Nervous System Effects

Headache and insomnia are common initial side effects that usually disappear after the first few weeks of treatment. 

MAOIs fall between TCAs and SSRIs in terms of lethality in overdose. Most complications related to MAOI overdose arise from the drugs stimulation of the sympathetic nervous system. MAOIs are most dangerous when patients experience hypertensive crises as the result of ingesting foods with high tyramine content. 

Inhibition of MAO can cause severe interactions with other drugs, as detailed in the Hypertensive Crisis and Serotonin Syndrome subsections earlier in this section. A list of drugs that interact with the nonselective MAOIs is provided in Table 2-5. 

An overdosage of local anesthetics can produce dose-dependent central nervous system (CNS) side effects such as insomnia, visual and auditory disturbances, nystagmus, shivering, tonic-clonic convulsions, and finally fatal CNS depression. The initial CNS excitation and convulsions may be brought under control by diazepam or thiopental. 

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Endrin 0.002 0.002 Nervous system effects Residue of banned insecticide... 

Oxamyl (Vydate) 0.2 0.2 Slight nervous system effects Runoff/leaching from insecticide used on apples, potatoes, and tomatoes... 

TCDD is the most potent inducer of chloracne. This has been well known since the accident in Seveso, Italy, in 1976 in which large amounts of TCDD were distributed in the environment subsequent to an explosion in a factory that produced a chlorophenoxy herbicide, 2,4,5-T. TCDD is an impurity produced during the production of 2,4,5-T. The most common long-term effect of TCDD exposure was chloracne. Exposed individuals also suffered increased excretion of porphyrins, hyper-pigmentation, central nervous system effects, and liver damage and increased risk of cancer was a long-term consequence of the exposure. In addition to TCDD, polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans, and polychloronaphthalens cause chloracne as well as other effects typical of TCDD. 7i... 

The various stimulants have no obvious chemical relationships and do not share primary neurochemical effects, despite their similar behavioral effects. Cocaines chemical strucmre does not resemble that of caffeine, nicotine, or amphetamine. Cocaine binds to the dopamine reuptake transporter in the central nervous system, effectively inhibiting dopamine reuptake. It has similar effects on the transporters that mediate norepinephrine and serotonin reuptake. As discussed later in this chapter in the section on neurochemical actions mediating stimulant reward, dopamine is very important in the reward system of the brain the increase of dopamine associated with use of cocaine probably accounts for the high dependence potential of the drug. 

Children are affected by methyl parathion in the same manner as adults. Exposure to high levels of methyl parathion, even for short periods, may result in changes in the nervous system, leading to headaches, dizziness, confusion, blurred vision, difficulty breathing, vomiting, diarrhea, loss of consciousness, and death (see also Section 1.5 for a more complete description of how methyl parathion affects human health). It is not known whether children are more sensitive to the effects of methyl parathion than adults. There is some indication that young rats may be more sensitive than adults to nervous system effects. 

Dille JR, Smith WS. 1964. Central nervous system effects of chronic exposure to organophosphate insecticides. Aerospace Medicine May 475-478. 

Symptoms of endosulfan poisoning have been seen in some people who were exposed to very large amounts of this pesticide during its manufacture. Symptoms of endosulfan poisoning have also been seen in people who intentionally or accidentally ate or drank large amounts of endosulfan. Most of these people experienced convulsions or other nervous system effects. 

Irregular respiration was observed in both male and female rats after a 4-hour nose-only inhalation exposure to aerosolized endosulfan (Hoechst 1983a). In both male and female rats, dyspnea was observed at the lowest concentrations tested (12.3 and 3.6 mg/m for males and females, respectively). Autopsies of the rats that died revealed dark-red, pinhead-sized foci on the lungs. It is unclear whether these effects represent direct effects of inhaled endosulfan on respiratory tissues or whether they are secondary to central nervous system effects on respiratory function. No treatment-related effects were... 

Some of the severe central nervous system effects described above have not been described in some intermediate or chronic ingestion studies of endosulfan in experimental animals (FMC 1959a, 1965,... 

Trichloroethylene levels in the workplace are regulated by the Occupational Safety and Health Administration (OSHA). The occupational exposure limit for an 8-hour workday, 40-hour workweek, is an average concentration of 100 ppm in air. The 15-minute average exposure in air that should not be exceeded at any time during a workday is 300 ppm. The OSHA standards are based on preventing central nervous system effects after trichloroethylene exposure. For more information, see Chapter 7. 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans after inhalation exposure to trichloroethylene. Trichloroethylene exposure can result in nervous system effects that result in secondary effects on muscle strength, especially in the face (Leandri et al. 1995). See Section 2.2.1.4 for further discussion of nervous system effects following trichloroethylene exposure. 

In the past, trichloroethylene was used as a human anesthetic. Trichloroethylene has also been used by individuals who intentionally inhale it for its narcotic properties. Therefore, most of the information regarding the effects of trichloroethylene in humans comes from case studies and experiments describing effects of trichloroethylene after inhalation exposure. These studies indicate that the primary effect of exposure to trichloroethylene is on the central nervous system. Effects include headache, vertigo, fatigue, short-term memory loss, decreased word associations, central nervous system depression, and anesthesia. 

A PPI may be warranted in patients older than 60 years of age.29 Proton pump inhibitors are the most useful option because they have superior efficacy and are dosed once daily. Elderly patients maybe sensitive to the central nervous system effects of metoclopramide and H2RAs. 

Cycloserine Adults8 10-15 mg/kg per day, usually 500-750 mg/day in two doses Children 10-15 mg/kg per day Central nervous system effects Monthly assessments of neuropsychiatric status Serum concentration may be necessary until appropriate dose is established... 

Zahn, T. and Rapoport, J., Autonomic nervous system effects of acute doses of caffeine in caffeine users and abstainers. Int J Psychophslol 5, 33-41, 1987. 

Govoni S, Battaini F, Rius RA, et al. 1988. Central nervous system effects of lead A study model in neurotoxicology. NATO ASI Ser 100(A) 259-275. 

Murata K, Araki S, Yokoyama K, et al. 1995. Autonomic and central nervous system effects of lead in female glass workers in China. Am J Ind Med 28(2) 233-244. 

Several bis-heterocyclopyridines have been previously demonstrated to have various central nervous system effects <1996CHEC-II(8)967>. Pyrrolo[l, 2- ]thieno[3,2-f ]pyrazines have been demonstrated to be high-affinity ligands for 5-HT3 receptors <1996JME2068>. Pyrazolo[4,3- ]pyrrolo[ l,2-tf]pyrazines have moderate antibacterial and antifungal activity <2005M217>. 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

A casualty with mild peripheral or central nervous system effects. However these patients will not be able to manage themselves and should be controlled. 

Inhaled nickel is at least 100 times more toxic than ingested nickel because it is more readily absorbed from the lungs than from the gastrointestinal tract, and death is more often the result of respiratory failure than of nervous system effects. For example, oral ingestion of 0.05 mg Ni/kg BW and inhalation at 0.005 Ni/m3 are equally effective threshold doses in rats (USPHS 1977). 

Chlorpyrifos inhibits substrate-borne reception and emission of sex pheromone in Tri-chogramma brassicae, an entomophagus insect massively used as a biological control agent of com borers, among survivors of an LC20 dose. Inhibition was probably due to nervous system effects and was not specific to pheromone communication (Delpuech et al. 1998). 

Fed diets of >100 or >1000 mg toxaphene/kg ration for 12 weeks Liver pathology at >100 mg/kg ration and central nervous system effects at >1000 mg/kg diet 7... 

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