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Hyperactivity and

Health and Safety Factors. Clinical side effects and LD q values of most commercially available analeptics have been summarized (2). Overdoses produce symptoms of extreme CNS excitation, including resdessness, hyperexcitabiUty, skeletal muscle hyperactivity, and ia some cases convulsions. [Pg.463]

Psychostimulants are drugs that substantially influence cognitive and affective functioning and behaviors. Effects are increased motivational desire, agitation, heightened vigilance, euphoria, hyperactivity, and... [Pg.1038]

The effects of endosulfan have not been studied in children, but they would likely experience the same health effects seen in adults exposed to endosulfan. Data in adults, mostly derived from cases of accidental or intentional acute exposure (ingestion) to large amounts of endosulfan, indicate that the primary target of endosulfan toxicity is the nervous system. The effects are manifested as hyperactivity and convulsions and in some cases have resulted in death (Aleksandrowicz 1979 Blanco-Coronado et al. 1992 Boereboom et al. 1998 Cable and Doherty 1999 Lo et al. 1995 Terziev et al. 1974). These effects have been reproduced in experimental animals. [Pg.173]

Randrup, A., and Munkvad, I. Pharmaeologieal studies on the brain mechanisms underlying two forms of behavioral excitation Stereotyped hyperactivity and rage. Ann NY Acad Sci 159 928-938, 1969. [Pg.97]

The administration of low doses of PCP to rodents induces hyperactivity and stereotypy (Chen et al. 1959 ). The observation that neuroleptics such as chlorpromazine, haloperidol, and pimozide, and adrenolytics such as alpha-methyl paratyrosine antagonize these behavioral effects of PCP suggests that they are mediated by facilitation of central dopaminergic neurotransmission (Murray and Horita 1979). The actions of PCP on central dopaminergic neurotransmission may be similar to amphetamine. A dose of PCP (2.5 mg/kg) in rats, which has no effects when given alone, enhances the behavioral effects of 1 and 3 mg/kg of d-amphetamine (Balster and Chait 1978). PCP, like dopamine, has also been shown to suppress plasma prolactin (Bayorh et al. 1983). However, the firm establishment of an excl usive relationship between dopamine neuro-transmission and PCP effects is difficult because of the prominent interactions of this drug with other neurotransmitter systems. [Pg.141]

Consroe, P. Boren, J.L. and Hsu, C.H. Propranolol antagonizes phencyclidine-induced hyperactivity and stereotypy in rats. Pharmacology 24 96-104, 1982. [Pg.144]

The close resemblance between schizophrenia and PCP-induced psychosis suggests that the behavioral effects produced by PCP might be useful as a model of psychosis. On this basis, most animal studies have examined the ability of various agents to modify PCP-induced hyperactivity and stereotypy. While some studies suggest that neuroleptics such as haloperidol (Castellani and Adams 1981 Garey et al. 1980), chlorpromazine, or clozapine (Freed et al. [Pg.147]

In some pathological states, fibrinolysis is hyperactive and inhibitors have a hemostatic value. [Pg.8]

I I. A 10-yea.r-old male displays hyperactivity and is unable to focus on his schoolwork because of an inability to focus on the activity Which of the following might prove effective in this patient ... [Pg.178]

All stages Sublethal Dose-dependent increase in hyperactivity and oxygen consumption 9... [Pg.1171]

M. salmoides 67 Exposure for 8 weeks produced hyperactivity and reductions in feeding rate and in prey capture 40... [Pg.1211]

Glutamatergic dysfunction. A deficiency of glutamatergic activity produces symptoms similar to those of dopaminergic hyperactivity and possibly symptoms seen in schizophrenia. [Pg.812]

Yamamoto, T., and Ueki, S. (1978) Effects of drugs on hyperactivity and aggression induced by raphe lesions in rats. Pharmacol. Biochem. Behav., 9 821-826. [Pg.167]

Additionally, impulse-control and attention problems, hyperactivity, and even antisocial behavior could be caused by a prenatal exposure to psychoactive drugs that escaped detection. Research has linked these conditions with known prenatal toxicity, and the consequences of low levels of prenatal exposure to psychoactive substances can sometimes be missed. In these instances, the symptoms are more likely to be observed as behavioral and attributed to other causes (such as Attention-Deficit Disorder). Recent research also suggests that children of mothers who may have used substances during pregnancy also may be at risk for drug problems later in life (Baer, Sampson, Barr, Connor, Streissguth, 2003). [Pg.30]

Conners Teacher Questionnaire. The TQ form was designed to obtain teacher evaluations of children up to age 15 in terms of their interactions with peers and their ability to cope with the school environment and requirements. There are 41 items, and the first 39 have a four-point scale. Question 40 deals with the teacher s evaluation of the child s severity of illness, and question 41 deals with global improvement in four different areas. This test is used once at pretreatment and as needed afterwards. It takes about 15 minutes to complete and covers either the present or any interval period up to one month. A shorter 11-item PTQ is often used after the initial use of the 41-item TQ. The five subscales included are conduct, inattentive-passive, tension-anxiety, hyperactivity, and social ability. [Pg.817]

Ayub N, Donaldson D, Bedford D, Alloway R, Ryalls M. (1997). Lessons to be learned a case study approach. Hyperactivity and confusion in the presentation of hyoscine overdose. J Royal Soc Health. 117(4) 242-44. [Pg.535]

Most cases of mercury poisoning led to handicap, chronic disease, or death. The most frequent symptoms include numbness of limbs, lips and tongue, speech abnormalities, limb function disorders, visual acuity disorders, deafness, and muscular atrophy. Insomnia, hyperactivity, and coma have also been reported. Methylmercury penetrates the blood-brain barrier and causes central nervous system injuries. Mercury also has a teratogenic effect, leading to congenital abnormalities or congenital Minamata disease. [Pg.242]

What are these subclinical effects Very simply, they are effects that occur at blood lead levels below those that produce clinically measurable effects - they occur in the absence of any sign of overt lead poisoning. These effects can be detected only by studying various forms of behavior, such as degree of hyperactivity and classroom attention span, and performance on various tests of intelligence and mental development. Deficits in neurobehavioral development, as measured by two widely used tests - the Bayley and McCarthy Scales - have been reported in children exposed prenatally (via maternal blood) to blood... [Pg.127]

Methylphenidate (Ritalin). Methylphenidate was developed in the late 1950s and its first use was the treatment of what we now call ADHD. Since that time, it has also been approved for the treatment of narcolepsy. Its only other use is the treatment of severe refractory depression either in medically ill patients who need rapid clinical improvement or as an augmentation agent when added to other antidepressants. In the treatment of ADHD, methylphenidate not only improves attention but also reduces hyperactivity and impulsivity. Verbal and physical aggression typically decreases as well. [Pg.240]

Clonidine (Catapres). Clonidine is largely used to treat high blood pressure. Although we don t fully understand how clonidine acts, it appears to reduce norepinephrine activity by stimulating a norepinephrine receptor known as the alpha-2 receptor. When clonidine binds to alpha-2 receptors on norepinephrine neurons, so-called autoreceptors, the cells are tricked into believing that there is already sufficient norepinephrine released and thus decrease any additional release of norepinephrine. As one might anticipate, clonidine is somewhat effective at reducing the hyperactivity and impulsivity of ADHD. It does not, however, provide nearly as much benefit for the inattention of ADHD. [Pg.247]

Typical Antipsychotics. The high potency antipsychotic haloperidol (Haldol) and low potency antipsychotics chlorpromazine (Thorazine) and thioridazine (Mellaril) have also been used to treat ADHD. Although they provide a tranquilizing effect (they are in fact sometimes called major tranquilizers ) that can reduce hyperactivity and impulsivity, antipsychotics remain markedly less effective than stimulants. Antipsychotics do not noticeably improve attention in patients with ADHD, and at this time the typical antipsychotics cannot be considered a reasonable monotherapy in uncomplicated ADHD. [Pg.249]

The disease develops at 3 to 6 months of age and it is characterised by developmental delay, eczema, hyperactivity and mental retardation. Newborn babies are routinely screened for PKU in many countries. Treatment is a phenylalanine-restricted diet and supplementation with tyrosine. [Pg.63]


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See also in sourсe #XX -- [ Pg.15 , Pg.100 , Pg.101 , Pg.120 , Pg.153 ]




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Hyperactive

Hyperactivity

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