Long-term recovery of diaphragm strength in neuralgic amyotrophy.
(1/124)
Diaphragm paralysis is a recognized complication of neuralgic amyotrophy that causes severe dyspnoea. Although recovery of strength in the arm muscles, when affected, is common, there are little data on recovery of diaphragm function. This study, therefore, re-assessed diaphragm strength in cases of bilateral diaphragm paralysis due to neuralgic amyotrophy that had previously been diagnosed at the authors institutions. Fourteen patients were recalled between 2 and 11 yrs after the original diagnosis. Respiratory muscle and diaphragm strength were measured by volitional manoeuvres as maximal inspiratory pressure and sniff transdiaphragmatic pressure. Cervical magnetic phrenic nerve stimulation was used to give a nonvolitional measure of diaphragm strength: twitch transdiaphragmatic pressure. Only two patients remained severely breathless. Ten of the 14 patients had evidence of some recovery of diaphragm strength, in seven cases to within 50% of the lower limit of normal. The rate of recovery was variable: one patient had some recovery after 2 yrs, and the rest took 3 yrs or more. In conclusion, in most patients with diaphragm paralysis due to neuralgic amyotrophy, some recovery of the diaphragm strength occurs, but the rate of recovery may be slow. (+info)
Diaphragm electromyogram measured with unilateral magnetic stimulation.
(2/124)
The purpose of this study was to establish the phrenic nerve conduction time (PNCT) for magnetic stimulation and further assess the relatively new technique of anterior unilateral magnetic stimulation (UMS) of the phrenic nerves in evaluating the diaphragm electromyogram (EMG). An oesophageal electrode was used to record the diaphragm compound muscle action potential (CMAP) elicited by supramaximal percutaneous electrical phrenic nerve stimulation (ES) and UMS from eight normal subjects. The oesophageal electrode used for recording the CMAP was positioned at the level of the hiatus and 3 cm below. The diaphragm CMAP was also recorded from chest wall surface electrodes in five subjects. All of the phrenic nerves could be maximally stimulated with UMS. A clear plateau of the amplitude of the CMAP was achieved for the right and left phrenic nerves. The mean amplitudes of the CMAP recorded from the oesophageal electrode were, for the right side, 0.74+/-0.29 mV (mean+SD) for ES and 0.76+/-0.30 mV for UMS with maximal power output, and for the left side 0.88+/-0.33 mV for ES and 0.80+/-0.24 mV for UMS. PNCT measured by the oesophageal electrode with ES and UMS with maximal output were, for the right side, 7.0+/-0.8 ms and 6.9+/-0.8 ms, respectively, and for the left side 7.8+/-1.2 ms and 7.7+/-1.3 ms, respectively. However, the CMAP recorded from chest wall surface electrodes with UMS was unsuitable for the measurement of PNCT. The results suggest that unilateral magnetic stimulation of the phrenic nerves combined with an oesophageal electrode can be used to assess diaphragmatic electrical activity and measure the phrenic nerve conduction time. (+info)
Myasthenic syndrome of snake envenomation: a clinical and neurophysiological study.
(3/124)
In this prospective study, 65 consecutive patients with neurological manifestations after snake envenomation, were examined in order to describe the natural history of the reversible nature of muscle weakness. Snake envenoming led to a completely reversible muscle paralysis involving the external ocular muscles with sparing of the pupils, muscles of mastication, facial muscles, palatal muscles, neck and proximal limb muscles. The deep tendon reflexes were preserved with no sensory abnormalities. The muscular weakness usually set in within an hour of envenomation and lasted up to 10 days, with fatigability lasting for 12 days. Respiratory muscle paralysis led to ventilatory failure needing ventilation in severely envenomed patients. Motor and sensory nerve conduction were normal with normal resting compound motor action potentials on electromyography. Repetitive nerve stimulation gave rise to a decremental response during high frequency stimulation. The edrophonium test gave negative results. These manifestations are due to abnormalities of neuromuscular transmission and are not typical of myasthenia gravis. As the exact pathophysiology of venom-related neurotoxicity is not known, it is suggested that the neurological manifestations of snake envenoming be designated a myasthenic syndrome. Further studies to isolate the neurotoxin and its mechanism and exact site of blocking at the neuromuscular junction would pave the way for the development of a novel long-acting neuromuscular blocking agent. (+info)
Chronic aneurysm of the descending thoracic aorta presenting with right pleural effusion and left phrenic paralysis.
(4/124)
A 62-year-old man was admitted to the emergency department with chronic dysphagia and lower back pain. Chest radiography revealed a wide mediastinal shadow and an elevated left diaphragm, which proved to be secondary to left phrenic paralysis. The patient was diagnosed with an aneurysm of the descending thoracic aorta and was admitted to the hospital. After the patient was admitted, the aneurysm ruptured into the right chest. The patient underwent an emergency operation to replace the ruptured segment with a synthetic graft. Postoperative recovery and follow-up were uneventful. This report describes an unusual presentation of a thoracic aortic aneurysm. Hemidiaphragmatic paralysis caused by compression of the phrenic nerve is an unusual complication that, to our knowledge, has not been previously reported. (+info)
Diaphragmatic paralysis due to Lyme disease.
(5/124)
Lyme disease is a tick-borne spirochaete infection which, in a proportion of patients, can lead to neuropathy. This article describes a case of diaphragmatic paralysis due to Lyme disease. A 39-yr-old male presented to the hospital because of an acute left facial palsy. Six weeks prior to admission he had developed a circular rash on his left flank during a camping holiday. He also complained of shortness of breath and arthralgia for 1 week. His chest radiograph demonstrated a raised right hemi-diaphragm. Diaphragmatic paralysis was confirmed by fluoroscopy (a positive sniff test). Serology revealed evidence of recent infection by Borrelia burgdorferi. On the basis of the patient's clinical presentation, a recent history of erythema migrans, and positive Lyme serology, a diagnosis of neuroborreliosis was made. He received oral doxycycline therapy (200 mg x day(-1)) for three weeks. Facial and diaphragmatic palsies resolved within eight weeks. On the basis of this case, a diagnosis of Lyme disease should be considered in patients from endemic regions with otherwise unexplained phrenic nerve palsy. (+info)
Effect of brachial plexus co-activation on phrenic nerve conduction time.
(6/124)
BACKGROUND: Diaphragm function can be assessed by electromyography of the diaphragm during electrical phrenic nerve stimulation (ES). Whether phrenic nerve conduction time (PNCT) and diaphragm electrical activity can be reliably measured from chest wall electrodes with ES is uncertain. METHODS: The diaphragm compound muscle action potential (CMAP) was recorded using an oesophageal electrode and lower chest wall electrodes during ES in six normal subjects. Two patients with bilateral diaphragm paralysis were also studied. Stimulations were deliberately given in a manner designed to avoid or incur co-activation of the brachial plexus. RESULTS: For the oesophageal electrode the PNCT was similar with both stimulation techniques with mean (SE) values of 7.1 (0.2) and 6.8 (0.2) ms, respectively (pooled left and right values). However, for surface electrodes the PNCT was substantially shorter when the brachial plexus was activated (4.4 (0.1) ms) than when it was not (7.4 (0.2) ms) (mean difference 3.0 ms, 95% CI 2.7 to 3.4, p<0.0001). A small short latency CMAP was recorded from the lower chest wall electrodes during stimulation of the brachial plexus alone. CONCLUSIONS: The results of this study show that lower chest wall electrodes only accurately measure PNCT when care is taken to avoid stimulating the brachial plexus. A false positive CMAP response to phrenic stimulation could be caused by inadvertent stimulation of the brachial plexus. This finding may further explain why the diaphragm CMAP recorded from chest wall electrodes can be unreliable with cervical magnetic stimulation during which brachial plexus activation occurs. (+info)
Assessment of diaphragm paralysis with oesophageal electromyography and unilateral magnetic phrenic nerve stimulation.
(7/124)
The purpose of this study was to establish a sensitive and reliable method of diagnosing diaphragm paralysis by recording the diaphragm compound muscle action potential (CMAP) using a multipair oesophageal electrode and unilateral magnetic phrenic nerve stimulation. An oesophageal electrode catheter was designed containing six coils (1 cm wide and 3 cm apart), creating an array of four sequential electrode pairs. The oesophageal catheter was taped at the nose with the proximal electrode pair 40 cm from the nares. Eight patients with unilateral (n=5) or bilateral (n=3) diaphragm paralysis were studied. Five to seven phrenic nerve stimulations were performed at 80% of maximum magnetic stimulator output and the CMAPs were recorded simultaneously from the four pairs of electrodes. In the five patients with unilateral diaphragm paralysis, the CMAP amplitudes and latencies were 1.16+/-0.29 mV and 7.6+/-1.5 ms for functioning sides. No diaphragm CMAP could be detected when stimulating nonfunctioning phrenic nerves. This study shows that diaphragm paralysis can be reliably diagnosed by unilateral magnetic stimulation combined with a multipaired oesophageal electrode. (+info)
Reversibility of paraneoplastic bilateral diaphragmatic paralysis after nephrectomy for renal cell carcinoma.
(8/124)
Bilateral diaphragmatic paralysis is usually caused by anatomic lesions of both phrenic nerves (e.g., after cardiothoracic surgery), generalized neurologic diseases (e.g., primary motor neuron disease, amyotrophic lateral sclerosis) or is without a known cause (idiopathic). We report a case of a patient with renal cell carcinoma complicated by an isolated bilateral diaphragmatic paralysis without clinical or electromyographic signs of other muscle or nerve involvement. There has been progressive, though till now partial, recovery of his vital capacity rising from 44% to 72% of predicted values, and maximal inspiratory pressures during the two years following the curative resection of his renal cell carcinoma. We believe this is the first report of a paraneoplastic bilateral diaphragmatic paralysis with actual recovery after tumour therapy. (+info)