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Thalamic ventrobasal (VB) stimulation, first performed by Mazars, in 1961, is a valuable means for treating central and deafferentation pain. The way it acts to achieve pain relief, however, is still a matter of controversy. In this paper, the author examines previously proposed hypotheses and suggests that VB stimulation induces pain relief by activation of a multisynaptic inhibitory pathway to the medial thalamus, in which the dopaminergic nigrostriatal system exerts an important role and by modulation of abnormal activity in VB itself. The multisynaptic pathway involved, as well as the neurotransmitters, are suggested: VB stimulation excites somatosensory cortex through the glutaminergic thalamocortical pathway, which in turn, sends excitatory glutaminergic axons to the motor cortex. The sensorymotor cortex originates the excitatory glutaminergic corticostriatal pathway to the anterior putamen. The anterior putamen sends excitatory peptidergic (substance P) pathways to the globus pallidus internus (striatopallidal pathway) and to the substantia nigra reticulata (striatonigral pathway). The globus pallidus internus inhibits the medial thalamus through the pallidothalamic GABAergic pathway. The substantia nigra reticulata sends inhibitory GABAergic projections to the medial thalamus (nigrothalamic pathway) and excites the substantia nigra compacta. The substantia nigra compacta projects excitatory dopaminergic axons to the striatal neurons (nigrostriatal pathway) with output to the globus pallidus internus and substantia nigra reticulata and so on. Data to support this hypothesis are provided by an extensive review of the literature.

Thalamic ventrobasal stimulation for pain relief: probable mechanisms, pathways and neurotransmitters