Ultrasound-Guided Proximal and Distal Tarsal Decompression: An Analysis of Pressures in the Tarsal, Medial Plantar, and Lateral Plantar Tunnels.

Objectives. To analyze the reliability of measurements of tarsal tunnel and medial and lateral plantar tunnel pressures before and after ultrasound-guided release. Measurements taken were guided by ultrasound to improve reliability. This novel approach may help surgeons make surgical decisions. The second objective was to confirm that decompression using ultrasound-guided surgery as previously described by the authors is technically effective, reducing pressure to the tarsal and medial and lateral plantar tunnels. Methods. The study included 23 patients with symptoms compatible with idiopathic tarsal tunnel syndrome (TTS). The first step was to measure intracompartmental pressure of the tarsal tunnel, medial plantar tunnel, and lateral plantar tunnel preoperatively. The second step was ultrasound-guided decompression of the tibial nerve and its branches. Subsequently, pressure was measured again immediately after decompression in the 3 tunnels. Results. After surgery, the mean values significantly dropped to normal values. This represents a validation of effective decompression of the tibial nerve and its branches in TTS with ultra-minimally invasive surgery. Conclusions. The ultrasound-guided surgical technique to release the tibial nerve and its branches is effective, significantly reducing pressure in the tunnels and, thereby, decompressing the nerves.Level of evidence: Level IV.

Effects of the CRF receptor antagonist D-Phe CRF(12-41) and the alpha2-adrenergic receptor agonist clonidine on stress-induced reinstatement of nicotine-seeking behavior in rats.

Tobacco dependence is a chronic disorder that is characterized by relapse after periods of abstinence. It has been hypothesized that the activation of brain stress systems mediates stress-induced relapse to smoking. The aim of these experiments was to investigate the role of corticotropin-releasing factor (CRF) and norepinephrine in stress-induced reinstatement of extinguished nicotine-seeking behavior. Rats were allowed to self-administer nicotine under a fixed-ratio 5 schedule for 14 days and then nicotine-seeking behavior was extinguished by substituting saline for nicotine. In experiment 1, footshocks reinstated extinguished nicotine-seeking behavior. In experiment 2, there was a trend for the CRF(1/2) receptor antagonist D-Phe CRF((12-41)) (5, 25microg, icv) to decrease stress-induced reinstatement of nicotine-seeking behavior. Footshock-induced reinstatement of nicotine-seeking behavior was observed only in a subset of stress-responsive rats (71%). D-Phe CRF((12-41)) significantly attenuated stress-induced reinstatement of nicotine-seeking behavior in this subset of rats. In experiment 3, the alpha2-adrenergic receptor agonist clonidine (20, 40microg/kg, sc) attenuated footshock-induced reinstatement of nicotine-seeking behavior. In experiment 4, the effects of D-Phe CRF((12-41)) and clonidine on responding for chocolate-flavored food pellets was investigated in order to determine if these compounds have sedative effects. D-Phe CRF((12-41)) did not affect responding for food pellets. Clonidine slightly, but significantly, decreased responding for food pellets. Clonidine decreased responding for food to a lesser degree than it decreased stress-induced reinstatement of nicotine-seeking behavior. These data provide support for the hypothesis that an increased activity of brain CRF and norepinephrine systems mediates stress-induced relapse to nicotine-seeking behavior.

Antagonism of CRF receptors prevents the deficit in brain reward function associated with precipitated nicotine withdrawal in rats.

Nicotine dependence is a chronic mental illness that is characterized by a negative affective state upon tobacco smoking cessation and relapse after periods of abstinence. It has been hypothesized that cessation of nicotine administration results in the activation of brain corticotropin-releasing factor (CRF) systems that leads to the negative affective state of withdrawal. The aim of our experiments was to investigate the role of brain CRF systems in the deficit in brain reward function associated with the cessation of nicotine administration in rats. The intracranial self-stimulation procedure was used to assess to negative affective aspects of nicotine withdrawal as this procedure can provide a quantitative measure of emotional distress in rats. In the first experiment, mecamylamine induced a dose-dependent elevation in brain reward thresholds in nicotine-treated rats. In the follow-up experiment, it was shown that pretreatment with the corticotropin-receptor antagonist D-Phe CRF((12-41)) prevents the elevations in brain reward thresholds associated with precipitated nicotine withdrawal. In the third experiment, the effect of D-Phe CRF((12-41)) on the elevations in brain reward thresholds associated with spontaneous nicotine withdrawal was investigated. Administration of D-Phe CRF((12-41)) 6 h after the explantation of the nicotine pumps, did not result in a lowering of the brain reward thresholds. These findings indicate that antagonism of CRF receptors prevents, but not reverses, the deficit in brain associated with nicotine withdrawal. These data provide support for the hypothesis that a hyperactivity of brain CRF systems may at least partly mediate the initiation of the negative affective aspects of nicotine withdrawal.