Saiyun Hou - Academia.edu (original) (raw)

Papers by Saiyun Hou

Neuromodulation : journal of the International Neuromodulation Society, 2016

Traditional tonic spinal cord stimulation (SCS) has been approved by FDA for chronic pain of intr... more Traditional tonic spinal cord stimulation (SCS) has been approved by FDA for chronic pain of intractable back and limb pain. However, it induces paresthesia and relieves pain poorly to some extent. Recently, burst SCS has been developed for pain reduction without the mandatory paresthesia. A systematic review of burst SCS for chronic back and limb pain. The objective of this systematic review is to determine the effects of burst SCS on pain relief without paresthesia for various conditions including failed back surgery syndrome, painful diabetic neuropathy, and radiculopathy. The available literature on burst SCS in managing chronic pain without paresthesia was reviewed. The 2011 American Academy of Neurology (AAN) Classification of Evidence Guidelines Process Manual was used to grade the evidence and risk of bias. Data sources included relevant literature identified through searches of PubMed, MEDLINE/OVID, SCOPUS, and manual searches of the bibliographies of known primary and revi...

Molecular Pain, 2012

Background: Distal limb fracture in man can induce a complex regional pain syndrome (CRPS) with p... more Background: Distal limb fracture in man can induce a complex regional pain syndrome (CRPS) with pain, warmth, edema, and cutaneous inflammation. In the present study substance P (SP, Tac1 −/− ) and CGRP receptor (RAMP1 −/− ) deficient mice were used to investigate the contribution of neuropeptide signaling to CRPS-like changes in a tibia fracture mouse model. Wildtype, Tac1 −/− , and RAMP1 −/− mice underwent tibia fracture and casting for 3 weeks, then the cast was removed and hindpaw mechanical allodynia, unweighting, warmth, and edema were tested over time. Hindpaw skin was collected at 3 weeks post-fracture for immunoassay and femurs were collected for micro-CT analysis. Results: Wildtype mice developed hindpaw allodynia, unweighting, warmth, and edema at 3 weeks post-fracture, but in the Tac1 −/− fracture mice allodynia and unweighting were attenuated and there was no warmth and edema. RAMP1 −/− fracture mice had a similar presentation, except there was no reduction in hindpaw edema. Hindpaw skin TNFα, IL-1β, IL-6 and NGF levels were up-regulated in wildtype fracture mice at 3 weeks post-fracture, but in the Tac1 −/− and RAMP1 −/− fracture mice only IL-6 was increased. The epidermal keratinocytes were the cellular source for these inflammatory mediators. An IL-6 receptor antagonist partially reversed post-fracture pain behaviors in wildtype mice.

Journal of Neuroinflammation, 2012

Tibia fracture in rats followed by cast immobilization leads to nociceptive, trophic, vascular an... more Tibia fracture in rats followed by cast immobilization leads to nociceptive, trophic, vascular and bone-related changes similar to those seen in Complex Regional Pain Syndrome (CRPS). Substance P (SP) mediated neurogenic inflammation may be responsible for some of the signs of CRPS in humans. We therefore hypothesized that SP acting through the SP receptor (NK1) leads to the CRPS-like changes found in the rat model. In the present study, we intradermally injected rats with SP and monitored hindpaw mechanical allodynia, temperature, and thickness as well as tissue levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6), and nerve growth factor-β (NGF) for 72 h. Anti-NGF antibody was utilized to block the effects of SP-induced NGF up-regulation. Fracture rats treated with the selective NK1 receptor antagonist LY303870 prior to cast removal were assessed for BrdU, a DNA synthesis marker, incorporation in skin cells to examine cellular proliferation. Bone microarchitecture was measured using micro computed tomography (μCT). We observed that: (1) SP intraplantar injection induced mechanical allodynia, warmth and edema as well as the expression of nociceptive mediators in the hindpaw skin of normal rats, (2) LY303870 administered intraperitoneally after fracture attenuated allodynia, hindpaw unweighting, warmth, and edema, as well as cytokine and NGF expression, (3) LY303870 blocked fracture-induced epidermal thickening and BrdU incorporation after fracture, (4) anti-NGF antibody blocked SP-induced allodynia but not warmth or edema, and (5) LY303870 had no effect on bone microarchitecture. Collectively our data indicate that SP acting through NK1 receptors supports the nociceptive and vascular components of CRPS, but not the bone-related changes.

Neuromodulation : journal of the International Neuromodulation Society, 2016

Traditional tonic spinal cord stimulation (SCS) has been approved by FDA for chronic pain of intr... more Traditional tonic spinal cord stimulation (SCS) has been approved by FDA for chronic pain of intractable back and limb pain. However, it induces paresthesia and relieves pain poorly to some extent. Recently, burst SCS has been developed for pain reduction without the mandatory paresthesia. A systematic review of burst SCS for chronic back and limb pain. The objective of this systematic review is to determine the effects of burst SCS on pain relief without paresthesia for various conditions including failed back surgery syndrome, painful diabetic neuropathy, and radiculopathy. The available literature on burst SCS in managing chronic pain without paresthesia was reviewed. The 2011 American Academy of Neurology (AAN) Classification of Evidence Guidelines Process Manual was used to grade the evidence and risk of bias. Data sources included relevant literature identified through searches of PubMed, MEDLINE/OVID, SCOPUS, and manual searches of the bibliographies of known primary and revi...

Molecular Pain, 2012

Background: Distal limb fracture in man can induce a complex regional pain syndrome (CRPS) with p... more Background: Distal limb fracture in man can induce a complex regional pain syndrome (CRPS) with pain, warmth, edema, and cutaneous inflammation. In the present study substance P (SP, Tac1 −/− ) and CGRP receptor (RAMP1 −/− ) deficient mice were used to investigate the contribution of neuropeptide signaling to CRPS-like changes in a tibia fracture mouse model. Wildtype, Tac1 −/− , and RAMP1 −/− mice underwent tibia fracture and casting for 3 weeks, then the cast was removed and hindpaw mechanical allodynia, unweighting, warmth, and edema were tested over time. Hindpaw skin was collected at 3 weeks post-fracture for immunoassay and femurs were collected for micro-CT analysis. Results: Wildtype mice developed hindpaw allodynia, unweighting, warmth, and edema at 3 weeks post-fracture, but in the Tac1 −/− fracture mice allodynia and unweighting were attenuated and there was no warmth and edema. RAMP1 −/− fracture mice had a similar presentation, except there was no reduction in hindpaw edema. Hindpaw skin TNFα, IL-1β, IL-6 and NGF levels were up-regulated in wildtype fracture mice at 3 weeks post-fracture, but in the Tac1 −/− and RAMP1 −/− fracture mice only IL-6 was increased. The epidermal keratinocytes were the cellular source for these inflammatory mediators. An IL-6 receptor antagonist partially reversed post-fracture pain behaviors in wildtype mice.

Journal of Neuroinflammation, 2012

Tibia fracture in rats followed by cast immobilization leads to nociceptive, trophic, vascular an... more Tibia fracture in rats followed by cast immobilization leads to nociceptive, trophic, vascular and bone-related changes similar to those seen in Complex Regional Pain Syndrome (CRPS). Substance P (SP) mediated neurogenic inflammation may be responsible for some of the signs of CRPS in humans. We therefore hypothesized that SP acting through the SP receptor (NK1) leads to the CRPS-like changes found in the rat model. In the present study, we intradermally injected rats with SP and monitored hindpaw mechanical allodynia, temperature, and thickness as well as tissue levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6), and nerve growth factor-β (NGF) for 72 h. Anti-NGF antibody was utilized to block the effects of SP-induced NGF up-regulation. Fracture rats treated with the selective NK1 receptor antagonist LY303870 prior to cast removal were assessed for BrdU, a DNA synthesis marker, incorporation in skin cells to examine cellular proliferation. Bone microarchitecture was measured using micro computed tomography (μCT). We observed that: (1) SP intraplantar injection induced mechanical allodynia, warmth and edema as well as the expression of nociceptive mediators in the hindpaw skin of normal rats, (2) LY303870 administered intraperitoneally after fracture attenuated allodynia, hindpaw unweighting, warmth, and edema, as well as cytokine and NGF expression, (3) LY303870 blocked fracture-induced epidermal thickening and BrdU incorporation after fracture, (4) anti-NGF antibody blocked SP-induced allodynia but not warmth or edema, and (5) LY303870 had no effect on bone microarchitecture. Collectively our data indicate that SP acting through NK1 receptors supports the nociceptive and vascular components of CRPS, but not the bone-related changes.