Richard G. Gillette

Characterization of spinal somatosensory neurons having receptive fields in lumbar tissues of cats

&NA; In pentobarbital anesthetized cats, extracellular unitary recordings were made from neurons in the extreme lateral dorsal horn of spinal segments L4–5. All 118 units reported had receptive fields in deep somatic tissues and/or skin of the lumbar region, hip and/or proximal leg. Neurons were functionally characterized according to their responses to non‐noxious and noxious mechanical stimuli and to injections of algogens. Most neurons (92%) were either wide‐dynamic range (WDR) or nociceptive specific (NS), and most of these had very large nociceptive receptive fields in the back/hip/leg that included both skin and deep somatic tissues innervated through both the dorsal (back/hip) and ventral (leg/ventral spine) rami. Most (72%) were ‘hyperconvergent’ in that they were responsive to stimulation of many different somatic tissues including skin, muscles, facet joint capsules, ligaments, and periosteum. Some units were tested and found also to be activated by noxious stimulation of spinal dura and ventral annulus fibrosis and ventral longitudinal ligament. Twelve of 22 neurons tested were found to have ascending axons extending beyond Th10. The nocireceptive neurons (NS and WDR) in the population tested are suitable for processing information about tissue damage in deep somatic tissues in the back, hip and proximal leg. The apparent relative paucity of such neurons and their very large hyperconvergent receptive fields suggest that sensations served by these neurons, such as low back and referred leg pain, would be neither well localized nor attributable to pathology in a specific tissue. These deductions, based on physiological characteristics in cats, are consistent with clinical reports from humans who experience pain as a consequence of spinal or paraspinal injuries.

Sympathetic activation of cat spinal neurons responsive to noxious stimulation of deep tissues in the low back

&NA; Prior findings from diverse studies have indicated that activity in axons located in the lumbar sympathetic chains contributes to the activation of spinal pain pathways and to low back pain; these studies have utilized sympathetic blocks in patients, electrical stimulation of the chain in conscious humans, and neuroanatomical mapping of afferent fiber projections. In the present study, dorsal horn neurons receiving nociceptor input from lumbar paraspinal tissues were tested for activation by electrical stimulation of the lumbar sympathetic chain in anesthetized cats. Of 83 neurons tested, 70% were responsive to sympathetic trunk stimulation. Excitatory responses, observed in both nociceptive specific and wide‐dynamic‐range neurons, were differentiable into two classes: non‐entrained and entrained responses. Non‐entrained responses were attenuated or blocked by systemic administration of the &agr;‐adrenergic antagonist phentolamine and are thought to result from sympathetic efferent activation of primary afferents in the units receptive fields. Entrained responses were unaffected by phentolamine and are thought to result from electrical activation of somatic and/or visceral afferent fibers ascending through the sympathetic trunk into the dorsal horn. These findings from nocireceptive neurons serving lumbar paraspinal tissues suggest that low back pain may be exacerbated by activity in both efferent and afferent fibers located in the lumbar sympathetic chain, the efferent actions being mediated indirectly through sympathetic‐sensory interactions in somatic and/or visceral tissues.

Slowly developing placebo responses confound tests of intravenous phentolamine to determine mechanisms underlying idiopathic chronic low back pain.

&NA; Phentolamine (30 mg) was administered intravenously to subjects with idiopathic chronic low back pain in a novel placebo‐controlled test to determine whether this &agr;‐adrenergic antagonist would reduce their pain. The effects of infusions on spontaneous pain and stimulus‐evoked pains (touch, cold, tapping and deep pressure) were evaluated separately. All subjects gave strong placebo responses (reduced pain) that prevented assessment of specific drug effects. The placebo responses had onset latencies of 15–60 min, developed slowly over the next 15–45 min and persisted for hours or several days. These results not only reinforce the understanding that placebo controls are essential in the evaluation of drugs or other palliative procedures on patients with chronic pain but also indicate that the control paradigms must allow for placebo effects that are slow to develop and very persistent.

Post-sympathectomy neuralgia: hypotheses on peripheral and central neuronal mechanisms

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome dependent on: (a) the transection, during sympathectomy, of paraspinal somatic and visceral afferent axons within the sympathetic trunk; (b) the subsequent cell death of many of the axotomized afferent neurons, resulting in central deafferentation; and (c) the persistent sensitization of spinal nociceptive neurons by painful conditions present prior to sympathectomy. Viscerosomatic convergence, collateral sprouting of afferents, and mechanisms associated with sympathetically maintained pain are all proposed to be important to the development of the syndrome.

Training the evidence-based practitioner: university of Western States document on standards and competencies.

An important goal of chiropractic clinical education should be to teach specific evidence-based practice (EBP) skills to chiropractic students, interns, and doctors. Using a nominal group process, the authors produced a document similar to the Council of Chiropractic Education standards for clinical competencies that can be used to drive an EBP curriculum. Standard texts and journal articles were consulted to create the standards for this program and each standard and corresponding learning objective was discussed in detail and was then graded by the committee in terms of importance and the level of competency that should be attained. Six standards and 31 learning objectives were generated with the learning objectives being further divided into lists of specific competencies. It is the hope of these authors that by sharing this document it can serve as a comprehensive and detailed seed document for other institutions.

Suppression of activity in spinal nocireceptive `low back' neurons by paravertebral somatic stimuli in the cat

Single-unit recording techniques were used to investigate spinal cord neurons likely to be involved in low back pain. Most dorsal horn neurons with somatic receptive fields in the low back region have complex receptive fields involving deep and superficial tissues. This report shows, for the first time, that activity in some nocireceptive low back neurons is suppressed by somatic stimulation of discrete sites within the larger excitatory receptive field. Both weak and intense mechanical stimulation of skin or deep tissues suppressed activity in some neurons. The neurons in this population tested for rostral projections had long ascending axons.

Utilizing Molecular Details of the Pain System to Illustrate Biochemical Principles

To capture student interest and show clinical relevance, molecular details from the pain system can be used as supplemental examples to basic biochemistry lectures. Lecture topics include glutamate, substance P, calmodulin-dependent protein kinase II, synaptic proteases, calcitonin gene-related peptide, and neuronal protein synthesis. These topics are utilized to illustrate basic biochemical issues and are linked to pain-related topics such as pain transmission, synaptic plasticity, long-term potentiation, and central sensitization. For analysis, a brief survey was administered to evaluate student attitudes toward a representative lecture segment. Survey results support the premise that utilizing the pain system is an effective tool to engage chiropractic students during basic biochemistry lectures.

Response to Comment by Boas

block or the technique of ablation used? For our ischemic cases the existence of prior pain is usually more distal, with spinal projection neurones similarly at a different level from that likely to be mediating the secondary complaint. Would this tend to discredit prior sensitisation as the basis for subsequent pain? If the original sensitising pain is resolved, why does the secondary post sympathectomy pain become manifest? Why is there no evidence clinically for actual deafferentation? Why are sodium channel blocking drugs so effective? If deafferentation is the basis for pain, why do most cases resolve? One is tempted to propose whether there is some other common factor which might also be considered. This might include the release of neuropeptides, nerve growth factor or other processes which could induce a central sensitisation in neurones subserving the same level as those from the damaged sympathetic nerve or ganglion. There could also be a form of signal cross-talk or chemical sensitisation at a dorsal root ganglion level induced by similar mechanisms. Post-sympathectomy pain deserves closer examination in a clinical setting with quantitative sensory testing and nerve function studies, and a search for an animal model as a means to help elaborate yet another form of complex neuropathic pain.