Objective evaluation of pain in various spinal diseases: neuropeptide immunoreactivity in the cerebrospinal fluid

Imasato, Hiroshi; Nagata, Kensei; Hashimoto, Sanshiro; Komori, Hironori; Inoue, Akio

doi:10.1038/sj.sc.3100537

Cited by 17 publications

(5 citation statements)

References 8 publications

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“…Accordingly, penetration of E through this barrier is highly variable, and its non-conjugated forms cannot traverse the BBB at all (King et al 2001). Often, no correlation can be observed between E levels in the CSF and pain intensity measured by a visual analogue scale (Imasato et al 1997). Although tiredness following physical exercise is inXuenced by both central and peripheral factors, it is not known in humans, whether the centrally and peripherally released BE correlate with each other or not (Nybo and 123 Secher 2004).…”

Section: Introductionmentioning

confidence: 98%

The effect of physical therapy on beta-endorphin levels

Bender¹,

Nagy²,

Barna

et al. 2007

Eur J Appl Physiol

115

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Beta-endorphin (betaE) is an important reliever of pain. Various stressors and certain modalities of physiotherapy are potent inducers of the release of endogenous betaE to the blood stream. Most forms of exercise also increase blood betaE level, especially when exercise intensity involves reaching the anaerobic threshold and is associated with the elevation of serum lactate level. Age, gender, and mental activity during exercise also may influence betaE levels. Publications on the potential stimulating effect of manual therapy and massage on betaE release are controversial. Sauna, mud bath, and thermal water increase betaE levels through conveying heat to the tissues. The majority of the techniques for electrical stimulation have a similar effect, which is exerted both centrally and--to a lesser extent--peripherally. However, the parameters of electrotherapy have not yet been standardised. The efficacy of analgesia and the improvement of general well-being do not necessarily correlate with betaE level. Although in addition to blood, increased brain and cerebrospinal fluid betaE levels are also associated with pain, the majority of studies have concerned blood betaE levels. In general, various modalities of physical therapy might influence endorphin levels in the serum or in the cerebrospinal fluid--this is usually manifested by elevation with potential mitigation of pain. However, a causal relationship between the elevation of blood, cerebrospinal fluid or brain betaE levels and the onset of the analgesic action cannot be demonstrated with certainty.

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Section: Introductionmentioning

confidence: 98%

The effect of physical therapy on beta-endorphin levels

Bender¹,

Nagy²,

Barna

et al. 2007

Eur J Appl Physiol

115

View full text Add to dashboard Cite

show abstract

“…Although the results of the present work indicate that they process somatic stimuli in a manner similar to those in the deeper dorsal horn, they may also serve to integrate internal and external stimuli: their dorsally projecting dendrites are in close proximity to the cerebrospinal fluid, and they internalize the NK1 receptor upon intrathecal SP administration (Abbadie et al, 1999). Numerous disease and injury conditions are associated with increased SP in the CSF, including posttraumatic stress disorder and major depression (Geracioti et al, 2006), late-stage Alzheimer's disease (Rosler et al, 2001), lumbar disc herniation, lumbar canal stenosis, and cervical myelopathy (Imasato et al, 1997). It is tempting to speculate that GF neurons may participate in adjusting behavioral responses to somatic stimuli in these and other pathological states.…”

Section: Discussionmentioning

confidence: 97%

Anatomical and functional characterization of neuropil in the gracile fasciculus

Ramer¹

2008

J of Comparative Neurology

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A fundamental organizational principle of the central nervous system is that gray matter is the province of neuronal somata, white matter their processes. However, the rat and primate dorsal columns (archetypal spinal "white matter" tracts) are actually of intermediate character, insofar as they contain a surprisingly prominent neuropil of unknown function. Here I report on the morphology, inputs, projections, and functional properties of these neurons. Small fusiform and larger lentiform neurons are most abundant in the gracile fasciculus of the cervical and lumbar enlargements and are absent from the cuneate fasciculus and corticospinal tract. Many have dendrites that run along the dorsal pia, and, although in transverse sections these neurons appear isolated from the gray matter, they are also connected to area X by varicose and sometimes loosely fasciculated dendrites. These neurons receive neurochemically diverse, compartmentalized synaptic inputs (primary afferent, intrinsic and descending), half express the substance P receptor, and some project supraspinally. Unlike substantia gelatinosa neurons, they do not express protein kinase C gamma. Functionally, they have small receptive fields, which are somatotopically appropriate with respect to their anterior-posterior position along the neuraxis. They respond to innocuous and/or noxious mechanical stimulation of the distal extremities, and some are prone to central sensitization or "windup." Morphologically, neurochemically, and functionally, therefore, these cells most closely resemble neurons in laminae III-VI in the dorsal horn. The proximity of their dorsal dendrites to the pia mater may also reflect an ability to integrate internal (e.g., changes in cerebrospinal fluid compostition) and external (e.g., somatic) stimuli.

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“…In different spinal cord compression syndromes and pain conditions, CSF substance P concentrations were significantly increased when compared with healthy controls (18.5 ± 3.6 pg/ml) [162]. The maximum concentration occurred in fractures of the lower extremities (57.7 ± 5.5 pg/ml).…”

Section: Degenerative Vertebral Spine Disordersmentioning

confidence: 97%

Substance P in Rheumatic Diseases

Seidel

Tsalik²,

Vetter³

et al. 2007

CRR

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Inflammation in many autoimmune syndromes is modulated by the nervous system. This paper reviews important principles of neurogenic inflammation and findings of substance P overexpression in rheumatic diseases. Substance P is a key molecule in activating inflammation after antidromal axoplasmic transport and secretion at the nociceptor. We summarize the results from studies with rheumatoid arthritis, osteoarthritis, psoriatic arthritis, systemic lupus erythematodes, systemic sclerosis, vasculitides, Sjögren syndrome, vasculitides, reflex sympathetic dystrophy, gouty arthritis, fibromyalgia syndrome, chronic fatigue syndrome and degenerative vertebral spine disorders. Although substance P is associated with many of these diseases, selective receptor blockers have not been effective in therapy. In contrast, the nonselective antagonist capsaicin is beneficial in some conditions. We also discuss a novel therapeutic principle with selective serotonin antagonists that may induce a powerful downregulation of neurogenic inflammation.

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Objective evaluation of pain in various spinal diseases: neuropeptide immunoreactivity in the cerebrospinal fluid

Cited by 17 publications

References 8 publications

The effect of physical therapy on beta-endorphin levels

The effect of physical therapy on beta-endorphin levels

Anatomical and functional characterization of neuropil in the gracile fasciculus

Substance P in Rheumatic Diseases

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