Pub Date : 1998-12-01DOI: 10.1016/S1082-3174(98)70001-7
Andrew C.N. Chen , Lars Arendt-Nielsen , Leon Plaghki
In Part I, this Focus article describes characteristics of laser-evoked brain potentials (LEPs) in human pain and examines some of the methodological inconsistencies. Evidence both cautioning and supporting the use of LEPs is contrasted. A host of neurological mechanisms clearly illustrates the relation of LEPs and pain processing: Lasers elicit selectively the cutaneous receptors of thin afferent fibers, the anterolateral spinal tract, and the lateral tracts of the brainstem. Implication for clinical use is briefly suggested. We raise three contending issues: (1) measurement standard, (2) association and dissociation of the LEP amplitude and pain, and (3) dynamic spatiotemporal specificity of LEPs. We conclude that LEPs may reflect nociceptive processing but may not be the entire pain experience. We emphasize the proper use of LEPs in understanding the mechanisms of nociceptive activation in pain experience. To achieve this, we address the technological advance required in studying the dynamic spatiotemporal specificity of LEPs and human pain.
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Pub Date : 1998-12-01DOI: 10.1016/S1082-3174(98)80009-3
Andrew C.N. Chen , Lars Arendt-Nielsen , Leon Plaghki
Our current positions (Focus articles I and II) regarding the cerebral processing of human pain in the research of LEPs are the following:
1.
Discrete, repeated sensory stimulation in evoked potential research, including laser stimulation in LEPs, is not a usual, natural experience, but an artificial convenience for probing into the window of human brain function.
2.
LEP methodology requires fundamental standardization.
3.
LEPs largely reflected neural pathways associated with some aspects of nociceptive processing (the LEPs focused on are those arising from activation of A-δ fibers).
4.
LEPs, in some circumstances, may dissociate from pain perception.
5.
Absence of evidence is not evidence of absence. Some neural events (eg, silent generators) and other biophysical constraints (eg, scalp smearing of cortical potentials) can occur. Consequently, no detectable trace of neural activity as ensured in the cortex or at the scalp. Thus, LEPs can never be used to validate the absence of nociception/pain in a person.
6.
Conversely, non-nociceptive events can influence some aspects of LEPs. Thus, interpretation of LEPs demands full control and understanding of the experimental conditions.
7.
LEPs attributes are likely to reflect the sensory—discriminatory dimension, but are not sufficient for equating the full multidimensional aspects of human pain.
8.
The pain experience can be correlated with changes of the amplitudes/latencies in LEPs; but it is not true to state that pain can be inversely inferred from the parameters of the LEPs since other nonpain-related factors can also, simultaneously, affect the LEPs.
9.
Exploration of the nociceptive processing using LEPs requires quantification of the temporospatial dynamics of the topographic brain activities.
10.
The precision of measuring the brain topography associated with human pain requires high-resolution EEG (>64 channel), based on the spatial sampling principle (the shallow generators and refined small focal activation demand higher density of electrode arrays than the deep generators; detection of tangent generators demand different assumptions than the radial generators).
11.
Equivalent current dipole modeling is useful, it can be approximated by the spherical model, but requires the realistic epilloid head model coregistered with MRI for concise analysis.
12.
Without proper MRI coregistration, the isolated dipole parameters should be reported in the coordinate terms only, and not anatomic attribution.
{"title":"Understanding of cerebral processing of human pain (II) by source modeling of laser-evoked potentials in conjunction with neuroimaging","authors":"Andrew C.N. Chen , Lars Arendt-Nielsen , Leon Plaghki","doi":"10.1016/S1082-3174(98)80009-3","DOIUrl":"10.1016/S1082-3174(98)80009-3","url":null,"abstract":"<div><p>Our current positions (Focus articles I and II) regarding the cerebral processing of human pain in the research of LEPs are the following:</p><ul><li><span>1.</span><span><p>Discrete, repeated sensory stimulation in evoked potential research, including laser stimulation in LEPs, is not a usual, natural experience, but an artificial convenience for probing into the window of human brain function.</p></span></li><li><span>2.</span><span><p>LEP methodology requires fundamental standardization.</p></span></li><li><span>3.</span><span><p>LEPs largely reflected neural pathways associated with some aspects of nociceptive processing (the LEPs focused on are those arising from activation of A-δ fibers).</p></span></li><li><span>4.</span><span><p>LEPs, in some circumstances, may dissociate from pain perception.</p></span></li><li><span>5.</span><span><p>Absence of evidence is not evidence of absence. Some neural events (eg, silent generators) and other biophysical constraints (eg, scalp smearing of cortical potentials) can occur. Consequently, no detectable trace of neural activity as ensured in the cortex or at the scalp. Thus, LEPs can never be used to validate the absence of nociception/pain in a person.</p></span></li><li><span>6.</span><span><p>Conversely, non-nociceptive events can influence some aspects of LEPs. Thus, interpretation of LEPs demands full control and understanding of the experimental conditions.</p></span></li><li><span>7.</span><span><p>LEPs attributes are likely to reflect the sensory—discriminatory dimension, but are not sufficient for equating the full multidimensional aspects of human pain.</p></span></li><li><span>8.</span><span><p>The pain experience can be correlated with changes of the amplitudes/latencies in LEPs; but it is not true to state that pain can be inversely inferred from the parameters of the LEPs since other nonpain-related factors can also, simultaneously, affect the LEPs.</p></span></li><li><span>9.</span><span><p>Exploration of the nociceptive processing using LEPs requires quantification of the temporospatial dynamics of the topographic brain activities.</p></span></li><li><span>10.</span><span><p>The precision of measuring the brain topography associated with human pain requires high-resolution EEG (>64 channel), based on the spatial sampling principle (the shallow generators and refined small focal activation demand higher density of electrode arrays than the deep generators; detection of tangent generators demand different assumptions than the radial generators).</p></span></li><li><span>11.</span><span><p>Equivalent current dipole modeling is useful, it can be approximated by the spherical model, but requires the realistic epilloid head model coregistered with MRI for concise analysis.</p></span></li><li><span>12.</span><span><p>Without proper MRI coregistration, the isolated dipole parameters should be reported in the coordinate terms only, and not anatomic attribution.</p></span></li><li><spa","PeriodicalId":101001,"journal":{"name":"Pain Forum","volume":"7 4","pages":"Pages 221-230"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1082-3174(98)80009-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90518616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-12-01DOI: 10.1016/S1082-3174(98)70003-0
Michael C. Rowbotham , Karin Lottrup Petersen , Howard L. Fields
Acute herpes zoster is a highly stereotyped condition of viral recrudescence producing inflammation in a dorsal root ganglion, a segmental vesicular rash, and pain. The long-term outcome is unpredictable. Those acute zoster patients that develop postherpetic neuralgia (PHN) fall into three subtypes: (1) an “irritable nociceptor” group with minimal deafferentation and touch-evoked allodynia due to peripheral nociceptor input, (2) a deafferentation group with marked sensory loss and no allodynia, and (3) a deafferentation group with sensory loss and allodynia due to central reorganization. Response to therapy also shows significant inhomogeneity. Some patients obtain nearly complete relief by either topical agents or oral monotherapy with opioids, antidepressants, or anticonvulsants. Other PHN sufferers are refractory to all measures, similar to patients with spinal cord injury and central poststroke pain. Because the clinical picture of PHN falls into distinct patterns based on differing pathophysiology, PHN should be thought of as several disorders, which may respond differently to therapeutic interventions and which may or may not coexist in the same patient.
{"title":"Is postherpetic neuralgia more than one disorder?","authors":"Michael C. Rowbotham , Karin Lottrup Petersen , Howard L. Fields","doi":"10.1016/S1082-3174(98)70003-0","DOIUrl":"10.1016/S1082-3174(98)70003-0","url":null,"abstract":"<div><p>Acute herpes zoster is a highly stereotyped condition of viral recrudescence producing inflammation in a dorsal root ganglion, a segmental vesicular rash, and pain. The long-term outcome is unpredictable. Those acute zoster patients that develop postherpetic neuralgia (PHN) fall into three subtypes: (1) an “irritable nociceptor” group with minimal deafferentation and touch-evoked allodynia due to peripheral nociceptor input, (2) a deafferentation group with marked sensory loss and no allodynia, and (3) a deafferentation group with sensory loss and allodynia due to central reorganization. Response to therapy also shows significant inhomogeneity. Some patients obtain nearly complete relief by either topical agents or oral monotherapy with opioids, antidepressants, or anticonvulsants. Other PHN sufferers are refractory to all measures, similar to patients with spinal cord injury and central poststroke pain. Because the clinical picture of PHN falls into distinct patterns based on differing pathophysiology, PHN should be thought of as several disorders, which may respond differently to therapeutic interventions and which may or may not coexist in the same patient.</p></div>","PeriodicalId":101001,"journal":{"name":"Pain Forum","volume":"7 4","pages":"Pages 231-237"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1082-3174(98)70003-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83721665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}