[Phrenic nerve palsy (phrenic nerve injury, diaphragmatic paralysis].
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Phrenic nerve conduction was studied in 19 volunteers using two different percutaneous methods of stimulation, mono and bipolar. A response was obtained in all nerves studied. The results are comparable using mono or bipolar stimulation method. No significant difference in latency, amplitude, or intensity stimulation applied was found between left and right sides. There was no correlation of age or height with the latency. Latencies above 10 ms or differences between right and left above 1.6 ms are abnormal values. We studied two patients with neurological disorders, one of them with Guillain-Barré syndrome and the other with a bulbar form of Amyotrophic Lateral Sclerosis and respiratory failure. Both of them had prolonged conduction time. This method permits reliable analysis of localized phrenic lesions and abnormalities induced in either the phrenic nerveor diaphragm by generalized disease processes.
The compound-action potential (cAP) of the nerve evoked at 1 Hz was reversibly inhibited and the threshold for nerve stimulation increased between 0.065 and 0.97 mM eugenol. The inhibition showed a sigmoid log10 dose-response relationship. With 2.44 mM or higher concentrations the block became irreversible. The inhibition was enhanced during stimulation at 100 Hz in 5 s with 0.487 mM or higher concentrations. The muscle tetanic tension also showed this high frequency inhibition (HFI). After 40-min exposure to 0.65 mM eugenol, the twitch contractions were unaffected. The indirectly induced tetanic tension was inhibited to 16.6 per cent of control in the initial and to 0.5 per cent in the terminal phase of a 5-s period of 100-Hz stimulation, whereas the directly-induced tetanic tension was inhibited to 38.0 and 13.6 per cent, respectively. Thus, eugenol had affected the neuromuscular transmission during tetanic stimulation in addition to its effect on the directly-stimulated preparation. Intracellular recordings of the end-plate potential (EPP) and miniature end-plate potential (MEPP) indicated both a pre- and a post-synaptic mechanism of action for eugenol. Experiments with eugenol plus d-tubocurarine showed a synergistic effect between these two drugs, suggesting a curare-like effect by eugenol. The resting membrane potential of the muscle was unaffected by eugenol. The following findings suggest that eugenol is a membrane-stabilizing (local anaesthetic) drug at low concentrations: reversible cAP inhibition, increased threshold, high-frequency inhibition, and unresponsiveness of the resting membrane potential of the muscle to the drug.
OBJECTIVE: To explore of the anatomic basis of the anastomosis of the facial nerve with the phrenic nerve. METHOD: Bilateral microsurgical dissection was performed on eleven human cadavers fixed with formalin. The following length data were measured with calipers: the distance between the bifurcation of the facial nerve trunk and the phrenic nerve root, the useful length of the facial nerve trunk and the phrenic nerve, and the distance between the overlapped nerve ends. RESULT: The length from the root of the the phrenic nerve to the level of the subclavian vein was (7.2 +/- 1.6) cm. The length from the root of the phrenic nerve to the bifurcation of the facial nerve trunk was (7.23 +/- 0.9) cm. The length from the bifurcation of the facial nerve trunk to the level below the horizontal semicircular canal was 2.7-3.5 cm, 1.0-1.5 cm longer than that cut below the level of the stylomastoid foramen. The cutting nerve ends were placed side by side. The distance between the overlapped nerve ends was 0.4-1.8 cm. CONCLUSION: In 20 specimens the tension-free anastomosis of the facial nerve with the phrenic nerve that cut in the subclavian vein level can be achieved, in 2 specimens the tension-free anastomosis can not be achieved.
Cervical magnetic stimulation (CMS), a nonvolitional test of diaphragm function, is an easy means for measuring the latency of the diaphragm motor response to phrenic nerve stimulation, namely, phrenic nerve conduction time (PNCT). In this application, CMS has some practical advantages over electrical stimulation of the phrenic nerve in the neck (ES). Although normal ES-PNCTs have been consistently reported between 7 and 8 ms, data are less homogeneous for CMS-PNCTs, with some reports suggesting lower values. This study systematically compares ES- and CMS-PNCTs for the same subjects. Surface recordings of diaphragmatic electromyographic activity were obtained for seven healthy volunteers during ES and CMS of varying intensities. On average, ES-PNCTs amounted to 6.41 +/- 0.84 ms and were little influenced by stimulation intensity. With CMS, PNCTs were significantly lower (average difference 1.05 ms), showing a marked increase as CMS intensity lessened. ES and CMS values became comparable for a CMS intensity 65% of the maximal possible intensity of 2.5 Tesla. These findings may be the result of phrenic nerve depolarization occurring more distally than expected with CMS, which may have clinical implications regarding the diagnosis and follow-up of phrenic nerve lesions.
The treatment outcome of nerve transfer using the C7 nerve root or phrenic nerve was compared in a rat experiment. One hundred and twenty SD rats were divided into two groups, one undergoing phrenic nerve transfer to the musculocutaneous nerve, and the other partial ipsilateral C7 (anteriolateral fascicles of the anterior division) to the musculocutaneous nerve. Neurotization outcomes of the two groups were evaluated by comparing the electrophysiologic, histologic, and myophysiologic changes of the biceps muscle. No significant differences were found between parameters from the phrenic nerve transfer group and those from the ipsilateral C7 nerve transfer group. This indicates that the treatment outcome of selective ipsilateral C7 transfer is comparable to that of phrenic nerve transfer. It is the surgery of choice in treating brachial plexus upper-trunk avulsion accompanied by phrenic nerve injury.
One reason for the reported conflicting results of the effect of ketamine on hemodynamics and respiration may be variations in afferent inputs from peripheral receptors to the central nervous system. In order to evaluate unmasked direct effects of ketamine on sympathetic nerve and phrenic nerve outflow, totally deafferented (involving vagus, sinus nerve, aortic depressor nerve) rabbits (n = 18), rabbits with vagotomy (n = 21), and neuraxis-intact rabbits (n = 6) were used in this study. The animals were anesthetized with urethane and mechanically ventilated. Ketamine 0.5, 1, or 2 mg/kg was injected intravenously and mean arterial pressure (MAP), heart rate (HR), and integrated renal sympathetic nerve and phrenic nerve activity (IRSNA, IPNA) were recorded before, and 1, 2, 3, 5, and 10 min after injection. MAP and IRSNA were significantly decreased, even by the smallest dose of ketamine, in the totally deafferented group. IPNA was decreased by the largest dose of ketamine only in the totally deafferented group. On the other hand, spontaneous respiratory frequency was decreased in the totally deafferented and vagotomy groups, but more so in the totally deafferented group. In the neuraxis-intact group, the only significant change with the largest dose of ketamine, 2 mg/kg was a slight increase in HR. We conclude that ketamine can suppress vasomotor and respiratory centers directly, and that the suppression is counterbalanced by afferent inputs from peripheral receptors.
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Electromyographic (EMG) activities of forelimb muscles and the diaphragm following cross-reinnervation of the elbow flexor nerve by the phrenic nerve sampled simultaneously with cinematographic recording of forelimb movements, in order to examine whether the respiratory nervous system in adult cats is capable of compensation for movement disorders. The right phrenic and musculocutaneous nerves were cut preparatory to cross-union, the proximal stump of the phrenic nerve being joined to the peripheral stump of the musculocutaneous nerve. Reinnervation of the elbow flexor muscles (m. biceps brachii and m. brachialis) was confirmed in terminal experiments by observing muscular contractions induced by nerve stimulations and/or retrogradely labeled motoneurons in cervical (C5-C7) segments following treatment for horseradish peroxidase (HRP) which had been injected previously into the m. biceps brachii of both sides. Behavioral observations were made in the chronically cross-reinnervated cats. Bipolar EMG recording electrodes were implanted chronically in the right m. biceps brachii, m. triceps brachii and in the left intact diaphragm. In freely moving cats 3-22 months after cross-union surgery, EMG activities in the elbow flexor usually were synchronized with those of the left diaphragm. However, occasionally, in cats cross-reinnervated more than 6 months previously, EMG activities in the right biceps muscle were dissociated from those of the left diaphragm during voluntary movements. During walking, EMG activities in the cross-reinnervated biceps muscle were not coordinated with the walking cycle. By contrast, during voluntary goal directed movements, the cats were capable of reaching their right forepaws to the target in a smooth manner using elbow flexion that was associated with EMG activity of the biceps muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
Phrenic nerve function was evaluated by transcutaneous stimulation in the neck and recording the diaphragmatic potential from surface electrodes placed at the ipsilateral seventh intercostal space (7CS) and the xiphoid process (XP). Simultaneous recordings from 7CS and XP electrodes connected together (XP-7CS) and each connected to a remote reference (knee-7CS and knee-XP) disclosed that the 7CS electrode was always more active and showed electropositive activity, whereas the XP electrode, which was only minimally active, showed electronegative response. Out-of-phase summation of opposite polarity activity at the two electrodes resulted in a higher amplitude response in XP-7CS derivation. Phrenic nerve studies are useful in establishing phrenic nerve injury following cardiothoracic operation. They may also provide evidence of phrenic nerve or diaphragmatic involvement in demyelinative neuropathies, motor neuron disease, and muscular dystrophies.
Formaldehyde, 0.5-4.5 mM, increased the threshold for electrical excitation of the nerve, and led to a partial and reversible inhibition of the compound action potential (cAP). The depression was not enhanced by high frequency stimulation. At 8.9 mM or higher, the depression of the nerve excitability could not be reversed. The inhibition of the nerve developed more slowly than that of the muscle, and the nerve was unaffected after 10 min exposure to 2.2 mM. Formaldehyde, 2.2 mM, caused an immediate depression of the indirectly (through the nerve) and directory (at the muscle) elicited twitch tension. After 10 min the tensions were reduced to respectively, 56% and 49% of control. However, the electromyogram was not changed, indicating that the effect was localized to the excitation-contraction coupling. Tetanic tension (100 Hz in 5 sec) was inhibited more than twitch tension during indirect stimulation, whereas the opposite was found during direct stimulation of the muscle. Thus, during high frequency stimulation, formaldehyde must have an additional effect on the neuromuscular transmission. This effect was localized presynaptically since a fall out of endplate potentials was observed in the formaldehyde-treated diaphragm. In 6.7 mM or higher concentrations the directly or indirectly induced contractions were irreversibly blocked. The resting membrane potential of the muscle cells was unchanged after exposure to formaldehyde. Formaldehyde caused myotonia-like contractions of the diaphragm, occasionally after exposure to low concentrations (2.2 mM), and always after exposure to higher concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Phase-locked slow rhythms in sympathetic nerve discharge (SND) and phrenic nerve activity (PNA) are generally thought to arise from a common brain stem "cardiorespiratory" oscillator. The results obtained in vagotomized and baroreceptor-denervated cats anesthetized with pentobarbital sodium do not support this view. First, partial coherence analysis revealed that the discharges of pairs of sympathetic nerves remained correlated at the frequency of the central respiratory cycle after mathematical removal of the portion of these signals common to PNA. The residual coherence suggests that the slow rhythm in SND is dependent on central mechanisms in addition to those responsible for rhythmic PNA. Second, the rhythms in SND and PNA became coupled in a 2:1 relationship during either moderate systemic hypocapnia or hypercapnia. Third, the slow rhythm in SND was maintained when rhythmic PNA was eliminated during extreme hypocapnia. Fourth, during extreme hypercapnia, coherence of the rhythms in SND and PNA was drastically reduced. These results suggest that the slow rhythms in SND and PNA arise from separate oscillators that are normally coupled.
Nine infants and children, referred for phrenic nerve pacemakers, had measurements of phrenic nerve conduction times and diaphragmatic action potential amplitudes. In these pediatric patients, phrenic nerve conduction times varied from 2.7 to 7.8 msec, were quite reproducible, and were shorter than phrenic nerve conduction times in adults; phrenic nerve conduction time increased with age and with increasing distance between the stimulating electrode and the diaphragm. Diaphragmatic action potential amplitudes varied from 0.08 to 4.1 mV, roughly equivalent to amplitudes in adults, but were variable between patients and within patients on different days. Lower amplitudes were obtained after percutaneous stimulation than after direct phrenic nerve stimulation. Five patients underwent preoperative, percutaneous phrenic nerve stimulation. Strong diaphragmatic contractions allowed us to advise for pacemaker insertion in three patients; weak or absent diaphragmatic contractions allowed us to advise against pacemaker insertion in two patients. Postoperatively, noninvasive measurements of oxygen, carbon dioxide, tidal volume, and diaphragmatic action potential amplitudes have been used to adjust the phrenic nerve pacemaker settings. Phrenic nerve pacemakers have facilitated discharge from the hospital to a home-based ventilation program in six of the seven patients in whom they were inserted. We conclude that phrenic nerve pacing is a practical method of supporting ventilation in carefully selected infants and children. Phrenic nerve stimulation studies are useful in selecting patients for pacing and in adjusting the pacemaker settings.
Phrenic nerve lesions as a result of birth trauma have been reported as a cause of acute respiratory distress infrequently. We report recent diagnostic and therapeutic experiences in four newborns with birth-traumatic phrenic nerve injury: one bilaterally, and three unilaterally, all right-sided. In each case, mechanical ventilation was required for at least 16 days. Ultrasound examination of the diaphragm and phrenic nerve conduction studies turned out to be the diagnostic methods of choice. Spontaneous recovery occurred in two children and two became asymptomatic after operative treatment. One improved after plication of diaphragm and one after autologous nerve transplantation.
Phrenic nerve paralysis frequently follows operations on the neck such as resection of a cervical or first rib. It all too often passes unrecognised or is incorrectly treated, leading to permanent lung damage which may be severe enough as to result in a functional pneumonectomy. This is particularly unfortunate since the phrenic nerve paralysis is usually temporary. Three case histories are described of reversible paralysis of the phrenic nerve in which, due to prompt diagnosis, the ensuing lung changes were either prevented or immediatley treated. Intermittent assisted respiration with a Monaghan respirator was used to provide nebulised inhalations of Mesna several times a day. The method is applicable via a tracheostomy, an endotracheal tube or a simple mouthpiece. The latter is illustrated. The therapy is not hindered by immobilisation of the head and neck and the level of consciousness of the patients is of no importance. Many chest X-rays demonstrate the rapid clearing of the lungs achieved. All three patients were discharged with perfectly normal lungs.
Phrenic nerve involvement is a rare feature in patients with neuralgic amyotrophy (Parsonage-Turner syndrome). We report four patients who initially presented with severe dyspnea in the absence of lung disease. All patients had a history of infectious disease or surgery and of pain of sudden onset in the shoulder region. Weakness of the proximal arm was observed in only one. Radiographic and pulmonary function studies, phrenic nerve conduction studies, and needle electromyogram (EMG) of the diaphragm documented diaphragmatic paralysis which was unilateral in one patient, bilateral in two patients, and recurrent on alternating sides in another one. Follow-up studies remained abnormal for up to 4 years. Neuralgic amyotrophy with phrenic nerve involvement should be considered in patients presenting with severe, unexplained dyspnea of sudden onset.
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