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Right hemi-diaphragm paralysis following cardiac radiofrequency ablation.

Diaphragm paralysis may occur after traumatic phrenic nerve injury. Here we report three patients in whom right hemi-diaphragmatic paralysis developed after cardiac radiofrequency ablation. We hypothesise that local focused thermal energy at the time of the ablation may have caused direct neuronal damage by axonal coagulation necrosis. The prognosis for this type of injury may be reasonably good; two of the three patients fully recovered diaphragm function by 1 year.

Adult↗

Botulinum type A toxin neutralisation by specific IgG and its fragments: a comparison of mouse systemic toxicity and local flaccid paralysis assays.

In this study, we have compared two in vivo assay methods to measure the type A botulinum toxin neutralising activity of specific immunoglobulin G (IgG) and its fragments (F(ab')(2), Fab', Fab) purified from pentavalent botulinum antisera raised in goats. Each assay method was repeated on three separate occasions in mice and relative potencies calculated with respect to a type A equine reference antitoxin. The conventional assay, which measures the number of mice surviving typically after 72 or 96 h following the intraperitoneal administration of a mixture of toxin and antitoxin, gave the following order of potency IgG>F(ab')(2)>Fab'>Fab (6.8>4.7>3.5>2.6 IU/mg). Differences in potency are likely to be due to differences in the pharmacokinetics of the antitoxins, which are related to their molecular weight. The alternative local flaccid paralysis assay, where toxin and antitoxin are injected subcutaneously into the left inguinocrural region, gave results with a narrower range of activities: IgG>Fab'>F(ab')(2)>Fab (6.0>5.9>5.5>4.6 IU/mg). Comparison of the two assay methods showed no significant differences for IgG, F(ab')(2) or Fab', although the Fab fragment was significantly more potent in the non-lethal assay probably because of the reduced influence of antitoxin pharmacokinetics in this localised assay. These findings show that a local flaccid paralysis assay provides a less time consuming and more humane alternative to the lethal assay for the potency testing of botulinum IgG and F(ab')(2) antitoxins.

Animals↗

Medialization thyroplasty for unilateral vocal cord paralysis.

Unilateral vocal cord paralysis causes disturbances with vocal function and swallowing, to include aspiration. Thyroplasty type I has become one of the preferred surgical treatments for unilateral vocal cord paralysis. It is tolerated better by the patient, improves predictability of surgical results, and provides good voice results when compared to more traditional procedures, such as teflon injection. Use of a premade thyroplasty implant has made it possible to accomplish permanent medial displacement of a paralyzed vocal cord, avoiding the complications of other surgical options.

Humans↗

Absorbable gelatin powder injection for transient vocal cord paralysis.

In the early 1900s, glottic insufficiency in patients with vocal cord paralysis was corrected by injecting paraffin intralaryngeally. Since then, injecting absorbable gelatin powder into the vocal cord has become an acceptable short-term solution for transient paralysis of a single vocal cord. Although relatively uncommon, this procedure has few complications and is an option for patients when vocal cord function is expected to return within one year.

Absorption↗

Thyroplasty type I for unilateral vocal cord paralysis.

Unilateral vocal cord paralysis may occur with trauma, neoplasms, mechanical or central nervous system dysfunction, or following extensive aortic and mediastinal vascular surgery or thyroidectomy. Thyroplasty type I is a form of laryngeal framework surgery (ie, phonosurgery) used to treat unilateral vocal cord paralysis. A silicone implant is placed inside a surgically created window in the thyroid cartilage and pushes the paralyzed cord medially, allowing the moving cord to touch the paralyzed cord and close the opening. The procedure is performed under monitored local anesthesia with sedation so the patient can phonate during the procedure. Airway compromise is the main complication associated with this procedure.

Contraindications↗

Motor initiation and execution in patients with conversion paralysis.

Motor initiation and motor execution in four patients with conversion paralysis were investigated in a non-affected motor modality (speech). In line with the hypothesis of dissociated control in conversion disorder [Cognit. Neuropsychiatry 8 (1) (2001) 21] motor initiation, but not response duration, was expected to be impaired. The motor initiation times (reaction time: RT) and motor execution times (response duration: RD) were compared on four RT-tasks that required the production of a verbal response: a simple choice RT-task, a mental letter rotation task, and an implicit and an explicit mental hand rotation task. Because conversion disorder is expected to primarily involve an impairment in the initiation of movement, we expected the following task characteristics to uniquely affect RT and not RD: type of instruction (implicit versus explicit instructed imagery), angle of rotation, and target arm (affected versus non-affected arm). The results indeed showed the task characteristics to significantly affect the participants' RT and not their RD. It was concluded that conversion paralysis is associated with a specific impairment in the explicit initiation of processes with a spatial and motor component.

Adult↗

Surgical treatment of lateral rectus muscle paralysis.

We conducted a retrospective study of 55 cases to investigate the effectiveness of three different surgical procedures (medial rectus muscle recession and lateral rectus muscle resection in 16 cases, the Hummelsheim procedure in 27 cases, and the Jensen procedure in 12 cases) in the treatment of lateral rectus muscle paralysis. All three procedures were equally effective. Shorter duration of lateral rectus muscle paralysis, greater preoperative lateral version, less contracture of the medial rectus muscle, and a traumatic origin for the sixth cranial nerve damage had a significant effect (P less than .05) on the final results of surgery.

Adult↗

[Treatment of recurrent unilateral paralysis with thyroplasty with Montgomery implant].

OBJECTIVES: An analysis of thyroplasty with Montgomery implant under local anesthesia for unilateral laryngeal nerve paralysis. PATIENTS AND METHOD: An inception cohort of 21 patients was operated on with a minimum follow-up of 9 months. All patients had severe dysphonia and breathlessness. Seven patients had aspiration with a non efficient cough. RESULTS: The only adverse side effect was a subcutaneous cervical hematoma in one patient. Aspiration disappeared immediately after completion of the thyroplasty. Immediate improvement of speech, cough, and breathlessness was achieved in all patients. Over time, speech and voice remained stable in all patients. Recurrence of aspiration was not encountered. CONCLUSION: Such data supported the notion that the thyroplasty with Montgomery implant under local anesthesia is an extremely valuable option in patients with unilateral laryngeal nerve paralysis.

Adult↗

Tuberculous lymphadenopathy of superior mediastinum causing vocal cord paralysis.

Vocal cord paralysis because of involvement of recurrent laryngeal nerve by benign and acute inflammatory lymphadenopathy is a rare condition. Presented here is a case of tuberculous lymphadenopathy of superior mediastinum causing left recurrent laryngeal nerve paralysis, which was successfully treated by antituberculosis treatment, with complete recovery of vocal cord function.

Adult↗

Adenosine A2A agonist reduces paralysis after spinal cord ischemia: correlation with A2A receptor expression on motor neurons.

BACKGROUND: The adenosine A2A agonist ATL-146e ameliorates reperfusion inflammation, reducing subsequent paralysis and neuronal apoptosis after spinal cord ischemia. We hypothesized that neuroprotection with ATL-146e involves inducible neuronal adenosine A2A receptors (A2A-R) that are upregulated after ischemia. METHODS: Eighteen rabbits underwent laparotomy, and 14 sustained spinal cord ischemia from cross-clamping the infrarenal aorta for 45 minutes. One group (ischemia-reperfusion [I/R] + ATL) received ATL-146e intravenously for 3 hours during spinal cord reperfusion. A second group (I/R) received equivolume intravenous saline solution for 3 hours and served as an ischemic control, and a third group (Sham) underwent sham laparotomy. At 48 hours, all subjects were assessed for motor impairment using the Tarlov scoring system (0 to 5). Lumbar spinal cord sections were immunolabeled for A2A-R and graded in a blinded fashion using light microscopy. RESULTS: There was a significant improvement in Tarlov scores in I/R + ATL animals compared with the I/R group. Sham-operated animals demonstrated no A2A-R immunoreactivity. There was a dramatic increase in A2A-R immunoreactivity in neurons of lumbar spinal cord sections from I/R compared with I/R + ATL and sham-operated animals. CONCLUSIONS: Reduction in paralysis in animals receiving ATL-146e correlates with the new finding of A2A-R expression on lumbar spinal cord motor neurons after ischemia. Adenosine A2A agonists may exert neuroprotective effects by binding to inducible neuronal A2A-R that are upregulated during spinal cord reperfusion, and reduced in response to administration of an A2A-R-specific agonist.

Animals↗

Aggressive treatment of acquired phrenic nerve paralysis in infants and small children.

Transthoracic diaphragmatic plication is a simple and effective means of treatment for phrenic nerve injury and resultant diaphragmatic paralysis, and should be undertaken as soon as the diagnosis of diaphragmatic paralysis is established in a child with substantial respiratory difficulty. Seven of more than 1,500 patients sustained phrenic nerve injury during operation for congenital heart disease at our institution over the past five years. All but 1 patient were less than 5 months old, and the average weight was 3.8 kg. Five of the 7 could not be weaned from the ventilator, and the other 2 had persistent postoperative tachypnea and stridor. Before 1980, 3 patients were intubated for an average of 16 days prior to diagnosis by fluoroscopy. Since then, 4 patients have been intubated for an average of 7.8 days before diagnosis. All 7 underwent transthoracic diaphragmatic plication and were extubated by 6 days after operation (mean, 3.7 days). Six patients survived and are doing well. The 1 death occurred in 1976 in a premature infant with multiple congenital cardiac lesions; diagnosis was delayed until the twenty-eighth day after intubation and transthoracic diaphragmatic plication, until the sixty-second day. This infant died of pneumonia one month after extubation. These data support our policy of establishing an early diagnosis of phrenic nerve injury and early treatment utilizing transthoracic diaphragmatic plication in symptomatic children.

Cardiac Surgical Procedures↗

Thyrotoxic periodic paralysis: two case studies.

Thyrotoxic periodic paralysis (TPP) is a disorder that affects a small percentage of patients with hyperthyroidism; the patients are predominantly Asian men. Two typical cases are presented here; both patients came to the emergency room with complaints of sudden onset of weakness. Their symptoms were initially resolved through treatment for acute hypokalemia. Additional tests identified the patients as being thyrotoxic for which condition they underwent thyroid ablation with radioiodine. No further episodes were reported for either patient. Often the underlying cause of the weakness or paralysis is undetected because of the absence of clinical symptoms of hyperthyroidism and because clinicians are unfamiliar with the disorder. It is imperative that TPP be recognized in the differential diagnosis of weakness and that the underlying thyrotoxicity is treated to permanently alleviate the condition. The authors discuss the epidemiology, etiology, clinical manifestations, and treatments of TPP.

Adult↗

Change in gene expression in facial nerve nuclei and the effect of superoxide dismutase in a rat model of ischemic facial paralysis.

Peripheral nerve injury induces changes in gene expressions of a variety of neuroactive substances in cell somata, which may have roles in the adaptive response to the injury, neuronal survival, growth and regeneration. In this study, we designed a rat model of ischemic peripheral facial paralysis with a selective embolization technique, and observed mRNA expression of calcitonin gene-related peptide (CGRP), c-jun, and growth associated protein (GAP)-43 in facial nerve nuclei using in situ hybridization histochemistry. The rats were demonstrated to have a transient facial paralysis consistently, and thus this method was regarded as a model of minor peripheral nerve injury. The mRNA of CGRP, c-jun and GAP-43 showed a distinct pattern of induction and time course of increase after the ischemic nerve injury. The results suggest that the small injury to the peripheral nerve was able to induce changes in mRNA expression in the cell body of motoneurons. We also investigated the protective effect of superoxide dismutase (SOD), which is a free radical-scavenging enzyme involved in cellular antioxidant defenses. The SOD treatment clearly alleviated the behavioral impairment and decreased the CGRP mRNA expression at 3rd day after injury. These data suggest that a free radical generated by the ischemia may be partially responsible for ischemic nerve damage and the change in gene expression in motoneurons.

Animals↗

Effects of paralysis with pancuronium bromide on joint mobility in premature infants.

To study the effects of muscle paralysis on joint mobility, we compared eight premature infants treated with pancuronium bromide with a control group. A significant reduction was observed in hip and knee flexion, and in ankle dorsal extension, which tended to resolve in time. We conclude that muscle paralysis reduces the mobility of selected joints; spontaneous activity appears to prevent long-term contractures.

Ankle↗

Different mechanism of vocal cord paralysis between spinocerebellar ataxia (SCA 1 and SCA 3) and multiple system atrophy.

While multiple system atrophy (MSA) is frequently associated with vocal cord paralysis (VCP) causing severe respiratory failure, it is still unknown whether hereditary types of spinocerebellar degeneration develop similar laryngeal paralysis. We analyzed the laryngeal function from the viewpoints of fiberoptic laryngoscopy and laryngeal myopathology and then attempted to clarify the difference of the mechanism of VCP among the patients with spinocerebellar ataxia type 1 (SCA 1), type 3 (SCA 3), and MSA. Seven patients with SCA 1, nineteen with SCA 3, and eleven with MSA were studied. Vocal cord movement was analyzed by fiberoptic laryngoscopy during wakefulness and diazepam-induced sleep (sleep load test). Paraffin-embedded sections or cryosections of the intrinsic laryngeal muscles from five autopsied cases (one with SCA 1 and four with SCA 3) were histologically examined. VCP was found in two of the seven SCA 1 patients (29%), three of the nineteen SCA 3 patients (16%), and in nine of the eleven MSA patients (82%). VCP observed in SCA 1 and SCA 3 was various in the severity and showed no exacerbation on sleep load test in all of the eight patients but one SCA 3 patient. In this patient, the findings of fiberoptic laryngoscopy were quite similar to those found in MSA. All the intrinsic laryngeal muscles including cricothyroid (CT), interarytenoid (IA), and posterior cricoarytenoid (PCA) muscles showed neurogenic atrophy in one autopsied SCA 1 and four SCA 3 patients. Our conclusion is that VCP in SCA 1 and SCA 3 contrasts with that in MSA in its occurrence, response to the sleep load test, and the distribution of the neurogenic abnormalities among the intrinsic laryngeal muscles.

Adult↗

Primary motor cortex isolation: complete paralysis with preserved primary motor cortex.

We present a left-sided hemiplegic patient with a cerebrovascular lesion involving the medial part of the right frontal and parietal lobes and the corpus callosum, but sparing the hand area of right primary motor cortex (M1). Several studies using transcranial magnetic stimulation demonstrated functional integrity of the efferent pathways from the right M1, intact sensory afferents to M1, an impairment of transcallosal connection between the bilateral motor cortices, and reduced ipsilateral cortico-cortical inhibition within the right M1. Based on these results, we conclude that the paralysis of this patient was caused by disconnection of the intact M1 from any structures requisite for initiation of movements. The present patient also suggests the importance of various afferents to M1 in voluntary movement. We propose a term of 'primary motor cortex isolation' to designate the paralysis reported here.

Electromyography↗

Thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis (TPP), a hyperthyroidism-related hypokalemia and muscle-weakening condition resulting from a sudden shift of potassium into cells, has been seen increasingly in Western countries. Failure to recognize TPP may lead to improper management. Many patients with TPP have no obvious symptoms related to hyperthyroidism. Therefore, several important clues may help in diagnosing and managing TPP: presentation in an adult male with no family history of periodic paralysis; presence of systolic hypertension, tachycardia, high QRS voltage, first-degree atrioventricular block on electrocardiography; presence of low-amplitude electrical compound muscle action potential on electromyography and no notable changes in amplitudes after low doses of epinephrinine; and typical acid-base and electrolyte findings such as normal blood acid-base state, hypokalemia with low urinary potassium excretion, hypophosphatemia associated with hypophosphaturia, and hypercalciuria. Immediate therapy with potassium chloride supplementation may foster a rapid recovery of muscle strength, but with a risk of rebound hyperkalemia. Nonselective beta-blockers may provide an alternative choice. Long-term therapy with definite control of hyperthyroidism completely abolishes attacks. Early diagnosis and prompt treatment of TPP prevent life-threatening complications of this treatable and curable disorder.

Calcium↗

Tick paralysis.

Tick paralysis is a preventable cause of morbidity and death that, when diagnosed promptly, requires a simple low-cost intervention. The key to success is to consider tick paralysis in the differential diagnosis of ascending weakness, particularly in children, in geographic areas where this disease predominates.

Acetylcholine↗