A comparison of the burst activity of lateral thalamic neurons in chronic pain and non-pain patients
Identifieur interne : 001162 ( PascalFrancis/Curation ); précédent : 001161; suivant : 001163A comparison of the burst activity of lateral thalamic neurons in chronic pain and non-pain patients
Auteurs : V. Radhakrishnan [Canada] ; J. Tsoukatos [Canada] ; K. D. Davis [Canada] ; R. R. Tasker [Canada] ; A. M. Lozano [Canada] ; J. O. Dostrovsky [Canada]Source :
- Pain : (Amsterdam) [ 0304-3959 ] ; 1999.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
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Abstract
Thalamic neurons are known to switch their firing from a tonic pattern during wakefulness to a bursting pattern during sleep. Several studies have described the existence of bursting activity in awake chronic pain patients and have suggested that this activity is abnormal and may be related to their pain. However, we have frequently observed bursting activity in awake non-pain patients suggesting that there may not be a causal relationship between thalamic bursting activity and chronic pain. To examine this issue more rigorously we compared the incidence and pattern of bursting activity of lateral thalamic neurons of both pain and non-pain patients in a state of wakefulness. Recordings were obtained from lateral thalamic areas of different groups of patients (n = 91) suffering from pain disorders (e.g. anaesthesia dolorosa, phantom limb pain, trigeminal neuralgia, post-stroke pain) and motor disorders (e.g. Parkinson's disease, essential tremor) during stereotactic surgical procedures for the treatment of pain and movement disorders. Burst indices (the number of bursting cells per electrode track) were computed for all the explorations in the two groups. The burst indices in the pain and non-pain groups (1.73 ± 0.28 and 1.14 ± 0.16, respectively) were not significantly different from each other. The bursts were analyzed to see if they fulfilled the criteria of low-threshold calcium spike (LTS)-evoked bursts characterized by (i) a shortening of the first interspike interval with an increase in the number of interspike intervals in the burst and also (ii) a progressive prolongation of successive interspike intervals. LTS-evoked bursts were identified in 27/47 (57%) bursting cells in pain patients and 15/32 (47%) cells in non-pain patients. These data demonstrate that the occurrence of bursting activity and of LTS-evoked bursts in the human thalamus is prevalent in both pain and non-pain patients. This suggests that the bursting activity of thalamic neurons in pain patients is not necessarily related to the occurrence of their pain.
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Tsoukatos</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author><author><name sortKey="Davis, K D" sort="Davis, K D" uniqKey="Davis K" first="K. D." last="Davis">K. D. Davis</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Surgery, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Playfair Neuroscience Unit, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author><author><name sortKey="Tasker, R R" sort="Tasker, R R" uniqKey="Tasker R" first="R. R." last="Tasker">R. R. 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Radhakrishnan</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author><author><name sortKey="Tsoukatos, J" sort="Tsoukatos, J" uniqKey="Tsoukatos J" first="J." last="Tsoukatos">J. Tsoukatos</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author><author><name sortKey="Davis, K D" sort="Davis, K D" uniqKey="Davis K" first="K. D." last="Davis">K. D. Davis</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Surgery, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Playfair Neuroscience Unit, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author><author><name sortKey="Tasker, R R" sort="Tasker, R R" uniqKey="Tasker R" first="R. R." last="Tasker">R. R. Tasker</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Surgery, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Playfair Neuroscience Unit, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author><author><name sortKey="Lozano, A M" sort="Lozano, A M" uniqKey="Lozano A" first="A. M." last="Lozano">A. M. Lozano</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Surgery, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Playfair Neuroscience Unit, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author><author><name sortKey="Dostrovsky, J O" sort="Dostrovsky, J O" uniqKey="Dostrovsky J" first="J. O." last="Dostrovsky">J. O. Dostrovsky</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Physiology, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Playfair Neuroscience Unit, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country></affiliation></author></analytic><series><title level="j" type="main">Pain : (Amsterdam)</title><title level="j" type="abbreviated">Pain : (Amst.)</title><idno type="ISSN">0304-3959</idno><imprint><date when="1999">1999</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Pain : (Amsterdam)</title><title level="j" type="abbreviated">Pain : (Amst.)</title><idno type="ISSN">0304-3959</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Discharge pattern</term><term>Electrical activity</term><term>Electrodiagnosis</term><term>Human</term><term>Nervous system diseases</term><term>Pain</term><term>Thalamus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term><term>Douleur</term><term>Thalamus</term><term>Mode décharge</term><term>Activité électrique</term><term>Electrodiagnostic</term><term>Homme</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Thalamic neurons are known to switch their firing from a tonic pattern during wakefulness to a bursting pattern during sleep. Several studies have described the existence of bursting activity in awake chronic pain patients and have suggested that this activity is abnormal and may be related to their pain. However, we have frequently observed bursting activity in awake non-pain patients suggesting that there may not be a causal relationship between thalamic bursting activity and chronic pain. To examine this issue more rigorously we compared the incidence and pattern of bursting activity of lateral thalamic neurons of both pain and non-pain patients in a state of wakefulness. Recordings were obtained from lateral thalamic areas of different groups of patients (n = 91) suffering from pain disorders (e.g. anaesthesia dolorosa, phantom limb pain, trigeminal neuralgia, post-stroke pain) and motor disorders (e.g. Parkinson's disease, essential tremor) during stereotactic surgical procedures for the treatment of pain and movement disorders. Burst indices (the number of bursting cells per electrode track) were computed for all the explorations in the two groups. The burst indices in the pain and non-pain groups (1.73 ± 0.28 and 1.14 ± 0.16, respectively) were not significantly different from each other. The bursts were analyzed to see if they fulfilled the criteria of low-threshold calcium spike (LTS)-evoked bursts characterized by (i) a shortening of the first interspike interval with an increase in the number of interspike intervals in the burst and also (ii) a progressive prolongation of successive interspike intervals. LTS-evoked bursts were identified in 27/47 (57%) bursting cells in pain patients and 15/32 (47%) cells in non-pain patients. These data demonstrate that the occurrence of bursting activity and of LTS-evoked bursts in the human thalamus is prevalent in both pain and non-pain patients. This suggests that the bursting activity of thalamic neurons in pain patients is not necessarily related to the occurrence of their pain.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0304-3959</s0></fA01><fA02 i1="01"><s0>PAINDB</s0></fA02><fA03 i2="1"><s0>Pain : (Amst.)</s0></fA03><fA05><s2>80</s2></fA05><fA06><s2>3</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>A comparison of the burst activity of lateral thalamic neurons in chronic pain and non-pain patients</s1></fA08><fA11 i1="01" i2="1"><s1>RADHAKRISHNAN (V.)</s1></fA11><fA11 i1="02" i2="1"><s1>TSOUKATOS (J.)</s1></fA11><fA11 i1="03" i2="1"><s1>DAVIS (K. D.)</s1></fA11><fA11 i1="04" i2="1"><s1>TASKER (R. R.)</s1></fA11><fA11 i1="05" i2="1"><s1>LOZANO (A. M.)</s1></fA11><fA11 i1="06" i2="1"><s1>DOSTROVSKY (J. 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All rights reserved.</s1></fA44><fA45><s0>25 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>99-0308855</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Pain : (Amsterdam)</s0></fA64><fA66 i1="01"><s0>NLD</s0></fA66><fC01 i1="01" l="ENG"><s0>Thalamic neurons are known to switch their firing from a tonic pattern during wakefulness to a bursting pattern during sleep. Several studies have described the existence of bursting activity in awake chronic pain patients and have suggested that this activity is abnormal and may be related to their pain. However, we have frequently observed bursting activity in awake non-pain patients suggesting that there may not be a causal relationship between thalamic bursting activity and chronic pain. To examine this issue more rigorously we compared the incidence and pattern of bursting activity of lateral thalamic neurons of both pain and non-pain patients in a state of wakefulness. Recordings were obtained from lateral thalamic areas of different groups of patients (n = 91) suffering from pain disorders (e.g. anaesthesia dolorosa, phantom limb pain, trigeminal neuralgia, post-stroke pain) and motor disorders (e.g. Parkinson's disease, essential tremor) during stereotactic surgical procedures for the treatment of pain and movement disorders. Burst indices (the number of bursting cells per electrode track) were computed for all the explorations in the two groups. The burst indices in the pain and non-pain groups (1.73 ± 0.28 and 1.14 ± 0.16, respectively) were not significantly different from each other. The bursts were analyzed to see if they fulfilled the criteria of low-threshold calcium spike (LTS)-evoked bursts characterized by (i) a shortening of the first interspike interval with an increase in the number of interspike intervals in the burst and also (ii) a progressive prolongation of successive interspike intervals. LTS-evoked bursts were identified in 27/47 (57%) bursting cells in pain patients and 15/32 (47%) cells in non-pain patients. These data demonstrate that the occurrence of bursting activity and of LTS-evoked bursts in the human thalamus is prevalent in both pain and non-pain patients. 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