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.
- Key wordscentral pain syndrome
- excitatory amino acids
- thalamic pain mechanisms
ASJC Scopus subject areas
- Clinical Neurology
- Anesthesiology and Pain Medicine