SEARCH · Search PubMed

Results for “Paralysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources

PubMed1991

Different gene loci for hyperkalemic and hypokalemic periodic paralysis.

The periodic paralyses are dominantly inherited disorders in which patients acutely develop muscle weakness in association with changes in the level of blood potassium. We recently reported genetic linkage of hyperkalemic periodic paralysis (HIKPP) to the gene encoding the adult form of the skeletal muscle sodium channel on the long arm of chromosome 17. In this paper, we exclude genetic linkage between hypokalemic periodic paralysis (HOKPP) and this sodium channel gene, demonstrating that there is non-allelic genetic heterogeneity among different forms of periodic paralysis. Electrophysiological abnormalities in muscle sodium conductance have been reported for both HIKPP and HOKPP as well as other muscle disorders characterized by membrane hyperexcitability or myotonia (myotonia congenita, paramyotonia congenita and the Schwartz-Jampel syndrome). The possibility that there may be a family of human muscle diseases arising from mutations in the sodium channel suggests these disorders may be classified by categories of mutations within this critical voltage-sensitive membrane protein.

Chromosome Mapping↗

PubMed2004

Cardiovascular effects of the toxin(s) of the Australian paralysis tick, Ixodes holocyclus, in the rat.

An extract of toxin(s) from the Australian paralysis tick, Ixodes holocyclus, produced positive inotropic responses in rat left ventricular papillary muscles and positive contractile responses in rat thoracic aortic rings. There was no measurable chronotropic response in rat right atria, but positive inotropic concentrations in papillary muscles produced arrhythmias in right atria. Positive inotropic responses were attenuated by verapamil, but unaffected by metoprolol, cimetidine, pyrilamine, tetrodotoxin and pinacidil. Microelectrode studies on isolated left ventricular papillary muscles demonstrated that the extract prolonged action potential duration at 20, 50 and 90% of repolarisation and delayed ventricular papillary muscle relaxation. Cardiovascular tissues isolated from rats with experimentally induced tick paralysis showed no myocardial damage as identified by histological and ultrastructural examination. The basal rate and force of contraction of isolated cardiac tissues were lower from tick-paralysed than normal rats. Concentration-response curves to dobutamine and calcium chloride were similar between tissues from tick-paralysed and normal rats. Thus, the Australian paralysis tick, I. holocyclus, produces one or more toxins with direct cardiovascular effects which mimic the effects produced by direct blockade of cardiac and vascular K+ channels.

Action Potentials↗

PubMed1997

Enhanced magnetic resonance imaging in a patient with acute paralysis of the inferior division of the oculomotor nerve.

PURPOSE: To describe the characteristics of enhanced magnetic resonance imaging of the orbit in a patient with acute paralysis of the inferior division of the oculomotor nerve. METHOD: Using a fat-suppression technique, we performed enhanced magnetic resonance imaging of the orbit of a 36-year-old woman with acute paralysis of the inferior division of the left oculomotor nerve. RESULTS: The inferior division of the left oculomotor nerve in the orbit was markedly enhanced, suggesting inflammation of the inferior division of the oculomotor nerve. The severity of paralysis decreased immediately after intravenous corticosteroid (prednisolone acetate) administration. CONCLUSION: These findings suggest that enhanced magnetic resonance imaging with a fat-suppression technique is useful for diagnosing peripheral nerve lesions in the orbit.

Acute Disease↗

PubMed1993

Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.

Muscle fibers from individuals with hyperkalemic periodic paralysis generate repetitive trains of action potentials (myotonia) or large depolarizations and block of spike production (paralysis) when the extracellular K+ is elevated. These pathologic features are thought to arise from mutations of the sodium channel alpha subunit which cause a partial loss of inactivation (steady-state Popen approximately 0.02, compared to < 0.001 in normal channels). We present a model that provides a possible mechanism for how this small persistent sodium current leads to repetitive firing, why the integrity of the T-tubule system is required to produce myotonia, and why paralysis will occur when a slightly larger proportion of channels fails to inactivate. The model consists of a two-compartment system to simulate the surface and T-tubule membranes. When the steady-state sodium channel open probability exceeds 0.0075, trains of repetitive discharges occur in response to constant current injection. At the end of the current injection, the membrane potential may either return to the normal resting value, continue to discharge repetitive spikes, or settle to a new depolarized equilibrium potential. This after-response depends on both the proportion of noninactivating sodium channels and the magnitude of the activity-driven K+ accumulation in the T-tubular space. A reduced form of model is presented in which a two-dimensional phase-plane analysis shows graphically how this diversity of after-responses arises as extracellular [K+] and the proportion of noninactivating sodium channels are varied.

Animals↗

PubMed1989

Hypokalaemic, hypophosphatemic thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis is an uncommon neuromuscular disorder frequently associated with severe hypokalemia. We describe a patient with hypophosphatemia occurring in the setting of hypokalemic thyrotoxic periodic paralysis, an association reported only once previously. A review of the literature indicates that this combined biochemical derangement may not be uncommon and that thyrotoxic periodic paralysis should be recognized as a potential cause of hypophosphatemia. The correction of both hypokalemia and hypophosphatemia may lead to a more rapid resolution of the associated acute neurologic syndrome.

Adult↗

PubMed2000

Neuromuscular paralysis as a pharmacodynamic probe to assess organ function during liver transplantation.

Potential for assessing liver function during liver transplantation surgery by monitoring muscle paralysis from nondepolarizing neuromuscular blockers that are hepatically cleared is critically assessed. Rocuronium is strongly favored as a promising pharmacodynamic probe for predicting allograft liver function because it is predominantly eliminated via the liver and its putative metabolites are not active. Prolongation of recovery from rocuronium paralysis is closely correlated with allograft liver function postoperatively. Vecuronium, pancuronium, and perhaps pipecuronium may also prove to be useful probes, but the two former blockers have active metabolites. Further prospective studies are necessary with more precise measurement of neuromuscular function to confirm the predictive value of this method. Alterations in neuromuscular blocker plasma concentrations that are correlated with changes in liver function and either the dose required or the intensity or duration of paralysis needs to be demonstrated for this technique to be clinically useful.

Androstanols↗

PubMed2003

Rocuronium infusion requirements and plasma concentrations at constant levels of neuromuscular paralysis during three phases of liver transplantation.

STUDY OBJECTIVE: To develop a rapid online test of graft liver function during liver transplantation. DESIGN: Prospective, observational study. SETTING: University hospital transplant unit. PATIENTS: 17 adult patients with end-stage liver disease who underwent liver transplantation surgery. INTERVENTIONS: Rocuronium infusion dose requirements and plasma concentrations to maintain constant levels of neuromuscular paralysis during three phases of liver transplantation and their relationship with early postoperative liver function tests were studied. MEASUREMENTS: Infusion dose requirements of rocuronium, assay of rocuronium plasma concentrations using gas chromatography-mass spectrometry, and intensity of neuromuscular blockade were measured. MAIN RESULTS: A 24% decrease in rocuronium infusion requirements was observed during the an-hepatic phase. Rocuronium requirement during the neohepatic phase was increased only modestly or remained unchanged in 14 of the 16 patients who had normal graft function in the immediate postoperative period. Rocuronium plasma concentrations for maintaining constant levels of paralysis were significantly lower during the neohepatic phase than during the paleohepatic and anhepatic phases, indicating that there is likely to be a change in pharmacodynamics during this phase. Significant reduction in rocuronium infusion requirements during the neohepatic phase was observed in the only patient who had poor graft function in the early postoperative stage, suggesting that the reduced infusion requirement to maintain a constant neuromuscular paralysis may be related to the functional state of the graft liver after reperfusion. CONCLUSIONS: A significant reduction in rocuronium infusion requirement during the neohepatic phase may be suggestive of impaired organ function after reperfusion of the graft liver. Rocuronium may serve as a potential online indicator of graft liver function during liver transplantation by measurement of its infusion requirements during transplantation.

Adolescent↗

PubMed1999

Dysfunction of sensory nerves during attacks of hypokalemic periodic paralysis.

Reversible electrophysiologic abnormalities of sensory nerve function were found by chance in three patients with hypokalemic periodic paralysis, a disorder previously considered to affect the function of muscle membranes only. A formal, prospective study was therefore conducted. Serial nerve conduction studies were done in ten additional patients. Amplitude of sensory action potentials was significantly smaller during paralytic attacks, but did not differ from controls after normalization of serum potassium concentration. These apparently novel findings might be explained by previous electrodiagnostic studies either not involving the testing of sensory nerves at all, or not being repeated after recovery from an attack. Involvement of sensory nerves in hypokalemic periodic paralysis is suggested to arise through dorsal root ganglia having an incomplete blood-nerve barrier and sensory neurons being particularly vulnerable to derangements affecting nerve cell metabolism. Neuronal inexcitability is postulated to occur consequent upon possible inactivation of the sodium-potassium pump by the low concentration of extracellular potassium. In patients with acute areflexic limb weakness, the diagnosis of hypokalemic periodic paralysis should not be excluded by abnormal results of sensory nerve conduction studies.

Adult↗

PubMed2003

Isolated unilateral hypoglossal nerve paralysis caused by an atlanto-occipital joint synovial cyst.

An isolated unilateral hypoglossal nerve lesion is an uncommon cranial nerve palsy. We report a case of isolated hypoglossal nerve paralysis caused by an intra-dural synovial cyst. To our knowledge, this is the first reported case of a twelfth nerve paralysis caused by a synovial cyst. The anatomy of the hypoglossal nerve, its blood supply and the relationship of the nerve to the atlanto-occipital joint are reviewed, along with the common causes of isolated hypoglossal nerve paralysis.

Cranial Nerve Diseases↗

PubMedDate not supplied

Scapulothoracic fusion for serratus anterior paralysis.

Paralysis of the serratus anterior may lead to severe disability. Many surgical options are available, from soft-tissue procedures to scapulothoracic fusion. We report the results of 10 consecutive scapulothoracic fusions in 10 patients (7 men and 3 women) treated between 1980 and 1997. The mean age at surgery was 39 years (range, 22-57 years). Paralysis of the serratus anterior was isolated in five patients. One patient was lost to follow-up, and one patient died from an unrelated cause. Fusion was not achieved in three patients, two of whom had successful revision within 1 year postoperatively. One patient with an excellent result had a traumatic arthrodesis fracture and underwent successful revision. Results were assessed in 8 patients, including 3 who had reoperation. At a mean follow-up of 6.2 years (range, 1-15 years), 6 patients had a very good or good result and returned to manual labor. The mean active mobility was limited to 93 degrees in abduction and 101 degrees in forward elevation but was well tolerated. Two patients had a poor result because of nonunion and frozen shoulder, respectively. Scapulothoracic fusion may not be recommended as a primary procedure in the treatment of winging of the scapula due to serratus anterior paralysis. However, with the use of a careful technique, this method may be an alternative to muscle transfer, especially in patients in whom a previous soft-tissue procedure has failed or in patients with strenuous activities or combined muscular lesions.

Adult↗

PubMed2005

Paralysis after aortic surgery: in search of lost cord function.

During the early 1980s, the rate of paralysis after aortic surgery was as high as 41% in patients for the most complex thoracoabdominal aortic operations. After comparing human and chacma baboon (papio ursinus) spinal cord vascular anatomy, an animal model was established to study the pathophysiology of aortic cross-clamping and the aetiology of the paralysis. Techniques, including motor evoked responses for monitoring spinal cord function, were developed that were tried in humans and later culminated in prospective and randomized studies. These established that the following were protective: combining cerebrospinal fluid with intrathecal papaverine; cooling systemically to moderate or profound hypothermia; minimizing intercostal ischaemia time; using a sequential segmental repair approach; re-attaching all patent and segmental intercostal arteries below T8 for descending thoracic aortic repair and from T6 to L2 for thoracoabdominal repairs; continuing cerebrospinal fluid drainage for at least two days and maintaining patients hypertensive after surgery. The net result has been that, in two of our recent series, the risk of permanent paralysis has been reduced to between 3.1% and 3.8%.

Animals↗

PubMed2005

Cruciate paralysis and hemiplegia cruciata: report of three cases.

STUDY DESIGN: Report of three cases of cruciate paralysis and hemiplegia cruciata. OBJECTIVE: To stress the importance of upper cervical spine lesions causing neurological symptoms and signs. SETTING: Neuro-orthopedic service, Fukui University Hospital, Japan. RESULTS: Three patients (all females; one with congenital anomaly at the occiput-atlas level, one with assimilation of the atlas, and one with rheumatoid arthritis-related proliferative synovium) had clinical features of cruciate paralysis and hemiplegia cruciata. All three cases underwent decompressive surgeries. CONCLUSION: Neurological symptoms and signs of cruciate paralysis and hemiplegia cruciata should be carefully assessed, and surgical therapy should be based on the pathological condition.

Aged↗

PubMed2002

Preoperative stress conditioning prevents paralysis after experimental aortic surgery: increased heat shock protein content is associated with ischemic tolerance of the spinal cord.

BACKGROUND: All forms of surgical therapy are stressful and injurious. The problems of paralysis, renal dysfunction, and colonic ischemia associated with aortic occlusion are due to acute ischemia-reperfusion injury at the cellular level. Acute-anterior spinal cord ischemia is the most devastating outcome of these iatrogenic-ischemic events. The majority of surgical procedures are performed electively and therefore provide an opportunity to preoperatively condition the patient to minimize these ischemia-related morbidities. OBJECTIVES: We sought to determine whether acute spinal cord injury associated with aortic occlusion can be prevented by induction of the cellular stress response by means of preoperative administration of whole-body hyperthermia or stannous chloride. METHODS: The study consisted of an experimental rabbit model of infrarenal aortic occlusion for 20 minutes at normothermic body temperature. RESULTS: Control rabbits experienced an 88% (7/8) incidence of paralysis after spinal cord ischemia induced by 20 minutes of aortic occlusion, whereas animals treated preoperatively with either whole-body hyperthermia (0/9) or stannous chloride (0/4) never became paralyzed (P <.001 for control vs treated groups). Ischemic protection of the spinal cord was associated with increased content of stress proteins within tissues of pretreated animals. CONCLUSION: Prior induction of the heat shock response in the whole animal will increase the content of stress proteins within the spinal cord and other tissues and result in the prevention of hind-limb paralysis associated with aortic occlusion. We have designated the preoperative induction of the cellular stress response for the prevention of ischemic tissue injury stress conditioning. We suggest that stress-conditioning protocols represent the opportunity to practice preventative medicine at the molecular level.

Animals↗

PubMed2003

Hyperkalaemic paralysis.

BACKGROUND: hyperkalaemic paralysis is a rare, treatable, and potentially fatal entity presenting with flaccid motor weakness. CASE REPORT: a patient with acute hyperkalaemic paralysis caused by erroneous oral potassium supplementation in the context of chronic renal failure. The clinical picture of quadriplegia was initially interpreted as spinal cord injury due to a pathological cervical fracture. DISCUSSION: the diagnosis of hyperkalaemic paralysis requires a high index of suspicion. Instructions for over-the-counter supplements must be clear and concise to prevent life-threatening medication errors.

Aged↗

PubMed1993

Prolonged paralysis after long-term, high-dose infusion of pancuronium in anaesthetized cats.

We have studied the neuromuscular effects of a 48-h infusion of high-dose pancuronium (400 micrograms kg-1 h-1) in four cats anaesthetized with pentobarbitone, using contraction of tibialis anterior muscles after direct and indirect stimulation. After cessation of the pancuronium infusion, prolonged paralysis existed. The first twitch in the train-of-four stimuli (TOF) reappeared 8-12 h after termination of the pancuronium infusion. Twenty-four hours after termination of the infusion, TOF ratios were less than 0.08 and twitch contraction averaged 39 (SE 8)% of initial values. Twitch contraction after direct stimulation did not differ from initial values. Antagonism of paralysis was accomplished with neostigmine 60 micrograms kg-1 in two animals and neostigmine 90 micrograms kg-1 and 4-aminopyridine 500 micrograms kg-1 in the others. Steady-state plasma concentration of pancuronium (2000 ng ml-1) decreased rapidly after termination of the infusion, but then stabilized at about 130 ng ml-1. These results indicate that prolonged paralysis after long-term administration of high-dose pancuronium is caused primarily by failure of neuromuscular transmission, most likely caused by the persistent plasma concentrations of the drug in the pharmacologically active range.

4-Aminopyridine↗

PubMed1992

Progressive bulbar paralysis of childhood. A reappraisal of Fazio-Londe disease.

Fazio-Londe disease is a label sometimes applied to a degenerative disease of the motor neurons characterized by progressive bulbar paralysis in children. It is very rare with only 22 case reports describing 24 children including four sibling pairs. In two reports mothers and sons were affected. The neuropathology is described in only four cases. Previous authors have recognized that the condition is very heterogeneous. The clinical features of five children with this type of progressive bulbar paralysis, diagnosed at this hospital between 1969 and 1989, are reviewed, and in two cases neuropathological findings are detailed. Based on this experience, suggested criteria for diagnosis include clinical features of a pure motor neuronopathy affecting the bulbar nuclei, exclusion of other causes of progressive bulbar paralysis and positive support for the diagnosis from electromyography and/or pathological examination. A review of the literature, combined with the present series, suggests that there are at least three distinct subtypes: a very rare autosomal dominant form (as described by Fazio) and two variants with probable autosomal recessive inheritance either with early onset of respiratory symptoms and rapid progression to death or later onset, less prominent respiratory symptoms and protracted clinical course. There is strong concordance for each clinical pattern within families.

Bulbar Palsy, Progressive↗

PubMed1997

Eradication of wild poliovirus from the Americas: acute flaccid paralysis surveillance, 1988-1995.

In May 1985, the Pan American Health Organization proposed the goal of interruption of wild poliovirus transmission in the Western Hemisphere. An important component of the polio eradication strategy was conducting surveillance for cases of acute flaccid paralysis. Reported cases were thoroughly investigated, including the collection of stool samples for testing for the presence of wild poliovirus. The last patient with poliomyelitis due to wild poliovirus in the Americas had onset of paralysis on 23 August 1991 in Peru. Since then, >9000 cases of acute flaccid paralysis have been reported and thoroughly investigated; none has been confirmed as paralytic poliomyelitis due to wild poliovirus. On 29 September 1994, the International Commission for the Certification of Poliomyelitis Eradication declared the Americas to be polio-free.

Americas↗

PubMedDate not supplied

Tourniquet paralysis after primary nerve repair.

Paralysis after use of a tourniquet during surgery is a well recognized complication. Based on the electrophysiologic findings, 35 cases referred to our electromyography laboratory have been diagnosed as tourniquet paralysis within a 3-yr period. This preliminary report suggests that tourniquet paralysis should be considered during clinical and electrophysiologic evaluations after primary nerve repairs.

Electromyography↗