Comparison of the effects of venlafaxine, paroxetine and desipramine on the pupillary light reflex in man

Bitsios, Panos; Szabadi, E.; Bradshaw, C. M.

doi:10.1007/s002130050949

Cited by 62 publications

(56 citation statements)

References 25 publications

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“…The diameter of the pupil at any time reflects the balance between the physiologically antagonistic sympathetic (pupil dilatation) and parasympathetic (pupil constriction) influence on the iris. On the other hand, the amplitude of the light reflex response is almost exclusively determined by parasympathetic activity, parasympathomimetic drugs increasing [42,43] and parasympatholytic drugs decreasing light reflex response amplitude [44].…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

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

Hou

Scaife

Freeman

et al. 2006

Brit J Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…Modern pupillometry systems use infrared digital video systems that automatically detect and measure pupil diameter with high temporal resolution. This technique has been increasingly used in research and clinical applications, including preoperative assessment before ocular surgery (Rosen et al, 2002, Wickremasinghe et al, 2005, clinical assessment of coma after closed head injury (Larson and Muhiudeen, 1995), studies of drug metabolism (Bitsios et al, 1999, Knaggs et al, 2004, psychology (Fukuda et al, 2005, Steinhauer andHakerem, 1992) and behavioral disorders (Granholm et al, 2003). Pupillometry can detect subtle abnormalities when the pupil response appears normal or may demonstrate a small pupillary light reflex when no pupil response is apparent clinically.…”

Section: Introductionmentioning

confidence: 99%

Dysfunction of the pupillary light reflex in experimental autoimmune autonomic ganglionopathy

Mukherjee¹,

Vernino²

2007

Autonomic Neuroscience

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Autoimmune autonomic ganglionopathy (AAG) is an antibody-mediated form of severe autonomic failure. AAG is associated with serum antibodies against ganglionic acetycholine receptors (AChR) and appears to result from impaired synaptic transmission in autonomic ganglia. The rabbit model of experimental AAG (EAAG), induced by immunization, reproduces the cardinal features of the human disease. Pupillary dysfunction is a prominent and defining feature in both AAG and EAAG. We adapted infrared computer-assisted video pupillometry to record direct pupil light responses in control and EAAG rabbits. Offline analysis algorithms were used to determine latency, velocity and amplitude of the constriction and redilation phases of the light reflex. Following immunization, pupillary abnormalities were the earliest sign of evolving autonomic failure. EAAG rabbits showed significant reduction in velocity and amplitude of pupil constriction while redilation parameters were only mildly affected. Fatigue in pupillary constriction, evidenced by premature redilation of the pupil prior to termination of the light stimulus, was observed only in seropositive rabbits. The severity of pupillary abnormalities was significantly correlated with ganglionic AChR antibody level. In chronic EAAG, treatment with pyridostigmine produced a partial recovery of pupil function. We conclude that pupillometry is a robust and sensitive diagnostic tool to assess autonomic dysfunction, distinguish AAG from other disorders, and assess responses to therapy. In EAAG, pupillary dysfunction is partially reversible, parasympathetic pupil function is more severely compromised than sympathetic function, and fatigue of pupillary constriction may be seen. These characteristic abnormalities of the pupillary light reflex may prove to have diagnostic value.

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“…However, in vivo data suggest a noradrenergic effect for venlafaxine at doses within the 'therapeutic range' -it produces tyramine pressor response at 225 mg and 375 mg in patients with depression (Debonnel 2007) and at 375 mg in healthy volunteers (Harvey 2000). Furthermore, the increased pupillary dilatation and prolonged reflex latency found in healthy volunteers on 150 mg venlafaxine has been attributed to a central noradrenergic effect (Bitsios 1999). Dr Gillman's advocacy for venlafaxine and reboxetine combination on the basis of the 'floor effect' of venlafaxine requires further consideration.…”

Section: Authors' Replymentioning

confidence: 99%

Authors' reply

Palaniyappan

Insole

Ferrier³

2010

Adv. psychiatr. treat

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Comparison of the effects of venlafaxine, paroxetine and desipramine on the pupillary light reflex in man

Cited by 62 publications

References 25 publications

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

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

Dysfunction of the pupillary light reflex in experimental autoimmune autonomic ganglionopathy

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