Abnormal stress responses in patients with diseases affecting the sympathetic nervous system. 841 84

Patients with severe hypertension with retinoscopic bilateral papilloedema only are not classically regarded as having malignant hypertension (MHT). We have encountered 23 such patients between 1965-1993, whilst over a similar period we have seen 315 patients who fulfilled the conventional criteria for MHT with bilateral retinal haemorrhages, exudates with or without papilloedema. We hypothesised that patients with "lone" papilloedema and severe hypertension were suffering from a disease which was identical in aetiology and outcome to conventional MHT. There were no significant differences in age, mean blood pressure, proteinuria or renal function at presentation, ethnic composition, smoking status and followup blood pressure control between the papilloedema group and those presenting with conventional MHT. Clinical features at presentation in the papilloedema only group included strokes in 4, visual disturbance in 2, headaches in 3 and heart failure in 1 patient. Many patients however had no complications at presentation. After a mean followup of 59.8 months, of the "lone" papilloedema group, 7 patients (30.4%) were still alive, 1 patient was on renal dialysis therapy, 13 were dead (56.5%) and 2 (8.7%) were lost to followup. The commonest causes of death were stroke in 4 patients, renal failure in 4 and heart disease in 2. This was a similar pattern of mortality to those patients with "conventional" MHT. Lifetable analyses showed a median survival of 35.9 months for the papilloedema group which was significantly worse than the 108.7 months for the conventional MHT group (Lee-Desu statistic 4.04, p = 0.045). We suggest that patients with high blood pressure and lone bilateral papilloedema may comprise a hitherto unrecognised subgroup of patients with MHT. Once intracerebral pathology has been excluded, these patients need to be treated as aggressively as those with MHT.
 ...
PMID:Severe hypertension with lone bilateral papilloedema: a variant of malignant hypertension. 874

Levosimendan belongs to a new group of heart failure drugs, the calcium sensitizers. Because these compounds are not yet available for clinical use, the adverse drug events (ADEs) during levosimendan treatment cannot be predicted in detail. To evaluate the tolerability of levosimendan in human subjects, ADEs, safety laboratory values before and after treatment, and ambulatory ECG findings have been collected from several phase I and phase II clinical studies. By June 1994, approximately 200 subjects had received levosimendan. The most common ADE seen in healthy volunteers is headache, reported by some 40% of subjects in oral dosing but only 10% in i.v. dosing. The incidence of headache does not correlate well with the total daily dose of the drug. However, the controlled release formulations tested appear to cause vasodilatory symptoms more frequently than i.v. or rapid release oral formulations. The other typical vasodilatory ADEs seen in healthy volunteers are nausea, palpitation, and dizziness. Symptomatic hypotension is rarely encountered. It appears that heart failure patients tolerate the vasodilatory actions of the drug better than healthy volunteers. Only individual cases of headache, vertigo, and flushing have been reported, and injection site irritation has been the most commonly reported ADE (with an incidence <5%). However, because the longest administration of the i.v. infusion has been only 24 h, the duration of exposure to the drug is too short to allow any definitive conclusions to be drawn. All patients who have received levosimendan have been monitored with an ambulatory ECG. Even though some increase in heart rate is seen with high doses of the drug, there are thus far no signs of an increased incidence of ventricular tachyarrhythmias, nor have there been any noteworthy changes in the clinical laboratory safety tests. The experience with levosimendan is limited thus far and long-term data are lacking. It can be concluded, however, that at least in i.v. dosing the drug is devoid of ADEs with significant medical seriousness.
 ...
PMID:Safety of levosimendan and other calcium sensitizers. 890 34

A drug surveillance study was performed to determine the tolerance and safety of quinapril in the treatment of patients with stage 1 or 2 hypertension. The trial was noncomparative, open-label, uncontrolled, and nonrandomized. Patients with secondary hypertension, heart failure, other heart diseases, and other serious conditions were excluded. After a washout period of 2 weeks, 752 patients (316 men and 436 women) with diastolic blood pressure (DBP) between 90 and 115 mm Hg and systolic blood pressure (SBP) between 140 and 200 mm Hg were entered into the treatment phase. The mean age of patients (+/- SD) was 53.1 +/- 11.4 years. Patients initially received 10 mg/d quinapril for 4 weeks. For nonresponders, the dosage was titrated up to a maximum of 40 mg. Active treatment continued for 12 weeks. Initial blood pressures (mean +/- SD) were DBP, 102 +/- 6.1 mm Hg, and SBP, 163 +/- 14.4 mm Hg. Final blood pressures were DBP, 83 +/- 6.5 mm Hg, and SBP, 135 +/- 11.6 mm Hg. The response rate for the therapeutic goal (DBP < 90 mm Hg and SBP < 140 mm Hg, or a reduction in SBP > or = 20 mm Hg) was 67.1%; 41 patients did not complete the study. The most common adverse events were cough, headache, and dizziness; only 10 patients (1.3%) failed to complete the study because of adverse events. Quinapril, as used in current private clinical practice, is well tolerated and effective for the treatment of patients with stage 1 or 2 hypertension.
 ...
PMID:Usefulness of low-dose, once-daily quinapril as monotherapy for patients with hypertension. 893 Apr 30

Nisoldipine coat-core is an extended-release once-daily formulation of a dihydropyridine calcium antagonist effective in the treatment of chronic stable angina pectoris. With immediate-release formulations of nisoldipine, plasma drug concentrations that produce therapeutic effects result rapidly, but are not sustained and do not maintain the effects throughout a 12-hour dosage interval. In contrast, with nisoldipine coat-core, a gradual increase in plasma nisoldipine concentrations occurs over 12 hours and therapeutic concentrations are then maintained for the duration of a 24-hour dosage interval. In dosages of 10 to 60 mg once daily, nisoldipine coat-core controls symptoms of angina and improves exercise-induced signs of ischaemia in patients with stable angina. Compared with placebo, daily nisoldipine coat-core doses of > or = 20 mg provide statistically significant increases in total exercise time and time to produce angina and a trend towards an increase in the time to produce 1 mm ST segment depression, in exercise tests conducted approximately 23 hours postdose. When administered in 20 and 40 mg daily doses, nisoldipine coat-core produces improvements in exercise test parameters that are similar to those seen with amlodipine 5 or 10 mg/day or regular-release or sustained-release (SR) diltiazem 240 mg/day. The frequency of daily angina attacks and consumption of short-acting nitrates are also reduced by nisoldipine to a similar extent to that observed with these other agents. After longer term (1 year) administration of 10 to 60 mg daily, improvements in exercise test parameters are maintained, with equivalent anti-ischaemic efficacy seen in patients receiving nisoldipine coat-core alone or with background nitrate or beta-blocker therapy. Adverse events associated with nisoldipine coat-core are typical of the dihydropyridine class of calcium antagonists, with peripheral oedema and headache being most common. Nisoldipine coat-core appears to be associated with fewer deaths than placebo, notably in the DEFIANT-II (Doppler Flow and Echocardiography in Functional Cardiac Insufficiency: Assessment of Nisoldipine Therapy II) study, where only 1 death occurred with nisoldipine compared with 7 in the placebo group. Nisoldipine should not be taken during phenytoin therapy. In addition, grapefruit juice should be avoided during nisoldipine therapy and nisoldipine should not be taken concurrently with high-fat meals. Thus, the coat-core formulation of nisoldipine appears to have overcome the limitations of the shorter duration of action of immediate-release nisoldipine. Nisoldipine coat-core is well tolerated and once-daily administration produces a long duration of effective anti-ischaemic relief in patients with chronic stable angina pectoris.
 ...
PMID:Nisoldipine coat-core. A review of its pharmacodynamic and pharmacokinetic properties and clinical efficacy in the management of ischaemic heart disease. 912 71

The recognized incidence of extra- and intracranial carotid artery dissection has increased concomitantly with the progress and development of diagnostic methods. However, management for this condition is still controversial. We report in the present study the management and long-term follow-up results of 15 patients with carotid artery dissection. Mean age of the patients at onset was 47.8 years old, and male/female ratio was 12:3. Two patients were considered to be traumatic dissections and the other 13 patients were spontaneous dissections. Dissection occurred in 10 patients at the extracranial carotid artery, in 4 at the intracranial carotid artery and in 1 at the middle cerebral artery. Nine of 15 patients demonstrated hemiparesis and 5 complained of headache or facial pain. However, it was not possible to identify a characteristic symptom of dissection. Final diagnosis of dissection was made by cerebral angiography in all patients. Serial angiography was carried out in 10 of those, and 5 of the 10 patients showed some improvements of dissection in the cerebral angiogram. Treatment for those patients was selected according to the neurological and angiographical changes. Five patients were managed conservatively and 10 patients underwent surgical revascularization. During the follow-up period (mean 77.6 months), none of them showed any symptoms of reattack, and all but one, who died of heart failure 193 months after revascularization surgery, have lived independently. Although diagnosis of dissection was difficult because of the lack of characteristic symptom, serial angiography was a useful method for diagnosis and adequate management has led to a good clinical outcome.
 ...
PMID:[Management and long-term follow-up results in patients with carotid artery dissection]. 914 99

Monoclonal antibodies (mAb) are antibodies, produced by cell clones, directed against specific antigens (Ag), which act by binding specifically to the target Ag. Depending on the mAb used, this binding may have different effects on the target (neutralizing, lytic, opsonizing or antibody dependent cytotoxicity, ADCC). In clinical practice, mAb are used as immunosuppressants, antineoplastic agents, or for diagnostic purposes. mAb are given i.v. by slow infusion; the dosage depends on the mAb used. Contraindications include allergic, neoplastic, infective diseases, but also hypertension, cardiac failure and pregnancy. Infusions are usually well tolerated, headache and skin rashes being recorded only rarely; however, little is known about long-term effects (possible derangement of the immune response and/or increase in neoplasms). mAb are potentially a powerful tool in medicine, but more studies are required to define their role and establish their possible adverse effects in humans.
 ...
PMID:[Monoclonal antibody therapy]. 917 70

Carvedilol competitively blocks beta 1, beta 2 and alpha 1 receptors. The drug lacks sympathomimetic activity and has vasodilating properties that are exerted primarily through alpha 1-blockade. Animal models indicate that carvedilol confers protection against myocardial necrosis, arrhythmia and cell damage caused by oxidising free radicals, and the drug has no adverse effects on plasma lipid profiles. Recent data have confirmed the antihypertensive efficacy of carvedilol in patients with mild to moderate essential hypertension. Carvedilol has similar efficacy to other beta-blocking agents, calcium antagonists, ACE inhibitors and hydrochlorothiazide. Carvedilol also improves exercise tolerance and ischaemic symptoms in patients with stable angina pectoris. Significant reductions in serious cardiac events after acute myocardial infarction and in frequency and severity of ischaemic events in patients with unstable angina have also been demonstrated. Interest in the use of carvedilol in patients with congestive heart failure (CHF) has culminated in the publication of a cumulative analysis of data from 1094 patients with mild to severe CHF who participated in the US Carvedilol Heart Failure Study Program (4 trials). After a median follow-up of 6.5 months, a significant overall reduction in mortality relative to placebo (3.2 vs 7.8%) was revealed in patients who had received carvedilol 6.25 to 50 mg twice daily (plus diuretics and ACE inhibitors). All-cause mortality, risk of hospitalisation for cardiovascular reasons and hospitalisation costs were also reduced significantly (by 65, 28% and 62%, respectively) in these trials. In addition, the Australia and New Zealand Heart Failure Research Collaborative Group showed a 26% reduction in the combined risk of death or hospitalisation with carvedilol 12.5 to 50 mg/day relative to placebo after a mean 19-month follow-up period in 415 patients with CHF (relative risk 0.74). Adverse events with carvedilol appear to be less frequent than with other beta-blocking agents, are dosage-related and are usually seen early in therapy. Events most commonly reported are related to the vasodilating (postural hypotension, dizziness and headaches) and the beta-blocking (dyspnoea, bronchospasm, bradycardia, malaise and asthenia) properties of the drug. Carvedilol appears to date to have little effect on the incidence of worsening heart failure. Concomitant administration of carvedilol with some medications requires monitoring. Carvedilol is therefore likely to have a beneficial role in the management of controlled CHF, but further clinical studies are required to show the place of beta-adrenoceptor blocking therapy in general in this indication, and the position of carvedilol relative to other similar agents. Carvedilol is also confirmed as effective in the management of mild to moderate hypertension and ischaemic heart disease.
 ...
PMID:Carvedilol. A reappraisal of its pharmacological properties and therapeutic use in cardiovascular disorders. 921 Oct 87

Losartan is a novel orally active nonpeptidal antihypertensive agent that specifically blocks the angiotensin II type 1 receptor. This paper compares the short- and long-term safety and tolerability of losartan with those of placebo. Approximately 3800 patients with mild-to-severe essential hypertension were enrolled in 16 double-masked and 4 open clinical trials worldwide. Of these, approximately 2900 were treated with losartan either alone or in combination with other antihypertensive drugs. These trials included patients with diabetes mellitus (n = 133). An additional 5 trials enrolled hypertensive patients with compromised renal function (n = 115) or heart failure (n = 220). Losartan dosages primarily ranged from 10 to 150 mg once daily, with most patients receiving 50 to 100 mg per day. Hypertension trials generally lasted 12 weeks. The most frequently reported adverse events were headache, upper respiratory tract infection, dizziness, and asthenia/fatigue, but only dizziness occurred more frequently (> or = 1%) in the losartan-treated groups. Cough occurred in 3.1% of patients treated with losartan and 2.6% of patients treated with placebo. The overall incidence of clinical and laboratory adverse events in the losartan- and placebo-treated groups was similar among patients with hypertension and either diabetes mellitus, renal impairment, or heart failure. The data suggest that losartan can be safely administered in hypertensive patients with concomitant illnesses. It can be considered for first-line therapy and is suitable as an alternative therapy in patients already experiencing side effects with other agents.
 ...
PMID:Clinical safety and tolerability of losartan. 937 6

Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. Diagnosis of obstructive, central and mixed apneas, hypopneas, and hypoventilation is best made using polysomnography. Therapeutic options include noninvasive ventilation such as continuous positive airway pressure, bilevel positive airway pressure, intermittent positive pressure ventilation and, rarely, tracheostomy, oxygen, or protriptyline. Evaluation by a sleep specialist should be initiated in any neuromuscular patient with nocturnal symptoms such as air hunger, intermittent snoring or breathing, orthopnea, cyanosis, restlessness, and insomnia. Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.
 ...
PMID:Nocturnal respiratory failure as an indication of noninvasive ventilation in the patient with neuromuscular disease. 967 Mar 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>