Nervous system excitation

Health Hazard Information - Recommended Personal Protective Equipment Goggles or face shield plastic gloves (as for gasoline) Symptoms Following Exposure Vapor causes mild irritation of eyes and mild Irritation of respiratory tract if inhaled. Ingestion causes irritation to stomach. Aspiration causes severe lung irritation and rapidly developing pulmonary edema central nervous system excitement... 

Class II— sympathoplegic drugs that reduce heart responsiveness to sympathetic autonomic nervous system excitation molecules that reduce adrenergic stimulation of the heart, usually P-adrenergic blocking agents... 

Behavioral and Pharmacological Tests. Behavioral and pharmacological tests involve the observation of clinical signs and behavior. These include signs of changes in awareness, mood, motor activity, central nervous system excitation, posture, motor incoordination, muscle tone, reflexes, and autonomic functions. If these tests so indicate, more specialized tests can be carried out that evaluate spontaneous motor activity, conditioned avoidance responses, operant conditioning, as well as tests for motor incoordination such as the inclined plane or rotarod tests. 

Opioid analgesics interact with non-selective monoamine oxidase inhibitors, causing nervous system excitation and hypertension (70). These interactions have been reviewed (SEDA-18, 14). 

Only six of 36 children who took overdoses of co-phenotrope had signs of atropine overdose (central nervous system excitement, hypertension, fever, flushed dry skin) (1). Opioid overdose (central nervous system and respiratory depression with miosis) predominated or occurred without any signs of atropine toxicity in 33 cases (92%). Diphenoxylate-induced hjrpoxia was the major problem and was associated with slow or fast respiration, hypotonia or rigidity, cardiac arrest, and in three cases cerebral edema and death. Respiratory depression recurred 13-24 hours after the ingestion in seven cases and was probably due to accumulation of difenoxine, an active metabolite of diphenoxylate. Recommended treatment is an intravenous bolus dose of naloxone, followed by a continuous intravenous infusion, prompt gastric lavage, repeated administration of activated charcoal, and close monitoring for 24 hours. 

Signs of central nervous system excitation, including convulsions, have been seen with the use of large parenteral doses of mepacrine in the treatment of malignancies (SEDA-11, 592). 

Carbapenems (imipenem more than meropenem) are believed to increase central nervous system excitation by inhibition of GABA binding to receptors. Combinations with other GABA-inhibiting drugs, such as theophylline or quinolones, have been reported to provoke seizures (59,60). 

Feline ingestion of philodendron results in central nervous system excitability, seizures, renal failure, and encephalitis. 

Acute ingestion of lindane shampoo does have the potential to cause central nervous system excitation. 

Acute toxicity in dogs has been reported. Vomiting and lethargy are often reported. Central nervous system excitation leading to seizures, ataxia, agitation, and hyperthermia are possible. In one case, tachycardia and premature ventricular contractions were documented. 

Another condition that could be confused with botulism is nerve agent and/or atropine poisoning (28). Unlike botulinum toxin, which results in decreased secretions, nerve agent poisoning (see Chap. 3) causes patients to develop copious respiratory secretions and miotic pupils. As compared to the clear sensorium of botulism patients, atropine overdose causes nervous system excitation, including hallucinations and delirium, even though the mucous membranes are dry and patients have mydriasis (see Chap. 3). 

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