scholarly journals Abnormal Anterior Pretectal Nucleus Activity Contributes to Central Pain Syndrome

2010 ◽  
Vol 103 (6) ◽  
pp. 3044-3053 ◽  
Author(s):  
Peter D. Murray ◽  
Radi Masri ◽  
Asaf Keller
Keyword(s):  
Spinal Cord ◽  
Pain Syndrome ◽  
Zona Incerta ◽  
Central Pain ◽  
Number Of Patients ◽  
Cord Injury ◽  
Pretectal Nucleus ◽  
Evoked Activity ◽  
Selective Increase ◽  
Central Pain Syndrome

Central pain syndrome (CPS) is a debilitating condition that affects a large number of patients with a primary lesion or dysfunction in the CNS, most commonly due to spinal cord injury, stroke, and multiple sclerosis lesions. The pathophysiological processes underlying the development and maintenance of CPS are poorly understood. We have recently shown, in an animal model of CPS, that neurons in the posterior thalamic nucleus (PO) have increased spontaneous and evoked activity. We also demonstrated that these changes are due to suppressed inhibitory inputs from the zona incerta (ZI). The anterior pretectal nucleus (APT) is a diencephalic nucleus that projects on both the PO and ZI, suggesting that it might be involved in the pathophysiology of CPS. Here we test the hypothesis that CPS is associated with abnormal APT activity by recording single units from APT in anesthetized rats with CPS resulting from spinal cord lesions. The firing rate of APT neurons was increased in spinal-lesioned animals, compared with sham-operated controls. This increase was due to a selective increase in firing of tonic neurons that project to and inhibit ZI and an increase in bursts in fast bursting and slow rhythmic neurons. We also show that, in normal animals, suppressing APT results in increased PO spontaneous activity and evoked responses in a subpopulation of PO neurons. Taken together, these findings suggest that APT regulates ZI inputs to PO and that enhanced APT activity during CPS contributes to the abnormally high activity of PO neurons in CPS.

scholarly journals Treatment of central pain syndrome with spinal cord stimulation

2018 ◽  
Vol 25 (3-4) ◽  
pp. 99-103
Author(s):  
A. E Yakovlev
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Stimulation ◽  
Pain Syndrome ◽  
Phantom Pain ◽  
Central Pain ◽  
Pain Medications ◽  
Postoperative Changes ◽  
Cord Injury ◽  
Central Pain Syndrome

Central pain syndrome (CPS) is a neurological disorder caused by damage or dysfunction of the central nervous system. Both conservative and operative methods of treatment are used in its treatment, but in most cases their effectiveness is rather low. We are presenting the clinical observation of a 60-year-old patient with spinal cord injury at the level of Th10 due to a car accident that occurred 44 years before the treatment in our clinic, who suffered from phantom pain that occurred after bilateral above the knee amputation because of advanced peripheral vascular disease. Due to the ineffectiveness of the conservative treatment, it was decided to proceed with spinal cord stimulation. The presence of pronounced postoperative changes in the area of spinal cord injury has complicated the transcutaneous placement of trial leads at the L1-L2 and Th12-L1 level. We managed to introduce leads at the level of Th7-Th8 and position them at the level of Th5-Th7. During continuous neurostimulation the pain in the sacrum, in the area of the hip joints, the phantom pain was relieved. The patient stopped using all pain medications. Spinal cord stimulation can be utilized as an alternative treatment for patients with intractable CPS.

scholarly journals Abnormal Activity of Primary Somatosensory Cortex in Central Pain Syndrome

2010 ◽  
Vol 104 (3) ◽  
pp. 1717-1725 ◽  
Author(s):  
Raimi L. Quiton ◽  
Radi Masri ◽  
Scott M. Thompson ◽  
Asaf Keller
Keyword(s):  
Somatosensory Cortex ◽  
Pain Syndrome ◽  
Zona Incerta ◽  
Primary Somatosensory Cortex ◽  
Central Pain ◽  
Chronic Pain Condition ◽  
Recorded Activity ◽  
Noxious Mechanical Stimulation ◽  
Increased Activity ◽  
Central Pain Syndrome

Central pain syndrome (CPS) is a debilitating and chronic pain condition that results from a lesion or dysfunction in the CNS. The pathophysiological mechanisms underlying CPS are poorly understood. We recently demonstrated that CPS is associated with suppressed inputs from the inhibitory nucleus zona incerta to the posterior thalamus (PO). As a consequence, activity in PO is abnormally increased in CPS. Because the perception of pain requires activity in the cerebral cortex, CPS must also involve abnormal cortical activity. Here we test the hypothesis that CPS is associated with increased activity in the primary somatosensory cortex (SI), a major projection target of PO that plays an important role in processing sensory-discriminative aspects of pain. We recorded activity of single units in SI in rats with CPS resulting from spinal cord lesions. Consistent with our hypothesis, SI neurons recorded from lesioned rats exhibited significantly higher spontaneous firing rates and greater responses evoked by innocuous and noxious mechanical stimulation of the hindpaw compared with control rats. Neurons from lesioned rats also showed a greater tendency than controls to fire bursts of action potentials in response to noxious stimuli. Thus, the excruciatingly painful symptoms of CPS may result, at least in part, from abnormally increased activity in SI.

scholarly journals Aromatase Inhibition Exacerbates Pain and Reactive Gliosis in the Dorsal Horn of the Spinal Cord of Female Rats Caused by Spinothalamic Tract Injury

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4341-4355 ◽  
Author(s):  
Samar Ghorbanpoor ◽  
Luis Miguel Garcia-Segura ◽  
Ali Haeri-Rohani ◽  
Fariba Khodagholi ◽  
Masoumeh Jorjani
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Mechanical Allodynia ◽  
Pain Syndrome ◽  
Female Rats ◽  
Central Pain ◽  
Mrna Levels ◽  
Aromatase Inhibition ◽  
Spinothalamic Tract ◽  
Central Pain Syndrome

Abstract Central pain syndrome is characterized by severe and excruciating pain resulting from a lesion in the central nervous system. Previous studies have shown that estradiol decreases pain and that inhibitors of the enzyme aromatase, which synthesizes estradiol from aromatizable androgens, increases pain sensitivity. In this study we have assessed whether aromatase expression in the dorsal horns of the spinal cord is altered in a rat model of central pain syndrome, induced by the unilateral electrolytic lesion of the spinothalamic tract. Protein and mRNA levels of aromatase, as well as the protein and mRNA levels of estrogen receptors α and β, were increased in the dorsal horn of female rats after spinothalamic tract injury, suggesting that the injury increased estradiol synthesis and signaling in the dorsal horn. To determine whether the increased aromatase expression in this pain model may participate in the control of pain, mechanical allodynia thresholds were determined in both hind paws after the intrathecal administration of letrozole, an aromatase inhibitor. Aromatase inhibition enhanced mechanical allodynia in both hind paws. Because estradiol is known to regulate gliosis we assessed whether the spinothalamic tract injury and aromatase inhibition regulated gliosis in the dorsal horn. The proportion of microglia with a reactive phenotype and the number of glial fibrillary acidic protein–immunoreactive astrocytes were increased by the injury in the dorsal horn. Aromatase inhibition enhanced the effect of the injury on gliosis. Furthermore, a significant a positive correlation of mechanical allodynia and gliosis in the dorsal horn was detected. These findings suggest that aromatase is up-regulated in the dorsal horn in a model of central pain syndrome and that aromatase activity in the spinal cord reduces mechanical allodynia by controlling reactive gliosis in the dorsal horn.

scholarly journals Zona Incerta: A Role in Central Pain

2009 ◽  
Vol 102 (1) ◽  
pp. 181-191 ◽  
Author(s):  
Radi Masri ◽  
Raimi L. Quiton ◽  
Jessica M. Lucas ◽  
Peter D. Murray ◽  
Scott M. Thompson ◽  
...  
Keyword(s):  
Pain Syndrome ◽  
Zona Incerta ◽  
Central Pain ◽  
Spontaneous Firing ◽  
Spinal Trigeminal Nucleus ◽  
Posterior Thalamus ◽  
Number Of Patients ◽  
The Face ◽  
Spontaneous Firing Rate ◽  
Inhibitory Regulation

Central pain syndrome (CPS) is a debilitating condition that affects a large number of patients with a primary lesion or dysfunction in the CNS. Despite its discovery over a century ago, the pathophysiological processes underlying the development and maintenance of CPS are poorly understood. We recently demonstrated that activity in the posterior thalamus (PO) is tightly regulated by inhibitory inputs from zona incerta (ZI). Here we test the hypothesis that CPS is associated with abnormal inhibitory regulation of PO by ZI. We recorded single units from ZI and PO in animals with CPS resulting from spinal cord lesions. Consistent with our hypothesis, the spontaneous firing rate and somatosensory evoked responses of ZI neurons were lower in lesioned animals compared with sham-operated controls. In PO, neurons recorded from lesioned rats exhibited significantly higher spontaneous firing rates and greater responses to noxious and innocuous stimuli applied to the hindpaw and to the face. These changes were not associated with increased afferent drive from the spinal trigeminal nucleus or changes in the ventroposterior thalamus. Thus CPS can result from suppressed inputs from the inhibitory nucleus zona incerta to the posterior thalamus.

Neuropathic pain syndrome as an occult manifestation of injury of the spinal cord after surgical repair of aortic coarctation

2000 ◽  
Vol 10 (4) ◽  
pp. 413-415 ◽  
Author(s):  
Luc M Beauchesne ◽  
Angela Mailis ◽  
Gary D Webb
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Aortic Coarctation ◽  
Surgical Repair ◽  
Rare Complication ◽  
Pain Syndrome ◽  
Neuropathic Pain Syndrome ◽  
Cord Injury ◽  
Unusual Symptoms ◽  
Arterial Branch

AbstractInjury to the spinal cord injury with paraplegia, is a rare complication of surgical repair of aortic coarctation recognized immediately post-operatively. We present the case of a 41-year-old male undergoing surgery for restenosis at the site of a repair. Intra-operatively, he suffered inadvertent injury to an intercostal arterial branch during isolation of the aorta below the graft. Over the following months, he developed unusual symptoms involving the legs and genitourinary tract which, only after extensive investigations, were attributed to ischemic damage to the spinal cord related to the surgery. We suspect that similar syndromes reflecting injury to the spinal cord injury may be unrecognized following surgical repair of coarctation.

First experience with chronic epidural spinal cord stimulation in Khanty-Mansi autonomous okrug — clinical observations

2021 ◽  
Vol LIII (2) ◽  
pp. 94-100
Author(s):  
Olga A. Bondarenko ◽  
Gaspar V. Gavrilov ◽  
Vadim A. Padurets ◽  
Roman V. Kasich
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Spinal Cord Stimulation ◽  
Pain Syndrome ◽  
Chronic Neuropathic Pain ◽  
Neuropathic Pain Syndrome ◽  
Epidural Stimulation ◽  
Cord Injury ◽  
Epidural Spinal Cord Stimulation ◽  
And Migration

Purpose of the work. The article is devoted to the first experience of epidural stimulation in the Khanty-Mansiysk Autonomous Okrug at the budgetary institution Surgut Clinical Trauma Hospital. Clinical examples are presented for two main indications for the application of this technique (disease of the operated spine, a consequence of spinal cord injury in combination with chronic neuropathic pain syndrome). Research methods. An assessment of the intensity of pain syndrome was given according to a visual analogue scale, the Pain Detect questionnaire; indicators of anxiety, depression on the HADS scale; quality of life according to the Oswestry questionnaire for a follow-up period of 6-12 months in patients with chronic epidural stimulation. Results. A positive assessment of the action during test neurostimulation was 63.3% (38 patients). Of the established permanent systems, a good result was achieved and persisted for 12 months or more in 96% (24 patients). It was necessary to change the stimulation parameters in 13% (3 patients). Revision of permanent systems was performed in 20% (5 patients), due to the progression of the degenerative-dystrophic process of the spine, damage and migration of system elements. Conclusions. Chronic epidural spinal cord stimulation has established itself as a personalized, highly effective, minimally invasive and safe method of treating chronic neuropathic pain syndromes. Multicomponent corrective action is of scientific interest and requires further study.

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