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Nervous system drugs reactive

We believe that L.S.D.-25 is a drug which induces a controllable toxic state within the nervous system, that reactivates anxiety and fear with apparently just enough euphoria to permit recall of the provoking experiences. It does this without the sluggishness or speech difficulties so frequently encountered during I.S.T. [Insulin Shock Therapy] and following E.C.T. [Electroconvulsive Therapy]. [Pg.133]

The main systems affected by adverse effects of the quinolones are the skin, liver, and nervous system. The best-known adverse effect is phototoxicity, the risk of which varies markedly among the quinolones lomefloxacin and sparfloxacin carry a particularly high risk. The development of phototoxicity is based on an interaction between hght and the drug. Neurotoxicity also occurs, with marked variation of incidence between the various compounds. Hypersensitivity reactions to quinolones are rare, and include anaphylactic shock and anaphylactoid reactions. Organ-specific reactions attributed to hypersensitivity involve the liver and kidneys. If hypersensitivity reactions occur, switching from one qui-nolone compound to another is probably not advisable, since there is cross-reactivity. [Pg.1397]

Vasculitis affecting the central nervous system (CNS) represents a heterogeneous group of inflammatory diseases that may be idiopathic or associated with autoimmune diseases, infections, drug exposure, radiation, or cancer. Inflammatory cells invade vessel walls, and neuropeptide release increases vasomotor reactivity. These properties lead to vessel narrowing. There is also loss of normal endothelial anticoagulant properties and vessels have increased susceptibility to thrombosis. Consequently, patients with vasculitis develop ischemic and thrombotic infarctions. There is also altered wall competence, which can result in dissection or vessel wall disruption with intracranial hemorrhage. MRA is clinically used to screen for vasculitis, but is less sensitive than DSA (Fig. 6.20). One study of 14 patients with suspected vasculitis reported that MRA can detect distal stenoses in vasculitis with a... [Pg.139]

The inhibition of AChE leads to the accumulation of the neurotransmitter ACh in synapses of the central and peripheral nervous systems and over-stimulation of post-synaptic cholinergic receptors. Exposure to even small amounts of an organophosphorus compound can be fatal as the poison causes seizures, convulsions and lesions of the central nervous system. The current standard treatment for poisoning usually consists of combined administration of anticholinergic drugs (preferably atropine) and AChE reactivators (called oximes). [Pg.174]

During its many years of use as a consumer product, carbon tetrachloride compiled a grim record of toxic effects that led the U.S. Food and Drug Administration (FDA) to prohibit its household use in 1970. It is a systemic poison that affects the nervous system when inhaled, and the gastrointestinal tract, liver, and kidneys when ingested. The biochemical mechanism of carbon tetrachloride toxicity involves reactive radical species, including... [Pg.759]


See other pages where Nervous system drugs reactive is mentioned: [Pg.276]    [Pg.177]    [Pg.11]    [Pg.1140]    [Pg.184]    [Pg.80]    [Pg.1217]    [Pg.1253]    [Pg.69]    [Pg.137]    [Pg.582]    [Pg.398]    [Pg.40]    [Pg.877]    [Pg.286]    [Pg.118]    [Pg.219]    [Pg.775]    [Pg.156]    [Pg.190]    [Pg.286]    [Pg.485]    [Pg.89]    [Pg.89]    [Pg.346]    [Pg.2315]    [Pg.150]    [Pg.15]   
See also in sourсe #XX -- [ Pg.298 ]




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Nervous system drugs

Reactive system

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