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

We describe an alloimmunized female patient who developed serious adverse reactions when receiving HPA-incompatible platelet transfusions. She had received 13 transfusions with random platelets before the first allergic reactions. Antibodies against both the human leucocyte antigens (HLA) and several human platelet antigens (HPA) were detected at the time of transfusions. When the patient received HLA- and HPA-compatible platelets, no reactions followed the transfusions and platelet count increments were good. When she was transfused with platelets from donors with one foreign HLA antigen, her reactions were fever, chills and headache and the response to platelet transfusions was poor. When the platelets were HLA compatible but HPA incompatible, the reactions were repeatedly rapid pulse, shortness of breath, tightness of chest and wheezing interpretable as anaphylactoid reactions. Platelet count increments were satisfactory. When rare side-effects occur after transfusion, detailed immunohaematological studies are indicated.
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PMID:Serious adverse events after HPA-incompatible platelet transfusions in an alloimmunized patient with leukaemia. 980 Feb 95

OBJECTIVE AND IMPORTANCE: Brain stem and cerebellar edema rarely have been described as the principal manifestation of hypertensive encephalopathy. In addition, secondary hydrocephalus has been described in only a few cases in the literature. We present an unusual case of posterior fossa swelling and hydrocephalus resulting from hypertensive encephalopathy. CLINICAL PRESENTATION: A 53-year-old man presented with increased shortness of breath, headache, and visual changes, which had been worsening for several months. Blood pressure on presentation was 253/140 mm Hg. Neuroradiological studies revealed brain stem swelling predominantly affecting the pons, with compression of the adjacent cisterns and fourth ventricle and resultant hydrocephalus. The diagnosis of brain stem glioma was briefly entertained. INTERVENTION: The patient's blood pressure was brought under control with medical management, and he was treated with dexamethasone for 48 hours. Subsequent neuroradiological studies revealed decreased posterior fossa edema as well as marked improvement in the hydrocephalus. CONCLUSION: Hypertensive encephalopathy can present principally in the posterior fossa and can give rise to obstructive hydrocephalus. Invasive treatment of the hydrocephalus is not necessarily required in this clinical setting because reduction of the blood pressure may result in rapid improvement of the hydrocephalus.
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PMID:Posterior fossa swelling and hydrocephalus resulting from hypertensive encephalopathy: case report and review of the literature 1037 34

EDS type IV presents a diagnostic and therapeutic challenge to the primary care physician, surgeon, and rheumatologist. In patients for whom the diagnosis is known, avoidance of trauma, contact sports, or strenuous activities, joint bracing and protection, and counseling on contraception are helpful preventive strategies. In patients presenting with vascular, gastrointestinal, or obstetric complications, a history of hypermobility and skin fragility (easy bruising, abnormal scarring, poor wound healing) should lead to a suspicion of this diagnosis, and to caution in the use of certain invasive diagnostic and operative techniques. Efforts should be made to examine family members. Most importantly, when caring for such patients, the acute onset of headaches, chest pain, shortness of breath, and abdominal pain should arouse suspicion of a potentially catastrophic vascular or visceral event.
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PMID:Aneurysms and hypermobility in a 45-year-old woman. 1041 Apr 41

Histamine-induced food intolerance is not IgE-mediated. Skin-prick testing and specific IgE to food allergens are typically negative. Food rich in histamine or red wine may cause allergy-like symptoms such as sneezing, flush, skin itching, diarrhoea and even shortness of breath. The suspected reason is a diminished histamine degradation based on a deficiency of diamine oxidase. As diamine oxidase cannot be supplemented, a histamine-free diet was implemented to reduce histamine intake. Forty-five patients with a history of suffering from intolerance to food or wine (n = 17) and chronic headache (n = 28) were put on the diet over months to years. Fish, cheese, hard cured sausages, pickled cabbage and alcoholic beverages had to be avoided. Complaint intensity and drug-use per week prior to and 4 weeks after a histamine-free diet were compared. After 4 weeks on the diet 33/45 patients improved considerably (P < 0.01), eight of them had total remission. In 12/45 patients, however, no changes in symptoms were observed. Symptoms of food or wine intolerance significantly decreased (P < 0.02; treatment of choice), headaches decreased in frequency (P < 0.001), duration and intensity. After eating histamine-rich food symptoms were reproducible and could be eliminated by anti-histamines in most patients. These data indicate the role of histamine in food and wine intolerance and that histamine-rich food causes a worsening of symptoms in patients suffering from chronic headaches. Results obtained support the hypothesis of a deficiency of diamine oxidase in patients with intolerance to food or wine.
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PMID:Histamine-free diet: treatment of choice for histamine-induced food intolerance and supporting treatment for chronic headaches. 1077 86

With the FDA approval of Rituximab in 1998 for the treatment of lymphoma, and Trastuzumab in 1999 for the treatment of breast cancer, monoclonal antibodies were officially added to the therapeutic armamentarium against malignancy. Most of the side effects associated with these agents are due to antigen-antibody interactions on specific cells and tissues. One of the most predictable side effects of these products is a constellation of various systemic effects including flu-like symptoms such as headache, fever, sweats, skin rash, shortness of breath, hypotension, nausea, and asthenia that occurs with the first infusion of such products. Rarely severe hypotension, bronchospasm, and hypoxia and even death have occurred. The pathophysiology of these reactions appears to be secondary to the release of cytokines as the antibodies bind do circulating antigen-expressing cells that are then removed in the reticuloendothelial system of the lungs, spleen and liver. In patients with large numbers of antigen-dense cells that have a high mitotic index, such as prolymphocytic leukemia, mantle cell lymphoma, or lymphosarcoma cell leukemia, there is a risk of true tumor lysis syndrome. One should be particularly cautious when treating patients with high numbers of circulating antigen-expressing cells in the setting of underlying cardiovascular or respiratory disease.
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PMID:Infusion reactions associated with the therapeutic use of monoclonal antibodies in the treatment of malignancy. 1085 89

A 44-year-old patient died from amyotrophic lateral sclerosis (ALS) after nine years of heavy exposure to cadmium (Cd) in a nickel cadmium (Ni-Cd) battery factory. Two years after starting work he and co-workers had experienced pruritus, loss of smell, nasal congestion, nosebleeds, cough, shortness of breath, severe headaches, bone pain, and proteinuria. Upper back pain and muscle weakness progressed to flaccid paralysis. EMG findings were consistent with motor neuron disease. Cd impairs the blood-brain barrier, reduces levels of brain copper-zinc (Cu-Zn) superoxide dismutase (SOD), and enhances excitoxicity of glutamate via up-regulation of glutamate dehydrogenase and down-regulation of glutamate uptake in glial cells. High levels of methallothionein, a sign of exposure to heavy metals, have been found in brain tissue of deceased ALS patients. The effects of Cd on enzyme systems that mediate neurotoxicity and motor neuron disease suggest a cause effect relationship between Cd and ALS in this worker.
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PMID:Amyotrophic lateral sclerosis in a battery-factory worker exposed to cadmium. 1137 40

The human illness designated as possible estuarine-associated syndrome (PEAS) by the Centers for Disease Control and Prevention (CDC) has been associated with exposure to estuaries inhabited by toxin-forming dinoflagellates, including members of the fish-killing toxic Pfiesteria complex (TPC), Pfiesteria piscicida and Pfiesteria shumwayae. Humans may be exposed through direct contact with estuarine water or by inhalation of aerosolized or volatilized toxin(s). The five cases reported here demonstrate the full spectrum of symptoms experienced during acute and chronic stages of this suspected neurotoxin-mediated illness. The nonspecific symptoms most commonly reported are cough, secretory diarrhea, headache, fatigue, memory impairment, rash, difficulty in concentrating, light sensitivity, burning skin upon water contact, muscle ache, and abdominal pain. Less frequently encountered symptoms are upper airway obstruction, shortness of breath, confusion, red or tearing eyes, weakness, and vertigo. Some patients experience as few as four of these symptoms. The discovery that an indicator of visual pattern-detection ability, visual contrast sensitivity (VCS), is sharply reduced in affected individuals has provided an objective indicator that is useful in diagnosing and monitoring PEAS. VCS deficits are present in both acute and chronic PEAS, and VCS recovers during cholestyramine treatment coincident with symptom abatement. Although PEAS cannot yet be definitively associated with TPC exposure, resolution with cholestyramine treatment suggests a neurotoxin-mediated illness.
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PMID:Possible estuary-associated syndrome: symptoms, vision, and treatment. 1188 86

A 47-year-old man reported becoming confused, disoriented, and anxious while driving his car. He recalled sweating and having blurred vision, palpitations, and a diffuse headache shortly before pulling to the side of the road and losing consciousness. Emergency service personnel arrived about 15 minutes later and administered a 50% solution of dextrose intravenously. On regaining consciousness, the patient had no weakness,shortness of breath, chest pain, or loss of bowel or bladder function. He had experienced a similar episode one week earlier and several others in the distant past. Each time, symptoms had been alleviated by eating.
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PMID:An obese man with anxiety, sweating, and headache. 1156 39

During January 1998, a cluster of illnesses occurred among hotel guests in Wisconsin. Ill persons had been exposed to the hotel's whirlpool spa and swimming pool. Symptoms included headache, fever, chills, myalgia, shortness of breath, and fatigue. A diagnosis of Pontiac fever was made, based on serologic evidence of acute infection with Legionella micdadei. High concentrations of heterotrophic bacteria were recovered from the spa, despite apparently high disinfectant levels. L. micdadei was isolated from the swimming pool filter and water from the spa after heat enrichment but not from pools and spas at nearby hotels. Water from hotel pools and spas was tested to determine endotoxin levels; water from the spa of the implicated hotel contained the highest concentration of endotoxin (14,400 endotoxin units/mL). Additional studies are needed to determine the role of endotoxin from legionellae or other bacteria in the pathogenesis of Pontiac fever.
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PMID:Pontiac fever due to Legionella micdadei from a whirlpool spa: possible role of bacterial endotoxin. 1167 17

This article describes a previously unreported cultural syndrome among Khmer refugees. This common presentation of distress centers on the complaint of a sore neck, the sufferer fearing that wind-and-blood pressure may burst the vessels in this area. During an acute episode, a Khmer endures many--if not all--of the following neck-and-head complaints: headache, blurry vision, a buzzing in the ear, and dizziness. While in the throes of the sore-neck attack, the patient frequently experiences palpitations as well as other symptoms of autonomic arousal, such as diaphoresis, shortness of breath, and trembling. A sufferer of sore-neck episodes often meets panic disorder criteria. In a clinic survey, thirty-five out of eighty-five patients (41%) were found to currently suffer the "sore-neck syndrome" (i.e., to have endured at least one episode in the last month), with almost all of these thirty-five patients (80%) fearing death during the acute event. The sore-neck syndrome represents a common and important way in which distress becomes embodied. The clinician must learn this body language; otherwise, the patient's communication of psychic, interpersonal, and physical pain goes unheard--and grave somatic suffering and disability unattended to--discounted as puzzling somatic complaints and unreasonable obsessionalism about blood pressure.
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PMID:A unique panic-disorder presentation among Khmer refugees: the sore-neck syndrome. 1168 Apr 77


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