PubMed · 14168439
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A CARAYON, P BOURREL. 1964. [CAUSALGIA].. https://pubmed.ncbi.nlm.nih.gov/14168439/
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We applied chronic deep brain stimulation (DBS) of the thalamic nucleus ventralis caudalis (Vc) for the treatment of peripheral deafferentation pain. The subjects included 11 cases of phantom limb pain and 7 of root or nerve injury pain without phantom sensation. In the phantom limb pain patients, the spike density markedly increased in the same area of the Vc where microstimulation induced paresthesia in the part with phantom sensation. Reorganization of the receptive field representation within the Vc was also demonstrated by microrecording and microstimulation. In the root or nerve injury pain patients with severe allodynia and without phantom sensation, oscillating neural hyperactivity appeared when the allodynia was induced during single-cell recording in the Vc. In both groups stimulation of these areas with the DBS electrode was useful for achieving pain reduction. Inhibition of spinothalamic tract neurons, restoration of the original receptive field representation and modulation of thalamocortical rhythmic oscillations are proposed to play important roles in a possible mechanism of Vc-DBS for the treatment of deafferentation pain.
Decrease of thalamic blood flow contralateral to neuropathic pain has been described by several groups, but its relation with sensory deafferentation remains unclear. Here we report one instance where the thalamic effects of sensory deafferentation could be dissociated from those of neuropathic pain. A 50-year-old patient underwent a left medullary infarct leading to right-sided thermal and pain hypaesthesia up to the third right trigeminal division, as well as in the left face. During the following months the patient developed neuropathic pain limited to the left side of the face. Although the territory with sensory loss was much wider in the right (non painful) than in the left (painful) side of the body, PET-scan demonstrated significant reduction of blood flow in the right thalamus (contralateral to the small painful area) relative to its homologous region. After 3 months of right motor cortex stimulation the patient reported 60% relief of his left facial pain, and a new PET-scan showed correction of the thalamic asymmetry. We conclude that thalamic PET-scan hypoactivity contralateral to neuropathic pain does not merely reflect deafferentation, but appears related to the pain pathophysiology, and may be normalized in parallel with pain relief. The possible mechanisms linking thalamic hypoactivity and pain are discussed in relation with findings in epileptic patients, possible compensation phenomena and bursting thalamic discharges described in animals and humans. Restoration of thalamic activity in neuropathic pain might represent one important condition to obtain successful relief by analgesic procedures, including cortical neurostimulation.
Complex regional pain syndrome is a clinically challenging entity both in terms of accurate diagnosis and effective treatment. Complex regional pain syndrome is a post-traumatic painful neurologic syndrome involving the somatosensory, sympathetic and often the somatomotor systems. This complex condition consists of local neurogenic inflammation out of proportion to injury; severe pain in the skin, subcutaneous tissues and joints; and a central hyperexcitability that is often compounded with a sympathetic component. The syndrome is multifaceted manifesting both central and peripheral neurologic pathophysiology, frequently including a prominent psychosocial component. The wide array of possible patient presentations and antecedent pathologies also complicate successful treatment. To further add to the clinical challenges of complex regional pain syndrome, the epidemiology and natural history of complex regional pain syndrome are only partially known; evidence concerning complex regional pain syndrome treatment has grown slowly, due in large part to the vagaries of diagnosis; and research data--when they are available--are difficult to interpret. Thus, in spite of our evolving understanding of this neurologic disorder, in many cases complex regional pain syndrome remains difficult to diagnose and treat successfully.