The Possible Role of the Cerebral Cortex Adjacent to the Central Sulcus for the Genesis of Central (Thalamic) Pain—a Metabolic Study

Hirato, Masafumi; Horikoshi, Satoru; Kawashima, Yasuhiro; Satake, K; Shibasaki, Takashi; Ohye, Chihiro

doi:10.1007/978-3-7091-9297-9_32

Cited by 14 publications

(7 citation statements)

References 4 publications

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“…Contrary to earlier belief, less than one third of CP of brain origin is purely thalamic [2,[63][64][65][66][67] and complete thalamic syndromes are exceptional.…”

Section: Thalamuscontrasting

confidence: 59%

Central post-stroke pain: Current evidence

Kumar

Soni

2009

Journal of the Neurological Sciences

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“…Contrary to earlier belief, less than one third of CP of brain origin is purely thalamic [2,[63][64][65][66][67] and complete thalamic syndromes are exceptional.…”

Section: Thalamuscontrasting

confidence: 59%

Central post-stroke pain: Current evidence

Kumar

Soni

2009

Journal of the Neurological Sciences

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“…The decrease in basal activity in the thalamus is not unexpected, as thalamic dysfunction has long been thought to play a role in chronic pain. Clinical studies have reported spontaneous pain and disturbed sensations produced by thalamic lesions (Riddoch, 1938;Garcin et al, 1968) and several recent PET studies have demonstrated that there is reduced thalamic rCBF and/or regional glucose metabolism in patients with chronic pain (Canavero et al, 1993;Hirato et al, 1993Hirato et al, ,1994Iadarola et al, 1995;Hsieh et al, 1995). It is possible that thalamic rCBF is down because of reduced inhibitory background activity, but this cannot be proved based on this study.…”

Section: Discussionmentioning

confidence: 77%

Long-term changes in behavior and regional cerebral blood flow associated with painful peripheral mononeuropathy in the rat

Paulson

Casey

Morrow

2002

Pain

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We identified long-term (up to 12 weeks), bilateral changes in spontaneous and evoked pain behavior and baseline forebrain activity following a chronic constriction injury (CCI) of the sciatic nerve. The long-term changes in basal forebrain activation following CCI were region-specific and can be divided into forebrain structures that showed either: (1) no change, (2) an increase, or (3) a decrease in activity with regard to the short-term (2 weeks) changes we previously reported. All the rats showed spontaneous pain behaviors that persisted throughout the 12-week observation period, resembling the pattern of change found in four limbic system structures: the anterior dorsal thalamus, habenular complex, and the cingulate and retrosplenial cortices. In contrast, heat hyperalgesia was delayed in onset until 4 weeks following CCI, but then persisted, showing a nearly constant level of increased responsiveness. The forebrain activation that resembles this behavioral pattern of change is found in somatosensory cortex, and in the hypothalamic paraventricular nucleus and the basolateral amygdala. Finally, mechanical allodynia, which was maximal during the first 2 weeks following nerve injury and gradually recovered by the seventh post-operative week uniquely matches the time course of changes in ventrolateral and ventroposterolateral thalamic activity. Our results indicate that peripheral nerve damage results in persistent changes in behavior and resting forebrain systems that modulate pain perception. The persistent abnormalities in the somatosensory cortex and thalamus suggest that the sensory thalamocortical axis is functionally deranged in certain chronic pain states.

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“…Our previous study indicated that the rate of appearance of irregular burst discharges showed reverse correlation with that of kinesthetic responses to peripheral stimulation on the sensory thalamus 15) . Moreover, regional CBF and metabolism increased on the cortical motor area on the side ipsilateral to the CVD lesion in those cases 9,10,15) . The widespread dysfunction of the thalamocortical system occurred in cases with central (thalamic) pain.…”

Section: Discussionmentioning

confidence: 93%

“…Electrophysiological studies clarifying thalamic neural mechanism from data obtained during the course of stereotactic thalamotomy using depth microelectrode have been performed 4,6~10,12,13,15~19,25) . Neuroimaging studies also clarifying cortical and subcortical neural mecha-nism from the data obtained by PET scan or functional MRI have been carried out 1,7,9,10,12,13,15,16,24) . Though several kinds of surgical treatment have been attempted for central pain, those results were not always satisfying.…”

Section: Introductionmentioning

confidence: 99%

<b>Indication of various kinds of surgical treatment </b><b>for central (thalamic) pain </b>

Hirato

Saitoh

2003

Pain Research

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We studied the effect and the indication of various kinds of surgical treatment for central (thalamic) pain in 10 cases. In 3 cases with localized pain, epidural spinal cord stimulation was effective. In 7 cases with diffuse pain (hemibody), stereotactic Vim-Vcpc thalamotomy was performed with the aid of depth microrecording. In 4 of these cases in which pain relief was obtained, we could find responses to peripheral natural stimulation on the sensory thalamus during the operation. Preoperative PET study also revealed an increase of rCBF on the sensory cortex ipsilateral to the thalamic CVD lesion during contralateral thumb brushing. On the other hand, in the 3 cases in which we failed to obtain pain relief, we frequently encountered irregular burst discharges on the thalamus. Gamma thalamotomy was added after the conventional thalamotomy in these 3 cases. Though transient pain relief was obtained, pain recurred thereafter. Precentral electrical cortical stimulation was also carried out in 3 recurrent cases, resulting in the failure of pain relief. In one of these cases, internal capsular (posterior limb) stimulation was performed, obtaining encouraging result. In cases of localized thalamic pain, epidural spinal cord stimulation proved to be an effective treatment. Thalamic surgery achieved pain relief in those cases with diffuse type pain, limited to preserving sensory function on the sensory thalamocortical system. Precentral electrical cortical stimulation, internal capsular (posterior limb) stimulation or Gamma thalamotomy may be an alternative treatment for central (thalamic) pain.

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The Possible Role of the Cerebral Cortex Adjacent to the Central Sulcus for the Genesis of Central (Thalamic) Pain—a Metabolic Study

Cited by 14 publications

References 4 publications

Central post-stroke pain: Current evidence

Central post-stroke pain: Current evidence

Long-term changes in behavior and regional cerebral blood flow associated with painful peripheral mononeuropathy in the rat

<b>Indication of various kinds of surgical treatment </b><b>for central (thalamic) pain </b>

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