Spontaneous eye blink rate in winter seasonal affective disorder

Barbato, Giuseppe; Moul, Douglas E.; Schwartz, Paul J.; Rosenthal, Norman E.; Oren, Dan A.

doi:10.1016/0165-1781(93)90057-n

Cited by 25 publications

(7 citation statements)

References 22 publications

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“…Attention has been given to the ‘awareness’ issue and also adaptation to the environment of the experimental room. So, for example, some investigators have opted for an initial three minute ‘adaptation’ period or perhaps even a five minute ‘accommodation’ period at the start of blink observations. Details of any differences in SBR were not reported.…”

Section: Discussionmentioning

confidence: 99%

“…The chair height was adjusted, so that the target was aligned at the height of the primary gaze position. A fixation target was used to minimise eye movements during the measurements since asking a subject to simply look straight ahead at a blank neutral wall for an extended period of time without some sort of unambiguous reference, is likely to lead to some saccadic eye movements.…”

Section: Discussionmentioning

confidence: 99%

“…Some investigators have advocated that the initial period of recording should not be considered as a subject adapts to having their blink activity recorded. This could be a three minute ‘adaptation’ period or perhaps even a five minute ‘accommodation’ period, followed by just two minutes for calculation of blink rates. Similarly, the SBR could progressively increase (or decrease) from initial values especially under extended periods of observation and with subjects required to undertake prescriptive visual tasks or are being exposed to visual glare …”

mentioning

confidence: 99%

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Assessment of short‐term variability in human spontaneous blink rate during video observation with or without head / chin support

Doughty

2016

Clinical and Experimental Optometry

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Assessment of short‐term variability in human spontaneous blink rate during video observation with or without head / chin support

Doughty

2016

Clinical and Experimental Optometry

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“…Reduced dopaminergic function in SAD is supported by findings of abnormalities of basal serum pro-lactin levels in winter and summer (Depue et al 1989(Depue et al , 1990 and reduced heat-loss response to thermal challenge in winter (Arbisi et al 1989(Arbisi et al , 1994. Reduced eye blink rates indicative of lower dopaminergic tone were found in some studies (Depue et al 1988) but not in others (Barbato et al 1993). Negative findings include normal levels of catecholamine metabolites in the cerebrospinal fluid (CSF) of SAD patients before and after light therapy (Rudorfer et al 1993).…”

mentioning

confidence: 90%

Effects of Alpha-Methyl-Para-Tyrosine-Induced Catecholamine Depletion in Patients with Seasonal Affective Disorder in Summer Remission

Lam

Tam

Grewal

et al. 2001

Neuropsychopharmacology

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Noradrenergic and dopaminergic mechanisms have been proposed for the pathophysiology of seasonal affective disorder (SAD). We investigated the effects of catecholamine depletion using alpha-methyl-para-tyrosine (AMPT), an inhibitor of tyrosine hydroxylase, in patients with SAD in natural summer remission. Nine drug-free patients with SAD by DSM-IV criteria, in summer remission for at least eight weeks, completed a double-blind, crossover study. Behavioral ratings and serum HVA and MHPG levels were obtained for 3-day sessions during which patients took AMPT or an active control drug, diphenhydramine. The active AMPT session significantly reduced serum levels of HVA and MHPG compared with the control diphenhydramine session. The AMPT session resulted in higher depression ratings with all nine patients having significant clinical relapse, compared with two patients during the diphenhydramine session. All patients returned to baseline scores after drug discontinuation. Catecholamine depletion results in significant clinical relapse in patients with SAD in the untreated, summer-remitted state. AMPT-induced depressive relapse may be a trait marker for SAD, and/or brain catecholamines may play a direct role in the pathogenesis of SAD.

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“…So far, the studies have revealed inconsistent results : studies report increased (Jacobsen et al, 1987), but also decreased (Depue et al, 1990 ;Oren et al, 1996) basal prolactin levels in SAD patients compared with controls. One study (Depue et al, 1990), but not another (Barbato et al, 1993) showed that SAD patients have an increased eyeblink rate. Initial findings of an abnormal thermoregulatory response to a thermal challenge in SAD patients compared to controls (Arbisi et al, 1989) were not replicated.…”

Section: Catecholaminergic Mechanisms In Sad and Light Therapymentioning

confidence: 97%

Monoaminergic function in the pathogenesis of seasonal affective disorder

Neumeister

Konstantinidis

Praschak-Rieder

et al. 2001

Int. J. Neuropsychopharm.

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Seasonal affective disorder\winter type (SAD) is characterized by recurrent depressive episodes during autumn and winter alternating with non-depressive episodes during spring and summer. Light therapy with fullspectrum, bright white light has been shown to be effective for this condition. Several hypotheses have been discussed in the literature about the pathogenesis of SAD. The most prominent includes disturbances in central monoaminergic transmission. Evidence can be inferred from studies showing a seasonal rhythm of central and peripheral serotonergic functioning which may be a predisposing factor for SAD. Some of the symptoms of SAD are believed to represent an attempt to overcome a putative deficit in brain serotonergic transmission. Moreover, 5-HT receptor challenge studies suggest altered activity at or downstream to central 5-HT receptors. Monoamine depletion studies support hypotheses about serotonergic and catecholaminergic dysfunctions in SAD and suggest that light therapy may well compensate for this underlying deficit. Further, albeit indirect, support for the importance of monoaminergic mechanisms in SAD and its involvement in the mechanism of the action of light therapy comes from studies showing antidepressant efficacy of serotonergic and noradrenergic antidepressants in the treatment of SAD. Altogether, disturbances in brain monoaminergic transmission seem to play a key role in the pathogenesis of SAD ; monoaminergic systems may also play an important role in the mechanisms of the action of light therapy.

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Spontaneous eye blink rate in winter seasonal affective disorder

Cited by 25 publications

References 22 publications

Assessment of short‐term variability in human spontaneous blink rate during video observation with or without head / chin support

Assessment of short‐term variability in human spontaneous blink rate during video observation with or without head / chin support

Effects of Alpha-Methyl-Para-Tyrosine-Induced Catecholamine Depletion in Patients with Seasonal Affective Disorder in Summer Remission

Monoaminergic function in the pathogenesis of seasonal affective disorder

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