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Ruth Defrin - One of the best experts on this subject based on the ideXlab platform.

  • Hemiplegic shoulder pain: Evidence of a neuropathic origin
    Pain, 2013
    Co-Authors: Gabi Zeilig, Michal Rivel, Harold Weingarden, Evgeni Gaidoukov, Ruth Defrin
    Abstract:

    Hemiplegic shoulder pain (HSP) is common after stroke. Whereas most studies have concentrated on the possible musculoskeletal factors underlying HSP, neuropathic aspects have hardly been studied. Our aim was to explore the possible neuropathic components in HSP, and if identified, whether they are specific to the shoulder or characteristic of the entire affected side. Participants included 30 poststroke patients, 16 with and 14 without HSP, and 15 healthy controls. The thresholds of warmth, cold, heat-pain, touch, and graphesthesia were measured in the intact and affected shoulder and in the affected lower leg. They were also assessed for the presence of allodynia and Hyperpathia, and computed tomography/magnetic resonance imaging scans of the brain were reviewed. In addition, chronic pain was characterized. Participants with HSP exhibited higher rates of parietal lobe damage (P < 0.05) compared to those without HSP. Both poststroke groups exhibited higher sensory thresholds than healthy controls. Those with HSP had higher heat-pain thresholds in both the affected shoulder (P < 0.001) and leg (P < 0.01), exhibited higher rates of Hyperpathia in both these regions (each P < 0.001), and more often reported chronic pain throughout the affected side (P < 0.001) than those without HSP. The more prominent sensory alterations in the shoulder region suggest that neuropathic factors play a role in HSP. The clinical evidence of damage to the spinothalamic-thalamocortical system in the affected shoulder and leg, the presence of chronic pain throughout the affected side, and the more frequent involvement of the parietal cortex all suggest that the neuropathic component is of central origin.

  • The nature and course of sensory changes following spinal cord injury: predictive properties and implications on the mechanism of central pain
    Brain, 2011
    Co-Authors: Gabi Zeilig, Shavit Enosh, Deborah Rubin-asher, Benjamin Lehr, Ruth Defrin
    Abstract:

    Central pain below the injury level after spinal cord injury is excruciating, chronic and resistive to treatment. Animal studies suggest that pretreatment may prevent central pain, but to date there are no measures to predict its development. Our aim was to monitor changes in the sensory profile below the lesion prior to the development of below-level central pain in order to search for a parameter that could predict its risk and to further explore its pathophysiology. Thirty patients with spinal cord injury and 27 healthy controls underwent measurement of warm, cold, heat-pain and touch thresholds as well as graphaesthesia, allodynia, Hyperpathia and wind-up pain in intact region and in the shin and feet (below level). Patients were tested at 2-4 weeks, 1-2.5 months and 2.5-6 months after the injury or until central pain had developed. At the end of the follow-up, 46% of patients developed below-level central pain. During the testing periods, individuals who eventually developed central pain had higher thermal thresholds than those who did not and displayed high rates of abnormal sensations (allodynia and Hyperpathia), which gradually increased with time until central pain developed. Logistic regressions revealed that the best predictor for the risk of below-level central pain was allodynia in the foot in the second testing session with a 77% probability (90.9% confidence). The results suggest that neuronal hyperexcitability, which may develop consequent to damage to spinothalamic tracts, precedes central pain. Furthermore, it appears that below-level central pain develops after a substantial build-up of hyperexcitability. To the best of our knowledge, this is the first systematic report establishing that neuronal hyperexcitability precedes central pain. Predicting the risk for central pain can be utilized to initiate early treatment in order to prevent its development.

  • The characteristics of chronic central pain after traumatic brain injury.
    Pain, 2007
    Co-Authors: Hadas Ofek, Ruth Defrin
    Abstract:

    Central pain following traumatic brain injury (TBI) has not been studied in depth. Our purpose was to conduct a systematic study of patients with TBI suffering from chronic central pain, and to describe the characteristics of the central pain. Groups were TBI patients with (TBIP) and without central pain (TBINP) and healthy controls. TBI patients with other pain mechanisms were excluded from the study. Participants underwent quantitative somatosensory testing in the painful and pain-free body regions. Thresholds for warmth, cold, heat-pain, touch and graphesthesia were measured and pathologically evoked pain (allodynia, Hyperpathia and wind-up pain) evaluated. Chronic pain was mapped and characterized. Chronic pain developed at a relatively late onset (6.6+/-9 months) was almost exclusively unilateral and reported as pricking, throbbing and burning. Although both TBIP and TBINP exhibited a significant reduction in thermal and tactile sensations compared to controls, thermal sensations in the painful regions of TBIP were significantly more impaired than pain-free regions in the same patients (p

  • Characterization of chronic pain and somatosensory function in spinal cord injury subjects.
    Pain, 2001
    Co-Authors: Ruth Defrin, Avi Ohry, Nava Blumen, Gideon Urca
    Abstract:

    The pathophysiology of the chronic pain following spinal cord injury (SCI) is unclear. In order to study it's underlying mechanism we characterized the neurological profile of SCI subjects with (SCIP) and without (SCINP) chronic pain. Characterization comprised of thermal threshold testing for warmth, cold and heat pain and tactile sensibility testing of touch, graphesthesia and identification of speed of movement of touch stimuli on the skin. In addition, spontaneously painful areas were mapped in SCIP and evoked pathological pain--allodynia, Hyperpathia and wind-up pain evaluated for both groups. Both SCIP and SCINP showed similar reductions in both thermal and tactile sensations. In both groups thermal sensations were significantly more impaired than tactile sensations. Chronic pain was present only in skin areas below the lesion with impaired or absent temperature and heat-pain sensibilities. Conversely, all the thermally impaired skin areas in SCIP were painful while painfree areas in the same subjects were normal. In contrast, chronic pain could be found in skin areas without any impairment in tactile sensibilities. Allodynia could only be elicited in SCIP and a significantly higher incidence of pathologically evoked pain (i.e. Hyperpathia and wind-up pain) was seen in the chronic pain areas compared to SCINP. We conclude that damage to the spinothalamic tract (STT) is a necessary condition for the occurrence of chronic pain following SCI. However, STT lesion is not a sufficient condition since it could also be found in SCINP. The abnormal evoked pain seen in SCIP is probably due to neuronal hyperexcitability in these subjects. The fact that apparently identical sensory impairments manifest as chronic pain and hyperexcitability in one subject but not in another implies that either genetic predisposition or subtle differences in the nature of spinal injury determine the emergence of chronic pain following SCI.

Alan I. Faden - One of the best experts on this subject based on the ideXlab platform.

  • Ablation of the transcription factors E2F1-2 limits neuroinflammation and associated neurological deficits after contusive spinal cord injury.
    Cell Cycle, 2015
    Co-Authors: Boris Sabirzhanov, Bogdan A. Stoica, Marta M. Lipinski, Zaorui Zhao, Shuxin Zhao, Nicole Ward, Dianer Yang, Alan I. Faden
    Abstract:

    Traumatic spinal cord injury (SCI) induces cell cycle activation (CCA) that contributes to secondary injury and related functional impairments such as motor deficits and Hyperpathia. E2F1 and E2F2 are members of the activator sub-family of E2F transcription factors that play an important role in proliferating cells and in cell cycle-related neuronal death, but no comprehensive study have been performed in SCI to determine the relative importance of these factors. Here we examined the temporal distribution and cell-type specificity of E2F1 and E2F2 expression following mouse SCI, as well as the effects of genetic deletion of E2F1-2 on neuronal cell death, neuroinflammation and associated neurological dysfunction. SCI significantly increased E2F1 and E2F2 expression in active caspase-3(+) neurons/oligodendrocytes as well as in activated microglia/astrocytes. Injury-induced up-regulation of cell cycle-related genes and protein was significantly reduced by intrathecal injection of high specificity E2F decoy oligodeoxynucleotides against the E2F-binding site or in E2F1-2 null mice. Combined E2F1+2 siRNA treatment show greater neuroprotection in vivo than E2F1 or E2F2 single siRNA treatment. Knockout of both E2F1 and E2F2 genes (E2Fdko) significantly reduced neuronal death, neuroinflammation, and tissue damage, as well as limiting motor dysfunction and Hyperpathia after SCI. Both CCA reduction and functional improvement in E2Fdko mice were greater than those in E2F2ko model. These studies demonstrate that SCI-induced activation of E2F1-2 mediates CCA, contributing to gliopathy and neuronal/tissue loss associated with motor impairments and post-traumatic hyperesthesia. Thus, E2F1-2 provide a therapeutic target for decreasing secondary tissue damage and promoting recovery of function after SCI.

  • Cell Cycle Activation Contributes to Increased Neuronal Activity in the Posterior Thalamic Nucleus and Associated Chronic Hyperesthesia after Rat Spinal Cord Contusion
    Neurotherapeutics, 2013
    Co-Authors: Charles Raver, Chunshu Piao, Asaf Keller, Alan I. Faden
    Abstract:

    Spinal cord injury (SCI) causes not only sensorimotor and cognitive deficits, but frequently also severe chronic pain that is difficult to treat (SCI pain). We previously showed that hyperesthesia, as well as spontaneous pain induced by electrolytic lesions in the rat spinothalamic tract, is associated with increased spontaneous and sensory-evoked activity in the posterior thalamic nucleus (PO). We have also demonstrated that rodent impact SCI increases cell cycle activation (CCA) in the injury region and that post-traumatic treatment with cyclin dependent kinase inhibitors reduces lesion volume and motor dysfunction. Here we examined whether CCA contributes to neuronal hyperexcitability of PO and Hyperpathia after rat contusion SCI, as well as to microglial and astroglial activation (gliopathy) that has been implicated in delayed SCI pain. Trauma caused enhanced pain sensitivity, which developed weeks after injury and was correlated with increased PO neuronal activity. Increased CCA was found at the thoracic spinal lesion site, the lumbar dorsal horn, and the PO. Increased microglial activation and cysteine–cysteine chemokine ligand 21 expression was also observed in the PO after SCI. In vitro , neurons co-cultured with activated microglia showed up-regulation of cyclin D1 and cysteine–cysteine chemokine ligand 21 expression. In vivo , post-injury treatment with a selective cyclin dependent kinase inhibitor (CR8) significantly reduced cell cycle protein induction, microglial activation, and neuronal activity in the PO nucleus, as well as limiting chronic SCI-induced Hyperpathia. These results suggest a mechanistic role for CCA in the development of SCI pain, through effects mediated in part by the PO nucleus. Moreover, cell cycle modulation may provide an effective therapeutic strategy to improve reduce both Hyperpathia and motor dysfunction after SCI.

John M. Gregg - One of the best experts on this subject based on the ideXlab platform.

  • Studies of traumatic neuralgias in the maxillofacial region: Surgical pathology and neural mechanisms
    Journal of Oral and Maxillofacial Surgery, 1990
    Co-Authors: John M. Gregg
    Abstract:

    Microsurgical exploration of injured trigeminal nerves in patients with neuralgia revealed four variations of traumatic neuroma, associated foreign objects, and a sprouting of nerve collaterals from adjacent uninjured nerve. A comprehensive theory of traumatic trigeminal pain is proposed based on three sites of pathosis: peripheral neuroma, somatic and autonomic collateralization, and central deafferentation pathoses. Anesthesia dolorosa is related in this model to amputation neuromas and central pathosis. Sympathetic mediated pain is attributed to autonomic C-fiber units in peripheral injured zones. Hyperalgesia is attributed to mechanosensitive A-fiber units in the nerves being linked to corresponding irritable central nervous system neurons. Hyperpathia is explained on the basis of ephaptic transmission between adjacent fibers in neuromas.

  • Studies of traumatic neuralgia in the maxillofacial region: symptom complexes and response to microsurgery.
    Journal of Oral and Maxillofacial Surgery, 1990
    Co-Authors: John M. Gregg
    Abstract:

    Patients with chronic pain following trigeminal nerve injuries were studied before and after microsurgical repairs using the McGill Pain Language Inventory, sensory reflex testing, and assessment of pain relief from nerve blocks. This protocol differentiated four syndrome types that appeared singly or in combination: anesthesia dolorosa (AD), sympathetic mediated pain (SMP), hyperalgesia, and Hyperpathia. Trigeminal nerve blocks proved to be good predictors of pain relief from microsurgical treatments. Surgical pain reduction was poor for AD and SMP (14.6% and 20.7%) as compared with hyperalgesia and Hyperpathia (60.5% and 56.3%).

Gianpietro Sechi - One of the best experts on this subject based on the ideXlab platform.

  • id 411 diffuse Hyperpathia in a case of wernicke s like encephalopathy
    Clinical Neurophysiology, 2016
    Co-Authors: Alberto Addis, Elia Sechi, Anna Laura Rassu, R. Piredda, Gianpietro Sechi
    Abstract:

    Objective Bilateral thalamic lesion is highly suggestive of thiamine deficiency. Thalamic Hyperpathia has never been reported as a feature of thiamine-related disorders. We propose a case of Wernicke‘s-like encephalopathy manifesting as intolerable touch-evoked pain resembling thalamic Hyperpathia. Methods A 22-year-old female was admitted for reduced level of consciousness after four days history of fever complicated with drowsiness and ataxia. A previous evaluation by the EMS had been obstructed by the fact that she felt an intense pain whenever touched, even lightly. Brain-MRI showed T2 hyperintensity of bilateral thalami, heads of caudate nuclei and periaqueductal region. Laboratory investigation excluded infectious-autoimmune etiology. Despite serum levels within normal range, high dose thiamine was administered with prompt improvement of symptoms supporting the suspicion of a genetic origin of the disorder. Results Gene sequencing disclosed a novel mutation of THTR-2 gene encoding for human thiamine transporter type 2. Conclusions The patient manifested a diffuse, touch-evoked, intense pain, not restricted to any radicular/peripheral nerve territory, as occurs in typical thalamic Hyperpathia. This symptom could be related to the thalamic lesions documented on MRI. Both the painful condition and the radiological findings resolved after thiamine supplementation. Key message Thiamine-related thalamic lesions could be a cause of thalamic Hyperpathia.

  • ID 411 – Diffuse Hyperpathia in a case of Wernicke’s-like encephalopathy
    Clinical Neurophysiology, 2016
    Co-Authors: Alberto Addis, Elia Sechi, Anna Laura Rassu, R. Piredda, Gianpietro Sechi
    Abstract:

    Objective Bilateral thalamic lesion is highly suggestive of thiamine deficiency. Thalamic Hyperpathia has never been reported as a feature of thiamine-related disorders. We propose a case of Wernicke‘s-like encephalopathy manifesting as intolerable touch-evoked pain resembling thalamic Hyperpathia. Methods A 22-year-old female was admitted for reduced level of consciousness after four days history of fever complicated with drowsiness and ataxia. A previous evaluation by the EMS had been obstructed by the fact that she felt an intense pain whenever touched, even lightly. Brain-MRI showed T2 hyperintensity of bilateral thalami, heads of caudate nuclei and periaqueductal region. Laboratory investigation excluded infectious-autoimmune etiology. Despite serum levels within normal range, high dose thiamine was administered with prompt improvement of symptoms supporting the suspicion of a genetic origin of the disorder. Results Gene sequencing disclosed a novel mutation of THTR-2 gene encoding for human thiamine transporter type 2. Conclusions The patient manifested a diffuse, touch-evoked, intense pain, not restricted to any radicular/peripheral nerve territory, as occurs in typical thalamic Hyperpathia. This symptom could be related to the thalamic lesions documented on MRI. Both the painful condition and the radiological findings resolved after thiamine supplementation. Key message Thiamine-related thalamic lesions could be a cause of thalamic Hyperpathia.

P.h.j.m. Veldman - One of the best experts on this subject based on the ideXlab platform.

  • Amputation for reflex sympathetic dystrophy
    Journal of Bone and Joint Surgery-british Volume, 1995
    Co-Authors: P.w. Dielissen, A.t.p.m. Claassen, P.h.j.m. Veldman, R.j.a. Goris
    Abstract:

    We have reviewed 28 patients with reflex sympathetic dystrophy (RSD) who had 34 amputations in 31 limbs. The amputations had been performed for untenable pain (5), recurrent infection (14) or to improve residual function (15). Only two patients were relieved of pain by amputation, and this could not be predicted. Ten of 14 patients were cured of infection and 9 of 15 patients had improvement of residual function. In 28 of the amputations, RSD recurred in the stump, especially after amputation at a level which was not free from symptoms. Because of recurrence of RSD in the stump or severe Hyperpathia only two patients wear a prosthesis. Despite this 24 patients were satisfied with the results.

  • Reflex sympathetic dystrophy of the head: case report and discussion of diagnostic criteria.
    The Journal of Trauma: Injury Infection and Critical Care, 1994
    Co-Authors: P.h.j.m. Veldman, Peter B. Dunki Jacobs
    Abstract:

    The case of a patient who was involved in a car crash is presented. On the right side her wrist and zygomatic arch were fractured. At both localizations she developed a painful syndrome. The diagnosis of reflex sympathetic dystrophy of her arm was made within 3 weeks after the injury and therapy instituted. The pain in her face and skull were accompanied by vasomotor changes which increased after exercise and by hypesthesia, Hyperpathia, paresis, and hyperhidrosis. Disorders of the cranial nerves were excluded by physical examination and electromyography and structural disorders by CT scanning