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PubMed1980

Pathogenesis of human poliovirus infection in mice. II. Age-dependency of paralysis.

The mechanism of resistance of newborn mice to poliovirus-induced paralysis was studied by comparing regional virus replication in the adult and in the newborn central nervous systems (CNS) after intracerebral (ic) and intraspinal inoculation. Initial virus replication in the brains was similar in both age groups. Paralysis correlated with replication of virus in the spinal cord to a constant threshold, and this replication in newborns was delayed. Intraspinal inoculation of newborns eliminated the delay, indicating that neonatal anterior horn motor neurons were fully susceptible to infection. Cordectomy prevented the spread of virus, despite patent cerebrospinal fluid (CSF) pathways. Thus, poliovirus appeared to spread within the CNS via an axonal transport system. Known maturational changes in the fast transport system may explain the relative resistance of immature mice to poliovirus-induced paralysis.

Age Factors↗
PubMed2002

Current approach to radial nerve paralysis.

LEARNING OBJECTIVES: After studying this article, the participant should be able to: 1. Identify all potential points of radial nerve compression and other likely causes of radial nerve injury. 2. Accurately diagnose both surgical and nonsurgical causes of radial nerve paralysis. 3. Define a safe and effective approach to the surgical release and reconstruction of the radial nerve. Radial nerve paralysis, which can result from a complex humerus fracture, direct nerve trauma, compressive neuropathies, neuritis, or (rarely) from malignant tumor formation, has been reported throughout the literature, with some controversy regarding its diagnosis and management. The appropriate management of any radial nerve palsy depends primarily on an accurate determination of its cause, severity, duration, and level of involvement. The radial nerve can be injured as proximally as the brachial plexus or as distally as the posterior interosseous or radial sensory nerve. This article reviews the etiology, prognosis, and various treatments available for radial nerve paralysis. It also provides a new classification system and treatment algorithm to assist in the management of patients with radial nerve palsies, and it offers a simple, five-step approach to radial nerve release in the forearm.

Algorithms↗
PubMed1989

Erythrocyte sodium-potassium pump in thyrotoxic periodic paralysis.

To search for a genetic marker in patients with thyrotoxic periodic paralysis (TPP), we studied the erythrocyte sodium-potassium pump activity in 13 patients with TPP; 30 thyrotoxic patients with no history of paralysis (T) and 69 euthyroid controls. In thyrotoxic patients (TPP and T), erythrocyte ouabain binding and ouabain sensitive sodium efflux rate constant were decreased while erythrocyte sodium content was increased. All these changes reverted to normal when the patients became euthyroid. Maximal ouabain binding capacity correlated positively with ouabain sensitive sodium efflux rate constant (r = 0.542; p less than 0.001; n = 155) and negatively with serum thyroxine concentration (r = -0.571; p less than 0.001; n = 60) and erythrocyte sodium content (r = -0.521; p less than 0.001; n = 155). In the thyrotoxic state, maximal ouabain binding capacity was just significantly higher in TPP when compared with T (0.268 +/- 0.014 and 0.234 +/- 0.009 pmol/10(9) cells respectively; p less than 0.05). This difference could not be demonstrated when the patients became euthyroid. Our findings suggest that patients with TPP respond to thyrotoxicosis with a smaller decrement in erythrocyte sodium-potassium ATPase activity than patients without a history of paralysis. However, the difference is too small to represent a useful genetic marker for this disease entity

Erythrocytes↗
PubMed1977

Effect upon serum insulin, glucose and potassium concentrations of acetazolamide during attacks of familial periodic hypokalemic paralysis.

In four patients with periodic hypokalemic paralysis paralytic attacks were induced in the untreated state and later, after the patients had been treated with acetazolamide. There was a distinct, clinically favourable effect of acetazolamide upon the length as well as the severity of paralysis. The maximum fall in serum potassium was less marked during acetazolamide therapy. After treatment all four patients showed significantly reduced serum levels of glucose and insulin during induced attacks of paralysis as compared with the levels obtained during paretic attacks in the untreated state. These findings indicate that the prophylactic effect of this drug does not relate merely to metabolic acidosis. The hypothesis is advanced that the lower serum insulin and glucose levels might represent reduced absorption which would amount to an indirect prophylactic action.

Acetazolamide↗
PubMed1982

Prevention of human poliovirus-induced paralysis and death in mice by the novel antiviral agent arildone.

Arildone, a novel antiviral agent which blocks virion uncoating, was assessed for its ability to prevent paralysis and death in mice infected intracerebrally with a lethal dose of human poliovirus type-2 (strain MEF). Intraperitoneal administration of arildone suspended in gum tragacanth prevented paralysis and death in a dose-dependent manner (minimal inhibitory dose = 32 mg/kg, twice daily) and protected animals from virus challenges in excess of 20 50% lethal doses. Oral medication with arildone solubilized in corn oil was similarly effective in preventing poliovirus-induced paralysis and death. Arildone was therapeutically effective even when intraperitoneal medication was delayed for 48 h postinfection. Analysis of the virus titers in the central nervous system tissues of animals infected with 200 50% lethal doses demonstrated that arildone reduced titers in the brain and spine by approximately 3 and 4 log10 PFU per g of tissue, respectively, implying that direct inhibition of virus replication was responsible for host survival. Arildone is the first antiviral agent capable of preventing poliovirus-induced death in mice. The efficient inhibition of poliovirus replication described here demonstrates the potential usefulness of uncoating blockers in the systemic treatment of viral diseases.

Animals↗
PubMed1980

Characterization of cricket paralysis virus-induced polypeptides in Drosophila cells.

Cricket paralysis virus purified from Galleria mellonella larvae was shown to be similar to virus purified from Drosophila melanogaster cells. Cricket paralysis virus contained three major structural polypeptides of similar molecular weight (around 30,000), had a buoyant density of 1.344 g/ml, and had a capsid diameter of 27 nm. Twenty virus-induced polypeptides could be detected in CrPV-infected Drosophila cells. Two major polypeptides found in the infected cells corresponded to two structural viral polypeptides (VP1 and VP3), whereas the third major intracellular polypeptide was the apparent precursor of the third viral structural polypeptide (VP2). Three of the primary virus-induced polypeptides had molecular weights of 144,000, 124,000, and 115,000. These and other polypeptides were chased into lower-molecular-weight proteins when excess cold methionine was added after a short [(35)S]methionine pulse. Although cricket paralysis virus has a number of characteristics in common with the mammalian enteroviruses, the extremely fast processing of high-molecular-weight polypeptides into viral proteins seems atypical. Also, no VP4 (8,000 to 10,000 molecular weight) has been found in the virus particles.

Journal Article↗
PubMed1993

Randomised trial of routine versus selective paralysis during ventilation for neonatal respiratory distress syndrome.

The strategy of non-selective neuromuscular paralysis was compared with that of synchronised (fast rate) ventilation and selective paralysis in infants receiving mechanical ventilation for respiratory distress syndrome with chronic lung disease as the primary outcome measure. One hundred and ninety three infants weighing under 2000 g were randomly allocated to receive either pancuronium during mechanical ventilation in the acute phase of respiratory distress syndrome (non-selective group) or synchronised ventilation (initial ventilatory rate at or above that of the infant's) (selective group). Infants in the selective group received pancuronium if they were consistently expiring during the inspiratory phase of the ventilator cycle. There was no significant difference between the groups with respect to birth weight, gestation, and sex distribution. There was no significant difference between the group with respect to death (selective 19%, non-selective 16%), pneumothorax (selective 14%, non-selective 14%), chronic lung disease (selective 49%), non-selective 47%), and oxygen dependency at 36 weeks' postmenstrual age (selective 32%, non-selective 39%). Routine paralysis of ventilated infants has potential complications that may be avoided by using synchronised ventilation. As the latter is not associated with an increased incidence of long term respiratory complications, it is concluded that it is the optimum strategy of the two for ventilating infants with respiratory distress syndrome.

Chronic Disease↗
PubMed2002

Thyrotoxic periodic paralysis: reports of seven patients presenting with weakness in an Asian emergency department.

OBJECTIVES: This study was done to describe the features of thyrotoxic periodic paralysis in young Asian men. METHODS: Seven male patients were enlisted who presented to the emergency department over a period of three years with weakness and paralysis in the morning. RESULTS: Initial electrolyte studies revealed hypokalaemia in these patients, and later thyroid function tests confirmed thyrotoxicosis for all. Only two of these patients had clinical symptoms and signs of thyrotoxicosis, the others being asymptomatic. CONCLUSIONS: Early morning paralysis can be the first manifestation of hyperthyroidism in Asian men, without the other more typical symptoms of weight loss, increased appetite, excitability, sweaty palms or goitre. Treatment to a euthyroid state will ameliorate the syndrome.

Adult↗
PubMed2002

Thyrotoxic periodic paralysis in a white woman.

A 24 year old white woman presented with sudden onset of flaccid quadriparesis and hypokalaemia. She was later found to be thyrotoxic. Paralysis resolved with potassium supplements, and after initiation of antithyroid medication she had no further episodes of hypokalaemic paralysis. To the best of the authors' knowledge, and after a Medline search, thyrotoxic periodic paralysis has not been described previously in a white woman.

Adult↗
PubMed1988

Diaphragm strength in patients with recent hemidiaphragm paralysis.

Eleven patients with unilateral diaphragm paralysis of recent onset were studied to investigate the effect of the paralysis on inspiratory muscle function. Nine of the patients had noticed a decrease in exercise tolerance, which was not explained by any other pathological condition. Hemidiaphragm dysfunction was confirmed by the demonstration of a greatly reduced or absent transdiaphragmatic pressure on stimulation of the phrenic nerve in the neck, by means of surface bipolar electrodes (unilateral twitch Pdi), compared with normal values on the contralateral side. Transdiaphragmatic pressure was 44.6% (9.4%) predicted during a maximal sniff and 30.3% (16.8%) predicted during a maximal static inspiration against a closed airway, confirming diaphragm weakness. Maximum static inspiratory mouth pressures were also low (61.7% (12.7%) predicted), consistent with a reduction in inspiratory muscle capacity. Phrenic nerve conduction time was prolonged on the affected side in nine patients, consistent with phrenic nerve dysfunction, whereas on the unaffected side it was normal. It is concluded that recent hemidiaphragm paralysis causes a reduction in transdiaphragmatic pressure that is associated with a reduction in maximum inspiratory mouth pressure. Phrenic nerve stimulation is a useful technique with which to confirm and quantify hemidiaphragm dysfunction. Measurement of phrenic nerve conduction time provides useful information about the underlying pathology.

Diaphragm↗
PubMed1976

Ischemic paralysis of the facial nerve: a possible etiologic factor in Bell's palsy.

Numerous causes of peripheral facial nerve paralyses have been described; however, none has satisfactorily explained the genesis of the most common type of paralysis, Bell's palsy. Two patients undergoing an experimental embolization of vascular intracranial tumors suffered a total peripheral facial nerve paralysis when occlusion of the middle meningeal artery had been accomplished. It is speculated that this paralysis resulted from ischemia of the horizontal portion of the facial nerve, an observation that has not previously been described and that might be applicable as well to the etiology of Bell's palsy.

Adult↗
PubMed1999

"Cell paralysis" as an intermediate stage in the programmed cell death of epiphyseal chondrocytes during development.

The efficient elimination of apoptotic cells depends on heterophagocytosis by other cells, which is difficult or impossible when the dying cells are embedded in an extracellular matrix. This situation is exemplified by the epiphyseal chondrocytes during the development of the chondroepiphyses of long bones. A detailed ultrastructural study identified an unusual type of epiphyseal chondrocyte which contained a very dark nucleus with irregular patches of condensed chromatin and a crenated nuclear membrane. The cytosol consisted of excessively expanded endoplasmic reticulum lumen, containing "islands" of cytoplasm and organelles. Since these cells appeared to be "in limbo," neither viable nor dead, they are referred to as "paralyzed" cells. By studying cells of intermediate morphologies, we were able to demonstrate the sequence of events leading to cell paralysis. It is proposed that the paralysis represents an intermediate state in the physiological cell death of epiphyseal chondrocytes in which destruction is orderly and avoids a inflammatory, potentially locally destructive, reaction. The cell is rendered paralyzed in terms of function but impotent in respect of damaging consequences. Paralysis is compared and contrasted with apoptosis, autophagocytosis, and necrosis and may represent another mode of programmed cell death in situations where cells are immature and/or where phagocytosis by neighboring cells is difficult.

Animals↗
PubMed2004

Mutations that rescue the paralysis of Caenorhabditis elegans ric-8 (synembryn) mutants activate the G alpha(s) pathway and define a third major branch of the synaptic signaling network.

To identify hypothesized missing components of the synaptic G alpha(o)-G alpha(q) signaling network, which tightly regulates neurotransmitter release, we undertook two large forward genetic screens in the model organism C. elegans and focused first on mutations that strongly rescue the paralysis of ric-8(md303) reduction-of-function mutants, previously shown to be defective in G alpha(q) pathway activation. Through high-resolution mapping followed by sequence analysis, we show that these mutations affect four genes. Two activate the G alpha(q) pathway through gain-of-function mutations in G alpha(q); however, all of the remaining mutations activate components of the G alpha(s) pathway, including G alpha(s), adenylyl cyclase, and protein kinase A. Pharmacological assays suggest that the G alpha(s) pathway-activating mutations increase steady-state neurotransmitter release, and the strongly impaired neurotransmitter release of ric-8(md303) mutants is rescued to greater than wild-type levels by the strongest G alpha(s) pathway activating mutations. Using transgene induction studies, we show that activating the G alpha(s) pathway in adult animals rapidly induces hyperactive locomotion and rapidly rescues the paralysis of the ric-8 mutant. Using cell-specific promoters we show that neuronal, but not muscle, G alpha(s) pathway activation is sufficient to rescue ric-8(md303)'s paralysis. Our results appear to link RIC-8 (synembryn) and a third major G alpha pathway, the G alpha(s) pathway, with the previously discovered G alpha(o) and G alpha(q) pathways of the synaptic signaling network.

Adenylyl Cyclases↗
PubMed1994

[Periodic paralysis: anatomo-pathological study of skeletal muscles in 14 patients].

Periodic paralysis is a rare disease, characterized by transient weakness associated with abnormal levels of serum potassium. Muscle biopsy may show a wide range of abnormalities, vacuoles being more specifically linked to the disease. We analysed 17 muscle biopsies from 14 patients with periodic paralysis (14 hypokalemic, 2 hyperkalemic). All of them showed at least one histological abnormality. Fourteen specimens showed vacuoles that were peripheral, single, frequent and preferentially found in type I fibers. Frequency or severity of attacks did not correlate with the presence of vacuoles but those were more easily found in patients with long term disease. Ten biopsies showed tubular aggregates, specially on the patients with frequent crises or long term disease. A second biopsy was done in three patients and in two we observed a worsening of the histopathologic picture. One patient manifested interictal weakness with evident myopathic changes on the muscle biopsy. Nonspecific changes were found in variable degrees in 15 biopsies. Our study shows that vacuoles and tubular aggregates are frequent changes in periodic paralysis and therefore helpful for the diagnosis. Important myopathic findings in the muscle biopsy suggest a permanent myopathy which probably develops after severe crises or long term disease.

Adolescent↗
PubMed2003

[Hopkins' syndrome in the differential diagnosis of flaccid paralysis in children: clinical and neurophysiological features. Case report].

INTRODUCTION: Hopkins syndrome is a motor neuron disease which leads to a flaccid paralysis affecting one or more limbs resembling poliomyelites. It follows an asthmatic attack and the prognosis is poor. All the 34 related cases occured after 13 months of age and there is no report in South America. Our objective is to describe a case of Hopkins Syndrome in Brazil affecting a patient younger than 1 year. CASE: Male 4 months-old infant, started presenting wheezing that turned into respiratory failure which required mecanical ventilation. Three days later he initiated with loss of strength in the lower limbs (LL). The patient was dismissed from hospital better of his respiratory complains but still paraparetic. Five months later, the patient returned with another episode of severe bronchospasm. At that time, he presented with flaccid paralysis, arreflexia and atrophy of the LL. There were no upper limbs and sensory abnormalities. The patient undergone to lumbar puncture, spinal MRI and SEPs which were all normal. MUSCLE BIOPSY: type grouping. EMG and NCS were in keeping with motor neuron disease affecting just the lumbosacral region. CONCLUSION: Hopkins syndrome should be included in the differential diagnosis of any flaccid paralysis when it is associated with an asthma attack.

Acute Disease↗
PubMed1982

Therapeutic neuromuscular paralysis in neonates: characteristic radiographic features.

Neonates with respiratory distress requiring mechanical ventilation may be treated with muscular paralysis to improve oxygenation. This results in characteristic radiographic features that relate in part to the specific drug used. The radiographic signs are: bell-shaped chest, decreased bowel gas, and soft-tissue edema. When all three findings are present, the use of neuromuscular blockade can be suggested from the radiographs alone without the aid of clinical history. Radiographs of 57 infants treated with muscular paralysis and mechanical ventilation were compared to 20 infants treated with mechanical ventilation alone. In paralyzed patients, a characteristic bell-shaped chest was seen in 24 of 57 and decreased bowel gas in 46 of 52. Soft-tissue edema was seen in patients treated with metocurine, and the incidence increased with duration of therapy (18 of 25 treated for 5 or more days); it was not radiographically detected in patients treated with d-tubocurarine (0 of 13). Bell-shaped chest, decreased bowel gas, and soft-tissue edema occurred one, three, and one times, respectively, in 20 nonparalyzed control infants, and each time the findings carried significantly different clinical implications. All cases were reviewed to determine if pulmonary edema can result from mobilization of soft-tissue edema fluid after cessation of neuromuscular paralysis, and this was found not to occur.

Clinical Trials as Topic↗
PubMed1995

Profound hypotension immediately following insertion of methyl methacrylate during bipolar endoprosthesis in a patient with long-term levodopa-treated paralysis agitans.

Insertion of methyl methacrylate polymer into newly reamed bony cavities has sometimes resulted in profound hypotension, cardiac arrest, or sudden death which are more common in patients with hemodynamic instability or hypovolemia. In paralysis agitans(Parkinson's disease), dramatic worsening of the disease often occurs when another illness or trauma accompanies it. And it is possible that chronic medication with levodopa can cause the loss of ability to support blood pressure. So, it involves some risk to use methyl methacrylate in chronic levodopa-treated paralysis agitans. We present a case of paralysis agitans who demonstrated profound hypotension immediately following insertion of methyl methacrylate polymer in spite of normovolemia and proper anesthetic management.

Aged↗
PubMedDate not supplied

Thyrotoxic hypokalemic periodic paralysis: six cases in non-Asian patients.

OBJECTIVE: To describe six cases of thyrotoxic hypokalemic periodic paralysis (THPP) in non-Asian men. METHODS: We present six cases of THPP, including clinical and laboratory findings, treatment, and outcome, and review the related literature. RESULTS: Hypokalemic periodic paralysis is a relatively common occurrence in Asian men with thyrotoxicosis; however, it is unusual in non-Asian patients with thyrotoxicosis. Among our six patients--four Caucasians, one African-American, and one Hispanic--the precipitating factors, initial manifestations, and clinical course varied. In general, treatment with 131 I or potassium eliminated the paralytic episodes. CONCLUSION: THPP needs to be distinguished from nonthyrotoxic hypokalemic periodic paralysis. Although THPP is unusual in non-Asian men, it must be recognized because of the severe and potentially fatal complications, which are reversible with potassium replacement and antithyroid therapy.

Journal Article↗