The ventral posterior nucleus of thalamus is involved in the generation of central pain syndromes

Research output: Contribution to journalArticle

Abstract

It is proposed that neurons in the principal sensory nucleus of human thalamus (ventralis posterior-VP) signal acute pain and that alterations in the activity of these neurons generate symptoms of central pain syndromes (CPS). During neurosurgical operations for treatment of pain, increased neuronal bursting activity is found in VP of patients with CPS. This bursting is of the type associated with a calcium conductance and is increased in areas of VP representing the part of the body where the patient experiences pain. Altered neuronal activity in CPS may be associated with the injuries to pain-signalling pathways that are found in all patients with CPS. In an animal model of pain following neural injury, dramatic changes in calcium-binding proteins occur in those areas of VP that represent the part of the body where the animal may experience pain. Inputs to VP from pain-signalling pathways may be mediated via excitatory amino acid neurotransmitters (EAA) acting at a receptor that gates a calcium conductance. These findings suggest that CPS are caused by injury to pain signalling pathways that in turn alter EAA-mediated calcium conductances at neurons in VP.

Original languageEnglish (US)
Pages (from-to)42-51
Number of pages10
JournalAPS Journal
Volume1
Issue number1
DOIs
StatePublished - 1992
Externally publishedYes

Fingerprint

Posterior Thalamic Nuclei
Ventral Thalamic Nuclei
Pain
Excitatory Amino Acids
Calcium
Human Body
Neurons
Neurotransmitter Agents
Wounds and Injuries
Calcium-Binding Proteins
Acute Pain
Thalamus

Keywords

  • excitatory amino acids
  • Key wordscentral pain syndrome
  • thalamic pain mechanisms

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine
  • Clinical Neurology
  • Neuroscience(all)

Cite this

The ventral posterior nucleus of thalamus is involved in the generation of central pain syndromes. / Lenz, Frederick.

In: APS Journal, Vol. 1, No. 1, 1992, p. 42-51.

Research output: Contribution to journalArticle

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