ABSTRACT
A complication of endoscopic carpal tunnel release (6/53 consecutive cases) is rupture of a digital branch. The objective of this study was to find a method for detecting neuropathy of the digital branch innervating the radial side of the fourth digit and the ulnar side of the third digit. This study examined whether the following sensory nerve conduction techniques would enhance diagnosis of this neuropathy: (1) recording with standard digital ring electrodes; (2) recording with ring electrodes from two adjacent fingers; and (3) disc electrodes placed between two fingers. Ten healthy individuals were studied before and after lidocaine anesthesia of the digital branch between the ring and middle finger. Statistical analysis was performed with a two-tailed, paired t test. Results show that after lidocaine injection there was a decrease in antidromic amplitude of 94% for ring electrodes on the fourth digit, 62% for rings on the third digit, 77% for disc electrodes between the fourth and third digits, and 74% for rings on digits 4 and 3 (P < 0.005), with no significant change in peak latency (P > 0.3). In conclusion, although all techniques used in this model yielded a significant change in amplitude, rings on the third digit compared with the second and discs between digits 4/3 compared with 3/2 were most specific without false-positives from normal data. It is hoped this study will aid the electromyographer in postoperative diagnosis.
Subject(s)
Carpal Tunnel Syndrome/surgery , Fingers/innervation , Median Nerve/physiology , Postoperative Complications/diagnosis , Adult , Aged , Carpal Tunnel Syndrome/diagnosis , Electrodes , Fingers/physiopathology , Humans , Median Nerve/injuries , Median Nerve/physiopathology , Middle Aged , Nerve Block , Neural Conduction , Peripheral Nervous System Diseases/diagnosis , Peripheral Nervous System Diseases/etiology , Postoperative Complications/etiology , Prospective StudiesABSTRACT
Administration of pirprofen may produce microvesicular steatosis of the liver in humans. The effects of pirprofen on the mitochondrial beta-oxidation of fatty acids have been investigated in mice. In vitro, addition of 2 mM pirprofen decreased by 50% the formation of [14C]acid-soluble beta-oxidation products, and decreased by 70% the formation of [14C]CO2 upon incubation of hepatic mitochondria with [14C]palmitic acid, ATP, carnitine and coenzyme A. In vivo, administration of pirprofen (2 mmol . kg-1 i.p.), 1 hr before that of [U-14C]palmitic acid, decreased by 70% the exhalation of [14C]CO2 during the next 6 hr. Administration of pirprofen (2 mmol . kg-1 i.p.), 1 hr before the measurement, decreased plasma beta-hydroxybutyrate by 60%, plasma acetoacetate by 30% and blood glucose by 40%. Administration of pirprofen (2 mmol . kg-1 i.p.) 6 hr before sacrifice, doubled hepatic triglycerides content and produced microvesicular steatosis of the liver. We conclude that pirprofen inhibits the mitochondrial beta-oxidation of fatty acids in mice, thus explaining the microvesicular steatosis observed in mice and in some human subjects.
