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At least 901 records · Page 50Linked to original sources
PubMed1992

Influence of cimetidine on gallamine-induced neuromuscular paralysis in rats.

1. The effect of cimetidine on gallamine-induced neuromuscular paralysis was evaluated in urethane-anaesthetized and mechanically ventilated rats. 2. Intravenous cimetidine (between 3.2 and 100 mg/kg) produced an immediate and sustained potentiation of gallamine-induced neuromuscular paralysis. 3. Intravenous calcium (0.35 mmol/kg) completely reversed the cimetidine-induced potentiation of gallamine's effect. 4. Cimetidine alone did not produce neuromuscular paralysis. 5. Cimetidine did not alter either the serum concentration or the total serum clearance of gallamine. 6. Cimetidine thus potentiates the action of gallamine via a pharmacodynamic and not a pharmacokinetic mechanism.

Animals↗
PubMed2004

Facial nerve paralysis secondary to acute otitis media in infants and children.

Nowadays, facial paralysis is an uncommon complication of acute inflammation of the middle ear, with an estimated incidence of 0.005%; it was not so rare in the pre-antibiotic era, occurring in 0.5-0.7% of middle ear inflammatory processes. We would like to highlight this complication of acute otitis media, a common paediatric complaint. We present three new cases of facial palsy in children with acute otitis media and discuss the etiological mechanisms and different approaches to the treatment; a flow chart for facial paralysis in acute otitis media is also presented. Our three patients recovered completely after mastoidectomy (first two cases) and myringotomy with antibiotic therapy (third case). Facial paralysis is an uncommon complication of otitis media which requires appropriate care. Following our experience and revision of literature on the subject, antibiotic therapy and myringotomy are the first-line procedures. Surgery should be employed in case of acute or coalescent mastoiditis, suppurative complications and lack of clinical regression.

Acute Disease↗
PubMed1998

Hypokalemic paralysis in association with acute gastroenteritis: a report of a sporadic case.

Hypokalemic periodic paralysis is a condition, characterized by episodic weakness of the skeletal muscle. It may be presented as familial or sporadic (secondary). In sporadic cases, the patient may present with paralysis without any previous self or familial history. It is known that these patients are more susceptible to hypokalemia than normal individuals. In low serum K+ concentrations that the normal population can tolerate, these patients may easily suffer from paralysis. A sporadic case of hypokalemic quadriparesis associated with acute gastroenteritis without any self or family history is reported. The patient had experienced two episodes of quadriparesis within a short interval and responded dramatically to potassium replacement therapy.

Acute Disease↗
PubMed1987

Hypokalemic periodic paralysis of thyrotoxic origin.

A 50-year-old Vietnamese man suffered recurrent episodes of hypokalemic periodic paralysis during treatment for thyrotoxicosis. Suspected precipitants of the paralysis were oral prednisolone, strenuous exertion and poor compliance with medications. Propranolol prevented the periodic paralysis. Control of the thyrotoxicosis was complicated by a florid skin reaction attributed to carbimazole, and was ultimately achieved using radioiodine.

Australia↗
PubMed1993

Comparison between the effects of botulinum toxin-induced paralysis and denervation on molecular forms of acetylcholinesterase in muscles.

Velocity sedimentation analysis of acetylcholinesterase (AChE) molecular forms in the fast extensor digitorum longus muscle and in the slow soleus muscle of the rat was carried out on days 4, 8, and 14 after induction of muscle paralysis by botulinum toxin type A (BoTx). The results were compared with those observed after muscle denervation. In addition, the ability of BoTx-paralyzed muscles to resynthesize AChE was studied after irreversible inhibition of the preexistent enzyme by diisopropyl phosphorofluoridate. Major differences were observed between the effects of BoTx treatment and nerve section on AChE in the junctional region of the muscles. A precipitous drop in content of the asymmetric A12 AChE form was observed after denervation, whereas its decrease was much slower and less extensive in the BoTx-paralyzed muscles. Recovery of junctional AChE and of its A12 form after irreversible inhibition of the preexistent AChE in BoTx-paralyzed muscles was nevertheless very slow. It seems that a greater part of the junctional A12 AChE form pertains to a fraction with a very slow turnover that is rapidly degraded after denervation but not after BoTx-produced muscle paralysis. The postdenervation decrease in content of junctional A12 AChE is therefore not primarily due to muscle inactivity. The extrajunctional molecular forms of AChE seem to be regulated mostly by muscle activity because they undergo virtually identical changes both after denervation and BoTx paralysis. The differences observed in this respect between the fast and slow muscles after their inactivation must be intrinsic to muscles.

Acetylcholinesterase↗
PubMedDate not supplied

Kawasaki disease with facial nerve paralysis.

Kawasaki disease (KD) is a multisystem disorder with varying clinical expression. We describe an instance of facial nerve paralysis in a patient with KD. A 5-month-old boy developed fever, irritability, and diarrhea, treated 8 days later with cefaclor and ibuprofen. Three days later a confluent, erythematous and papular rash appeared, his lips were reddened and swollen, and his white blood count and platelet count were 20,900/mm(3) and 558,000/mm(3), respectively. He was admitted to the hospital with a diagnosis of KD, and an echocardiogram showed a right coronary aneurysm. The patient then developed an acute, right-sided, facial nerve peripheral paralysis that resolved over the next 6 weeks. He was treated with intravenous immune globulin (IVIG) 2 g/kg and aspirin 100 mg/kg/day with improvement of signs and symptoms. This report documents facial nerve paralysis as an uncommon complication of KD and points out that it may be a marker of increased risk of cardiovascular disease in this disorder.

Coronary Aneurysm↗
PubMed1977

Paralysis of calves by the tick, Ixodes Holocyclus.

Adult female Ixodes holocyclus were collected from the field at Fig Tree Pocket, a Brisbane suburb, at Tamborine Mountain, Queensland and at Lismore, New South Wales, in November 1974. Females were also reared from engorged nymphs collected off bandicoots from Tamborine Mountain July 1974 and 1975. In November 1974 unexposed 2-3 week old British breed calves, weighing between 26 and 46 kg were infested with 2,4,8 or 10 ticks. Neither 2 nor 4 females per calf caused paralysis. A challenge of 8 to 10 females induced paralysis 6 to 9 days after infestation by which time most ticks had engorged. There was little difference between ticks from different geographic localities. The site of attachment had no influence on tick toxicity. In September 1975, 2-3 week old British breed and Sahiwal x Jersey calves were infested with female ticks which had moulted 2-4 weeks prior to infestation. All but one calf with 10 ticks and all calves with 4 ticks became paralysed 8 to 13 days after infestation. At the time of paralysis only 1 of the 86 ticks had engorged and the remainder were small (30 to 50 mg). The greater toxicity of the latter ticks may have been due to the different treatment of ticks prior to infestation or to variations in the production of toxin associated with slow feeding. Four of 7 paralysed calves were saved using canine antitick serum.

Animals↗
PubMed1998

The biophysical and pharmacological characteristics of skeletal muscle ATP-sensitive K+ channels are modified in K+-depleted rat, an animal model of hypokalemic periodic paralysis.

We evaluated the involvement of the sarcolemmal ATP-sensitive K+ channel in the depolarization of skeletal muscle fibers occurring in an animal model of human hypokalemic periodic paralysis, the K+-depleted rat. After 23-36 days of treatment with a K+-free diet, an hypokalemia was observed in the rats. No difference in the fasting insulinemia and glycemia was found between normokalemic and hypokalemic rats. The fibers of the hypokalemic rats were depolarized. In these fibers, the current of sarcolemmal ATP-sensitive K+ channels measured by the patch-clamp technique was abnormally reduced. Cromakalim, a K+ channel opener, enhanced the current and repolarized the fibers. At channel level, two open conductance states blocked by ATP and stimulated by cromakalim were found in the hypokalemic rats. The two states could be distinguished on the basis of their slope conductance and open probability and were never detected on muscle fibers of normokalemic rats. It is known that insulin in humans affected by hypokalemic periodic paralysis leads to fiber depolarization and provokes paralysis. We therefore examined the effects of insulin at macroscopic and single-channel level on hypokalemic rats. In normokalemic animals, insulin applied in vitro to the muscles induced a glybenclamide-sensitive hyperpolarization of the fibers and also stimulated the sarcolemmal ATP-sensitive K+ channels. In contrast, in hypokalemic rats, insulin caused a pronounced fiber depolarization and reduced the residual currents. Our data indicated that in hypokalemic rats, an abnormally low activity of ATP-sensitive K+ channel is responsible for the fiber depolarization that is aggravated by insulin.

ATP-Binding Cassette Transporters↗
PubMed1975

Mechanism of insulin-induced paralysis of muscles from potassium-depleted rats.

Zinc-free insulin elicited a reduction in the potassium conductance of muscle fibers from potassium-depleted muscle, which led to depolarization, blockage of action-poteintial mechanism, and paralysis. These changes are proposed as the mechanism of insulin-induced paralysis in patients with hypokalemic periodic paralysis. A similar effect by concanavalin a suggests that the effect may be mediated through the insulin receptors.

Action Potentials↗
PubMed1975

Detection of Clostridium botulinum toxin by local paralysis elicited with intramuscular challenge.

Clostridium botulinum toxin can be identified by a characteristic, acute local paralysis that follows its injection into the gastrocnemius ("calf" muscle) of mice. The local botulism can be elicited with slightly less than one-tenth the toxin amount that is needed to kill mice by the intraperitoneal (i.p.) challenge route. The practical sensitivities of the intramuscular (i.m.) versus i.p. tests are about equal, however, because maximum sample volume injectable i.m. is 0.1 ml as compared to the 0.5-ml range that can be given i.p. i.m. injection of 10 or more mouse i.p. mean lethal doses causes paralysis in about 1 h, and an i.m. injection of about 0.5 i.p. mean lethal doses causes paralysis in 3 to 4 h. Toxin neutralization by homologous type of antitoxin only can be demonstrated with an incubated mixture of toxin and antitoxin. Although not as convenient as the i.p. method for routine use to detect botulinum toxin, the i.m. method has characteristics which could make it a useful supplement to the presently accepted i.p. procedure.

Animals↗
PubMed1999

Hyperkalaemic paralysis--a bizarre presentation of renal failure.

Paralysis due to hyperkalaemia is rare and the diagnosis may be overlooked in the first instance. However it is rapidly reversible and so long as electro-cardiography and serum potassium measurement are urgently done in all patients presenting with paralysis, it will not be missed. A case of hyperkalaemic paralysis is described and a review of the emergency management discussed.

Acute Kidney Injury↗
PubMed1990

Familial congenital laryngeal abductor paralysis: different expression in a family with one male and three females affected.

A brother and two sisters of remotely consanguineous parents had congenital laryngeal abductor paralysis and moderate mental retardation. In the two older sibs, mental deficiency could have resulted from birth asphyxia, but the youngest girl was already microcephalic at birth and had no apparent asphyxia. The mother, who was healthy and of normal intelligence, was found on laryngoscopy to have unilateral laryngeal abductor paralysis. This is the first family with both mentally retarded and nonretarded affected members with congenital laryngeal abductor paralysis. Inheritance is most likely autosomal dominant with variable expression, but autosomal recessive inheritance, with both parents carriers and the mother an affected homozygote, and X linked inheritance are also possible.

Consanguinity↗
PubMed1992

Clinical features of Todd's post-epileptic paralysis.

Two hundred and twenty nine patients with generalised tonic-clonic seizures were prospectively evaluated. Fourteen were identified who had transient focal neurological deficits thought to be Todd's post-epileptic paralysis (PEP). Eight of these 14 patients had underlying focal brain lesions associated with the postictal deficits. All patients with PEP were weak, but there was wide variation in the pattern (any combination of face, arm, leg), severity (plegia to mild), tone (spastic, flaccid, or normal), and reflexes (increased, decreased, or normal). Significant sensory loss occurred in only one patient. The only other signs of PEP were aphasia (in five patients all with underlying lesions) and gaze palsy (in four patients). Post-epileptic paralysis persisted from half an hour to 36 hours (mean of 15 hours). Post-epileptic paralysis may occur with the first seizure or after many years of seizures and does not appear after every seizure. The clinical features of PEP are thus heterogeneous.

Electroencephalography↗
PubMed1981

Periodic paralysis complicating malaria.

Episodic muscular weakness, commonly associated with alterations of serum potassium, is the cardinal feature of periodic paralysis. The combination of transient hyperkalaemia and rigors occurring during febrile episodes of malaria is suggested as the underlying cause which precipitated the muscular paralysis. Three patients with malaria who developed a similar paralysis during the paroxysms of fever are described to illustrate this.

Adult↗
PubMed1983

Respiratory mechanics during halothane anesthesia and anesthesia-paralysis in humans.

In six spontaneously breathing anesthetized subjects [halothane approximately 1 maximum anesthetic concentration (MAC), 70% N2O-30% O2], we measured flow (V), volume (V), and tracheal pressure (Ptr). With airway occluded at end-inspiration tidal volume (VT), we measured Ptr when the subjects relaxed the respiratory muscles. Dividing relaxed Ptr by VT, total respiratory system elastance (Ers) was obtained. With the subject still relaxed, the occlusion was released to obtain the V-V relationship during the ensuing relaxed expiration. Under these conditions, the expiratory driving pressure is V X Ers, and thus the pressure-flow relationship of the system can be obtained. By subtracting the flow resistance of equipment, the intrinsic respiratory flow resistance (Rrs) is obtained. Similar measurements were repeated during anesthesia-paralysis (succinylcholine). Ers averaged 23.9 +/- 4 (+/- SD) during anesthesia and 21 +/- 1.8 cmH2O X 1(-1) during anesthesia-paralysis. The corresponding values of intrinsic Rrs were 1.6 +/- 0.7 and 1.9 +/- 0.9 cmH2O X 1(-1) X s, respectively. These results indicate that Ers increases substantially during anesthesia, whereas Rrs remains within the normal limits. Muscle paralysis has no significant effect on Ers and Rrs. We also provide the first measurements of inspiratory muscle activity and related negative work during spontaneous expiration in anesthetized humans. These show that 36-74% of the elastic energy stored during inspiration is wasted in terms of negative inspiratory muscle work.

Adult↗
PubMed1988

Breathing pattern of anesthetized humans during pancuronium-induced partial paralysis.

We investigated the breathing patterns of 17 subjects anesthetized with enflurane before and after partial muscle paralysis produced by pancuronium bromide. In the face of significant muscle weakness produced by pancuronium, breathing patterns are characterized by decreases in both tidal volume and respiratory frequency. The decreased tidal volume corresponded to the decrease in occlusion pressure, indicating that the decreased tidal volume results solely from a decreased contractile force of the respiratory muscles. The decreased respiratory frequency was due to prolongation of both inspiratory and expiratory time without changing the ratio of the inspiratory time to the total breath time. Withdrawal of phasic vagal influence by airway occlusion before partial muscle paralysis revealed that an active Breuer-Hering inflation reflex was operative in only 8 of all 17 subjects. Since the contribution of the Breuer-Hering inflation reflex alone does not seem to account for the consistent decrease in respiratory frequency, some other mechanisms modulating respiratory frequency might be involved in the characteristic breathing patterns during partial muscle paralysis under enflurane anesthesia.

Adult↗
PubMed1993

Effect of selective diaphragmatic paralysis on the inspiratory motor drive.

Using alpha-chloralose-anesthetized mechanically ventilated vagotomized dogs, we assessed the effects of selective diaphragmatic paralysis on the inspiratory motor drive. Diaphragmatic paralysis was accomplished by a bolus injection of vecuronium, a neuromuscular junction blocker, into the left phrenic artery of an in situ vascularly isolated and innervated left diaphragm. The inspiratory motor drive during spontaneous breathing attempts was assessed by measuring peak integrated electromyographic (EMG) activities of the left and right diaphragms and parasternal and alae nasi muscles. Respiratory timing parameters were measured from the integrated EMG signals of the diaphragm. Three groups of dogs were studied. In group 1 (n = 9), vecuronium was injected into the phrenic artery with the left diaphragmatic length adjusted at the functional residual capacity. Vecuronium injection (0.2 mg) resulted in a significant decline in left diaphragmatic tension and integrated EMG. Breathing frequency increased by 24% of the baseline value, whereas right diaphragm, parasternal, and alae nasi EMG activities rose to 136, 227, and 165% of their respective baseline values a few seconds after the vecuronium injection. In group 2 (n = 6), vecuronium injection in left phrenectomized animals did not alter the EMG activities of the inspiratory muscles (left EMG signal was abolished) nor did it alter respiratory timing. In group 3 (n = 4), the left diaphragm was placed in a flaccid position. Vecuronium injection in this group did not produce any changes in the EMG activities or respiratory timing. We conclude that selective diaphragmatic paralysis elicits a significant rise in the inspiratory motor drive. This effect is likely to be mediated through the inhibition of diaphragmatic Golgi tendon organ activity.

Animals↗
PubMedDate not supplied

Comparison between the GIRBAS Scale and the Acoustic and Aerodynamic Measures Provided by EVA for the Assessment of Dysphonia following Unilateral Vocal Fold Paralysis.

The aim of this study is to establish relevant objective parameters for evaluating dysphonia following unilateral vocal fold paralysis. To do so, the study compares objective and perceptual voice measures. The objective measures were obtained using a voice analysis software (Evaluation Vocale Assistée), whereas the perceptual measures were established with the GIRBAS Scale (grade, instability, roughness, breathiness, asthenia, and strain). All measurements were performed on 40 voice samples: 28 dysphonic subjects with unilateral laryngeal paralysis, and 12 control subjects. The intra- and inter-judge agreements were fairly good, at least for control subjects. The six GIRBAS measures obtained from the pathological voices were higher than those from the control voices (p < 0.001) and the correlation between both groups was good. Grade, breathiness and asthenia correlated with the objective parameters that express the aperiodicity of the phonatory signal (p < 0.01), namely, the coefficient of variability of the fundamental frequency, the coefficient of variability of intensity, and jitter. Our findings suggest that the perceptual reality of laryngeal paralysis-induced dysphonia depends more on grade, breathiness and asthenia than it does on roughness or instability.

Female↗