Percutaneous radiofrequency coagulation of osteoid osteoma in children and adolescents

The purpose of this paper was to evaluate the effectiveness of percutaneous radiofrequency ablation of osteoid osteoma in children and adolescents. Twenty-three patients aged 4.5-19.5 years were retrospectively reviewed. All patients with lower limb lesions were able to bear full weight on their operated limb immediately after the procedure, and to resume their daily activities within 24-48 h. Pain disappeared immediately after surgery in 21 cases, and in lower limb lesions the gait was back to normal after an average of 5 days. No septic or neurovascular complications were observed. At an average follow-up of 3.5 years, all the patients including two cases of initial failure were free of pain and had a normal gait. Clinical healing was confirmed by computed tomography and bone scan performed in 12 cases. This precise and minimally invasive method is safe, effective and associated with reduced health care resources. It could be recommended as the treatment of choice for osteoid osteoma of the limbs in children and adolescents.     

Neuropeptide FF attenuates allodynia in models of chronic inflammation and neuropathy following intrathecal or intracerebroventricular administration

Experiments were conducted to explore the effects of Neuropeptide FF acting at spinal and supraspinal sites in models of chronic inflammatory or neuropathic pain and of acute pain. Neuropeptide FF was administered intrathecally (i.t.; 10.0, 25.0 and 50.0 nmol) or intracerebroventricularly (i.c.v.; 10.0, 12.5 and 15.0 nmol) either 24 h after inflammation-inducing injections of Freund's Complete Adjuvant in one hind paw or 7 days after unilateral sciatic nerve constriction. Evoked pain was assessed by measuring the withdrawal response threshold (in grams of pressure) to a mechanical stimulus applied to the plantar surface of the injured paw. Neuropeptide FF dose-dependently attenuated the allodynic response (i.e., withdrawal from a normally innocuous stimulus) to mechanical stimulation in the inflammatory and neuropathic model following i.t. (ED50=20.86 nmol and ED50=18.91 nmol, respectively) and i.c.v. (ED50=12.31 nmol and ED50=11.68 nmol, respectively) administration. Pretreatment with naloxone (2.0 mg/kg; s.c.) attenuated the anti-allodynic effect of i.t. or i.c.v. Neuropeptide FF in rats experiencing inflammatory, but not neuropathic pain. In contrast, Neuropeptide FF administered i.t. (10.0, 25.0 and 50.0 nmol) or i.c.v. (10.0, 12.5 and 15.0 nmol) had no effect on the response to acute thermal or mechanical stimulation. Neuropeptide FF injected i.t. or i.c.v. in inflamed or neuropathic rats did not produce any sign of motor dysfunction. These results suggest that Neuropeptide FF acting at spinal and supraspinal sites plays a role in modulating chronic, but not acute pain. Furthermore, the results suggest that the anti-allodynic effect of Neuropeptide FF is mediated indirectly by naloxone-sensitive opioid mechanisms in rats subjected to inflammatory, but not neuropathic pain.     

Cellular mechanism of action of resiniferatoxin: a potent sensory neuron excitotoxin

The mechanism of activation of sensory neurons by the potent irritant resiniferatoxin (RTX) was compared with that of the pungent compound, capsaicin. RTX and capsaicin evoked an inward, depolarising current associated with an increase in membrane conductance in a subpopulation of dissociated cultured neurons from rat dorsal root ganglia. RTX also evoked an uptake of⁴⁵Ca into and an efflux of [¹⁴C]guanidinium and of⁸⁶Rb from these cells but was at least 100-fold potent than capsaicin. The levels of cGMP, but not cAMP were elevated by RTX. Prolonged exposure to RTX damaged DRG neurons by a predominantly osmotic process. RTX-sensitive cells were identified by a cobalt-staining method; neurofilament-containing DRG neurons were RTX-insensitive as were all sympathetic neurons and non-neuronal cells. Cultured DRG neurons from chick embryos were also unaffected by RTX. In a neonatal rat spinal cord-tail preparation in vitro, RTX activated capsaicin-sensitive peripheral noiciceptive fibres and caused a subsequent spinal cord depolarization measured in the ventral spinal roots. Neither prolonged exposure to a phorbol ester, to desensitize/down-regulate protein kinase C, nor inhibition of protein kinase C by staurosporine affected responses produced by RTX or capsaicin. The effects of capsaicin were abolished when preparations were exposed to desensitizing concentrations of RTX. RTX therefore acts as a highly potent capsaicin analogue to activate a subpopulation of rat sensory neurons.     

The effect of wavelength on glial fibrillary acidic protein immunoreactivity in laser-induced lesions in rabbit retina

Rabbit retinas were treated with low-intensity laser coagulation at five different wavelengths. Using an indirect immunocytochemical method, the retinas were stained for glial fibrillary acidic protein (GFAP) at 2, 4, 21 and 32 days after coagulation such that we could follow GFAP expression in the Müller cells during retinal repair. GFAP-positive staining was found in the end feet of the Müller cells at 2 days after laser coagulation. GFAP immunoreactivity was observed throughout the Müller cells, surrounding the central necrotic tissue, at days 4, 21 and 32 after laser coagulation. Scar tissue in the subretinal space at days 21 and 32, which was more pronounced for the longer wavelengths produced by the Krypton and Nd-YAG lasers, also showed GFAP immunoreactivity. The Müller cells remained GFAP-immunoreactive for at least 32 days after laser coagulation.Presented at the 17th meeting of the Club Jules Gonin, Lausanne, September 2–6, 1990 Offprint requests to: M.-J. Tassignon     

Release of luteinizing hormone-releasing hormone: interrelations between eicosanoids and catecholamines

The in vitro release of luteinizing hormone-releasing hormone (LHRH), prostaglandin (PG) E2 and leukotriene (LT) C4 from male rat median eminences (ME), was estimated by radioimmunoassay (RIA) in the presence of the catecholamines (CA), norepinephrine (NE) and dopamine (DA). NE increased the release of PGE2 in the presence and in the absence of the Ca2+ ionophore A23187 (5 x 10(-6) M), but it did not modify the A23187-induced release of LTC4 from endogenous precursors or radiolabelled arachidonic acid. DA also stimulated the A23187-induced release of PGE2 but inhibited that of LTC4. However, while NE increased both the basal and the A23187-induced release of LHRH, DA increased the basal release of LHRH and inhibited the A23187-induced LHRH release. Exogenous LTC4 cancelled the inhibitory effect of DA on LHRH release. Blockade of dopaminergic receptors with haloperidol suppressed the effects of DA on PGE2, LTC4 and LHRH release. Neither eicosanoid affected the K+-evoked [3H]DA release, whereas only PGE2 inhibited the K+-evoked [3H]NE release. We conclude that LTC4 does not interact with the noradrenergic pathway and that the stimulatory effect of both catecholamines on LHRH release involves PGE2, but the inhibitory effect of DA is associated with reduced LTC4 production.     

Barbiturates in severe head injuries?

Possible mechanisms for the therapeutic effects of barbituric acid derivatives in severe head injuries have been discussed for half a century. In the following, a survey of the literature, and a discussion of three controlled clinical studies available until now is presented. A proven effect in terms of a beneficial long-term outcome for all injured patients has not been established.On the other hand there might be a subgroup of patients with an intact CO₂ reactivity of the brain vessels who may profit from barbiturates administered after head trauma.Dedicated to Marianne and Gerhard Winkler