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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Involvement of the nervous system in infectious mononucleosis is common. About 50% have headache on presentation. Neck stiffness without meningitis is a frequent finding. Severe neurological complications are rare though, occurring in fewer than 0.5%. We describe two patients with unusual and severe neurological complications in association with serological evidence of EBV-infection: a 32-year old female developed a bilateral optic neuritis combined with a transverse myelitis and a 72-year old man developed mononeuritis multiplex, autonomic neuropathy and a salt-wasting nephropathy.
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PMID:Severe neurological complications in association with Epstein-Barr virus infection. 947 19

Although abortive treatment and nonpharmacologic interventions are effective for many if not most patients' occasional migraine attacks, patients who have frequent and/or severe attacks may benefit from preventive pharmacotherapy. This is particularly critical for those patients whose migraines are not treated effectively by acute-care medications because lack of pain control may lead to overuse syndromes that complicate further treatment. Inappropriate use of acute-care medication may contribute to chronic daily headache, tolerance to symptomatic medication, and headache refractory to all treatment. In addition, patients who increase use of acute-care medication due to lack of effect may suffer ergotism, GI problems, liver toxicity, analgesic nephropathy, drug induced-headache, and withdrawal symptoms when overused agents are withdrawn. Finally, overuse of acute-care medication may interfere with the effectiveness of preventive medication. The remainder of this article will focus on when to treat with preventive medication and which medications are currently available for prevention of migraine.
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PMID:Pharmacological prevention of migraine. 952 60

Tacrolimus (FK-506) is an important immunosuppressive agent most often given for maintenance immunosuppression to prevent acute cellular organ rejection. A 57-year-old woman with end-stage renal disease presumed secondary to chronic glomerulonephritis underwent a living related renal allograft transplantation. She tolerated the surgery well and was discharged on postoperative day 5. She was stabilized with prednisone, azathioprine, and tacrolimus. Two years after transplantation, nefazodone 50 mg twice/day orally was prescribed due to depression. After 1 week of nefazodone therapy the patient experienced headache, confusion, and "gray areas" in her vision, without abnormal ophthalmologic findings. Her serum creatinine was elevated to 2.2 mg/dl (baseline 1.5 mg/dl), and trough tacrolimus level was markedly elevated (> 30 ng/ml). Both tacrolimus and nefazodone are metabolized by the cytochrome P450 (CYP) 3A4 system. We suspect that nefazodone inhibits metabolism of tacrolimus. Coadministration of antidepressant agents such as nefazodone, or any other drug that inhibits the CYP3A4 isoenzyme subfamily, should be anticipated to interfere with tacrolimus metabolism. Monitoring blood concentrations of tacrolimus is vital, and appropriate dosage adjustments are required when the two drugs are administered concurrently to avoid serious interactions such as nephrotoxicity and neurotoxicity.
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PMID:Interaction between tacrolimus and nefazodone in a stable renal transplant recipient. 985 39

Indinavir is a protease inhibitor used in the treatment of patients with HIV infection. Combination antiretroviral therapy with indinavir plus 2 nucleoside reverse transcriptase inhibitors (NRTIs) is associated with greater reductions in viral load, greater increases in CD4+ cell counts, and reduced morbidity and mortality when compared with 2 NRTIs alone. In the landmark clinical trial ACTG 320, the rate of progression to AIDS or death (primary end-point) among zidovudine-experienced patients treated with indinavir, zidovudine and lamivudine was approximately half that of patients who received only zidovudine plus lamivudine (6 vs 11%; p < 0.001). The durability of an indinavir-containing regimen was demonstrated in Merck protocol 035, an ongoing trial in which a significant proportion of patients had sustained viral suppression for up to 3 years. Merck protocol 039, also an ongoing trial, showed a greater effect on surrogate markers of HIV disease progression with indinavir-based triple therapy than with zidovudine plus lamivudine or indinavir monotherapy in patients with advanced disease (median baseline CD4+ count 15 cells/microL). Numerous additional clinical trials have established the beneficial antiviral and immunological effects of indinavir in both antiretroviral-naive and -experienced patients with HIV infection. Indinavir is associated with various drug class-related adverse events, including gastrointestinal disturbances (e.g. nausea, diarrhoea), headache and asthenia/fatigue. A lipodystrophy syndrome has been commonly reported with indinavir and other protease inhibitors combined with NRTIs, but it has also been reported in many protease inhibitor-naive patients, and a definitive causal link has not been established between the syndrome and protease inhibitors. Nephrolithiasis may develop in about 9% of patients receiving indinavir but does not appear to be associated with other protease inhibitors; <0.5% of patients receiving indinavir discontinue the drug because of nephrolithiasis, which may be the extreme end of a continuum of crystal-related renal syndromes. Additional renal problems (e.g. nephropathy) have been reported in small numbers of patients receiving indinavir. In summary, indinavir is a protease inhibitor with well documented efficacy when used as part of combined therapy in patients with HIV infection. Both US and UK treatment guidelines continue to recommend protease inhibitor-based regimens including indinavir as a first-line option. Indinavir is being studied as a twice daily and once daily regimen with a low dosage of ritonavir as a way to alleviate tolerability, drug interaction and patient compliance/adherence issues. Indinavir-containing triple therapy has demonstrated positive effects not only on surrogate markers of disease progression, but also on clinical end-points of mortality and morbidity in patients with HIV disease. Protease inhibitors are a significant advance in the care of patients with HIV infection, and, in an era of evidence-based medicine, indinavir represents an important component of antiretroviral treatment strategies.
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PMID:Indinavir: a review of its use in the management of HIV infection. 1065 94

Treatment with intravenous human immunoglobulin (IVIG) has become a routine therapeutic method in immunodeficiency states and autoimmune diseases. Although it is a relatively safe therapeutic method it may have serious undesirable effects. Knowledge of these undesirable effects is the prerequisite for coping with them and in some instances it is possible to prevent them. Undesirable effects of IVIG administration can be divided into six groups: 1. Generalized reaction, in particular fever, shiver, nausea, vomiting, tachycardia, dyspnoea, changes of blood pressure are recorded in less than 5% patients, usually during infusion and depend on the rate of administration. 2. Hypersensitivity and anaphylactic reactions may be also severe to fatal and are usually the manifestation of the action of antibodies against IgA; they may be anticipated in particular in patients with deficiency of class A immunoglobulins and in patients with autoimmune diseases. 3. Haematological: rare and usually clinically irrelevant haemolytic anaemia. 4. Neurological: frequent and minor headache, rarely relapsing aseptic meningitis syndrome. 5. Nephrological: renal failure which developed by the mechanism of osmotic nephrosis, relatively very rare, affecting almost exclusively patients with nephropathy present before administration of IVIG. 6. Thrombotic complications manifested by cerebral ischaemia. They are however extremely rare and their relationship to IVIG administration is controversial. At present we can rule out transmission of viral infection by IVIG preparations with the exception of transmission of the hepatitis C virus.
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PMID:[Adverse effects of administration of intravenous human immunoglobulins]. 1074 20

Posterior leukoencephalopathy syndrome is a newly recognised brain disorder that predominantly affects the cerebral white matter. Oedematous lesions particularly involve the posterior parietal and occipital lobes, and may spread to basal ganglia, brain stem, and cerebellum. This rapidly evolving neurological condition is clinically characterised by headache, nausea and vomiting, seizures, visual disturbances, altered sensorium, and occasionally focal neurological deficit. Posterior leukoencephalopathy syndrome is often associated with an abrupt increase in blood pressure and is usually seen in patients with eclampsia, renal disease, and hypertensive encephalopathy. It is also seen in the patients treated with cytotoxic and immunosuppressive drugs such as cyclosporin, tacrolimus, and interferon alfa. The lesions of posterior leukoencephalopathy are best visualised with magnetic resonance (MR) imaging. T2 weighted MR images, at the height of symptoms, characteristically show diffuse hyperintensity selectively involving the parieto-occipital white matter. Occasionally the lesions also involve the grey matter. Computed tomography can also be used satisfactorily to detect hypodense lesions of posterior leukoencephalopathy. Early recognition of this condition is of paramount importance because prompt control of blood pressure or withdrawal of immunosuppressive agents will cause reversal of the syndrome. Delay in the diagnosis and treatment can result in permanent damage to affected brain tissues.
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PMID:Posterior leukoencephalopathy syndrome. 1150 3

This study was designed to investigate the effect of delapril, an ACE inhibitor, and manidipine, a long action calcium antagonist, on persistent microalbuminuria in normotensive type 2 diabetic patients. Sixty type 2 diabetic patients were randomized to take delapril 30 mg/day or manidipine 10 mg/day for 48 weeks, in an open label design. Twenty eight of thirty subjects in the delapril group and twenty nine of thirty in the manidipine group completed the study. Urine albumin excretion as measured by the urinary albumin creatinine ratio decreased significantly in both groups (112.0+/-60.9 to 95.3+/-64.9 mg/g and 108.5+/-51.0 to 96.4+/-53.5 mg/g in the delapril and manidipine group respectively, p < 0.05, by paired t-test). Systolic and diastolic blood pressure were not significantly changed after treatment in the delapril group but significantly decreased in the manidipine group (130.9+/-7.1/80.2+/-6.1 to 127.2+/-7.1/78.0+/-5.3 mm/Hg, p < 0.05, by student's paired t-test). After 48 weeks of treatment, two patients in the delapril group and one patient in the manidipine group converted to normoalbuminuria (urinary albumin:creatinine ratio < 30 mg/g) and one patient in each group progressed to overt nephropathy (urinary albumin:creatinine ratio > 300 mg/g). There were no significant changes in fasting plasma glucose, HbA1c, serum fructosamine, creatinine, potassium and lipid profiles after 48 weeks of treatment in both groups. Two cases in the delapril group were withdrawn during the study because of an intolerable cough and one case in the manidipine group because of intolerable dizziness and headache. In conclusion, both delapril and manidipine are effective in the reduction of microalbuminuria in normotensive type 2 diabetic patients with persistent microalbuminuria.
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PMID:Effects on urinary albumin excretion and renal function changes by delapril and manidipine in normotensive type 2 diabetic patients with microalbuminuria. 1133 83

Caffeine has been an additive in analgesics for many years. However, the analgesic adjuvant effects of caffeine have not been seriously investigated since a pooled analysis conducted in 1984 showed that caffeine reduces the amount of paracetamol (acetaminophen) necessary for the same effect by approximately 40%. In vitro and in vivo pharmacological research has provided some evidence that caffeine can have anti-nociceptive actions through blockade of adenosine receptors, inhibition of cyclo-oxygenase-2 enzyme synthesis, or by changes in emotion state. Nevertheless, these actions are only considered in some cases. It is suggested that the actual doses of analgesics and caffeine used can influence the analgesic adjuvant effects of caffeine, and doses that are either too low or too high lead to no analgesic enhancement. Clinical trials suggest that caffeine in doses of more than 65 mg may be useful for enhancement of analgesia. However, except for in headache pain, the benefits are equivocal. While adding caffeine to analgesics increases the number of patients who become free from headache [rate ratio = 1.36, 95% confidence interval (CI) 1.17 to 1.58], it also leads to more patients with nervousness and dizziness (relative risk = 1.60, 95% CI 1.26 to 2.03). It is suggested that long-term use or overuse of analgesic medications is associated with rebound headache. However, there is no robust evidence that headache after use or withdrawal of caffeine-containing analgesics is more frequent than after other analgesics. Case-control studies have shown that caffeine-containing analgesics are associated with analgesic nephropathy (odds ratio = 4.9, 95% CI 2.3 to 10.3). However, no specific contribution of caffeine to analgesic nephropathy can be identified from these studies. Whether caffeine produces nephrotoxicity on its own, or increases nephrotoxicity due to analgesics, is yet to be established.
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PMID:A benefit-risk assessment of caffeine as an analgesic adjuvant. 1177 46

After the synthesis of epoetins alpha and -beta, a third molecule of recombinant human erythropoietin (rHuEPO) was synthesized and was named epoetin-omega. The molecule of epoetin-omega is a sialoglycoprotein with smaller amounts of O-bound sugars, less acidic and with different hydrophylity than the other 2 epoetins. The purpose of the study was to assess the efficacy, safety and clinical tolerance of epoetin-omega for treatment of renal anemia. In an open-label, uncontrolled prospective clinical study, 22 end-stage renal disease patients (9 male and 13 female) were followed for 6 months. They all had a hemoglobin (Hb) value below 85 g/l, and were on regular hemodialysis therapy 3 times a week, 4 hours per session. The initial weekly dose of epoetin-omega was 90 units per kg of body weight (b.w.) divided in 3 equal portions and administered subcutaneously after each dialysis session. After correction of the hemoglobin, the dose of rHuEPO was individualized to keep Hb within target limits of 100-120 g/l. To follow efficacy and safety, a number of clinical and laboratory parameters were monitored. All patients responded well to the therapy with corrected hemoglobin after the 10th week of the study. The mean dose of epoetin-omega during the correction period never exceeded 100 U/kg b.w. per week. The average maintenance dose of rHuEPO was 50-60 U/kg b.w. per week. Iron was, where needed, supplied intravenously. We noted no change in serum urea. creatinine, phosphorus, and heparin dose per dialysis session. The prothrombin time improved during the study. Serum albumin increased. No change was observed in urea reduction ratio (URR), body weight and mean arterial pressure. One serious adverse event was noted: worsening of hypertension in 1 patient, with the development of hypertensive encephalopathy and severe headache. rHuEPO treatment was stopped. The blood pressure was effectively controlled by reducting her body weight by 5%. Thereafter, rHuEPO therapy was resumed with good blood pressure control. We could conclude that recombinant human erythropoietin-omega was an efficient and safe therapeutic agent for the treatment of renal anemia.
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PMID:Epoetin omega for treatment of anemia in maintenance hemodialysis patients. 1192 56

Sphenoid opacifications may be discovered during the radiological work up of patients presenting with fever, headache, or neurological changes. While most of these patients do not require surgical intervention, prompt assessment and management is nevertheless required. Ten patients who underwent sphenoidotomy for drainage or biopsy at Montefiore Hospital during a 4-year period from September 1995 through January 2000 are presented. Nine out of 10 patients had predisposing factors such as AIDS, diabetes, leukemia, and end-stage renal disease. The most common presentation was altered mental status. One patient rapidly developed cavernous sinus thrombosis. Microbiology of sphenoid cultures included various fungi, Mycobacterium avium intracellulare, coagulase negative Staphylococci, and Corynebacterium. Neoplastic processes included non-Hodgkin's lymphoma and sinonasal undifferentiated carcinoma. When evaluating hospitalized patients with sphenoid sinus disease, a thorough history and a bedside nasal endoscopy should be performed. Conservative management in the form of intravenous antibiotics and topical decongestion should always be the first line of treatment. Those patients with clinical or radiological evidence of disease extending beyond the confines of the sphenoid sinus require immediate surgical intervention.
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PMID:Infectious and neoplastic diseases of the sphenoid sinus--a report of 10 cases. 1201 52


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