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The recent years brought a growing awareness for the existence of complex neuronal structures within the spinal cord that act as movement controllers. The presented pilot study addresses an extension of pure non-invasive spinal cord stimulation by adding an afferent input from electrically stimulated peripheral nerve. The goal was to assess electrophysiologically the influence of peripheral nerve stimulation (peroneal nerve) on the function of the lumbar spinal cord neural circuitries.

Prior to a discussion of the development of descending motor pathways in amphibians, some aspects of the development of the CNS of urodeles and anurans will be discussed. Coghill’s and Herrick’s studies on the early development of the CNS in the tiger salamander, Ambystoma tigrinum, were aimed at determining the relation between early differentiation of the brain and the development of behavior. In anurans, particularly the development of the primary nervous system, a functionally complete, yet transient embryonic nervous system, has been extensively studied.

It was initially reported by Hunt et al.36 that physiological stimulation of rat primary sensory neurons causes the expression of c-fos-like protein immunoreactivity in nuclei of postsynaptic neurons of the dorsal horn of the spinal cord. In these experiments it was demonstrated that noxious heat or chemical stimuli resulted in a rapid appearance of Fos-like immunoreactivity (Fos-LI) in the superficial laminae of the dorsal horn, while activation of low threshold cutaneous afferents resulted in fewer labeled cells with a different laminar distribution. The work of Hunt et al.36 has been at the origin of numerous studies related to pain research. After several years of investigations, there is accumulating evidence that various nociceptive peripheral stimuli result in c-fos expression at the spinal cord level. These stimuli include noxious heat,10,11,35,36,48,56,57,58,59,61 noxious chemical stimulation,31,36,42,52,59 noxious mechanical stimulation,2,10,11,12,42 acute inflammation,25,37,46,48,49 intense electrical transcutaneous stimulation13,35,44 and visceral stimulation.7,8,9,32,45,54 These data are in good agreement with numerous electrophysiological investigations showing that a very high proportion of neurons located either in the superficial laminae or in the neck of the dorsal horn are driven by noxious stimuli (see Refs in 4). It is reasonable to assume therefore that those dorsal horn cells driven by noxious stimulation may be those which preferentially express c-fos. This assertion is strongly supported by the fact that stimulation of the sciatic nerve at Aδ/C intensity, but not at Aα/β, induced c-fos expression in lumbar spinal cord neurons 35

The introduction of intrathecal baclofen therapy in 1985 (Penn and Kroin 1985; Ochs and Struppler 1987) brought significant progress in treating severe forms of spasticity. With this new therapy, high drug concentrations are reached at the desired site of action in the lumbar spinal cord while the concentration in the brain remains very low. Thus, side effects from actions at the cerebral level, such as tiredness and hallucinations, can be circumvented. The concentration of baclofen in the CSF is 50 times higher with intrathecal administration than with systemic administration (Kroin 1992).

Hemisection of the spinal cord in the adult cat has been used repeatedly as an experimental model to investigate the mechanisms underlying spasticity. In many of these experiments low thoracic spinal cord lesions were performed, which spared the dorsal funiculi (McCouch et al. 1957; Murray and Goldberger 1974; Hultborn and Malmsten 1983). A recent study used hemisection of the lower lumbar spinal cord (Carter et al. 1991) to study the contributions of interneuronal relays located in these segments (Edgley et al. 1988).

The pathogenesis of intermittent claudication in spinal canal stenosis has attracted increasing attention as a blood flow problem in the spinal cord and cauda equina. It has been noted that the increased density and dilatation of blood vessels in the lumbar spinal cord or the ipsilateral limb can be induced after electrical stimulation of a limb.

The 36th Annual Meeting of the German Society for Neurosurgery discussed surgical approaches to the various parts of the spinal column, the ligaments, and the attachments of the spinal cord and its vasculature. In this paper, data are presented on the approaches to the craniocervical junction in particular, but also to the thoracic and lumbar spinal cord.

The effects of intrathecally administered morphine on the activity of single units in Rexed lamina V of the transected feline lumbar spinal cord were studied in order to investigate the mechanisms of intrathecally administered morphine analgesia. The activity of single units in Rexed lamina V was sampled utilizing an extracellular microelectrode recording technique. These cells respond preferentially to noxious peripheral stimuli. The results of the present study demonstrate a well-defined suppression of the activity of lamina V nociceptive neurons after intrathecally administered morphine (0.1 mg) on the spinal cord. The results also demonstrate that the degree and duration of this suppression by intrathecally administered morphine 0.1 mg were significantly greater than those by intravenously administered morphine 2.0 mg/kg. The suppressive effect continued for more than 2 and half hours. Naloxone promptly reversed the suppression effect of intrathecally administered morphine. Onset time of the suppressive effect was significantly slower in morphine intrathecally administered than in morphine intravenously administered.

The pathology of the spinal cord has for a long time been dominated by myelitis. Nowadays it is thought that many of the previously described “syndromes” are, in fact, vascular myelopathies. Three events have shed new light on spinal pathology: 1. Research into the blood supply and circulation of the central nervous system has not only recalled some long-standing and often neglected developments by Adamkiewicz (1882), Kadyi (1889), and Tanon (1910) but has also provided new details (Lazorthes, 1957, 1958, 1964; Corbin, 1961). 2. More systematic anatomic and clinical investigations of the pathologic spinal cord have also produced some very interesting observations (Ullman and Alajouanine, 1938; Zulch, 1954–1955; Lhermitte and Corbin, 1960; Garcin et al., 1963; Jellinger, 1966; Neumayer, 1967; Fazio, 1970). 3. New techniques of exploration and examination, especially angiography of the vessels of the spinal cord by selective injection, have placed the anatomic contributions in an appropriate clinical and surgical framework (Houdart et al., 1965; Di Chiro, 1967).