nitrophenols and Organophosphate-Poisoning

The clinical manifestations of acute poisoning by organophosphorus compounds in man are in accord with, initially, the stimulation and, later, the blocking of cholinergic transmission due to acetylcholinesterase inhibition. The manifestations involve mainly the para-sympathetic nerves, the neuromuscular junctions, and the central nerve synapses, and to a smaller degree the cholinergic sympathetic nerves. Miosis and muscle fasciculations are useful signs for diagnosis and for the control of therapy. Blood cholinesterase determination is the best diagnostic test. The cause of death is usually respiratory paralysis. Persistent manifestations have not been confirmed. Atropine and pralidoxime are effective for treatment and useful for diagnosis. Other oximes are promising but their clinical value has not been established. Poisoning by malathion is characterized by a prolonged course and by motor signs. Poisoning by organophosphorus compounds in man differs from animal experiments in several ways: in man, exposure may occur by several different routes, the manifestations are detected more easily, and therapy is given throughout the course of illness.

Topics: Acetylcholinesterase; Atropine; Chemical Phenomena; Chemistry; Child; Cholinesterase Inhibitors; Cholinesterases; Environmental Exposure; Glycosuria; Humans; Hyperglycemia; Neurologic Manifestations; Nitrophenols; Occupational Diseases; Organophosphate Poisoning; Organothiophosphorus Compounds; Oximes; Parasympatholytics; Parathion; Poisoning; Pralidoxime Compounds; Synapses

To determine the cerebral metabolism of patients with cortical visual loss.. Two observational case studies.. Two patients who survived acute organophosphate poisoning with respiratory failure experienced severe visual loss despite relatively normal ophthalmic examination results. Magnetic resonance imaging of the brain revealed no abnormality of the visual system in either patient. Positron emission tomography (PET) was performed in these 2 patients and in 12 normal subjects with fluorine-18 fluorodeoxyglucose (FDG) as a tracer to measure cerebral glucose metabolism for the estimation of neurologic deficit in the visual cortex.. The FDG uptake values were measured as nanoCurie per cubic centimeters of tissue (nCi/cc). The relative uptake index in visual cortex was computed as the ratio of uptake of FDG in each region of visual cortex to that of cerebellum (regional visual cortex/cerebellum).. Hypometabolism was observed in the visual cortex of both patients. The relative uptake index of FDG in visual cortex (visual cortex/cerebellum) was significantly decreased in those patients compared with normal subjects.. In patients with cortical visual loss, conventional neuroimaging techniques can fail to visualize damage that can be detected by PET scanning, and PET analysis may be helpful in estimating the metabolic deficit of visual cortex and in establishing the organic nature of cortical visual loss in these patients.

Topics: Adult; Blindness, Cortical; Female; Fluorescein Angiography; Fluorodeoxyglucose F18; Humans; Insecticides; Magnetic Resonance Imaging; Mevinphos; Middle Aged; Nitrophenols; Organophosphate Poisoning; Organophosphorus Compounds; Radiopharmaceuticals; Tomography, Emission-Computed; Visual Acuity; Visual Cortex

Topics: Adolescent; Adult; Aged; Autonomic Nervous System; Color; Eye Diseases; Eye Movements; Female; Humans; Insecticides; Liver Function Tests; Male; Middle Aged; Nervous System Diseases; Nitrophenols; Organophosphate Poisoning; Pupil; Refraction, Ocular; Vision Disorders; Visual Acuity; Visual Fields

Topics: Blood Pressure; Humans; Nitrophenols; Organophosphate Poisoning; Parathion; Pyridines; Urinary Tract

Topics: Body Fluids; Chromatography; Humans; Nitrophenols; Organophosphate Poisoning; Parathion