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

11 cases of cerebral venous thrombosis in adults are reported. Main clinical signs are: intracranial hypertension (headache, nausea, papilledema in 7 cases, loss of consciousness in 6 cases, neurological deficit in 6 cases, seizure in 4 cases. 1 patient is dead, who did not receive heparin treatment. Delay before diagnosis is between 2 and 20 days, and is shortened when arteriography or MRI are available and prescribed. At least one (or several) CT examination was performed in 10 patients. Direct signs of thrombosis are uneasily detected without contrast injection, seen here in 4 cases. Empty delta sign is observed in 7 patients, lately in 4 cases, and once only afterwards. Cerebral infarction is visualized in 7 cases over 10. Its features frequently seem evocative for cerebral venous thrombosis: triangularin 4 cases or nodular shape in 3 cases with hemorragic infarct in 7 cases, with bilateral topography in 6 cases, in frontal or central areas in 7 cases. 6 patients had a MRI examination. All cerebral infarctions appeared haemorragical, even at early stages. During subacute period, venous thrombosis is constantly and easily detected by the mean of methemoglobin high signal intensity on T1 weighted images. The prediagnosis delay is short, without necessity of arteriography. MRI should take the place of CT and arteriography in investigation of a clinically suspected cerebral venous thrombosis.
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PMID:[Thrombosis of the cerebral veins. X-ray computed tomography and MRI imaging. 11 cases]. 160 50

A 42-year-old black man, a physician, presented with a three week history of intermittent right arm and leg numbness and weakness, lasting about five minutes. This was not associated with headache, visual changes, seizures, aphasia or loss of consciousness. There was no history of head trauma, migraines, or previous attacks. Positive findings on physical examination were confined to a blood pressure of 182/80; evidence of hypertensive retinopathy; normal carotid pulses without bruits; and a Grade II/VI systolic ejection murmur with normal sinus rhythm. Initial hematocrit was 25.7%; white blood cell count 14,000 cu/mm with a normal differential; platelet count 532,000 cu/mm. An electrocardiogram showed left ventricular hypertrophy. Duplex scan demonstrated normal carotid bifurcations bilaterally, and arteriogram revealed no carotid or intracranial pathology. Hemoglobin electrophoresis revealed sickle cell disease of the SS type. He was treated with transfusion therapy and has remained asymptomatic at 40 months. Approximately 20% of children with the SS type sickle cell disease will have cerebrovascular symptoms caused by small intracranial artery occlusion due to sludging of the abnormal hemoglobin. This unusual cause of transient ischemic attacks can occur in older patients of African-American ancestry and must be recognized to enable early and effective therapy with exchange transfusion.
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PMID:An unusual cause of transient ischemic attacks: case report. 187

In the paper a thorough study of the influence of the methemoglobin levels and the occurrence of certain syndromes of clinical symptoms was made in the inhabitants living in the immediate vicinity of the large refuse dumps. During a 2.5-day clinical hospitalization the following examinations were done: general medical, specialistic and neuropsychological examinations, biochemical-analytical examination, EKG, chest X-ray, USG of the abdominal cave, spirometric tests, toxicological investigation of body fluids: carboxyhemoglobin, methemoglobin, lactates. The air pollution was measured and included: continuous measurement of the suspended particulate matter, carbon monoxide, sulfur dioxide, nitrogen oxide, nitrogen dioxide and the sum of nitrogen oxides. The evaluation of the refuse dumps gas showed that its main compounds were: carbon dioxide, methane in the amount of a few volume percent. Other pollutants were: carbon monoxide, hydrogen sulfide, methane homologues and aromatic hydrocarbons. The results of biochemical investigations were within normal limit. The elevated methemoglobin levels were found in 8 patients. The increased values of blood lactate concentration were found in 14 people and in 8 people the elevation of carboxyhemoglobin level was noted. The results of toxicological investigation do not unequivocally indicate the occurrence of toxic methemoglobinemia. However, the elevated levels of methemoglobin and lactates indicate a slight degree of oxygen deficiency in the body. In the examined people typical symptoms of methemoglobinemia were not observed, the only symptoms which may indicate their impact on the central nervous system were frequent headaches and neurovegetative disorders.
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PMID:The frequency of toxic methemoglobinemias in people living in the vicinity of refuse dumps in Barycz. 871 Nov 89

A 47-year-old woman unwittingly ingested an unknown substance together with her breakfast coffee. She suffered effects such as strong headache, generalized cyanosis, and a burning sensation of the lips and collapsed some minutes later. After admission into hospital a methemoglobin level of 35% was determined in the blood. Treatment by administration of tolonium chloride (toluidine blue) resulted in complete recovery of the patient. The toxic agent was identified as aniline by GC with mass selective detection after organic solvent extraction and 11 h after ingestion the plasma aniline level was 0.13 mg/l. Acetanilide (0.79 mg/ml) and acetaminophen (2.3 mg/ml) were identified in plasma as metabolites of aniline. It was assumed that a high metabolic capacity for acetylation protected the victim from more severe reactions. Her husband confessed later that he had tried to poison her.
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PMID:Acute intoxication with aniline: detection of acetaminophen as aniline metabolite. 1087 91

Previous research of our group demonstrated an increase in L-arginine/nitric oxide (NO) pathway activity in patients with chronic daily headache (CDH) with a previous history of migraine, which was associated with a reduced platelet serotonin content and increased Ca(2+) levels. In the present work, we assessed the variations in L-arginine/NO pathway activity and platelet cyclic guanosine 3',5'-monophosphate (cGMP) levels in 25 patients affected by chronic tension-type headache (CTTH) (8 M, 17 F; age range: 34-54 years). The NO production, shown spectrophotometrically by stoichiometric transformation of oxyhemoglobin to methemoglobin due to NO synthase (NOS) activity, and inter platelet cGMP concentration, assessed with a RIA method, were determined in parallel to variations of aggregation response to 0.3 microg/ml collagen. The intracellular platelet calcium concentrations were also determined using fluorescence polarisation spectrometry. Platelet serotonin content and collagen-induced secretion as well as glutamate content were also determined with high-performance liquid chromatography (HPLC). The above parameters were compared with those of an age-matched control group. A reduction in aggregation platelet response was found. The reduction in platelet aggregation was coupled with an increased NO and cGMP production (p<0.0002 and p<0.001, respectively). A significant increase in cytosolic Ca(2+) concentration was also detected compared to control individuals (p<0.001). This was accompanied by a reduced platelet content and collagen-induced secretion of serotonin and increased content of glutamate (p<0.0001, p<0.0001 and p<0.001, respectively). The above findings were more evident in patients with analgesic abuse. It can be hypothesized that the increased NOS activity shown in platelets of CTTH patients reflects an analogous central up-regulation of NOS activity in the spinal horn/trigeminal nucleus and supraspinal structures involved in the modulation of nociceptive input from myofascial cranial structures contributing to central sensitization. The increase in NOS activity seems to be associated with a hyposerotonergic status, particularly in patients with analgesic abuse, and this can contribute to central sensitization in CTTH patients. The increase in platelet glutamate content in the same patients suggests the implication of the above excitatory amino acid in spinal and supraspinal structures involved in head pain induction and maintenance.
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PMID:L-Arginine/nitric oxide pathway in chronic tension-type headache: relation with serotonin content and secretion and glutamate content. 1203 57

Methemoglobinemia is a rare complication that can occur with the use of benzocaine-containing compounds. Two cases of methemoglobinemia are reported, and the pathophysiology and treatment of methemoglobinemia are reviewed. Both patients received topical 20% benzocaine spray before endoscopy. Immediately following the procedure, there was a reduction in O2 saturation assessed by pulse oximetry that was refractory to O2 therapy. Dramatic peripheral and central cyanosis developed. O2 saturation measured by pulse oximetry ranged from 83% to 87% on O2 by nasal prongs and 100% O2 by a nonrebreathing mask. Both patients were mildly confused and one patient complained of a significant headache. The diagnosis of methemoglobinemia was considered and arterial blood gas sampling was performed. In both patients, the arterial blood had a chocolate brown colour. A methemoglobin level of 48% and 18% was noted in patient 1 and patient 2, respectively. Both patients were treated with methylene blue, resulting in a significant improvement with gradual normalization of their O2 saturation within 10 min to 30 min. The use of benzocaine spray may not markedly alter the patient's perception of endoscopy and thus, the routine use of these agents should be questioned. If such agents are used, the physician must be aware of this association to prevent a delay in the diagnosis and management of this rare, but potentially lethal, condition.
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PMID:Benzocaine-induced methemoglobinemia: a condition of which all endoscopists should be aware. 1549 3

Acute ingestion of copper sulfate has been reported to cause gastrointestinal injury, hemolysis, methemoglobinemia, hepatorenal failure, shock; or even death. The toxicity of organocopper compounds, however, remains largely unknown. A 40-y-old man attempted suicide by ingesting some 50 ml of Sesamine fungicide. He immediately developed headache, vomiting and abdominal pain, followed by progressive dyspnea, cyanosis, dark urine and diarrhea. Severe methemoglobinemia and hemolysis were documented, and treatment with ascorbic acid and hydration was commenced. He was referred to our service 3 d later for methylene blue treatment. Despite the above treatment, his symptomatology persisted and it was not until 5 d post-ingestion that the implicated fungicide was identified as copper-8-hydroxyquinolate. BAL therapy and plasma exchange were instituted, which decreased his plasma hemoglobin from 1,300 mg/dL to 29.1 mg/dL, and lowered his methemoglobin level from 20.9% to 1.1%. His serum and urine copper concentration dropped from 238 microg/dL to 96 microg/dL and from 112 microg/dL to 16 microg/dL, respectively. He was discharged uneventfully 18 d post-ingestion. Pre-existing glucose-6-phosphate dehydrogenase (G6PD) deficiency as well as copper-induced inhibition of G6PD activity was documented during hospitalization. Organocopper compounds may cause prolonged hemolysis and methemoglobinemia through oxidative stress, especially among patients with G6PD deficiency. Antidotal therapy with methylene blue is not likely to be effective in this setting: treatment with intensive supportive measures and other therapeutic options, such as plasma exchange, should be sought.
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PMID:Prolonged hemolysis and methemoglobinemia following organic copper fungicide ingestion. 1558 50

Methemoglobinemia and hemolysis are the most prominent side-effects of exposure to a wide variety of arylamine drugs, including agricultural and industrial chemicals. Recent studies with aniline and dapsone have identified N-hydroxyl metabolites as the red blood cell (RBC) mediators. This study examines the time-course methemoglobinemic potential of several halogenated aniline phenylhydroxylamines. Symptoms of aniline poisoning include headache, fatigue, dizziness, respiratory and cardiac arrest, and possibly death. Initial studies indicated that the parent compounds are converted to their toxic metabolites (N-hydroxylamine), which enter the RBC and react with oxyhemoglobin. Consequent reduction of molecular oxygen to active oxygen species occurs, leading to RBC damage. Our laboratory is investigating the role of redox cycling and an alternative hypothesis--that a "hydroxylamine-centered" radical formed during arylhydroxylamine-oxyhemoglobin reaction results in RBC injury. The methemoglobinemic capacities of several structurally related N-hydroxy derivatives of aniline--phenylhydroxylamine (PHA), p-fluoro-, p-chloro-, p-bromo-, and p-iodo-PHA--were studied spectrophotometri-cally by treating washed rat RBC at concentrations ranging from 30 to 300 microM of the test compounds for up to 240 minutes. The results showed dose- and time-dependent changes in the induction of methemoglobin (MetHb) by aniline derivatives. The MetHb levels peaked to as high as 75% and remained elevated up to 240 minutes, depending on the electronegativity of halogenated phenylhydroxylamine aniline. This study supports the previous findings that there may be several aniline-derived metabolites other than PHA that are capable of inducing MetHb. The minimum dose required to induce this effect and duration of the MetHb may vary with the test agent.
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PMID:Aniline derivative-induced methemoglobin in rats. 1571 9

There is a long list of prescribed and over the counter oxidizing agents that can induce methemoglobinemia. We report a case of methemoglobinemia in a 46-year-old man with a mayor depression disorder who ingested 30 pills of diphenhydramine, 30 pills of haloperidol, 20 pills of dolagesic, 20 pills of cyclobenzaprine, 20 pills of naproxen, 14 pills of cephalexin, and 48 pills of chlorzoxazone. On admission, he was on mechanical ventilation, and responded only to painful stimuli. Five hours later his face, hands and feet became cyanotic. The pulse oximetry revealed a Sp02 of 85%. The dark chocolate color arterial blood showed a Pa02 of 290.8 mm Hg and oxygen saturation (Sa02) of 99%. The chocolate color arterial blood and unchanged Sp02 suggested the diagnosis of methemoglobinemia. One mg per Klg of intravenous methylene blue was administered in 5 minutes. Twenty minutes later, the cyanosis began to fade and one hour later, it had disappeared and the Sp02 was 99%. Early treatment of methemoglobinernia is crucial in preventing tissue hypoxia. Methylene blue is the treatment of choice in symptomatic patients. The initial dose of methylene blue is 1-2 mg/kg of a 1% solution administered over 5 minutes. Reduction of methemoglobin is usually complete within 1 hour. If methemoglobinernia persists, a second dose not to exceed a total dose of 5-7 mg/kg may be administered. Because headache, nausea, vomiting, diarrhea, and angina may occur with therapeutic doses, methylene blue should only be administered to those patients with symptoms or signs of hypoxia.
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PMID:Methemoglobinemia: life-threatening hazard of multiple drug ingestions. 1960

The athletic performance supplement industry is a multibillion-dollar business and one popular category claims to increase nitric oxide (NO) production. We report three patients presenting to the emergency department with adverse effects. A 33-year-old man presented with palpitations, dizziness, vomiting, and syncope, after the use of NO(2) platinum. His examination and electrocardiogram (ECG) were normal. The dizziness persisted, requiring admission overnight. A 21-year-old man with palpitations and near syncope had used a "nitric oxide" supplement. He was tachycardic to 115 bpm with otherwise normal examination. Laboratory values including methemoglobin, and ECG were unremarkable. He was treated with 1 L of saline with no change in heart rate. He was admitted for observation. A 24-year-old man presented after taking NO-Xplode with palpitations and a headache. His examination, laboratory values, and ECG were normal. He was discharged. The purported active ingredient in these products is arginine alpha-ketoglutarate (AAKG), which is claimed to increase NO production by supplying the precursor L-arginine. The symptoms could be due to vasodilation from increased levels of NO, though other etiologies cannot be excluded. AAKG containing supplements may be associated with adverse effects requiring hospital admission.
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PMID:Adverse effects associated with arginine alpha-ketoglutarate containing supplements. 1975 57


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