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

Hyperprolactinemia is frequent in clinical endocrinology. Its commonest causes are, besides pregnancy and lactation, drugs, mainly involving the generally used psychopharmaca and the equally ubiquitously prescribed estrogens. The single most important cause is a pituitary tumor, the prolactinoma, but lesions of the hypothalamus or pituitary stalk, primary hypothyroidism, liver cirrhosis and chronic renal failure, among others, may also provoke hyperprolactinemia. The clinical features of hyperprolactinemia in women are mainly amenorrhea, or irregular menses, galactorrhea, hirsutism, infertility and loss of libido. In men loss of libido and/or impotence are the most important symptoms, accompanied by infertility. Macroadenoma, more frequently seen in men than in women, may cause tumor symptoms such as headache and ophthalmologic disorders (visual field loss). The main biochemical finding is hyperprolactinemia, which should be repeatedly checked. In general, high concentrations are mainly found in large adenomas, while microadenomas usually involve only mild hyperprolactinemia, though there are numerous exceptions. While dynamic tests of prolactin secretion have provided useful information about the pathophysiology of prolactin secretion, their use in routine clinical work is controversial and of limited value. As a routine neuroradiological examination, high resolution CT of the pituitary area is to be recommended. In all hyperprolactinemic patients with suspicion of macroadenoma, ophthalmologic evaluation of fundus and visual fields should be performed. Dopaminergic drugs such as bromocriptine rapidly reduce serum prolactin levels in hyperprolactinemic women and men with micro- or macroadenoma. With these drugs considerable tumor shrinkage is possible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hyperprolactinemia]. 395 83

Over the last ten years the efficacy of lithium salts in cluster headache has been well demonstrated. Our patient, who had been suffering from cluster headache for approximately 30 years, had been in haemodialysis treatment for the last ten years for chronic renal failure. Moreover, he was affected by heart failure and peptic ulcer. The patient was currently under therapy with Digitalis, Isorbide dinitrate, and ranitidine and was dialyzed three times a week for a total of five hours each time. Neither prophylactic headache therapy nor high doses of analgesic drugs had proved effective. Although this patient was in haemodialysis, lithium treatment was indicated. The administration of lithium carbonate 300 mg during dialysis days and 150 mg during non-dialysis days improved the attacks. Complete recovery from the attacks was obtained when the serum levels of lithium reached the therapeutic range. No side effects were noted.
Cephalalgia 1985 Jun
PMID:Cluster headache: clinical efficacy of lithium salts in a haemodialysis treated patient. 401 22

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

Diclofurime is a non-inotropic arterial vasodilator and an antagonist to calcium transport. We studied its antihypertensive effect in 16 hypertensive subjects. When given alone at an average dose of 240 mg/day, it induced an overall significant diminution of systolic and diastolic arterial pressure. Among the 16 subjects studied, diclofurime lowered arterial pressure below 150/90 mm Hg in seven, induced an improvement in arterial pressure in six, and showed no effect in three. When hypertension is not controlled with 450 mg diclofurime in 3 doses/day, it may be given in association with acebutolol. Diclofurime is well tolerated. The most troublesome side effects noted were headache, cardiac erethism, asthenia and edema in the lower limbs. These clinical signs were usually transient. Among these 32 patients side effects required interruption of treatment in three. Laboratory follow-up was made on day 78 and 180 after initiation of treatment. No significant change in results was noted. Renal function was studied in seven patients having normal renal function and in six chronic renal failure patients whose inulin clearance was about 30 ml min-I. It was observed that in the normal subject, the injection of a loading dose of 40 mg diclofurime followed by a maintenance dose of 80 mg during one hour induced a slight increase in glomerular filtration and a greater increase in renal blood flow; the filtered fraction was thus diminished. Diclofurime induced a clear and sustained increase in excretion of water and sodium chloride without modifying urinary excretion of potassium. In severe renal failure, no significant changes in glomerular filtration, renal blood flow or electrolyte excretion were observed with diclofurime.
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PMID:[Diclofurime: a new antihypertensive agent. Effectiveness and kidney tolerance]. 679 31

In 29 patients suffering from chronic renal failure intraocular pressure was measured during different therapeutic regimens. Conventional hemodialysis (principle of transport diffusion, n = 15) led to an increase in IOP after one hours treatment. In individuals complaining of headaches during dialysis a marked increase in IOP was observed indicating a disequilibrium syndrome. Hemofiltration is characterized by mass transfer and exchange of plasma water. When this treatment was applied to 6 patients IOP was elevated during the second hour. Simultaneous hemofiltration/hemodialysis (n = 8) had no influence on IOP behaviour. Statistically there was no correlation between the behaviour of serum osmolarity, arterial blood pressure, loss of body weight and IOP.
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PMID:[Effect of serum osmolarity, arterial blood pressure and volume loss on IOP during hemodialysis, hemofiltration and simultaneous hemofiltration/hemodialysis (author's transl)]. 690 45

Analgesic nephropathy is discussed. It has been estimated that 5-7% of all patients with chronic renal failure have a history of excessive analgesic use. Chronic analgesic abusers are predominantly women (3:1), and the peak incidence is between the ages of 40-60. Most analgesic abusers have some psychoneurosis with a history of headaches, backaches, arthritis, or ulcers. Several mechanisms for this nephrotoxicity have been proposed. It is thought that the ingestion of aspirin with phenacetin modifies the metabolism or alters the renal tissue response to one of these two drugs in such a manner as to increase toxicity. It has been proposed that the oxidative metabolites of phenacetin act in conjunction with aspirin to cause papillary necrosis. Chronic renal failure, a history of excessive analgesic use, radiological evidence of papillary necrosis, and clinical evidence of hematuria and mild proteinuria may confirm the diagnosis of analgesic nephropathy. Pharmacists should be aware of the indicence of analgesic nephropathy, and the general profile of patients who abuse analgesics. Early detection and cessation of analgesic use may avert progressive renal failure. Pharmacists should advise patients on the long-term complications of chronic analgesic use.
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PMID:Nephropathy as a hazard of analgesic abuse. 729 57

We have examined and subjected to statistical analysis the transient acute neurological complications arising in the course of hemodialysis in 103 patients with chronic renal failure (13,969 hemodialysis sessions). Our data show that such complications are multiform. Some of the symptoms are aspecific: headache, nausea and/or vomiting, muscle cramps. We have found these symptoms in over 96% of patients, often combined with extraneurological symptoms and phenomena, such as cardiocirculatory shock or increased blood pressure. The other symptoms denote real cerebral impairment: convulsions, consciousness disturbances, psychomotor agitation. They are present in 36% of the patients, but only 10.5% of the patients show a combination of at least two symptoms. In these patients the so-called "Disequilibrium syndrome" is present: its percentage in our case-series is similar to that reported in literature.
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PMID:Acute neurologic complications of hemodialysis. Study of 14,000 hemodialyses in 103 patients with chronic renal failure. 733 6

The effect of the oral slow-release formulation of Nifedipine in rapidly lowering blood pressure was studied in 20 severely hypertensive Nigerians (8 males, 12 females). A significant fall (p < 0.05) in mean systolic, diatolic, and mean arterial pressure was obtained 30 minutes after administration of Nifedipine. The fall in all three parameters of blood pressure remained sustained and significant (p < 0.05) 6 hours after a single dose administration. Side effects were minimal and limited to headaches in 20% of patients and palpitations in 10%. All patients showed a sustained control of blood pressure over a three month follow up period on slow release Nifedipine. Addition of methyldopa resulted in improved blood pressure control in one patient with chronic renal failure. It was concluded that oral slow release Nifedipine is a drug of choice in the rapid and sustained control of blood pressure in severely hypertensive patients especially in a setting where critical intensive monitoring facilities are limited.
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PMID:Oral slow-release nifedipine in the rapid treatment of severe hypertension in Nigerians. 780 25

Two cases of ruptured cerebral aneurysm with chronic renal failure were successfully treated by selecting an appropriate dialysis during the pre- and postoperative period. Case 1; a 41-year-old male, who had been receiving hemodialysis for 4 years, complained of sudden onset of headache, and his consciousness deteriorated abruptly afterwards. A ruptured basilar-left superior cerebellar artery aneurysm was diagnosed, and an external ventricular drainage device was installed. The patient slowly recovered consciousness and was scheduled for delayed operation. During this period hemodialysis was suspended and continuous ambulatory peritoneal dialysis (CAPD) was performed instead. On the 24th day, the aneurysm was clipped, and CAPD switched to ordinary hemodialysis three days after the operation. However, consciousness deteriorated and CT scan showed diffuse cerebral swelling due to disequilibrium syndrome. The patient recovered consciousness 24 hours after hemodialysis. Frequent short-term dialysis eventually eliminated this syndrome. Case 2; a 60-year-old male, who had been receiving hemodialysis for 6 years, complained of a sudden severe headache, and a ruptured anterior communicating artery aneurysm was diagnosed. Emergency clipping of the aneurysm was performed and, except for mild vasospasm on the seventh day, the patient's recovery was uneventful postoperatively, with non-anticoagulative agent hemodialysis. These two cases demonstrate that chronic renal failure of a ruptured cerebral aneurysm patient can, with good prognosis, be treated by CAPD preoperatively, and non-anticoagulative agent hemodialysis postoperatively, followed by ordinary dialysis carefully avoiding the disequilibrium syndrome.
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PMID:[Ruptured cerebral aneurysm associated with chronic renal failure: case report and evaluation of dialysis]. 842 92


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