Effects of centrally depressant drugs on pupillary function: significance for normal and diseased subjects.

Safran, A. B.

doi:10.1111/j.1365-2125.1984.tb02587.x

Cited by 5 publications

(8 citation statements)

References 13 publications

(13 reference statements)

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“…In agreement with previous reports (Karniol et al 1976;Safran 1984;Walser et al 1987;Loewenfeld 1993, pp 683827), in the present study we found that a benzodiazepine (diazepam) failed to alter resting pupil size. Furthermore, diazepam treatment with either dose had no signiÞcant e¤ect on the amplitude of the light reßex in the safe condition.…”

Section: Discussionsupporting

confidence: 95%

Sensitivity of the fear-inhibited light reflex to diazepam

1998

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We have shown previously that pupil diameter increases and the amplitude of the pupillary light reflex is reduced when subjects are under threat of an aversive event (electric shock), and that light reflex amplitude correlates negatively with subjective anxiety. We have suggested that the "fear-inhibited light reflex" paradigm could be used as a laboratory model of human anxiety. In the present study, we examined whether two doses (5 mg and 10 mg) of the anxiolytic drug diazepam would antagonize the effects of threat on the pupillary light reflex. Twelve healthy male volunteers participated in three weekly sessions, each associated with one of three treatments (diazepam 5 mg or 10 mg or placebo) in a double-blind, balanced, cross-over design. The light reflex was recorded during either the anticipation of a shock ("threat" blocks) or periods in which no shocks were anticipated ("safe" blocks). At the end of each "threat" or "safe" block, subjects rated their anxiety using visual analogue scales. Two-factor ANOVA (treatment x condition) showed that diazepam treatment antagonized the effect of threat on light reflex amplitude in a dose-dependent manner but it did not affect the threat-induced increase in pupil diameter. Diazepam had no effect on the pupillary light reflex in the "safe" condition. Diazepam also reduced subjective anxiety and alertness in the threat condition. These results show the sensitivity of the threat-induced reduction of light reflex amplitude to anxiolytic drugs, and provide further evidence for the utility of the fear-inhibited light reflex paradigm as a laboratory model of human anxiety.

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Section: Discussionsupporting

confidence: 95%

Sensitivity of the fear-inhibited light reflex to diazepam

1998

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“…recording changes in pupil diameter in unanaesthesized human subjects after the ingestion of a single dose of 10 mg diazepam vs recording from the short ciliary nerves, without monitoring pupil diameter, in anaesthetised cats after intravenous injection of 0.1-3 mg/kg diazepam). Indeed, a central parasympatholytic effect by diazepam would be expected to result in mydriasis and the attenuation of the light reflex response which is not the case when diazepam is administered to human subjects (Karnoil et al 1976;Safran 1984;Walser et al 1987;Loewenfeld 1993a;Bitsios et al 1998;Hou et al 2006b; see also present results).…”

Section: Effects Of Diazepam On Pupillary Reflexesmentioning

confidence: 78%

“…In fact, it is well documented that benzodiazepine-induced sedation is not accompanied by any change in pupil diameter (Karnoil et al 1976;Safran 1984;Walser et al 1987;Loewenfeld 1993a;Bitsios et al 1998;Huron et al 2002;Hou et al 2006b). Interestingly, according to one report, whilst sedation induced by the benzodiazepine lorazepam was not accompanied by miosis, it was associated with an increase in pupillary sleepiness waves (Huron et al 2002).…”

Section: Introductionmentioning

confidence: 94%

Arousal and the pupil: why diazepam-induced sedation is not accompanied by miosis

et al. 2007

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Section: Introductionmentioning

confidence: 99%

“…Another class of drug not conforming to the general rule of an association between sedation and miosis are the benzodiazepines. These drugs, although highly sedative, have been reported not to influence pupillary diameter [2][3][4][5][6]. Diphenhydramine is a first-generation antihistamine [7], which has high affinity for H1 histamine receptors [8,9], without any affinity for H2 histamine receptors [10].…”

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confidence: 99%

Relationship between sedation and pupillary function: comparison of diazepam and diphenhydramine

Hou

Scaife

Freeman

et al. 2006

Brit J Clinical Pharma

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AimsTo examine the relationship between sedation and pupillary function by comparing the effects of diazepam and diphenhydramine on arousal and pupillary activity. MethodsFifteen male volunteers participated in three weekly sessions in which they received (i) diazepam 10 mg, (ii) diphenhydramine 75 mg and (iii) placebo, according to a balanced, double-blind protocol. Pupil diameter was measured with infrared pupillometry under four luminance levels. Alertness was assessed by visual analogue scales (VAS) and by critical flicker fusion frequency (CFFF). Blood pressure, heart rate and skin conductance were recorded by conventional methods. Data were analysed with analysis of variance ( ANOVA ) with multiple comparisons. ResultsThere were significant effects of ambient luminance ( F 3,42 = 305.7, P < 0.001) and treatment condition ( F 2,28 = 9.0, P < 0.01) on pupil diameter; diphenhydramine caused miosis at all luminance levels ( P < 0.05). The light reflex response was not affected. Both active drugs reduced the pre-post treatment changes compared with placebo [mean difference from placebo (95% confidence interval)]: in CFFF (Hz), diazepam − 0.73 ( − 1.63, 0.17), diphenhydramine − 1.46 ( − 2.40, − 0.52); and VAS alertness (mm), diazepam − 11.49 ( − 19.19, − 3.79), diphenhydramine − 19.83 ( − 27.46, − 12.20). There were significant effects of both session ( F 2,26 = 145.1, P < 0.001) and treatment ( F 2,26 = 5.5, P < 0.01) on skin conductance; skin conductance was reduced by both drugs ( P < 0.05). ConclusionsThe miosis by diphenhydramine and the reduction in skin conductance by both drugs may indicate central sympatholytic effects. A lack of a sympatholytic effect of diazepam on the pupil may be due to the masking of the miosis by mydriasis resulting from the inhibition of the parasympathetic output to the iris. IntroductionIt is generally accepted that there is a close relationship between the level of arousal of the central nervous system and pupil diameter: any decrease in arousal is accompanied by a decrease in pupil diameter. In fact, it has been stated that sedative drugs 'all decrease pupillary diameter in proportion to their sedative-hypnotic effects: the closer the recipient drifts toward somnolence, the smaller the pupils' [1]. This relationship may not hold in the case of drugs which, apart from causing sedation, may directly influence, by a separate pharmacological action, the pupil control mechanism. An example of such a class of drug may be the firstgeneration antihistamines. Many of these drugs, apart from causing sedation, presumably due to the blockade of central H1 histamine receptors, also have anticholinergic effects, due to their affinity for muscarinic cholinoceptors. Thus the sedation caused by these drugs is expected to induce miosis, whereas their atropine-like effect on the iris is predicted to lead to mydriasis. Another class of drug not conforming to the general rule of an association between sedation and miosis are the benzodiazepines. These drugs, although highly sedative, have been r...

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Effects of centrally depressant drugs on pupillary function: significance for normal and diseased subjects.

Cited by 5 publications

References 13 publications

Sensitivity of the fear-inhibited light reflex to diazepam

Sensitivity of the fear-inhibited light reflex to diazepam

Arousal and the pupil: why diazepam-induced sedation is not accompanied by miosis

Relationship between sedation and pupillary function: comparison of diazepam and diphenhydramine

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