Efficient estimation of sensory thresholds

Harvey, Lewis O.

doi:10.3758/bf03201438

Cited by 242 publications

(165 citation statements)

References 33 publications

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“…Since the first intimation of a sequential maximum-likelihood procedure by Hall (1968Hall ( , 1981 several others have been suggested: QUEST (Watson & Pelli, 1979 BEST PEST (Pentland, 1980;Lieberman & Pentland, 1982), ML-TEsT (Harvey, 1986), QUADRATURE METHOD (Emerson, 1986b), IDEAL (Pelli, 1987a, b), YAAP (Treutwein, 1989(Treutwein, , 1991Treutwein & Rentschler, 1992), and ZEST (KingSmith, Grisby, Vingrys, Benes & Supowit, 1991;KingSmith et al, 1994). All use maximum-likelihood or Bayesian estimators and differ only in minor aspects (for an overview see Table 2).…”

Section: Psychophysical Incarnations Of Bayesian and Mlmethodsmentioning

confidence: 99%

“…Therefore, for a desired confidence level of y, solving the following equations leads to a condition where the best estimate of the threshold value lies in the interval (0t, 0u) with probability y In most cases equation (23) In a different approach, Watson and Pelli (1983) and Harvey (1986), referring back to Wiiks (1962), advised a likelihood-ratio test for determining a confidence interval. The arguments given by these authors for applying the test are not fully developed and three questions arise: first, the test does not account for the sequential nature of the estimation problem.…”

Section: Bayes' Estimationmentioning

confidence: 99%

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Adaptive psychophysical procedures

1995

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Section: Psychophysical Incarnations Of Bayesian and Mlmethodsmentioning

confidence: 99%

Section: Bayes' Estimationmentioning

confidence: 99%

Adaptive psychophysical procedures

1995

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“…Briefly, thresholds were estimated by fitting a Gaussian integral psychometric f unction to the observed withdrawal rates, for each of the tested von Frey hairs, using a maximum-likelihood fitting method (Harvey, 1986;Treutwein and Strasburger, 1999). This method is a streamlined, f unctionally equivalent version of methods used previously (Dixon, 1980;Chaplan et al, 1994) and yields exactly the same results for the same set of data (Dixon, 1980;Chaplan et al, 1994;Milligan et al, 2000).…”

Section: Behavioral Measuresmentioning

confidence: 99%

“…This method is a streamlined, f unctionally equivalent version of methods used previously (Dixon, 1980;Chaplan et al, 1994) and yields exactly the same results for the same set of data (Dixon, 1980;Chaplan et al, 1994;Milligan et al, 2000). Estimated thresholds derived from a Gaussian integral f unction yield a mathematical continuum and thus are appropriate for parametric statistical analyses (Harvey, 1986;Treutwein and Strasburger, 1999;Milligan et al, 2000). The computer program PsychoFit may be downloaded from L. O. Harvey's website (http://psych.colorado.edu /ϳlharvey).…”

Section: Behavioral Measuresmentioning

confidence: 99%

Intrathecal HIV-1 Envelope Glycoprotein gp120 Induces Enhanced Pain States Mediated by Spinal Cord Proinflammatory Cytokines

et al. 2001

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Perispinal (intrathecal) injection of the human immunodeficiency virus-1 (HIV-1) envelope glycoprotein gp120 creates exaggerated pain states. Decreases in response thresholds to both heat stimuli (thermal hyperalgesia) and light tactile stimuli (mechanical allodynia) are rapidly induced after gp120 administration. gp120 is the portion of HIV-1 that binds to and activates microglia and astrocytes. These glial cells have been proposed to be key mediators of gp120-induced hyperalgesia and allodynia because these pain changes are blocked by drugs thought to affect glial function preferentially. The aim of the present series of studies was to determine whether gp120-induced pain changes involve proinflammatory cytokines [interleukin-1␤ (IL-1) and tumor necrosis factor-␣ (TNF-␣)], substances released from activated glia. IL-1 and TNF antagonists each prevented gp120-induced pain changes. Intrathecal gp120 produced time-dependent, site-specific increases in TNF and IL-1 protein release into lumbosacral CSF; parallel cytokine increases in lumbar dorsal spinal cord were also observed. Intrathecal administration of fluorocitrate (a glial metabolic inhibitor), TNF antagonist, and IL-1 antagonist each blocked gp120-induced increases in spinal IL-1 protein. These results support the concept that activated glia in dorsal spinal cord can create exaggerated pain states via the release of proinflammatory cytokines.

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“…Because there were no differences in thresholds between left and right hind paws throughout testing, data obtained from the left and right hind paws were averaged. The behavioral responses were used to calculate the 50% paw withdrawal threshold (absolute threshold), by fitting a Gaussian integral psychometric function using a maximum-likelihood fitting method (Harvey, 1986;Treutwein and Strasburger, 1999), as described in detail previously (Milligan et al, 2000). This fitting method allows parametric statistical analyses.…”

Section: Von Frey Test For Mechanical Allodyniamentioning

confidence: 99%

Interleukin-6 mediates low-threshold mechanical allodynia induced by intrathecal HIV-1 envelope glycoprotein gp120

Schoeniger-Skinner

Ledeboer

Frank

et al. 2007

Brain, Behavior, and Immunity

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Spinal cord glia (microglia and astrocytes) contribute to enhanced pain states. One model that has been used to study this phenomenon is intrathecal (i.t.) administration of gp120, an envelope glycoprotein of HIV-1 known to activate spinal cord glia and thereby induce low-threshold mechanical allodynia, a pain symptom where normally innocuous (non-painful) stimuli are perceived as painful. Previous studies have shown that i.t. gp120-induced allodynia is mediated via the release of the glial pro-inflammatory cytokines, tumor necrosis factor-α (TNF), and interleukin-1β (IL-1). As we have recently reported that i.t. gp120 induces the release of interleukin-6 (IL-6), in addition to IL-1 and TNF, the present study tested whether this IL-6 release in spinal cord contributes to gp120-induced mechanical allodynia and/or to gp120-induced increases in TNF and IL-1. An i.t. anti-rat IL-6 neutralizing antibody was used to block IL-6 actions upon its release by i.t. gp120. This IL-6 blockade abolished gp120-induced mechanical allodynia. While the literature predominantly documents the cascade of pro-inflammatory cytokines as beginning with TNF, followed by the stimulation of IL-1, and finally TNF plus IL-1 stimulating the release of IL-6, the present findings indicate that a blockade of IL-6 inhibits the gp120-induced elevations of TNF, IL-1, and IL-6 mRNA in dorsal spinal cord, elevation of IL-1 protein in lumbar dorsal spinal cord, and TNF and IL-1 protein release into the surrounding lumbosacral cerebrospinal fluid. These results would suggest that IL-6 induces pain facilitation, and may do so in part by stimulating the production and release of other proinflammatory cytokines.

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Efficient estimation of sensory thresholds

Cited by 242 publications

References 33 publications

Adaptive psychophysical procedures

Adaptive psychophysical procedures

Intrathecal HIV-1 Envelope Glycoprotein gp120 Induces Enhanced Pain States Mediated by Spinal Cord Proinflammatory Cytokines

Interleukin-6 mediates low-threshold mechanical allodynia induced by intrathecal HIV-1 envelope glycoprotein gp120

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