Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 73-year-old woman with intravascular malignant lymphomatosis (IML) who showed generalized telangiectasia as well as various neurological symptoms. In July 1998, she developed fever, dizziness, and confusion followed by left hemiparesis, and was admitted to our hospital on August 11, 1998. Laboratory tests indicated a normochromic normocytic anemia, thrombocytopenia, elevated serum lactic dehydrogenase (LDH), C-reactive protein (CRP), and cerebrospinal fluid protein. Magnetic resonance imaging (MRI) of the brain revealed an infarct-like lesion in the left frontal lobe and multiple white matter lesions. After admission, her neurological status deteriorated and lapsed into coma and quadriplegia. At the end of September 1998, generalized telangiectasia appeared, and she was diagnosed as IML on skin biopsy. Although combination chemotherapy failed to improve her neurological symptoms, telangiectasia disappeared in a few days, and the infarct-like lesion on MRI decreased in size. Serum LDH, CRP, and thrombocyte counts were normalized. Autopsy findings revealed perivascular clustering of B cell type lymphoma cells in the left frontal lobe where abnormal signal intensity was found on MRI, as well as the spleen and the bone marrow. This case emphasizes the importance of early diagnosis and treatment in IML.
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PMID:[Intravascular malignant lymphomatosis: an autopsy case with generalized telangiectasia and various neurological manifestations]. 1148 51

The abuse of methylenedioxymethamphetamine (MDMA), flunitrazepam, ketamine hydrochloride, and gamma-hydroxybutyrate (GHB) is discussed. Club drugs are chemical substances used recreationally in social settings. Use is increasingly frequent among young people, especially during all-night dance parties. All four agents have been classified as controlled substances. MDMA ("ecstasy") is available as a tablet, a capsule, and a powder; formulations may contain many adulterants. MDMA increases the release of neurotransmitters. The desired effects are euphoria, a feeling of intimacy, altered visual perception, enhanced libido, and increased energy. The most common adverse effects are agitation, anxiety, tachycardia, and hypertension. More serious adverse effects include arrhythmias, hyperthermia, and rhabdomyolysis. Flunitrazepam is a potent benzodiazepine. At higher doses, the drug can cause lack of muscle control and loss of consciousness. Other adverse effects are hypotension, dizziness, confusion, and occasional aggression. Ketamine is a dissociative anesthetic used primarily in veterinary practice. It may be injected, swallowed, snorted, or smoked. Like phencyclidine, ketamine interacts with the N-methyl-D-aspartate channel. Analgesic effects occur at lower doses and amnestic effects at higher doses. Cardiovascular and respiratory toxicity may occur, as well as confusion, hostility, and delirium. GHB, a naturally occurring fatty acid derivative of gamma-aminobutyric acid, was introduced as a dietary supplement. Increasing doses progressively produce amnesia, drowsiness, dizziness, euphoria, seizures, coma, and death. Flunitrazepam, ketamine, and GHB have been used to facilitate sexual assault. Supportive care is indicated for most cases of club drug intoxication. The increasing abuse of MDMA, flunitrazepam, ketamine hydrochloride, and GHB, particularly by young people in social settings such as clubs, should put health care professionals on guard to recognize and manage serious reactions.
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PMID:Club drugs: methylenedioxymethamphetamine, flunitrazepam, ketamine hydrochloride, and gamma-hydroxybutyrate. 1206 92

George Gershwin, renowned composer and pianist, well known for his popular works, died on the 11th July 1937 due to a brain tumor. His neurological symptoms first appeared on that same year, in February, with a simple olfactory partial seizure, characterized by an unpleasant smell of burnt rubber (uncinated seizure). He later had a quick clinical descend, with severe headache that occurred in bouts, dizziness, coordination compromise and olfactory seizures, eventually lapsing into a coma on the 9th July 1937. It was then that a gliomatosus cyst was diagnosed, which on microscopic examination proved to be a "glioblastoma multiforme". Despite the surgical intervention, Gershwin died soon after the procedure without recovering his consciousness. We make a brief review of Gershwin's neurologic disease, with emphasis on the initial symptoms, namely the uncinated seizures.
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PMID:The uncinated crisis of George Gershwin. 1213 61

Highly effective medicinal herbs are being used successfully in China to treat malaria, for example, using Ching Hao Su, an extract from wormwood. There are 5000 varieties of medicinal herbs cataloged, some more effective than western drugs. China's barefoot doctors investigate diseases and collect effective drugs, one of which is Muching which has been highly effective in treating chronic bronchitis. Salvia miltiorrhiza, used in ancient times to activate blood circulation, is used to treat coronary artery diseases and has proved effective in 87% of angina pectoris cases. Medicinal herbs are used to treat burns, hypertension, and cancer and, although the herbs are readily available and inexpensive, they work slowly. Using medicinal herbs, a Shansi Medical College affiliated hospital successfully treated over 800 cases of extra-uterine pregnancy and, in 90% of the cases, no surgery was performed. Treatment showed medicinal herbs checked bleeding, improved circulation, and eradicated blood clots. Research is being conducted with herbal prescriptions to find safer, more effective and convenient contraceptives for men and women. A breakthrough for the Institute of Medicine of the Chinese Academy of Medicine Sciences was seen in the successful cultivation of gastrodia elata which has been used for 2000 years to treat dizziness, headaches, and infantile coma.
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PMID:China: a new medicine born of tradition. 1230 32

The Centers for Disease Control and Prevention urge physicians to become familiar with chemical and biological weapons. Preparedness among neurologists is especially important because several of these agents affect the nervous system. This article reviews 4 agents that have a history of military or terrorist use: cyanide poisons, organophosphate poisons, botulinum toxin, and anthrax. Cyanide and organophosphate poisons are characterized by dose-dependent impairment of neurological function with nonspecific symptoms such as headache or dizziness at one end of the spectrum and convulsions and coma at the other. Neurological examinations help clinicians to differentiate these agents from other intoxications. Botulinum toxin has a delayed onset of action and results in descending paralysis and prominent cranial nerve palsies. Anthrax frequently causes fulminating hemorrhagic meningitis. Early recognition of these chemical and biological weapons is key to instituting specific therapy and preventing casualties within the health care team and the community at large.
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PMID:Neurological aspects of biological and chemical terrorism: a review for neurologists. 1253 84

Carbon monoxide (CO) is a colorless, tasteless, odorless, and non-irritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb), the body's oxygen carrier, forming carboxyhemoglobin (COHb) and thereby reducing oxygen (O(2)) delivery to the body's organs and tissues. High COHb concentrations are poisonous. Central nervous system (CNS) effects in individuals suffering acute CO poisoning cover a wide range, depending on severity of exposure: headache, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma. At lower concentrations, CNS effects include reduction in visual perception, manual dexterity, learning, driving performance, and attention level. Earlier work is frequently cited to justify the statement that CO exposure sufficient to produce COHb levels of ca. 5% would be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits. In a recent literature re-evaluation, however, the best estimate was that [COHb] would have to rise to 15-20% before a 10% reduction in any behavioral or visual measurement could be observed. This conclusion was based on (1) critical review of the literature on behavioral and sensory effects, (2) review and interpretation of the physiological effects of COHb on the CNS, (3) extrapolation from the effects of hypoxic hypoxia to the effects of CO hypoxia, and (4) extrapolation from rat behavioral effects of CO to humans. Also covered in this review article are effects of chronic CO exposure, the discovery of neuroglobin, a summary of the relatively new role for endogenous CO in neurotransmission and vascular homeostasis, groups which might be especially sensitive to CO, and recommendations on further research. The interested reader is directed to other published reviews of the literature on CO and historically seminal references that form our understanding of this ubiquitous gas.
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PMID:Carbon monoxide and the nervous system. 1266 97

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.
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PMID:Human health effects of sodium azide exposure: a literature review and analysis. 1285 Nov 50

We report 43 cases of chlorodifluoromethane (Freon-22) intoxication that occurred on August 5, 2003 when a freezer in a seafood factory exploded. In this accident, 80 workers were exposed to Freon-22 gas and 43 workers developed symptoms and were transferred to six hospitals. Neurological symptoms including dizziness, headache, and nausea were most frequently observed (40 of 43 patients). One patient was comatose but recovered within 1 h with oxygen inhalation. Airway and respiratory symptoms including dysesthesia of the tongue, pharyngitis, and shortness of breath were also frequently observed (26 of 43 patients). These symptoms disappeared within a few days in all patients. There were no fatalities. Although Freon-22 has been considered to be a chlorofluorocarbon of relatively low toxicity, this incident suggests that potentially significant toxic effects may occur following large exposures.
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PMID:Acute inhalational exposure to chlorodifluoromethane (freon-22): a report of 43 cases. 1603 10

Gamma-hydroxybutyrate (GHB) is encountered in biological specimens as an endogenous neuromodulator, recreational drug, or therapeutic agent. Clinically, the drug is useful for the treatment of cataplexy. Illicit doses are typically 2-4 g, and the onset of action is rapid, occurring 15-30 min following oral ingestion. Dose-dependent effects include drowsiness, euphoria, dizziness, vomiting, respiratory depression, coma, and death. GHB was isolated from biological samples using a simple liquid-liquid extraction. The trimethylsilyl derivative (GHB-di-TMS) was analyzed using gas chromatography-mass spectrometry with positive chemical ionization. Deuterated internal standard and selective ion monitoring were used throughout. We report a GHB fatality involving a 35-year-old male who was partying with friends. Subjects at the party ingested unknown quantities of wine and GHB. A female companion at the party reported seeing the male alive before she herself passed out. She awoke to find the decedent cold and stiff. Postmortem specimens were submitted for comprehensive toxicology testing. No alcohol or common drugs of abuse were detected. A targeted analysis revealed GHB in urine, brain, vitreous fluid, femoral blood, heart blood, and liver at concentrations of 1665 mg/L, 102 mg/kg, 48 mg/L, 461 mg/L, 276 mg/L, and 52 mg/kg, respectively. Concentrations of the drug in urine and vitreous fluid are important in death investigations because of significant postmortem production of GHB in blood specimens. The cause of death was attributed to GHB intoxication, and the manner of death was accidental.
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PMID:Distribution of GHB in tissues and fluids following a fatal overdose. 1610 69

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29


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