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PubMed2005

Part 1. Injuries to the brachial plexus: mechanisms of injury and identification of risk factors.

Upper-arm weakness (paresis) or paralysis indicates peripheral-nerve damage to the brachial plexus, a network of lower cervical and upper thoracic spinal nerves supplying the arm, forearm, and hand. Physical findings reflect muscle paralysis from spinal nerve roots. The mechanism of injury includes maternal, obstetric, and infant factors that apply traction on or compression to the anatomically vulnerable brachial plexus. Nerve regeneration can occur if nerve tissue components are preserved. Recovery is affected by multiple factors, including the type and site of injury, intervention timing, and developmental factors. The majority of injuries recover in days or months; however, residual deficits can persist. Part 1 of 2 of this article provides an overview of the neurophysiology of peripheral-nerve damage and nerve regeneration. The multifactorial etiology of brachial plexus injuries will be reviewed. Photographs and on-line video clips will enhance the description of the brachial plexus injury classifications and illustrate mechanisms of shoulder dystocia and obstetric relief maneuvers. A systematic approach to the physical examination will be explored in Part 2. Serial evaluation of motor function recovery is essential and is accomplished by appropriate referrals and follow-up. Part 2 will also describe treatment options and discuss anticipatory parent guidance.

Birth Injuries↗
PubMed1990

Pancreatic and extrapancreatic galanin release during sympathetic neural activation.

To address the hypothesis that the neutropeptide, galanin, functions as a sympathetic neurotransmitter in the endocrine pancreas, we sought to determine if galanin is released from pancreatic sympathetic nerves during their direct electrical stimulation in halothane-anesthetized dogs. During bilateral thoracic splanchnic nerve stimulation (BTSNS), both peripheral arterial and pancreatic venous levels of galanin-like immunoreactivity (GLIR) increased (delta at 10 min = +92 +/- 31 and +88 +/- 25 fmol/ml, respectively). Systemic infusions of synthetic galanin demonstrated that 1) the increment of arterial GLIR observed during BTSNS was sufficient to modestly restrain basal insulin secretion and 2) only 25% of any given increment of arterial GLIR appears in the pancreatic vein, suggesting that the pancreas extracts galanin, as it does other neurotransmitters. By use of 75% for pancreatic extraction of circulating galanin, it was calculated that pancreatic galanin spillover (output) increased by 410 +/- 110 fmol/min during BTSNS. To reinforce the conclusion that pancreatic sympathetic nerves release galanin, GLIR spillover was next measured during direct local stimulation of the pancreatic sympathetic input produced by electrical stimulation of the mixed autonomic pancreatic nerves (MPNS) in the presence of the ganglionic blocker, hexamethonium. During this local pancreatic sympathetic nerve stimulation, arterial GLIR remained unchanged, but pancreatic venous GLIR increased by 123 +/- 34 fmol/ml. Thus pancreatic GLIR spillover increased by 420 +/- 110 fmol/min during MPNS in the presence of hexamethonium. We conclude that galanin is released from both pancreatic and extrapancreatic sources during sympathetic neural activation in dogs.

Animals↗
PubMed1982

Effects of individual cardiac nerve stimulation on atrioventricular conduction.

This study investigated the effects of individual canine cardiac nerve stimulation on atrioventricular conductions as measured by His bundle electrograms. A-H and H-V intervals were measured before and during stimulation of each nerve in paced hearts (200 beats/min) and before and after blocking doses of either atropine or propranolol. Increases in A-H or H-V intervals were evidence of parasympathetic innervation; decreases in intervals were evidence of sympathetic innervation. Separation by autonomic composition produced 3 categories: sympathetic, parasympathetic, and mixed input to the atrioventricular junction. The sympathetic nerves were the left and right ansae subclavia, the ventrolateral cardiac nerve, and the right stellate cardiac nerve. The parasympathetic nerve was the right thoracic vagus, and the mixed nerves were the left thoracic vagus, and the innominate, ventromedial, craniovagal, caudovagal, and right recurrent cardiac nerves. The cardiac nerves eliciting a major response were the left and right ansae subclavia, the ventrolateral, right recurrent, craniovagal, and caudovagal cardiac nerves, and the left and right thoracic vagi. In theory, the nerves of the right side, because of their innervation of both sinoatrial and atrioventricular nodes, may be expected to elicit a balanced heart rate-atrioventricular conduction response when stimulated, thus matching atrial and ventricular rates. On the other hand, stimulation of the ventrolateral cardiac nerve regularly produces dysrhythmia, due to increased automaticity at the atrioventricular junction. Production of such arrhythmias indicates the possible implication of imbalanced autonomic activity in arrhythmogenesis. Three cardiac nerves produced little or no effect on atrioventricular conduction. These were the innominate, ventromedial, and right stellate cardiac nerves. Because of its limited distribution and marked sinus rate effects, the right stellate cardiac nerve can be considered almost a purely positive chronotropic nerve. Its possible role in heart rate-atrioventricular conduction mismatching has not been delineated but, because of its nearly exclusive action at the sinoatrial node, may be of considerable importance.

Animals↗
PubMed2005

Temporary innervation of a primary coverage muscle: a new technique to optimize function in a subsequent functional microvascular muscle transplant.

The author describes the simple technique of innervating the coverage muscle in the staged reconstruction of an upper-extremity crush-avulsion injury with a functional microvascular muscle transplant (FMMT). The thoracodorsal nerve was repaired to the mixed motor-sensory radial nerve above the elbow. Contraction of the latissimus muscle at 8 months after nerve repair signaled the adequacy of the 10-cm thoracodorsal nerve graft as a target motor nerve for the eventual FMMT. Excursion of the latissimus muscle created a septo-alveolar plane similar to the plane between two healthy muscles into which the FMMT could be placed. The author also discusses the potential advantages of early thoracodorsal nerve repair for successful nerve regeneration. This simple technique helped overcome the potential limitations to functional muscle transplantation in the severely traumatized upper extremity, and deserves applied study.

Adult↗
PubMed1990

Responses of inspiratory neurons of the dorsal respiratory group to stimulation of expiratory muscle and vagal afferents.

In decerebrate, paralyzed and ventilated cats, we monitored the intracellular responses of 30 inspiratory neurons of the dorsal respiratory group (DRG) to stimulation of vagal and expiratory muscle (internal intercostal and abdominal) afferents. We hypothesized that the inhibitory effects of stimulation of expiratory muscle afferents, previously reported, would block the excitatory responses of inspiratory neurons of the DRG to vagal stimulation. Although prolonged stimulus trains to expiratory muscle afferents caused respiratory phase-switching, single shocks or short trains elicited no responses in 17 bulbospinal neurons, excitatory responses in 6, and inhibitory responses in 2. Of the 4 propriobulbar neurons tested, 2 had inhibitory responses and 2 did not respond. In only 2 neurons, both bulbospinal, did conditioning stimuli to expiratory muscle afferents block or reduce the excitatory effects of vagal stimulation. These results suggest that interaction of vagal and expiratory muscle afferents, which might account for the absence of a change in inspiratory duration despite increased vagal afferent feedback at elevated end-expiratory lung volumes, does not occur within the DRG.

Action Potentials↗
PubMedDate not supplied

Effects of morphine on somatocardiac sympathetic reflexes in spinalized cats.

The effects of morphine on sympathetic reflexes, recorded in the inferior cardiac nerve, to myelinated A and unmyelinated C afferent stimulation were tested in 17 acutely spinalized cats. Stable sympathetic A and C reflexes of short latency (approximately 30 ms and 140 ms in the case of the ulnar nerve, respectively) could be recorded in the inferior cardiac sympathetic nerve to stimulation of somatic A and C afferents in the ulnar and upper thoracic intercostal nerves, ipsilaterally. Spinal sympathetic A reflexes, which were primarily evoked from stimulation of A delta afferent fibers, could be elicited from more segmental levels than could sympathetic C reflexes. Additionally, smaller reflexes, only from A afferent fiber activation, were identified from stimulations on the contralateral side of the body. Small doses of morphine (0.02 mg kg-1, i.v.) proved to be ineffective at altering sympathetic A and C reflexes, while somewhat larger doses (0.2 mg kg-1, i.v.) produced a clear 62% decrease in C reflexes and a 33% decrease in A reflexes, Dosages of 1 and 2 mg kg-1 severely depressed both A and C reflexes. All of the above effects of morphine administration were completely and immediately reversible by naloxone (i.v.). The results are discussed with regard to the effects of morphine on sympathetic A and C reflexes in CNS intact, anesthetized cats.

Afferent Pathways↗
PubMed1975

Intercostal blocks with etidocaine. Preliminary report.

Although the results are few and should be considered as preliminary, the following conclusions may be drawn: 1. Etidocaine 0.5% and bupivacaine 0.5%, both with adrenaline (5 mug/ml), are comparable with regard to duration of sensory block. 2. Etidocaine 0.5% without adrenaline did not give the same duration of complete sensory block as when adrenaline was present. 3. Etidocaine 0.5% acts as a vasodilator at the site of injection. Adrenaline added to the solution counteracts the dilating effect. 4. Blood level studies of etidocaine do not at present show differences when 0.5% solution with or without adrenaline is used.

Acetanilides↗
PubMed1989

Internal intercostal nerve discharges in the cat: influence of chemical stimuli.

We studied the influence of central and peripheral chemoreceptor stimulation on the activities of the phrenic and internal intercostal (iic) nerves in decerebrate, vagotomized, and paralyzed cats with bilateral pneumothoraces. Whole iic nerves of the rostral thorax (T2-T5) usually discharged during neural inspiration, whereas those of the caudal thorax (T7-T11) were primarily active during neural expiration. Filaments of rostral iic nerves that terminated in iic muscles generally discharged during expiration, suggesting that inspiratory activity recorded in whole iic nerves may have innervated other structures, possibly parasternal muscles. All nerves were phasically active at hyperoxic normocapnia and increased their activities systematically with hypercapnia. Isocapnic hypoxia or intra-arterial NaCN injection consistently increased phrenic and inspiratory iic nerve activities. In contrast, expiratory iic nerve discharges were either decreased (10 cats) or increased (7 cats) by hypoxia. Furthermore, expiratory responses to NaCN were highly variable and could not be predicted from the corresponding response to hypoxia. The results show that central and peripheral chemoreceptor stimulation can affect inspiratory and expiratory motoneuron activities differentially. The variable effects of hypoxia on expiratory iic nerve activity may reflect a relatively weak influence of carotid body afferents on expiratory bulbospinal neurons. However, the possibility that the magnitude of expiratory motoneuron activity is influenced by the intensity of the preceding centrally generated inspiratory discharge is also discussed.

Action Potentials↗
PubMed1978

Failure of naloxone to reverse peripheral transcutaneous electro-analgesia in patients suffering from acute trauma.

Transcutaneous electrical stimulation of the intercostal nerves innervating the site of fractured ribs in 6 patients produced subjective and clinical evidence of decrease in the pain experienced by the patients. This analgesia was not significantly modified by naloxone, a pure narcotic antagonist. The possible role of endogenous morphine-like substances in peripheral electro-analgesia in man is discussed.

Acute Disease↗