Study design: Discussion of issues and development of consensus. Objective: Present the background, purpose, development process, format and definitions of the International Spinal Cord Injury Pain (ISCIP) Classification. Methods: An international group of spinal cord injury (SCI) and pain experts deliberated over 2 days, and then via e-mail communication developed a consensus classification of pain after SCI. The classification was reviewed by members of several professional organizations and their feedback was incorporated. The classification then underwent validation by an international group of clinicians with minimal exposure to the classification, using case study vignettes. Based upon the results of this study, further revisions were made to the ISCIP Classification. Results: An overall structure and terminology has been developed and partially validated as a merger of and improvement on previously published SCI pain classifications, combined with basic definitions proposed by the International Association for the Study of Pain and pain characteristics described in published empiric studies of pain. The classification is designed to be comprehensive and to include pains that are directly related to the SCI pathology as well as pains that are common after SCI but are not necessarily mechanistically related to the SCI itself. Conclusions:The format and definitions presented should help experienced and non-experienced clinicians as well as clinical researchers classify pain after SCI.
Astrocytes in vitro and in situ have been shown to express voltage- activated ion channels previously thought to be restricted to excitable cells, including voltage-activated Na+, Ca2+, and K+ channels. However, unlike neurons, astrocytes do not generate action potentials, and the functional role of voltage-activated channels in astrocytes has been an enigma. In order to study the function of Na+ channels in glial cells, we carried out ion flux measurements, patch-clamp recordings, and ratiometric imaging of [Na+]i during blockade of Na+ channels on rat spinal cord astrocytes cultured for 7–10 d. Acute blockade of astrocyte Na+ channels by TTX had multiple effects: (1) TTX reduced, in a dose- dependent manner, Na+/K(+)-ATPase activity measured as unidirectional influx of 86Rb+; (2) TTX depolarized astrocyte membrane potential at a rate of approximately 1 mV/min; (3) TTX (100 microM) reduced [Na+]i; and (4) prolonged exposure to micromolar TTX induced astrocyte death. All these effects of TTX could be mimicked by ouabain or strophanthidin, specific blockers of the Na+/K(+)-ATPase. The effects of TTX and ouabain (or strophanthidin) were not additive. These results suggest that TTX-blockable Na+ channels in glial cells serve functions that do not require their participation in action potential electrogenesis; in particular, we propose that glial Na+ channels constitute a “return” pathway for Na+/K(+)-ATPase function, which permits Na+ ions to enter the cells to maintain [Na+]i at concentrations necessary for activity of the Na+/K(+)-ATPase. Since astrocyte Na+/K(+)-ATPase is believed to participate in [K+]o homeostasis in the CNS, the coupling of Na+ flux through voltage- activated Na+ channels to ATPase activity may provide a feedback loop that participates in the regulation of K+ ion levels in the extracellular space.
The postnatal differentiation of rat optic nerve fibres was examined by transmission electron microscopy. The results show that many early developing axons contain clusters of vesiculotubular profiles prior to myelination. At places vesicular elements appear to fuse with the axolemma, and, in addition, some axons exhibit deep axolemmal invaginations and axoplasmic lamellated bodies. It is suggested that these features might reflect axolemmal remodelling, possibly involving axoglial signalling and/or functional differentiation of the axolemma. The size distribution of unmyelinated optic nerve axons changes little during development. Ensheathment of larger axons commences 6 days postnatally. The subsequent formation of compact myelin sheaths is accompanied by an increase in axonal diameter. The early sheaths are a few microns long and separated by long bare axon segments. In optic nerves from 10-12-day-old rat pups, a few sheaths consisting of about five layers border primitive asymmetric nodes with a patchy axolemmal undercoating. Extensions from one of the terminating sheaths are often associated with undercoated patches of axolemma. Relatively differentiated nodes of Ranvier first appear 14-16 days after birth. The continued nodal maturation involves establishment of a regular nodal geometry, increasing distinctness of the axolemmal undercoating, and formation of perinodal astrocytic processes embedded in an extracellular node gap substance. The results are compared with available data on the conduction properties of rat optic nerve fibres during development.
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