Neurones with Epileptiform Discharge in the Central Nervous System and Chronic Pain

Yamashiro, Katsumi; Iwayama, Kaoru; Kurihara, Masaki; Mori, Kazuo; Níwa, Masami; Tasker, Ronald R.; Albé-Fessard, D

doi:10.1007/978-3-7091-9160-6_35

Cited by 11 publications

(4 citation statements)

References 6 publications

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“…'8 Epileptiform discharge recorded in hyperactive neurons in the thalamus were also demonstrated in patients with central pain due to causes other than spinal cord injury. 19 In animals with a behavioural syndrome indicative of nerve injury pain due to dorsal rhizotomy, neuronal hyperactivity was recorded at the levels of the spinal cord dorsal horn, and at thalamic and cortical levels.20 Neuronal hyperactivity and hyperresponsiveness were also recorded at the thalamic and cortical levels in animals after chronic constriction injury to the sciatic nerve.2' The experimental data show that peripheral and central lesions cause similar changes in the activity of central neurons. This is of interest because central pain after spinal cord injury In conclusion, the present data provide clinical evidence that the development of central pain after spinal cord injury is not only dependent on the lesioning of spinothalamic or dorsal column-medial lemniscal pathways, but may involve the development of abnormal activity including hyperexcitability in nociceptive spinothalamic tract neurons.…”

Section: Discussionmentioning

confidence: 96%

“…The median intensity of allodynia recorded by means of a 100 mm visual analogue scale in 12 patients was 36 mm. Furthermore, the median duration of after-sensation pain was 10 seconds (ranges five seconds-i 5 minutes), and the median diameter of radiation of pain was 10 (range [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] cm. In the painful denervated skin areas, wind up-like pain provoked by a von Frey filament (6-65 units) was evoked in nine of the 14 patients tested.…”

Section: Somatosensory Findingsmentioning

confidence: 99%

See 1 more Smart Citation

Somatosensory findings in patients with spinal cord injury and central dysaesthesia pain.

Eide¹,

Jørum²,

Stenehjem³

1996

Journal of Neurology, Neurosurgery & Psychiatry

108

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Objective-To determine whether central pain in patients with spinal cord injury is only dependent on the lesioning of spinothalamic pathways. Methods-In sixteen patients with spinal cord injury and central dysaesthesia pain, somatosensory abnormalities in painful denervated skin areas were compared with somatosensory findings in normal skin areas as well as in non-painful denervated skin areas. Results-The threshold values for detection of thermal (heat, cold, heat pain, or cold pain) and tactile stimulation were significantly changed in denervated skin areas although there were no significant differences in the threshold values between painful and non-painful denervated skin areas. The reductions of sensations of touch, vibration, joint position, and two point discrimination in painful and non-painful denervated skin areas were not significantly different. Allodynia (pain caused by non-noxious stimulation) and wind up-like pain (pain caused by repeatedly pricking the skin) were significantly more common in painful than nonpainful denervated skin areas. Conclusions-Because pain and thermal sensory perception are primarily mediated to the brain via spinothalamic pathways, whereas the sensations of touch, vibration and joint position are primarily mediated by dorsal column-medial lemniscal pathways, the results indicate that central pain is not only dependent on the lesioning of either dorsal column-medial lemniscal pathways or spinothalamic pathways. The findings of abnormal evoked pain (allodynia and wind up-like pain) may be consistent with the experimental findings of hyperexcitability in nociceptive spinothalamic tract neurons, that may be involved in the pathogenesis of central pain. Severe and disabling chronic pain is a major sequel after spinal cord injury, with an estimated prevalence ranging from 18 to 63%.1 Pain in patients with spinal cord injury includes musculoskeletal pain, radicular pain, visceral pain, central dysaesthesia pain, psychogenic pain, lesional pain, reflex sympathetic dystrophy, and limb pain secondary to compressive mononeuropathies.2 Central dysaesthesia pain is characterised by spontaneous continuous and intermittent pain as well as by pain evoked by non-noxious stimulation (allodynia).2 It is difficult to treat this type of pain as central pain is not effectively relieved by traditional analgesics or neurosurgical procedures.34 Increased knowledge of the pathogenesis of central dysaesthesia pain after spinal cord injury is desired.An important hypothesis is that the development of central pain is dependent on the lesioning of spinothalamocortical pathways.35 The hypothesis is partly based on the finding that sensory perception mediated to the brain via spinothalamocortical pathways is more often affected than sensory perception mediated by dorsal column-medial lemniscal pathways in this group of patients.3 6In the present study, somatosensory testing of patients with spinal cord injury and central dysaesthesia pain was undertaken to further examine whether central pain is ...

show abstract

Section: Discussionmentioning

confidence: 96%

Section: Somatosensory Findingsmentioning

confidence: 99%

Somatosensory findings in patients with spinal cord injury and central dysaesthesia pain.

Eide¹,

Jørum²,

Stenehjem³

1996

Journal of Neurology, Neurosurgery & Psychiatry

108

View full text Add to dashboard Cite

show abstract

“…This taxonomy is divided into three tiers. 6,11,[17][18][19][20][21][22][23][24][25] Below-level pain is described as the "most severe or excruciating" of all SCI pain reported. 15,16 The most straightforward and logical classification scheme for clinical assessment simply categorizes pain below the lesion (true "central pain" phenomena), pain at the level of the lesion (most like radiculopathic/neuropathic), and pain above the lesion (often called "musculoskeletal" in the literature).…”

Section: Classification/taxonomymentioning

confidence: 99%

“…Furthermore, neuropathic lesions are easier to study (both with animal models and clinically), and there is considerably more evidence in the treatment of neuropathies. 1,24,34 Primary and secondary events also ultimately result in afferent dysesthesias and efferent modulation, which result in pathologic changes in the initiation, perception, and maintenance of injury-induced pain. 4,31,32 Traumatic or ischemic damage to the spinal cord triggers a dynamic cascade of molecular, biochemical, anatomic ("plasticity"), and cellular responses.…”

Section: Pathology and Mechanismsmentioning

confidence: 99%