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 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

1. The two major classifications of stroke are ischemic and hemorrhagic. Ischemic strokes account for 75% of all strokes and result from the complete occlusion of an artery. Hemorrhagic strokes, often caused by aneurysm or hypertension, are caused by the rupture of a cerebral blood vessel and bleeding into the surrounding tissue. 2. The signs and symptoms of stroke may include unilateral weakness or paralysis, a sagging of one side of the face, double or blurred vision, vertigo, numbness or tingling, and language disturbances. 3. Management of ischemic stroke may include thrombolytic agents (e.g., heparin, warfarin) if the individual is treated within 6 hours after the onset of symptoms. Diagnostic tests may include, computed tomography scan, transesophageal echocardiagraphy, Doppler ultrasonography, and electrocordiography. 4. Occupational health nurses can be actively involved in helping workers modify their risks for stroke, developing and implementing an action plan if an individual is experiencing a stroke, and facilitating the individual's reentry into the worksite after rehabilitation is completed.
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PMID:Stroke. Risks, recognition, and return to work. 1222 9

The efficacy of a recently marketed posttesticular male oral contraceptive, Contrasperm, was assessed in a clinical trial involving 32 Malaysian volunteers ages 21-39 years. Contrasperm is claimed to be a pure botanical extract free of toxic chemicals, steroids, and hormones. The drug is believed to cause cells surrounding the sperm in the seminiferous tubules to secrete carbon dioxide, producing a weakly acidic environment that greatly increases the sperms' metabolism and reduces the pH of semen from its normal level of 7.5 to 1.5. The manufacturer claims that this drop in pH decreases motility from 95% to 0%. Semen samples were collected by masturbation from subjects to provide baseline data. 3 days after the initial sperm analysis, subjects were given 1 capsule of Contrasperm containing 10 mcg of the active ingredient. Additional semen analyses were conducted 30 minutes, 6 hours, and 24 hours after ingestion. Sperm count and sperm motility were greatly reduced in most subjects 30 minutes after ingestion. However, 6 subjects had increased sperm counts and 4 subjects demonstrated increased sperm motility, indicating an enhancing effect. At 6 hours after ingestion, 20 subjects had lowered sperm motility and 12 subjects showed normal sperm motility, contradicting the manufacturer's claim that motility is reduced to 0%. Although Contrasperm is claimed to be effective for 6-8 hours after ingestion, its effect wore off in less than 6 hours in 37% of subjects. Both sperm count and sperm motility returned to normal levels 24 hours after ingestion, confirming the reversibility of this drug. Most subjects reported mild side effects such as muscle weakness, blurred vision, dizziness, perspiration, urgency, abnormal muscle tension, and dry throat which persisted longer than 24 hours. Further studies, with proper controls, are needed to assess the reliability and toxicity of this preparation.
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PMID:Efficacy of Contrasperm as a male contraceptive: clinical trials in Malaysian men. 1227 93

Sarin (O-isopropylmethylphosphonofluoridate) is a highly toxic nerve agent produced for chemical warfare. Sarin is an extremely potent acetylcholinesterase (AchE) inhibitor with high specificity and affinity for the enzyme. Death by sarin is due to anoxia resulting from airway obstruction, weakness of the muscles of respiration, convulsions and respiratory failure. The main clinical symptoms of acute toxicity of sarin are seizures, tremors and hypothermia. Exposure to sarin during incidents in Japan in 1994, 1995 and 1998, and possible exposure to low levels of sarin during the Gulf War, resulted in the deaths and injury of many people in Japan and caused possible long-term health effects on Gulf War veterans. Symptoms related to sarin poisoning in Japan still exist 1-3 years after the incident and include fatigue, asthenia, shoulder stiffness and blurred vision. Sarin produced seizures in rats and pigs. Recent studies showed that long-term exposure to low levels of sarin caused neurophysiological and behavioral alterations. Toxicity from sarin significantly increased following concurrent exposure to other chemicals such as pyridostigmine bromide. Further research to examine effects of sarin on the cellular and the molecular levels, gene transcription, endocrine system as well as its long-term impact is needed.
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PMID:Sarin: health effects, metabolism, and methods of analysis. 1238 97

The authors report a case of a 65-year-old woman with small cell lung cancer who had profound, progressive lower extremity weakness, intermittent blurred vision, a dry mouth, and orthostatic hypotension. Results of laboratory and electrodiagnostic studies were consistent with the diagnosis of Lambert-Eaton myasthenic syndrome. The patient was treated with one course of intravenous immunoglobulin and had significant improvement.
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PMID:Use of intravenous immunoglobulin in Lambert-Eaton myasthenic syndrome. 1250 87

Botulinum toxin is the most potent toxin known to humans and as little as 100 ng can be lethal. The toxin blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system by introducing an endopeptadase enzyme into the presynaptic side of the synapse. The endopeptadase cleaves acetylcholine vesicle docking proteins that are required for the synapse to release acetylcholine into the synaptic cleft. Botulism occurs from consumption or inhalation of preformed botulinum toxin or growth of Clostridium botulinum bacteria in the infant gastrointestinal tract or within a wound. Growth of C. botulinum in the immature gut or wound will release botulinum toxin that reaches the circulation. All forms of botulism cause progressive weakness, bulbar signs (blurred vision, diplopia, mydriasis, dysphagia, and dysarthria), and respiratory failure with normal sensation and mentation. Treatment is aimed at 1) maintaining respiration via intubation and mechanical ventilation, 2) stopping progression of weakness by administration of botulinum antitoxin (equine trivalent botulinum antitoxin for adults and botulism immune-globulin intravenous-human for infant botulism), and 3) preventing complications from weeks of paralysis with good supportive care. The source of the botulinum toxin should be identified to prevent additional cases. Patients can recover normal muscle strength within weeks to months, but usually complain of fatigue for years.
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PMID:Botulism. 1252 61

A 38-year-old subcutaneous injecting heroin addict had subacute blurred vision, dysarthria and dysphagia. The next day she could not swallow or speak and developed weakness of all limbs and respiratory failure. Electromyography showed abnormalities compatible with a presynaptic neuromuscular transmission deficit, which supported the diagnosis of botulism. The point of entry was probably a skin abscess due to injections. Treatment with antitoxin and antibiotics resulted in a favourable recovery. Wound botulism is caused by local production of toxin by Clostridium botulinum after wound infection. Although it is a rare variant of botulism, it is increasingly being reported in drug users who inject subcutaneously.
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PMID:[The clinical diagnosis 'wound botulism' in an injecting drug addict]. 1457 84

Toxoplasmosis is the most common opportunistic infection of the central nervous system in patients with AIDS. The standard treatment for toxoplasmic encephalitis is pyrimethamine and sulfadiazine. There have been few reports of concurrent Toxoplasma brain abscess and cavitary Pneumocystis carinii pneumonia (PCP) in Taiwan. We report the case of a 26-year-old homosexual man with coexisting infection with Toxoplasma gondii and P. carinii who was successfully treated for brain abscess with clindamycin and sulfadiazine. The cavitary lung lesions, initially diagnosed as pulmonary tuberculosis, were proved to be PCP by lung biopsy. HIV infection and syphilis had been diagnosed 1 year before admission. He presented with general weakness, ataxia, nausea, blurred vision and fever for 2 weeks. Magnetic resonance imaging of the brain revealed multiple ring-enhanced lesions over the cerebrum and cerebellum. Chest roentgenography showed a 3-cm lesion with cavitation over the right upper lung field. Diagnostic computerized tomography-guided lung biopsy revealed P. carinii cysts. Clindamycin, sulfadiazine and trimethoprim (TMP)-sulfamethoxazole (20 mg/kg/day TMP) were given with good response. His CD4 count rose from 40 to 280/microL 4 months later. All antibiotics were discontinued after 4.5 months due to the development of a skin rash. He was well at follow-up 1 year later. This case suggests that the combination of clindamycin and sulfadiazine is an effective treatment for Toxoplasma brain abscess and highlights the importance of diagnostic lung biopsy for cavitary lung lesions, particularly in a region endemic for tuberculosis.
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PMID:Treatment of Toxoplasma brain abscess with clindamycin and sulfadiazine in an AIDS patient with concurrent atypical Pneumocystis carinii pneumonia. 1264 93

During August 22-26, 2003, four injection-drug users (IDUs) in Yakima County, Washington, sought medical care at the same hospital with complaints of several days of weakness, drooping eyelids, blurred vision, and difficulty speaking and swallowing. All four were regular, nonintravenous injectors of black tar heroin (BTH), and one also snorted BTH. This report summarizes the investigation of these cases, which implicated wound botulism (WB) as the cause of illness.
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PMID:Wound botulism among black tar heroin users--Washington, 2003. 1367 92

The rat lungworm (Angiostrongylus cantonensis) is the principal cause of eosinophilic meningitis or meningoencephalitis worldwide. It is endemic in Taiwan and the Asia Pacific area. We report the case of a 10-year-old boy who was referred to us suffering from intermittent headache, low-grade fever and blurred vision of 4-5 days' duration. He had been treated for gastroenteritis just prior to referral. The patient's history was unremarkable, except that he raised snail (Ampullarium canaliculatus) as pet at home. On physical examination, the patient's consciousness was alert and well oriented. No papilledema was found on fundal examination. The neurological examination revealed normal cranial nerve function, mild weakness of both lower limbs and normal deep tendon reflexes, but positive Babinski and Kernig signs. Laboratory findings showed peripheral eosinophilia, elevated immunoglobulin E level, cerebrospinal fluid eosinophilic pleocytosis and the presence of stage 3 A. cantonensis larvae, which confirmed the diagnosis of eosinophilic meningitis. A 2-week course of mebendazole combined the glucocorticosteroids was beneficial in relieving headache, paresthesia and the other eosinophilic meningitis symptoms in the patient.
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PMID:Eosinophilic meningitis in a child raising snails as pets. 1473 22


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