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

Estimulação talâmica ventrobasal para alívio da dor: prováveis mecanismos, vias e neurotransmissores

Abstracts

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 multisynaptyic 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 interims (striatopallidal pathway) and to the substantia nigra reticulata (striatonigral pathway). The globus pallidus interims 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.

pain; analgesia; electrical stimulation; thalamic nuclei; thalamus; cerebral cortex; basal ganglia; neurotransmitters


A estimulação talâmica ventrobasal (VB), primeiramente realizada por Mazars em 1961, é método útil para o tratamento de dor central e dor de deaferentação. A maneira como ela atua para produzir alívio da dor, porém, é ainda questão de controvérsia. Neste estudo, o autor examina as hipóteses anteriormente propostas e sugere que o alívio da dor obtido pela estimulação de VB se deve a dois prováveis mecanismos: (1) Modulação da atividade anormal em VB e (2) Ativação de uma via multisináptica inibitória para os neurônios nociceptives do tálamo medial, na qual o sistema dopaminérgico nigroestriatal exerce importante papel. A via multisináptica envolvida, bem como os neurotransmissores, são sugeridos: a estimulação de VB, através da via tálamo-cortical glutaminérgica, excitaria o córtex somatosensitivo que, por sua vez, excitaria o córtex motor através dos neurotransmissores excitatórios glutamato e aspartate. No córtex sensitivo-motor se originaria a via corticoestriatal glutaminérgica excitatória para o putâmen anterior, o qual emitiria uma via peptidérgica (substância P) excitatória para o globo pálido interno (via estriatopalidal) e para a substância nigra reticulata (via estriatonigral). O globo pálido interno inibiria o tálamo medial através da via pálido-talâmica gabaérgica. A substância nigra reticulata emitiria projeções gabaérgicas inibitórias para o tálamo medial (via nigrotalâmica) e excitaria a substância nigra compacta. A substância nigra compacta projetaria axônios dopaminérgicos excitatórios para os neurônios estriatais com eferência para o globo pálido interno e substância nigra reticulata e assim por diante. Dados de suporte a esta hipótese são providos por extensa revisão da literatura.

dor; analgesia; estimulação elétrica; núcleos talâmicos; tálamo; córtex cerebral; gânglios da base; neurotransmissores


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

Estimulação talâmica ventrobasal para alívio da dor: prováveis mecanismos, vias e neurotransmissores

Osvaldo Vilela Filho

M.D., Head, Division of Neurosurgery, Instituto Ortopédico de Goiânia; Researcher, Department of Psysiology and Pharmacology, Institute of Biological Sciences, Universidade Federal de Goiás

SUMMARY

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 multisynaptyic 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 interims (striatopallidal pathway) and to the substantia nigra reticulata (striatonigral pathway). The globus pallidus interims 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.

Key words: pain, analgesia, electrical stimulation, thalamic nuclei, thalamus, cerebral cortex, basal ganglia, neurotransmitters.

RESUMO

A estimulação talâmica ventrobasal (VB), primeiramente realizada por Mazars em 1961, é método útil para o tratamento de dor central e dor de deaferentação. A maneira como ela atua para produzir alívio da dor, porém, é ainda questão de controvérsia. Neste estudo, o autor examina as hipóteses anteriormente propostas e sugere que o alívio da dor obtido pela estimulação de VB se deve a dois prováveis mecanismos: (1) Modulação da atividade anormal em VB e (2) Ativação de uma via multisináptica inibitória para os neurônios nociceptives do tálamo medial, na qual o sistema dopaminérgico nigroestriatal exerce importante papel. A via multisináptica envolvida, bem como os neurotransmissores, são sugeridos: a estimulação de VB, através da via tálamo-cortical glutaminérgica, excitaria o córtex somatosensitivo que, por sua vez, excitaria o córtex motor através dos neurotransmissores excitatórios glutamato e aspartate. No córtex sensitivo-motor se originaria a via corticoestriatal glutaminérgica excitatória para o putâmen anterior, o qual emitiria uma via peptidérgica (substância P) excitatória para o globo pálido interno (via estriatopalidal) e para a substância nigra reticulata (via estriatonigral). O globo pálido interno inibiria o tálamo medial através da via pálido-talâmica gabaérgica. A substância nigra reticulata emitiria projeções gabaérgicas inibitórias para o tálamo medial (via nigrotalâmica) e excitaria a substância nigra compacta. A substância nigra compacta projetaria axônios dopaminérgicos excitatórios para os neurônios estriatais com eferência para o globo pálido interno e substância nigra reticulata e assim por diante. Dados de suporte a esta hipótese são providos por extensa revisão da literatura.

Palavras-chave: dor, analgesia, estimulação elétrica, núcleos talâmicos, tálamo, córtex cerebral, gânglios da base, neurotransmissores.

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Full text available only in PDF format.

Acknowledgements - I am grateful to the arquitect Dimas Aidar for the illustration, and to the colleagues Dr. Ronald Tasker, Dr. Joaquim Tomé de Sousa, Dr. Herbert A. Oliveira e Souza and Dr. Andrew Parrent, for their critical review of this paper.

Aceite: 5-março-1994.

Paper prepared at the Division of Neurosurgery, Instituto Ortopédico de Goiânia

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Publication Dates

  • Publication in this collection
    19 Jan 2011
  • Date of issue
    Dec 1994
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