Antihistamines and visual function: studies on dynamic acuity and the pupillary response to light.

Nicholson, A. N.; Smith, PA; Spencer, M. B.

doi:10.1111/j.1365-2125.1982.tb04957.x

Cited by 61 publications

(22 citation statements)

References 22 publications

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“…In comparison to pheniramine maleate the side effects were also much less with Cetirizine and Astemizole (Table IV). However, in our study incidence of side effects were much higher in comparision of previous reported studies in whom Cetirizine and Astemizole were claimed to be devoid of CNS side effects and anti cholinergic effects (Callier et al, 1981), wilson and Hillas (1982), Nicolson et al, 1982 andVijay et al, 1994). The higher incidence of these side effects in our study might be because of the fact that we specifically asked regarding these effects from all such patients who failed to volunteer any adverse effects of the drug.…”

Section: Discussionsupporting

confidence: 74%

Cetirizine and astemizole in allergic rhinitis a comparative study

Jain

1999

IJO & HNS

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The efficacy, safety and side effects of Cetirizine and Astemizole were compared with Pheniramine maleate in sixty cases of allergic rhinitis. All medications were stopped one week prior to treatment. Cetirizine, Astemizole or Pheniramine maleate were given as a single daily dose for 15 days. On completion of treatment results were evaluated subjectively as well as objectively, Cetirizine and Astemizole were found to be more effective than Pheniramine maleate. The side effects were minimum with Cetirizine.

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Section: Discussionsupporting

confidence: 74%

Cetirizine and astemizole in allergic rhinitis a comparative study

Jain

1999

IJO & HNS

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“…HR1 antagonists decrease the critical flicker fusion frequency. [59][60][61][62] The responses of macaque parasol ganglion cells to luminance flicker are identical to those of human subjects under the same conditions, 63 and it is possible that the antihistamines act on the neural circuit providing input to parasol cells. In rats, dopaminergic neurons express HR1 (Fig.…”

Section: Retinopetal Axons Containing Histaminementioning

confidence: 71%

Retinopetal Axons in Mammals: Emphasis on Histamine and Serotonin

Gastinger

Tian

Horváth

et al. 2006

Current Eye Research

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Since 1892, anatomical studies have demonstrated that the retinas of mammals, including humans, receive input from the brain via axons emerging from the optic nerve. There are only a small number of these retinopetal axons, but their branches in the inner retina are very extensive. More recently, the neurons in the brain stem that give rise to these axons have been localized, and their neurotransmitters have been identified. One set of retinopetal axons arises from perikarya in the posterior hypothalamus and uses histamine, and the other arises from perikarya in the dorsal raphe and uses serotonin. These serotonergic and histaminergic neurons are not specialized to supply the retina; rather, they are a subset of the neurons that project via collaterals to many other targets in the central nervous system, as well. They are components of the ascending arousal system, firing most rapidly when the animal is awake and active. The contributions of these retinopetal axons to vision may be predicted from the known effects of serotonin and histamine on retinal neurons. There is also evidence suggesting that retinopetal axons play a role in the etiology of retinal diseases. Keywordscentrifugal; efferent; histamine; primate; serotonin MORPHOLOGY AND FUNCTIONS OF RETINOPETAL AXONS IN MAMMALSIn mammalian retinas, three types of retinopetal axons have been distinguished by morphological criteria. The first type gives rise to terminals in the outer strata of the inner plexiform layer (IPL). Typically, the axons terminate along the border with the inner nuclear Copyright (Figs. 1A and 1C). Using the Golgi method, axons with this pattern of branching have been identified in dog 1 and chimpanzee 2 retinas. The second type of retinopetal axon is larger in diameter, varicose, and terminates in the outer plexiform layer (OPL). In rats, these axons are labeled with antibodies to serotonin after loading the retina with a related indoleamine, 5,7-dihydroxytryptamine (5,7-DHT). They originate from perikarya in the optic chiasm or the preoptic area of the hypothalamus. 3 Retinopetal axons similar to these are labeled with neurofilament antibodies in the mouse retina. 4 Neurons that project from the anterior hypothalamus to the retina have been identified in a prosimian, 5 but their terminals in the retina have not been described.The third type of retinopetal axon branches extensively in IPL (Fig. 1B). Using the Golgi method, Polyak described axons like these in macaque retinas. 2 They run in the optic fiber layer (OFL), and they give off a nearly vertical branch to the IPL, where they branch extensively in a broad band in the center of the layer. In the mouse retina, axons with a similar branching pattern are labeled with neurofilament antibodies. 4 These axons are also labeled using reduced silver stains in monkey 6,7 and human 8,9 retinas. These studies confirmed and extended Polyak's descriptions, and they also demonstrated clear morphological differences between retinopetal axons and those of ganglion cells with intraretin...

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“…Mann, Crowe, & Tietze (1989) and Woodward (1990) have described the chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of many of the nonsedating histamine HIreceptor antagonists and their differences with traditional antihistamines such as diphenhydramine (Benadryl) and chlorpheniramine. Terfenadine has shown little or no performance impairment when compared to the significant performance impairments shown with centrally acting antihistamines such as diphenhydramine (Betts, Markman, L••benham, Mortiboy & McKevitt, 1984;Clarke & Nicholson, 1978;Cohen, Hamilton, & Peck, 1987;Fink & Irwin, 1979;Gaillard, Gruisen, & de Jong, 1988;Goetz, Jocobsen, Murnarne, Reid, Repperger, Goodyear, & Martin, 1989;Kulshrestha, Gupta, Turner, & Wadsworth, 1978;Moskowitz & Burns, 1988;Nicholson, Smith, & Spencer, 1982;Nicholson & Stone, 1986;and Schilling, Adamus, & Kuthan, 1990). Performance was assessed in asymptomatic adults with simple tasks such as reaction time, adaptive tracking, continuous memory, visual search, visuo-motor coordination, dynamic visual acuity, digit symbol substitution, divided attention, vigilance, finger tapping, body sway, eye movements, critical flicker fusion and wfth subjective scales such as mental status surveys, self-rating scales to assess mood state, and symptom questionnaires.…”

Section: Medicationsmentioning

confidence: 99%