Phrenic Nerve Conduction Studies Research Articles

Phrenic nerve conduction studies: Technical aspects and normative data

Muscle & NerveVolume 38, Issue 6 p. 1658-1659 Letter to the Editor Phrenic nerve conduction studies: Technical aspects and normative data Charles F. Bolton MD, Charles F. Bolton MD Queens University, Kingston, Ontario, CanadaSearch for more papers by this author Charles F. Bolton MD, Charles F. Bolton MD Queens University, Kingston, Ontario, CanadaSearch for more papers by this author First published: 18 November 2008 https://doi.org/10.1002/mus.21128Citations: 16Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume38, Issue6December 2008Pages 1658-1659 RelatedInformation

Vocal cord paresis and diaphragmatic dysfunction are severe and frequent symptoms of GDAP1-associated neuropathy

Cranial nerve involvement in Charcot-Marie-Tooth disease (CMT) is rare, though there are a number of CMT syndromes in which vocal cord paralysis is a characteristic feature. CMT disease due to mutations in the ganglioside-induced differentiation-associated protein 1 gene (GDAP1) has been reported to be associated with vocal cord and diaphragmatic palsy. In order to address the prevalence of these complications in patients with GDAP1 mutations we evaluated vocal cord and respiratory function in nine patients from eight unrelated families with this disorder. Hoarseness of the voice and inability to speak loudly were reported by eight patients and one had associated symptoms of respiratory insufficiency. Patients were investigated by means of peripheral and phrenic nerve conduction studies, flexible laryngoscopy, pulmonary function studies and polysomnography. Nerve conduction velocities and pathological studies were compatible with axonal CMT (CMT2). Flexible laryngoscopy showed left vocal cord palsy in four cases, bilateral cord palsies in four cases and was normal in one case. Restrictive respiratory dysfunction was seen in the eight patients with vocal cord paresis who were all chair-bound. These eight had confirmed phrenic nerve dysfunction on neurophysiology evaluation. The patient with normal vocal cord and pulmonary function had a less severe clinical course.This study shows that CMT patients with GDAP1 mutations develop severe disability due to weakness of limb muscles and that laryngeal and respiratory muscle involvement occurs late in the disease process when significant proximal upper limb weakness has developed. The early and predominant involvement of the left vocal cord innervated by the longer left recurrent laryngeal nerve suggests a length dependent pattern of nerve degeneration. In GDAP1 neuropathy, respiratory function should be thoroughly investigated because life expectancy can be compromised due to respiratory failure.

Predictors of Ventilator Weaning in Individuals With High Cervical Spinal Cord Injury

Background/Objective: To evaluate which tests best predict the ability of patients with ventilator-dependent tetraplegia to wean from the ventilator.Methods: Retrospective review of patients.Participants: Twenty-six ventilator-dependent patients with tetraplegia admitted to a university inpatient spinal cord-injury rehabilitation unit with American Spinal Injury Association (ASIA) injury levels C2 to C6, A or B.Results: Failure to wean off the ventilator completely was predicted by absence of motor unit recruitment of one hemidiaphragm or at least moderate decreased recruitment with needle electromyography (EMG) in both hemidiaphragms. Phrenic nerve conduction studies would have predicted that all patients who weaned off the ventilator would have failed. Fluoroscopic examination of the diaphragm and bedside spirometry were not as good predictors of ability to wean, failing to predict accurately in 44% and 19% of cases, respectively. ASIA examination was also not entirely predictive, and any outliers that may have been expected to wean based on ASIA examination (ie, C4 or lower neurological levels) were predicted not to wean by needle electromyography.Conclusions: Negative inspiration force diaphragm needle EMG best predicted the ability to wean from the ventilator. Bedside spirometry (negative inspiratory force and forced vital capacity) is an accurate bedside measure of a patient's readiness to wean. Fluoroscopic examination of the diaphragm and phrenic nerve conduction studies were not helpful in determining weaning potential in ventilator-dependent patients with cervical spine injury.

Phrenic nerve conduction studies: Technical aspects and normative data

In our clinical work we have occasionally encountered difficulties (e.g., no response, concomitant brachial plexus stimulation) in performing phrenic nerve conduction studies. The aim of this study was to overcome these difficulties and obtain our own set of normative data. In 29 healthy volunteers (15 men), aged 21-65 years, phrenic nerve conduction studies were performed using bipolar surface stimulation electrodes and a standard recording montage. Stimulation just above the clavicle, between the sternal and clavicular heads of the sternocleidomastoid muscles, elicited responses at the lowest stimulation strength, without concomitant brachial plexus stimulation. M-wave amplitude and duration changed with respiration, whereas latency and area did not. The normative limit for M-wave latency was 8.0 ms (upper), for amplitude it was 0.46/0.33 mV (lower: inspiration/expiration), and for area it was 4.4 mVms (lower). We suggest a slight modification of the generally used position for phrenic nerve stimulation, and the use of M-wave latency and area (unaffected by the respiratory cycle) in future phrenic nerve conduction studies.

Phrenic Nerve Stimulation in the Evaluation of Ventilator-Dependent Individuals with C4- and C5-Level Spinal Cord Injury

Three individuals with C4 or C5 spinal cord injuries (SCI) were seen in follow-up for management of their late complications, which included impaired ventilation. Electrodiagnostic studies were performed on all three as part of the assessment of the function of their phrenic nerves and diaphragm muscles in relation to their need for mechanical ventilator support. Each patient had evidence of lower-motor neuron injury to the phrenic nerves. Two of the patients who initially displayed small-amplitude (<0.1 mV) compound muscle action potentials (CMAP) bilaterally were later reevaluated during the course of their observation in the outpatient rehabilitation clinic. The CMAP amplitude of the diaphragm increased in these two cases during the 3-11 mos after SCI. Evidence of nerve recovery occurred in parallel with improvements in pulmonary function testing and was followed by successful weaning from the ventilator. These individuals both gained ventilator independence after the CMAP amplitude of least one hemidiaphragm was >0.4 mV. In the third case, early failure of ventilator weaning was reported to the patient as a poor prognostic sign. At the time of our first evaluation 11 mos after injury, a CMAP of 1.0 mV was seen on the right, with an absent response on the left. In case 3, the needle electromyogram demonstrated voluntary active motor unit action potentials that provided additional electrophysiologic support for phrenic nerve function. Phrenic nerve-conduction studies can provide useful measures in assessing the recovery of lower-motor neuron diaphragm function in relation to impaired ventilation in individuals with C4- or C5-level SCI.

N-ACETYLCYSTEINE PROTECTS THE RATS AGAINST PHRENIC NERVE DYSFUNCTION IN SEPSIS

This study investigates the association of oxidative stress with the function of the phrenic nerve and inquires whether N-acetylcysteine (NAC) may counteract the possible detrimental effects. Thirty rats were divided into three groups: sham, cecal ligation and puncture (CLP), and CLP plus NAC treatment. Sepsis was produced by the CLP procedure. NAC was administered at 70 mg/day for 7 days. Electrophysiology was evaluated by the needle electromyography of the diaphragm and phrenic nerve conduction study. Oxidative stress was evaluated by malondialdehyde (MDA), nitrite/nitrate (NN), and reduced-glutathione (ReGSH) levels and myeloperoxidase (MPO) and catalase (CAT) activities in the phrenic nerve. In the CLP group, ReGSH and CAT were decreased (P = 0.0001, P = 0.07, respectively); and MDA, MPO, and NN were increased (P = 0.02, P = 0.0001, P = 0.043, respectively), compared with the sham group. NAC administration increased the ReGSH (P = 0.036) and decreased the MDA, MPO, and NN (P = 0.008, P = 0.01, P = 0.032, respectively), compared with the CLP group. In the CLP group, electrophysiology revealed reductions in the number of motor unit action potentials (P = 0.0001) and prolongations in the latency of the compound nerve action potential (P = 0.0001), indicating phrenic nerve neuropathy. NAC administration significantly ameliorated these electrophysiological alterations (P = 0.011, P = 0.0001, respectively), compared with the CLP group. The present results showed that intraabdominal sepsis is closely associated with phrenic nerve neuropathy. In addition, NAC administration protects the rats against the detrimental events of sepsis.

Insidious Phrenic Nerve Involvement in Postpolio Syndrome

A 49-year-old woman with amyotrophic sequelae of poliomyelitis experienced progressive left upper limb weakness and breathing discomfort while walking that had developed over one year prior to presentation. She had flaccid quadriplegia which was more marked in the left upper limb, with the C4- and C5-innervated muscles being most severely affected. Chest radiographs double exposed at maximal inspiration and expiration revealed poor respiratory movements in the left hemidiaphragm. Phrenic nerve conduction study demonstrated conspicuous diaphragmatic paralysis on the left side. The electrophysiological study supports radiological findings and provides useful evidence for insidious phrenic nerve involvement in postpolio syndrome.

Sepsis induces early phrenic nerve neuropathy in rats

The aim of the present study was to investigate the electrophysiology of the phrenic nerve and the diaphragm muscle during sepsis. In total, 26 rats underwent either sham laparotomy or caecal ligation and puncture (CLP). Electrophysiology was evaluated via a phrenic nerve conduction study and needle electromyography of the diaphragm, prior to CLP, 6 and 24 h post-CLP and on day 7. The histopathology of the diaphragm muscle and phrenic nerve was also examined on day 7. In the sepsis group, the phrenic nerve conduction study showed decreased amplitude of compound action potential (CMAP), and prolongation in the duration and the latency of CMAP. The diaphragmatic needle electromyography showed decreased amplitude and frequency of the motor unit action potential (MUP), and prolongation in the duration of MUP, at all time points, compared with the pre-CLP values. The electrophysiological abnormalities were consistent with axonal and demyelinating phrenic nerve neuropathy. Electrophysiological abnormalities were present at 6 h with worsening at 24 h and on day 7. Histopathological examination showed normal muscular fibres and focally slight myelin degenerations of the phrenic nerve fibres. In conclusion, sepsis induced phrenic nerve neuropathy as early as the 6th h in rats.

Respiratory evoked potentials and occlusion elicited sympathetic skin response

Introduction. – Neurophysiological study of respiratory structures usually relies upon diaphragm electromyography and phrenic nerve conduction study, which do not assess the afferent sensory pathways. Objective. – To assess the feasibility of respiratory evoked potentials (REPs) and sympathetic skin responses (SSRs) elicited by inspiratory occlusion. Methods. – REPs and SSRs were studied in 12 healthy adults. REPs were elicited by inspiratory occlusions triggered by the physician within 1 s after the onset of a respiratory effort. They were recorded from C3, C4 and Cz needle electrodes (referenced to Fz). Each individual trial consisted of two superimposed 30-sweep averaged responses to inspiratory occlusions. SSRs were recorded from surface electrodes placed on the subject’s hand and elicited by similar inspiratory occlusions. Results. – Reproducible REPs and SSRs were obtained in all subjects. Mean latencies of initial P1 and N1 cortical responses were 41 and 72 ms, respectively. SSRs were similar to those usually elicited by peripheral nerve electrical stimulation. Conclusion. – Brief occlusion of inspiration induces cortical and sympathetic activation, both are easily recordable. Since REPs are considered to be the neurophysiological substrate of certain types of respiratory sensations and are altered in different chronic respiratory diseases, they, in addition to SSR, represent attractive new techniques that may provide better understanding of respiratory dysfunction.

Phrenic Nerve Pacing Via Intramuscular Diaphragm Electrodes in Tetraplegic Subjects

Diaphragm pacing in ventilator-dependent tetraplegic subjects is usually achieved by the placement of phrenic nerve electrodes via thoracotomy. However, this technique may be accomplished less invasively via laparoscopic placement of IM electrodes, at a lower cost and with less risk of injury to the phrenic nerve. To assess the feasibility of laparascopic placement of IM diaphragm electrodes to achieve long-term ventilatory support in ventilator-dependent tetraplegic subjects. Two IM diaphragm electrodes were placed laparoscopically in each hemidiaphragm in five subjects with ventilator-dependent tetraplegia. Studies were performed either on an outpatient basis or with a single overnight hospitalization. Ventilator-dependent tetraplegic subjects were identified in whom bilateral phrenic nerve function was present, as determined by phrenic nerve conduction studies. Following electrode placement, subjects participated in a conditioning program to improve the strength and endurance of the diaphragm over a period of 15 to 25 weeks. The duration of the study was variable depending on the time necessary to determine the maximum duration that individuals could be maintained without mechanical ventilation support. Magnitude of inspired volume generation and duration of ventilatory support with bilateral diaphragm pacing alone. In four of the five subjects studied, initial bilateral diaphragm stimulation resulted in inspired volumes between 430 and 1,060 mL. Reconditioning of the diaphragm over several weeks resulted in substantial increases in inspired volumes to 1,100 to 1,240 mL. These subjects were comfortably maintained without mechanical ventilatory support for prolonged time periods by diaphragm pacing, by full-time ventilatory support in three subjects, and 20 h per day, in the fourth subject. No response to stimulation was observed in one subject, most likely secondary to denervation atrophy. Diaphragm pacing in ventilator-dependent tetraplegic subjects can be successfully achieved via laparascopic placement of IM electrodes.

Chronic inflammatory demyelinating polyneuropathy, phrenic nerve and respiratory symptoms

Respiratory involvement in chronic inflammatory demyelinating polyneuropathy (CIDP) has been very recently described. Phrenic nerve conduction studies have been described as useful to detect respiratory impairment in these patients. This study describes two patients with CIDP, in whom neurophysiological studies of the respiratory muscles were performed. The first patient had severe respiratory insufficiency, and phrenic nerve studies disclosed no motor responses and electromyography (EMG) of the diaphragm confirmed severe loss of motor units, bilaterally. On treatment, we documented clinical and neurophysiological improvement. In the second patient, phrenic nerve studies showed abnormal results; however, EMG of the diaphragm ruled out loss of motor units. The first case represents the risk of phrenic nerve involvement in this disorder, and the potential recovery on treatment. The second case illustrates that the temporal dispersion of the motor responses can be misleading, and EMG of diaphragm should be performed to confirm the loss of motor units.

Dyspnea as the Predominant Manifestation of Bilateral Phrenic Neuropathy

Phrenic neuropathy associated with brachial neuritis has been well described; however, bilateral phrenic neuropathy with minimal or no involvement of the brachial plexus has not. We review the clinical features, as well as the results of radiographic studies, pulmonary function tests, and electrodiagnostic studies, of 3 patients in whom dyspnea was the presenting manifestation of bilateral phrenic neuropathy. All 3 patients had acute-onset dyspnea, which led to consideration of a pulmonary or cardiac etiology. Phrenic nerve conduction studies showed bilateral axonal degeneration of the phrenic nerves. Diaphragmatic paralysis should be considered in the differential diagnosis of acute-onset dyspnea. Dyspnea increases typically when the patient lies down, and paradoxical respiration may be present. Neck, shoulder, or upper limb pain may occur at onset. Inspiratory pressures may be reduced, but a comparison of the forced vital capacity when the patient is standing and supine is more specific for diaphragmatic weakness. Phrenic nerve conduction studies and diaphragmatic electromyography may provide evidence of bilateral involvement. Subclinical evidence of brachial plexus involvement may be present. The prognosis for patients with bilateral phrenic neuropathy may be more favorable than reported previously.

Phrenic nerve conduction study in CIDP

Background: Alterations of the phrenic nerve (FN), as well as of the pulmonary function tests (PFTs), have been described in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Objective: Our study was aimed at assessing the relationship between FN conduction study and respiratory function in 24 CIDP patients without clinical signs of respiratory failure. Material and Methods: Bilateral FN and right median nerve conduction studies were accomplished, along with emogasanalysis (EGA) and PFTs: maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), forced vital capacity (FVC) and partial CO2 pressure. Results: The amplitude of the compound muscle action potential (CMAP) of the FN was altered in 19 (79%) of our 24 patients, the latency in 22 (92%). Eighteen patients (75%) showed at least one PFT or the pCO2 abnormal. FN alterations showed a low sensitivity and specificity with respect to PFTs or pCO2. Discussion: Our results demonstrated electrophysiological alterations of the FN in a high percentage of CIDP patients. No significant correlation was observed between FN and PFTs alterations.

Phrenic Nerve Paralysis After Subclavian Revascularization Surgery: A Case Report

Phrenic nerve paralysis (PNP) has been reported following neck dissection and after instillation of local anesthetics in the interpleural space. We report a case of PNP which to our knowledge is the first case report following subclavian revascularization surgery. A 50-year-old female patient, ASA class 2 with normal preoperative chest-x-ray andlaboratory investigations, was operated for unilateral subclavian to subclavian artery bypass graft under general anesthesia. At the end of surgery atropine and neostigmine were given in the usual dosages guided by a peripheral nerve stimulator. The trachea was extubated and immediately thereafter the patient developed shortness of breath and became cyanotic. The trachea was then reintubated. In the ICU and on the 10th postoperative day a phrenic nerve study with recording the diaphragmatic compound muscle action potential (DCMAPs) revealed unilateral PNP, where delayed conduction was determined for the right phrenic nerve with a mean latency of 9.23msec and decreased amplitude 0.085mv. The patient was sedated and under controlled ventilation. On the 18th postoperative day, the test was repeated and showed shorter latency of 6.63msec (72% recovery) and high amplitude 0.45mv (5 fold improved). The weaning process was started and finally the trachea was extubated and the patient was breathing spontaneously and adequately with satisfactory arterial blood gases. We concluded that phrenic nerve conduction studies could be valuable in the diagnosis and follow up of these patients with PNP for better outcome.

Are the neurophysiological techniques useful for the diagnosis of diaphragmatic impairment in multiple sclerosis (MS)?

To characterize cortico-diaphragmatic pathway involvement in multiple sclerosis (MS) by means of transcranial magnetic stimulation (TMS), and verify its clinical impact. TMS from diaphragm (Dia), and abductor digiti minimi (AbdV degrees ) was performed in 26 MS patients. Phrenic nerve (PN) conduction study was also performed. Expanded disability status scale (EDSS) and fatigue descriptive scale (FDS) were measured. Forced vital capacity (FVC), forced expiratory volume at the first second (FEV1), peak expiratory flow (PEF) were tested: the predicted percentage value (% pred) was considered. Cortical motor evoked potential (Cx-MEP) latency and central motor conduction time (CMCT) were prolonged, respectively, in 31 and 23% of patients from Dia, in 76 and 79% from AbdV degrees. PN-compound motor action potential (CMAP) was normal. EDSS correlated to Cx-MEP from AbdV degrees (P<0.01), and PN-CMAP amplitude (P<0.05), FEV1 % pred (P<0.01), PEF % pred (P<0.01). PN-CMAP amplitude correlated to FVC % pred P=0.05, FEV1 % pred P<0.01, PEF % pred P<0.01. Fatigue was related to AbdV degrees Cx-MEP and CMCT (P<0.05 and P<0.01). Cortico-diaphragmatic pathway is impaired only in a minority of MS patients. Lack of correlation between TMS findings from Dia and respiratory tests argues against its routinary use to detect subclinical respiratory alterations. Fatigue seems to be related to the motor impairment rather than to respiratory distress.

Phrenic nerve dysfunction after heart-lung and lung transplantation

The incidence and consequences (ventilator days and ICU length of stay(ICU LOS)) of phrenic nerve dysfunction (PND) was studied by retrospective chart review of 27 heart-lung (HLTX) and 111 lung transplantations (LTX) for the period from 1991 to 6/2001 in our institution. On clinical suspicion of diaphramatic dysfunction a phrenic nerve conduction study( (1) MacLean I.C. et al. Arch Phys Med Rehab. 1981; 62: 71 Google Scholar ) was performed, completed with a needle electromyography (EMG) of the diaphragm( (2) Bolton C.F. et al. Muscle and Nerve. 1992; 15: 678 Crossref PubMed Scopus (115) Google Scholar ), when the nerve conduction study was not conclusive. PND is defined as an uni- or bilateral abnormal EMG of the phrenic nerve(s) or signs of denervation on the needle EMG of the diaphragm. Data are presented as mean +/-1 standard deviation. The incidence of PND in 21 evaluable HLTX patients was 42,8 % (9 patients), resulting in significantly more ventilator days (PND 37,6 +/-36,3 days(d) vs non-PND 5,3+/-3d,p<0,05) and a prolonged ICU LOS (PND 46,8+/-33d vs non-PND 9,8+/-4,9d,p<0.05). Thirteen out of the 42 phrenic nerves at risk developed PND (25%). In the 97 evaluable LTX patients 9 (9,3%) developed PND involving 12 of the 142 phrenic nerves at risk (8.45 %). This resulted in a significantly higher number of ventilator days (PND 30,6+/-14,8d vs non-PND 7,9+/-14,8d,p<0,05) and a longer ICU LOS (PND 37,9+/-18,7d vs non-PND 12,1+/-17,8d,p<0.05). In LTX patients suffering from PND more tracheostomies were performed (PND 4/9 patients or 44,4% vs non-PND 4/88 patients or 4,5%,p<0,005) and 8 out of 9 LTX PND patients had a sequential single LTX. The needle EMG of the diaphragm revealed denervation of the diaphragm in 1 HLTX and in 4 LTX.

Peripheral nerve injuries during cardiac surgery: risk factors, diagnosis, prognosis, and prevention.

Neuropathies involving the brachial plexus, phrenic, recurrent laryngeal, and saphenous nerves, as well as the sympathetic chain are complications of cardiac surgery. The reported frequency of nerve injuries varies from 1.5% to 24% for the brachial plexus and 10% to 60",,6 for the phrenic nerve (1-5). Neuropathies of the recurrent laryngeal, lower limb (saphenous) nerves, and the sympathetic chain are less frequent.

Phrenic nerve conduction study in demyelinating neuropathies and open-heart surgery

Objectives: The aim of this study was to determine normal values of phrenic nerve conduction (PNC) in healthy individuals; to evaluate the subclinical extent of phrenic nerve involvement in Guillain–Barré syndrome (G-B) and hereditary motor and sensory neuropathy-I (HMSN-I), and to evaluate phrenic nerve damage after cardiac surgery.Materials and methods: PNC was performed by transcutaneous stimulation in the neck and recording the diaphragmatic potential from surface electrodes placed at the seventh and eight intercostal spaces. PNC was performed bilaterally in 25 healthy volunteers and 25 patients before and after open-heart surgery. Right PNC was also performed in 5 cases with G-B and 5 patients with HMNS-I.Results: Latency and amplitude of the diaphragmatic potential were the same in controls and in patients with cardiac disease before surgery. After surgery, 28% of patients had left phrenic nerve inexcitability, and 8% had reduced amplitude of the response. These 9 patients demonstrated elevation of the left hemidiaphragm on chest radiography. Left PNC performed 1 year after the operation showed improvement in latency and amplitude of the responses in all except one patient. PNC was prolonged in 4 out of 5 cases with G-B and in all patients with HMNS-I.Conclussions: PNC is an easy and reliable method in evaluating phrenic nerve damage due to hypothermia or primary stretch injury in patients after cardiac surgery. PNC may be helpful in detecting diaphragmatic involvement before clinical ventilatory insufficiency in demyelinating neuropathies such as G-B and HMNS-I.

Phrenic nerve conduction studies in acute organophosphate poisoning

Phrenic nerve conduction studies were performed within 48 h of admission and subsequently in 29 patients (14 of whom required mechanical ventilation) with acute organophosphate (OP) poisoning. The mean (±SD) amplitude of the diaphragmatic compound muscle action potential (CMAP) in patients requiring mechanical ventilation (119.09 ± 173.85 μV) was significantly lower than in those not requiring mechanical ventilation (461.63 ± 138.69 μV) (P < 0.0001). Diaphragmatic CMAP amplitudes in ventilated patients increased with time during the course of hospitalization and were normal in 5 (36%) patients and only mildly reduced in another 6 (43%) patients prior to discontinuation of mechanical ventilation, which was undertaken 4–18 days (mean 7 ± 3 days) after poisoning. Eleven patients (79%) were successfully weaned from mechanical ventilation at the first attempt. In the 3 (21%) remaining patients, mechanical ventilation had to be reestablished because of weaning failure. The mean (±SD) diaphragmatic CMAP amplitude, prior to discontinuation of ventilatory assistance, was 242.6 ± 94.1 μV in these 3 patients. After ventilatory discontinuation, it fell to 95.5 ± 105.8 μV. Thus, reduced diaphragmatic CMAP amplitudes correlate with the need for mechanical ventilation in acute OP poisoning. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 627–632, 2000.

Phrenic nerve conduction studies in acute organophosphate poisoning.

Phrenic nerve conduction studies were performed within 48 h of admission and subsequently in 29 patients (14 of whom required mechanical ventilation) with acute organophosphate (OP) poisoning. The mean (+/-SD) amplitude of the diaphragmatic compound muscle action potential (CMAP) in patients requiring mechanical ventilation (119.09 +/- 173.85 microV) was significantly lower than in those not requiring mechanical ventilation (461.63 +/- 138.69 microV) (P < 0.0001). Diaphragmatic CMAP amplitudes in ventilated patients increased with time during the course of hospitalization and were normal in 5 (36%) patients and only mildly reduced in another 6 (43%) patients prior to discontinuation of mechanical ventilation, which was undertaken 4-18 days (mean 7 +/- 3 days) after poisoning. Eleven patients (79%) were successfully weaned from mechanical ventilation at the first attempt. In the 3 (21%) remaining patients, mechanical ventilation had to be reestablished because of weaning failure. The mean (+/-SD) diaphragmatic CMAP amplitude, prior to discontinuation of ventilatory assistance, was 242.6 +/- 94.1 microV in these 3 patients. After ventilatory discontinuation, it fell to 95.5 +/- 105.8 microV. Thus, reduced diaphragmatic CMAP amplitudes correlate with the need for mechanical ventilation in acute OP poisoning.