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Donald C Hood - One of the best experts on this subject based on the ideXlab platform.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    The pupillary light reflex (PLR) is a reflex that controls the constriction and dilation of the pupil in response to changes in light intensity. The PLR has been used in the clinic and in Clinical research as an objective measure of retinal and optic nerve function. Most Clinical studies have measured the latency and amplitude of pupil constriction to a brief, light stimulus.1–7 There is also a slow and sustained miosis after stimulus offset that was well known, although not necessarily well understood, at a neurophysiological level.8 The discovery of a class of retinal ganglion cells (RGCs) containing the photopigment melanopsin, which could be directly activated by light and which provide input to the pupillomotor center, provided a new understanding of the sustained PLR.9 The melanopsin-expressing intrinsic photosensitive RGCs (ipRGCs) show a delayed latency and a prolonged response that extend well after stimulus offset,10 similar to the sustained PLR. More recent studies, using pharmacologic blockades of the rod and cone input in primates11 and knockout mice,12,13 support the claim that the sustained PLR is mainly dependent on the ipRGCs. The use of the PLR as assay of the ipRGC is of potential Clinical value.5,14 First, a PLR technique to measure rod sensitivity to light has been developed as an objective measure of the effect of treatment in a Clinical trial.15–17 Second, a Protocol to evaluate the melanopsin contribution versus rod and cone contributions to the PLR may be of use in estimating the degree of damage to the RGCs versus to the retinal photoreceptors. Third, the presence of intact ipRGCs may help us to understand the currently unexplained phenomena (e.g., circadian rhythm) in some patients with little or no receptor function.18 Finally, considering the recent developments in retinal prosthesis (see, for example, Refs. 19–21), there is a need to know which patients with little or no receptor function have functioning RGCs and thus are viable candidates for recovery of vision. Kardon et al.14,22 provided evidence that a Clinical Protocol could assess the contributions of the rods, cones, and melanopsin to the PLR in patients with outer retinal disease. Although an important proof of concept, their original design was suboptimal. First, they did not establish conclusively that they had isolated the rod, cone, and melanopsin contributions to the human PLR, though their results did show evidence for discriminating patients with photoreceptor disease from healthy subjects. Second, they used a staircase stimulus paradigm of increasing intensity (13-second duration stimulus) to facilitate patient comfort and to observe both transient and sustained stimulus-on pupil responses. However, the 13-second duration stimuli, even at the highest stimulus intensity of blue light (100 cd/m2), did not reveal obvious sustained PLR after light termination, which is the characteristic electrophysiological signature of a melanopsin-mediated contribution. Recently, Kankipati et al.23,24 showed that there is a significant decrease in melanopsin-driven PLR in patients with glaucoma, a disease known to decrease the number of RGCs. The purpose here was to better understand the relative contributions of rod, cone, and melanopsin to the human PLRs and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    PURPOSE. To better understand the relative contributions of rod, cone, and melanopsin to the human pupillary light reflex (PLR) and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol. METHODS. PLR was measured with an eye tracker, and stimuli were controlled with a Ganzfeld system. In experiment 1, 2.5 log cd/m(2) red (640 ± 10 nm) and blue (467 ± 17 nm) stimuli of various durations were presented after dark adaptation. In experiments 2 and 3, 1-second red and blue stimuli were presented at different intensity levels in the dark (experiment 2) or on a 0.78 log cd/m(2) blue background (experiment 3). Based on the results of experiments 1 to 3, a Clinical Protocol was designed and tested on healthy control subjects and patients with retinitis pigmentosa and Leber's congenital amaurosis. RESULTS. The duration for producing the optimal melanopsin-driven sustained pupil response after termination of an intense blue stimulus was 1 second. PLR rod- and melanopsin-driven components are best studied with low- and high-intensity flashes, respectively, presented in the dark (experiment 2). A blue background suppressed rod and melanopsin responses, making it easy to assess the cone contribution with a red flash (experiment 3). With the Clinical Protocol, robust melanopsin responses could be seen in patients with few or no contributions from the rods and cones. CONCLUSIONS. It is possible to assess the rod, cone, and melanopsin contributions to the PLR with blue flashes at two or three intensity levels in the dark and one red flash on a blue background.

Randy H Kardon - One of the best experts on this subject based on the ideXlab platform.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    The pupillary light reflex (PLR) is a reflex that controls the constriction and dilation of the pupil in response to changes in light intensity. The PLR has been used in the clinic and in Clinical research as an objective measure of retinal and optic nerve function. Most Clinical studies have measured the latency and amplitude of pupil constriction to a brief, light stimulus.1–7 There is also a slow and sustained miosis after stimulus offset that was well known, although not necessarily well understood, at a neurophysiological level.8 The discovery of a class of retinal ganglion cells (RGCs) containing the photopigment melanopsin, which could be directly activated by light and which provide input to the pupillomotor center, provided a new understanding of the sustained PLR.9 The melanopsin-expressing intrinsic photosensitive RGCs (ipRGCs) show a delayed latency and a prolonged response that extend well after stimulus offset,10 similar to the sustained PLR. More recent studies, using pharmacologic blockades of the rod and cone input in primates11 and knockout mice,12,13 support the claim that the sustained PLR is mainly dependent on the ipRGCs. The use of the PLR as assay of the ipRGC is of potential Clinical value.5,14 First, a PLR technique to measure rod sensitivity to light has been developed as an objective measure of the effect of treatment in a Clinical trial.15–17 Second, a Protocol to evaluate the melanopsin contribution versus rod and cone contributions to the PLR may be of use in estimating the degree of damage to the RGCs versus to the retinal photoreceptors. Third, the presence of intact ipRGCs may help us to understand the currently unexplained phenomena (e.g., circadian rhythm) in some patients with little or no receptor function.18 Finally, considering the recent developments in retinal prosthesis (see, for example, Refs. 19–21), there is a need to know which patients with little or no receptor function have functioning RGCs and thus are viable candidates for recovery of vision. Kardon et al.14,22 provided evidence that a Clinical Protocol could assess the contributions of the rods, cones, and melanopsin to the PLR in patients with outer retinal disease. Although an important proof of concept, their original design was suboptimal. First, they did not establish conclusively that they had isolated the rod, cone, and melanopsin contributions to the human PLR, though their results did show evidence for discriminating patients with photoreceptor disease from healthy subjects. Second, they used a staircase stimulus paradigm of increasing intensity (13-second duration stimulus) to facilitate patient comfort and to observe both transient and sustained stimulus-on pupil responses. However, the 13-second duration stimuli, even at the highest stimulus intensity of blue light (100 cd/m2), did not reveal obvious sustained PLR after light termination, which is the characteristic electrophysiological signature of a melanopsin-mediated contribution. Recently, Kankipati et al.23,24 showed that there is a significant decrease in melanopsin-driven PLR in patients with glaucoma, a disease known to decrease the number of RGCs. The purpose here was to better understand the relative contributions of rod, cone, and melanopsin to the human PLRs and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    PURPOSE. To better understand the relative contributions of rod, cone, and melanopsin to the human pupillary light reflex (PLR) and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol. METHODS. PLR was measured with an eye tracker, and stimuli were controlled with a Ganzfeld system. In experiment 1, 2.5 log cd/m(2) red (640 ± 10 nm) and blue (467 ± 17 nm) stimuli of various durations were presented after dark adaptation. In experiments 2 and 3, 1-second red and blue stimuli were presented at different intensity levels in the dark (experiment 2) or on a 0.78 log cd/m(2) blue background (experiment 3). Based on the results of experiments 1 to 3, a Clinical Protocol was designed and tested on healthy control subjects and patients with retinitis pigmentosa and Leber's congenital amaurosis. RESULTS. The duration for producing the optimal melanopsin-driven sustained pupil response after termination of an intense blue stimulus was 1 second. PLR rod- and melanopsin-driven components are best studied with low- and high-intensity flashes, respectively, presented in the dark (experiment 2). A blue background suppressed rod and melanopsin responses, making it easy to assess the cone contribution with a red flash (experiment 3). With the Clinical Protocol, robust melanopsin responses could be seen in patients with few or no contributions from the rods and cones. CONCLUSIONS. It is possible to assess the rod, cone, and melanopsin contributions to the PLR with blue flashes at two or three intensity levels in the dark and one red flash on a blue background.

Jason C Park - One of the best experts on this subject based on the ideXlab platform.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    The pupillary light reflex (PLR) is a reflex that controls the constriction and dilation of the pupil in response to changes in light intensity. The PLR has been used in the clinic and in Clinical research as an objective measure of retinal and optic nerve function. Most Clinical studies have measured the latency and amplitude of pupil constriction to a brief, light stimulus.1–7 There is also a slow and sustained miosis after stimulus offset that was well known, although not necessarily well understood, at a neurophysiological level.8 The discovery of a class of retinal ganglion cells (RGCs) containing the photopigment melanopsin, which could be directly activated by light and which provide input to the pupillomotor center, provided a new understanding of the sustained PLR.9 The melanopsin-expressing intrinsic photosensitive RGCs (ipRGCs) show a delayed latency and a prolonged response that extend well after stimulus offset,10 similar to the sustained PLR. More recent studies, using pharmacologic blockades of the rod and cone input in primates11 and knockout mice,12,13 support the claim that the sustained PLR is mainly dependent on the ipRGCs. The use of the PLR as assay of the ipRGC is of potential Clinical value.5,14 First, a PLR technique to measure rod sensitivity to light has been developed as an objective measure of the effect of treatment in a Clinical trial.15–17 Second, a Protocol to evaluate the melanopsin contribution versus rod and cone contributions to the PLR may be of use in estimating the degree of damage to the RGCs versus to the retinal photoreceptors. Third, the presence of intact ipRGCs may help us to understand the currently unexplained phenomena (e.g., circadian rhythm) in some patients with little or no receptor function.18 Finally, considering the recent developments in retinal prosthesis (see, for example, Refs. 19–21), there is a need to know which patients with little or no receptor function have functioning RGCs and thus are viable candidates for recovery of vision. Kardon et al.14,22 provided evidence that a Clinical Protocol could assess the contributions of the rods, cones, and melanopsin to the PLR in patients with outer retinal disease. Although an important proof of concept, their original design was suboptimal. First, they did not establish conclusively that they had isolated the rod, cone, and melanopsin contributions to the human PLR, though their results did show evidence for discriminating patients with photoreceptor disease from healthy subjects. Second, they used a staircase stimulus paradigm of increasing intensity (13-second duration stimulus) to facilitate patient comfort and to observe both transient and sustained stimulus-on pupil responses. However, the 13-second duration stimuli, even at the highest stimulus intensity of blue light (100 cd/m2), did not reveal obvious sustained PLR after light termination, which is the characteristic electrophysiological signature of a melanopsin-mediated contribution. Recently, Kankipati et al.23,24 showed that there is a significant decrease in melanopsin-driven PLR in patients with glaucoma, a disease known to decrease the number of RGCs. The purpose here was to better understand the relative contributions of rod, cone, and melanopsin to the human PLRs and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    PURPOSE. To better understand the relative contributions of rod, cone, and melanopsin to the human pupillary light reflex (PLR) and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol. METHODS. PLR was measured with an eye tracker, and stimuli were controlled with a Ganzfeld system. In experiment 1, 2.5 log cd/m(2) red (640 ± 10 nm) and blue (467 ± 17 nm) stimuli of various durations were presented after dark adaptation. In experiments 2 and 3, 1-second red and blue stimuli were presented at different intensity levels in the dark (experiment 2) or on a 0.78 log cd/m(2) blue background (experiment 3). Based on the results of experiments 1 to 3, a Clinical Protocol was designed and tested on healthy control subjects and patients with retinitis pigmentosa and Leber's congenital amaurosis. RESULTS. The duration for producing the optimal melanopsin-driven sustained pupil response after termination of an intense blue stimulus was 1 second. PLR rod- and melanopsin-driven components are best studied with low- and high-intensity flashes, respectively, presented in the dark (experiment 2). A blue background suppressed rod and melanopsin responses, making it easy to assess the cone contribution with a red flash (experiment 3). With the Clinical Protocol, robust melanopsin responses could be seen in patients with few or no contributions from the rods and cones. CONCLUSIONS. It is possible to assess the rod, cone, and melanopsin contributions to the PLR with blue flashes at two or three intensity levels in the dark and one red flash on a blue background.

Virginia Rovnyak - One of the best experts on this subject based on the ideXlab platform.

  • evaluation of an office Protocol to increase exclusivity of breastfeeding
    Pediatrics, 2013
    Co-Authors: Sharon K Corriveau, Emily Drake, Ann Kellams, Virginia Rovnyak
    Abstract:

    OBJECTIVE: The purpose of this study was to determine whether implementing a program based on a Clinical Protocol affects breastfeeding rates within a pediatric primary care setting. Increasing breastfeeding rates is an important public health initiative identified by multiple agencies. METHODS: The Academy of Breastfeeding Medicine (ABM) Clinical Protocol (“The Breastfeeding-Friendly Physician’s Office, Part 1: Optimizing Care for Infants and Children”) was used as a template for the provision of breastfeeding services within a pediatric primary care clinic. There were 757 mother–infant pairs included in the study. A retrospective before-and-after study design was used. Data collection points included the hospital stay, the newborn visit, and the 2-, 4-, and 6-month health maintenance visits. The 2 groups were compared to estimate the Protocol’s effectiveness as a method of increasing breastfeeding rates. RESULTS: The results of this evaluation were positive for exclusive breastfeeding, with group comparisons showing a statistically significant increase in exclusive breastfeeding rates at all 5 time points. CONCLUSIONS: Our diverse patient population within a pediatric practice had increased initiation rates and exclusive breastfeeding rates after implementation of the ABM’s breastfeeding-friendly Protocol. Families who receive care in a pediatric primary care setting that has implemented the ABM Clinical Protocol may have increased rates of exclusive breastfeeding.

David W Rhee - One of the best experts on this subject based on the ideXlab platform.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    The pupillary light reflex (PLR) is a reflex that controls the constriction and dilation of the pupil in response to changes in light intensity. The PLR has been used in the clinic and in Clinical research as an objective measure of retinal and optic nerve function. Most Clinical studies have measured the latency and amplitude of pupil constriction to a brief, light stimulus.1–7 There is also a slow and sustained miosis after stimulus offset that was well known, although not necessarily well understood, at a neurophysiological level.8 The discovery of a class of retinal ganglion cells (RGCs) containing the photopigment melanopsin, which could be directly activated by light and which provide input to the pupillomotor center, provided a new understanding of the sustained PLR.9 The melanopsin-expressing intrinsic photosensitive RGCs (ipRGCs) show a delayed latency and a prolonged response that extend well after stimulus offset,10 similar to the sustained PLR. More recent studies, using pharmacologic blockades of the rod and cone input in primates11 and knockout mice,12,13 support the claim that the sustained PLR is mainly dependent on the ipRGCs. The use of the PLR as assay of the ipRGC is of potential Clinical value.5,14 First, a PLR technique to measure rod sensitivity to light has been developed as an objective measure of the effect of treatment in a Clinical trial.15–17 Second, a Protocol to evaluate the melanopsin contribution versus rod and cone contributions to the PLR may be of use in estimating the degree of damage to the RGCs versus to the retinal photoreceptors. Third, the presence of intact ipRGCs may help us to understand the currently unexplained phenomena (e.g., circadian rhythm) in some patients with little or no receptor function.18 Finally, considering the recent developments in retinal prosthesis (see, for example, Refs. 19–21), there is a need to know which patients with little or no receptor function have functioning RGCs and thus are viable candidates for recovery of vision. Kardon et al.14,22 provided evidence that a Clinical Protocol could assess the contributions of the rods, cones, and melanopsin to the PLR in patients with outer retinal disease. Although an important proof of concept, their original design was suboptimal. First, they did not establish conclusively that they had isolated the rod, cone, and melanopsin contributions to the human PLR, though their results did show evidence for discriminating patients with photoreceptor disease from healthy subjects. Second, they used a staircase stimulus paradigm of increasing intensity (13-second duration stimulus) to facilitate patient comfort and to observe both transient and sustained stimulus-on pupil responses. However, the 13-second duration stimuli, even at the highest stimulus intensity of blue light (100 cd/m2), did not reveal obvious sustained PLR after light termination, which is the characteristic electrophysiological signature of a melanopsin-mediated contribution. Recently, Kankipati et al.23,24 showed that there is a significant decrease in melanopsin-driven PLR in patients with glaucoma, a disease known to decrease the number of RGCs. The purpose here was to better understand the relative contributions of rod, cone, and melanopsin to the human PLRs and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol.

  • toward a Clinical Protocol for assessing rod cone and melanopsin contributions to the human pupil response
    Investigative Ophthalmology & Visual Science, 2011
    Co-Authors: Jason C Park, Ana Laura De Araujo Moura, Ali S Raza, David W Rhee, Randy H Kardon, Donald C Hood
    Abstract:

    PURPOSE. To better understand the relative contributions of rod, cone, and melanopsin to the human pupillary light reflex (PLR) and to determine the optimal conditions for assessing the health of the rod, cone, and melanopsin pathways with a relatively brief Clinical Protocol. METHODS. PLR was measured with an eye tracker, and stimuli were controlled with a Ganzfeld system. In experiment 1, 2.5 log cd/m(2) red (640 ± 10 nm) and blue (467 ± 17 nm) stimuli of various durations were presented after dark adaptation. In experiments 2 and 3, 1-second red and blue stimuli were presented at different intensity levels in the dark (experiment 2) or on a 0.78 log cd/m(2) blue background (experiment 3). Based on the results of experiments 1 to 3, a Clinical Protocol was designed and tested on healthy control subjects and patients with retinitis pigmentosa and Leber's congenital amaurosis. RESULTS. The duration for producing the optimal melanopsin-driven sustained pupil response after termination of an intense blue stimulus was 1 second. PLR rod- and melanopsin-driven components are best studied with low- and high-intensity flashes, respectively, presented in the dark (experiment 2). A blue background suppressed rod and melanopsin responses, making it easy to assess the cone contribution with a red flash (experiment 3). With the Clinical Protocol, robust melanopsin responses could be seen in patients with few or no contributions from the rods and cones. CONCLUSIONS. It is possible to assess the rod, cone, and melanopsin contributions to the PLR with blue flashes at two or three intensity levels in the dark and one red flash on a blue background.