Neurologia medico-chirurgica
Online ISSN : 1349-8029
Print ISSN : 0470-8105
ISSN-L : 0470-8105
頑痛に対する視床手術後の再発防止対策としての視床中継核刺激法 ―その基礎と臨床応用―
坪川 孝志小谷 昭夫西本 博片山 容一森安 信雄
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1976 年 16pt2 巻 3 号 p. 247-254

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Recurrence of intractable pain was observed following basomedial thalamotomy, in spite of making a lesion as wide as possible at both the neo and paleo-spinothalamic pathway.
As a last resort for prevention of recurrence, the relay nucleus stimulation for selection of the candidate among the cases suffered from intractable pain was applied in clinical cases. The mechanism of inhibitory modulating effect of relay nucleus stimulation upon the medial thalamic neuron responding to noxious stimuli was also studied in experimental animals.
Experimental Results: The neurons responded to noxious stimuli in the medial thalamic nucleus are divided into 2 types; one group (F-type neuron) shows activation of action potentials with about 20 msec. latency; the other (I-type neuron) shows inhibition upon the spontaneous activities. The F-type cell is pre or post-synaptically inhibited while the I-type cell disinhibited by conditioning stimulation in the thalamic relay nucleus, although the relay nucleus does not directly connect with the medial nucleus. The inhibitory modulating effect by stimulation of the thalamic relay nucleus is suppressed following the sensori-motor cortical ablation, or making lesion in the anteromedial thalamic area.
It may be concluded that the conditioning stimulation of the thalamic relay nucleus produces the inhibitory modulating effect through the cortical or intrathalamic fiber connections upon pain perceptive activity at the medial thalamic nucleus.
Clinical Observations: In clinical cases whose intractable pains were suppressed by conditioning stimulation of thalamic relay nucleus, the medial thalamotomy had excellent long lasting pain killing effects.
It is concluded that the pain relief effects of medial thalamotomy can be predicted before the destruction of thalamic nucleus by application of conditioning stimulation in the thalamic relay nucleus.

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