Pathophysiology of Central (Thalamic) Pain: Combined Change of Sensory Thalamus with Cerebral Cortex around Central Sulcus

Hirato, Masafumi; Watanabe, Katsushige; Takahashi, Akira; Hayase, Nobuaki; Horikoshi, Satoru; Shibasaki, Takashi; Ohye, C.

doi:10.1159/000098636

Cited by 36 publications

(25 citation statements)

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“…moved slowly" over the skin. When this stimulus was used on the affected side, it produced activation of structures very similar to those activated in response to 20°C waterbath stimulation of the affected hand in the present study (Table 4) (Peyron et al, 1998) (see also Cesaro et al, 1991;Hirato et al, 1994).…”

Section: Functional Imaging Studiessupporting

confidence: 63%

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

et al. 2007

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Central pain is neuropathic pain resulting from a lesion of the CNS, such as a stroke [poststroke central pain (CPSP)]. Lesions involving the posterior thalamus lead to reduction or loss of sensation and to CPSP, although the responsible nuclei have not been identified. We now examine the hypotheses that thalamic lesions must extend posterior to the ventral caudal nucleus (Vc) and include ventral medial posterior nucleus (VMpo), to result in loss of cold sensibility and CPSP. Patients with small thalamic strokes associated with CPSP were evaluated by atlas-based mapping of magnetic resonance imaging scans, and by somatosensory testing. All lesions involved posterior Vc; two lesions also involved nuclei posterior to Vc, but not VMpo. All patients tested had alterations of cold pain sensation and tactile sensation, as measured by von Frey hairs. Three patients had altered cool sensation, and the patient with the least involvement of Vc had normal cool thresholds, suggesting that a critical volume of Vc must be involved before cool sensation is impaired. Perception of warm was impaired only in lesions involving nuclei posterior to Vc. Heat pain perception was never affected. In a subject with cold allodynia, a single-subject protocol PET study measured the responses to immersion of either hand in a 20°C waterbath. The scan during stimulation of the affected hand was characterized by intense activation of contralateral sensorimotor cortex. Therefore, there are modality-specific subnuclear structures in the posterior thalamus, but lesions of Vc not involving VMpo are sufficient to impair cold sensibility and to produce CPSP.

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Section: Functional Imaging Studiessupporting

confidence: 63%

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

et al. 2007

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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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“…19) Irregular burst discharges were found in the posterolateral thalamus in patients with CPSP, and regional cerebral glucose metabolism decreased in the thalamus and cortical postcentral area, but increased in the cortical precentral area, suggesting that changes in cortical activity adjacent to the central sulcus might be related to the genesis of thalamic pain. 6) Differences in abnormal activities in the thalamic neurons and changes in cortical and thalamic activity may be one reason for the necessity of higher intensity stimulation parameters for MCS in the brainstem-spinal group.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Motor Cortex Stimulation for Intractable Central Neuropathic Pain: Comparison of Stimulation Parameters Between Post-stroke Pain and Other Central Pain

Tanei

Kajita

Noda

et al. 2011

Neurol. Med. Chir.(Tokyo)

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Motor cortex stimulation (MCS) has now become the preferred option for neurosurgical management of intractable central neuropathic pain such as post-stroke pain and trigeminal neuropathic pain. However, the efficacy of MCS for other central neuropathic pain such as pain resulting from spinal cord or brainstem lesions is unclear. We retrospectively reviewed 11 consecutive patients with intractable central neuropathic pain who underwent MCS in our institution. Eight patients had poststroke pain caused by thalamic hemorrhage (n ＝ 5) or infarction (n ＝ 3) (thalamic group). Two patients had postoperative neuropathic pain caused by spinal cord lesions, and one patient had facial pain caused by a brainstem lesion associated with multiple sclerosis (brainstem-spinal group). Visual analog scale and stimulation parameters were evaluated at 1 and 6 months postoperatively. MCS was effective for six of eight patients in the thalamic group, and all three patients in the brainstem-spinal group. These efficacies continued for 6 months after surgery without significant change in the stimulation parameters compared with the parameters at 1 month in both groups. The mean amplitude at 1 month and frequency at 6 months after surgery were significantly higher in the brainstem-spinal group than the thalamic group, although the patient number was small. MCS is effective for other central neuropathic pain, but higher intensity stimulation parameters may be necessary to gain adequate pain reduction.

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Pathophysiology of Central (Thalamic) Pain: Combined Change of Sensory Thalamus with Cerebral Cortex around Central Sulcus

Cited by 36 publications

References 0 publications

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

Lesions Limited to the Human Thalamic Principal Somatosensory Nucleus (Ventral Caudal) Are Associated with Loss of Cold Sensations and Central Pain

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

Efficacy of Motor Cortex Stimulation for Intractable Central Neuropathic Pain: Comparison of Stimulation Parameters Between Post-stroke Pain and Other Central Pain

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