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PubMed2005

[An unusual diagnostic of quadriparesia: hyperkalemic paralysis. Report of four non-familial cases].

INTRODUCTION: The classical cause of hyperkalemic paralysis is the hereditary hyperkalemic paralysis. Very rarely, secondary forms of hyperkalemic paralysis have been reported. EXEGESIS: Four cases of acute paralysis mimicking Guillain-Barre syndrome in three cases and revealing severe hyperkalemia are presented. All the four patients had moderate chronic renal insufficiency. In two cases, the patients received spironolactone. One case was associated with lysis syndrome. All the 4 cases dramatically improved with the treatment of hyperkalemia. CONCLUSION: These cases pointed out the possibility for acute peripheral paralysis to reveal severe hyperkalemia.

Aged↗
PubMed2000

Prediction of walking function in stroke patients with initial lower extremity paralysis: the Copenhagen Stroke Study.

OBJECTIVES: The majority of stroke patients with initial leg paralysis do not regain independent walking. We characterize the minority who, despite initial leg paralysis, regained independent walking. DESIGN: Consecutive and community based. SETTING: A stroke unit receiving all stroke patients from a well-defined community. PATIENTS: A total of 859 acute stroke patients; 157 (15%) initially had leg paralysis. MAIN OUTCOME MEASURES: Scandinavian Stroke Scale (SSS) and Barthel index (BI) on admission and weekly during rehabilitation. Univariate and multivariate statistics were considered. RESULTS: Of the 157 patients with initial leg paralysis, 84 (60%) died; 73 (40%) survived. Fifteen (21%) survivors regained walking function (the walking group), and 58 (79%) did not (the nonwalking group). The BI on admission was the only factor of significant predictive value (p < .03). Mean admission BI was 50 in the walking group versus 3 in the nonwalking group (p < .001). Age, gender, lesion size, total SSS score, and comorbidity had no predictive value. Within the first week, the walking group gained 3.2 points in the SSS subscore for leg strength versus 0.5 points in the nonwalking group (p < .02). CONCLUSION: Only 10% of stroke patients with initial leg paralysis regained independent walking. In these patients, BI on admission was high and leg strength improved quickly in the first week.

Aged↗
PubMedDate not supplied

Thyrotoxic periodic paralysis: a case report and review of the literature.

Hypokalemic periodic paralysis occurring in thyrotoxicosis is rare in Caucasians and is not often highlighted as an endocrine emergency. Periodic paralysis, without familial background, manifests only in the thyrotoxic patient. Thyrotoxic periodic paralysis is a self-limiting disorder that is cured by the treatment of the underlying hyperthyroidism. We report an unusual case of acute onset weakness from thyrotoxic periodic paralysis in a young Chinese migrant who had a normal serum potassium level at the time of initial presentation, though on subsequent presentation one week later, he had the typically associated hypokalemia. We also review the literature on thyrotoxic periodic paralysis.

Adult↗
PubMed2001

Sensitivity to diethylether anesthesia of fruit flies primarily depends on the genotypes of the sodium channel gene rather than the states of the membranes and the mechanisms might be different from heat-induced paralysis.

The para locus of Drosophila melanogaster encodes the alpha subunit of a voltage-sensitive sodium channel. Many of the mutants develop paralysis at the high temperature (37 degrees C) and are hypersensitive to diethylether anesthesia. We examined whether the two aspects of the phenotype are mediated by a same mechanism that involves the sodium channel molecule by investigating properties of the three para alleles (para(hd838), para(ts1) and para(ts3)). Larvae of the all para strains showed almost normal sensitivities to diethylether anesthesia while adult flies of them showed hypersensitivities to that in the following manner: para(hd838)<==para(ts1)<para(ts3)<Canton-S. Larvae of the two para strains showed hypersensitivities to heat-induced paralysis in the following manner: para(ts1)=para(ts3)<para(hd838)=Canton-S, while adult flies of the all para strains showed hypersensitivities to that in the following manner: para(ts1)=para(ts3)<para(hd838)<Canton-S. The distinct phenotype of para(hd838) from para(ts1) or para(ts3) observed in the larval and adult heat-induced paralysis, would be the reflection of the difference of the mutation sites between in para(hd838) and para(ts1) or para(ts3). In addition, because the rank of sensitivity in the adult anesthesia and heat-induced paralysis were reversed between para(hd838) and para(ts1) or para(ts3), the mechanisms of diethylether anesthesia and heat-induced paralysis are not the same. There would be the anesthesia-specific mechanisms because the sensitivity to anesthesia became more remarkable in para(hd838) than in para(ts1) or para(ts3). para(hd838) has an insertion of P-element, one of a transposable element, in the second intron of the para sodium channel gene. Excision of the P-element from the para locus of the para(hd838) conferred the flies the wild-typic phenotype and reduction of the para gene in para(hd838) dramatically enhanced the hypersensitivity to anesthesia, suggesting that the phenotype of the strain was caused exclusively by the mutation of the para locus. The susceptibility to anesthesia also depends on the temperature at which the flies were assayed, not at which they were cultured, but the dependence on the assay temperature was smaller than that on the genotype. By these findings we could assure that the sensitivity to diethylether anesthesia of para(hd838) primarily depends on the genotypes of the sodium channel gene rather than other reasons such as the fluidity of the membranes.

Journal Article↗
PubMed1993

Potassium channels in hypokalaemic periodic paralysis: a key to the pathogenesis?

1. A possible role for the ATP-sensitive potassium channels in the pathogenesis of hypokalaemic periodic paralysis was investigated. 2. We assessed insulin release and muscle strength after intravenous glucose loading with and without the potassium channel opener pinacidil and the potassium channel blocker glibenclamide in three patients with hypokalaemic periodic paralysis and in a pair of matched control subjects for each patient. 3. A significantly higher initial insulin response (1.5-30 min) was found in the patients with hypokalaemic periodic paralysis in comparison with the control subjects. During potassium channel blocking with glibenclamide the insulin release was more enhanced in patients than in control subjects. On the other hand, the potassium channel opener pinacidil impaired the insulin release in healthy control subjects but not in patients. The serum glucose levels showed no differences between patients and control subjects. In one of the patients with hypokalaemic periodic paralysis glucose loading resulted in a fall in muscle strength, which did not occur during the administration of pinacidil. 4. These findings suggest a disturbance in the ATP-sensitive potassium channel in patients with hypokalaemic periodic paralysis, which is not limited to pancreatic beta cells, but may be also involved in the abnormal behaviour of skeletal muscle.

Adult↗
PubMed2005

Role of T-lymphocyte subsets in facial nerve paralysis owing to the reactivation of herpes simplex virus type 1.

CONCLUSION: Although both T-cell subsets are essential for inhibiting HSV-1 reactivation in the GG, CD4 + T cells play a more important role in host defense against virus replication. OBJECTIVE: To elucidate the host immunological factors that participate in herpes simplex virus type 1 (HSV-1) reactivation in the geniculate ganglia (GG) and lead to facial paralysis, we developed a mouse model of facial paralysis that involved the reactivation of HSV-1 following general immune suppression. MATERIAL AND METHODS: Eight weeks after recovery from primary facial paralysis caused by inoculating the auricle with HSV-1 the auricle was scratched and mice (n = 69) were given an i.p. injection of either anti-CD4 (n = 46) or anti-CD8 (n = 23) monoclonal antibody to deplete specific T-lymphocyte subsets. Following this reactivation procedure, the rate of recurrent facial paralysis was compared between the two models. The GG were examined histopathologically and using polymerase chain reaction to detect HSV-1 DNA. RESULTS: Facial paralysis developed in 42% of mice in the anti-CD4 model and in 13% in the anti-CD8 model. HSV-1 DNA was detected in 50% of the mice in both models. Histopathologically, neurons were destroyed in parts of the GG and numerous virus particles were seen in the surviving neurons.

Animals↗
PubMed2003

Electrocardiographic manifestations in patients with thyrotoxic periodic paralysis.

BACKGROUND: Thyrotoxic periodic paralysis (TPP) commonly precedes the overt symptoms and signs of hyperthyroidism and may be misdiagnosed as other causes of paralysis (non-TPP). Because the cardiovascular system is very sensitive to elevation of thyroid hormone, we hypothesize that electrocardiographic manifestations may aid in early diagnosis of TPP. METHODS: We retrospectively identified 54 patients who presented to the emergency department (ED) with hypokalemic paralysis during a 3.5-year period. Thirty-one patients had TPP and 23 patients had non-TPP, including sporadic periodic paralysis, distal renal tubular acidosis, diuretic use, licorice intoxication, primary hyperaldosteronism, and Bartter-like syndrome. Electrocardiograms during attacks were analyzed for rate, rhythm, conduction, PR interval, QRS voltage, ST segment, QT interval, U waves, and T waves. RESULTS: There were no significant differences in age, sex distribution, and plasma K+ concentration between the TPP and non-TPP groups. Plasma phosphate was significantly lower in TPP than non-TPP. Heart rate, PR interval, and QRS voltage were significantly higher in TPP than non-TPP. Forty-five percent of TPP patients had first-degree atrioventricular block compared with 13% in the non-TPP group. There were no significant differences in QT shortening, ST depression, U wave appearance, or T wave flattening between the 2 groups. CONCLUSION: Relatively rapid heart rate, high QRS voltage, and first-degree AV block are important clues suggesting TPP in patients who present with hypokalemia and paralysis.

Acidosis, Renal Tubular↗
PubMed1998

Paralysis only slightly reduces the febrile response to interleukin-2 during isoflurane anesthesia.

BACKGROUND: Fever sometimes occurs during anesthesia. However, it is rare considering how often pyrogenic causes are likely to be present and how common fever is after surgery. This low incidence results in part from dose-dependent inhibition of fever by volatile anesthetics. Paralysis, however, may contribute by preventing shivering and the associated increase in metabolic heat production. Therefore the authors tested the hypothesis that paralysis during anesthesia decreases the febrile response to pyrogen administration. METHODS: Seven volunteers each participated on two study days. They were given 30 IU/g intravenous interleukin-2, followed 90 min later by an additional 70 IU/g dose. Anesthesia was induced 30 min after the second dose and maintained for 6 h with 0.6 minimum alveolar concentration isoflurane. The volunteers were randomly assigned to (1) paralysis with vecuronium or (2) no muscle relaxants. Body heat content and distribution were determined from measured tissue and skin temperatures. Data are presented as mean +/- SD; P < 0.05 was considered significant. RESULTS: There was no clinically important difference in peak core (tympanic membrane) temperatures on the unparalyzed (37.6+/-0.9 degrees C) and paralyzed (37.2+/-0.6 degrees C) days. Core heat content increased 1.2+/-0.7 kcal/kg over the last 5 h of anesthesia on the unparalyzed day, but only by 0.9+/-0.4 kcal/kg when the volunteers were paralyzed. Peripheral tissue heat content increased 0.1+/-1.1 kcal/kg on the unparalyzed day but decreased 1.1+/-0.7 kcal/kg when the volunteers were paralyzed. Consequently, body heat content increased 1.3+/-1.3 kcal/kg on the unparalyzed day but decreased significantly by 0.2+/-0.8 kcal/kg when the volunteers were paralyzed. CONCLUSIONS: Paralysis prevented shivering from increasing the metabolic rate. Consequently, body heat content decreased during paralysis, whereas otherwise it increased. Thermoregulatory vasoconstriction was nonetheless able to maintain similar peak and integrated core temperatures on each study day. Administration of muscle relaxants thus is not the primary explanation for the relative paucity of intraoperative fever.

Anesthesia↗
PubMed2006

Flexor pollicis brevis adductorplasty: an alternative method in ulnar nerve paralysis.

Loss of pinch power associated with loss of coordinated movement of thumb and index fingers is the major disability in patients with ulnar nerve paralysis. Several tendon transfer methods utilizing different donor muscles have been used to restore adductor pollicis muscle function in ulnar nerve paralysis. In this paper, we discuss the transfer of flexor digitorum brevis muscle to the tendon of adductor pollicis muscle as an alternative method to restore key pinch in ulnar nerve paralysis. The technique was applied to 4 patients with ulnar nerve paralysis. Before clinical application, an anatomic study was carried out in 6 cadaver hands. In cadavers, radial and ulnar arteries were injected with latex and arterial pedicles of flexor pollicis brevis muscle were dissected under 4x magnification. Also, motor branches from the median nerve were shown at the entrance point to the muscle. In surgical practice, the superficial head of the muscle is detached from its insertion and the minor pedicle of the muscle is cut. Muscle is dissected proximally up to two thirds of its length. The dominant pedicle of the muscle originating from superficial palmar arcus is preserved, and the muscle is sutured to the tendon of the adductor pollicis muscle close to its insertion. Patients were evaluated in terms of key pinch strength preoperatively and at the postoperative sixth month using a pinch meter (Chattanooga Group, Inc). Key pinch strengths were recorded and expressed as percentage of the strength of the contralateral uninvolved hand. Mean key pinch strength of our patients was 29.7%. In conclusion, we believe in that flexor pollicis brevis adductorplasty may be an alternative method for restoration of adductor pollicis muscle function in ulnar nerve paralysis.

Adult↗
PubMed1970

Function of the Reticuloendothelial System IV. Evidence for Two Types of Particle-Induced Reticuloendothelial Paralysis.

Reticuloendothelial system (RES) phagocytosis has been quantitated after intravenous injection of two different sets of particles by determining the clearance rate of subsequently injected identical or nonidentical particles. Injection of carbon produced a biphasic RES paralysis consisting of an early transient phase followed by a delayed sustained phase. The two phases were separated by a distinct interval of greatly augmented clearance rates. The injection of aggregated albumin was followed only by a single period of depressed clearance, which corresponded to the first phase of carbon-induced inhibition. This first phase, designated immediate RES paralysis, was initiated by particle injection and its duration was related to the rate of particle removal, to the dose of particles injected, and to the presence of the particles in the circulation. The second phase, designated delayed RES paralysis, began sometime after the particles had been engulfed by the cells, was independent of the rate of particle removal, and persisted without the presence of measurable particles in the circulation. The evidence indicates that the immediate paralysis arises from a competition between the particles in the circulation, whereas the delayed paralysis arises from a cellular derangement inhibitory to further phagocytosis. In contrast to the usual description of RES blockade as a single sustained period of depression, the present experiments indicate that the phenomenon has two phases which can be dissociated in time and mechanism.

Journal Article↗
PubMed1998

Secondary hyperkalaemic paralysis.

Besides the hereditary hyperkalaemic paralysis, a secondary form exists which often mimicks Guillain-Barre syndrome. A 62 year old patient is reported on who developed severe hyperkalaemic paralysis on the basis of mild renal failure and additive spironolactone intake. Neurophysiological examinations disclosed normal muscle fibre activity but delayed nerve conduction velocities indicating that the mechanism underlying secondary hyperkalaemic paralysis is different from channelopathies. Haemodialysis led to complete recovery. Review of the medical literature showed that spironolactone intake is the most common cause of secondary hyperkalaemic paralysis. Typical symptoms are flaccid tetraplegia sparing the cranial nerves with only mild or lacking sensory impairment. Symptoms promptly resolve after haemodialysis or after glucose and insulin infusion. Only three out of 18 patients reviewed died, because of cardiopulmonary complications. Thus the prognosis of secondary hyperkalaemic paralysis is good.

Diagnosis, Differential↗
PubMed1979

Regulation of plasma potassium in hyperkalemic periodic paralysis.

Hyperkalemic periodic paralysis is frequently considered a disorder in which episodes of weakness and an attendant rise in plasma potassium interrupt a baseline of normal strength and potassium. We studied venous potassium throughout a 36-hour period in two patients with hyperkalemic periodic paralysis and in nine normals under rigidly controlled conditions. At no time did the patients with periodic paralysis have an attack of weakness, but their mean potassium concentrations were above the normal range for 33 to 36 hours. In hyperkalemic periodic paralysis, the postprandial change in potassium relative to insulin release exceeded normal. There appears to be a continuous alteration in potassium regulation in our patients with hyperkalemic periodic paralysis.

Female↗
PubMed1999

Defective slow inactivation of sodium channels contributes to familial periodic paralysis.

OBJECTIVE: To evaluate the effects of missense mutations within the skeletal muscle sodium (Na) channel on slow inactivation (SI) in periodic paralysis and related myotonic disorders. BACKGROUND: Na channel mutations in hyperkalemic periodic paralysis and the nondystrophic myotonias interfere with the normally rapid inactivation of muscle Na currents following an action potential. This defect causes persistent inward Na currents that produce muscle depolarization, myotonia, or onset of weakness. Distinct from fast inactivation is the process called SI, which limits availability of Na channels on a time scale of seconds to minutes, thereby influencing muscle excitability. METHODS: Human Na channel cDNAs containing mutations associated with paralytic and nonparalytic phenotypes were transiently expressed in human embryonic kidney cells for whole-cell Na current recording. Extent of SI over a range of conditioning voltages (-120 to +20 mV) was defined as the fraction of Na current that failed to recover within 20 ms at - 100 mV. The time course of entry to SI at -30 mV was measured using a conditioning pulse duration of 20 ms to 60 seconds. Recovery from SI at -100 mV was assessed over 20 ms to 10 seconds. RESULTS: The two most common hyperkalemic periodic paralysis (HyperPP) mutations responsible for episodic attacks of weakness or paralysis, T704M and M1592V, showed clearly impaired SI, as we and others have observed previously for the rat homologs of these mutations. In addition, a new paralysis-associated mutant, I693T, with cold-induced weakness, exhibited a comparable defect in SI. However, SI remained intact for both the HyperPP/paramyotonia congenita (PMC) mutant, A1156T, and the nonparalytic potassium-aggravated myotonia (PAM) mutant, V1589M. CONCLUSIONS: SI is defective in a subset of mutant Na channels associated with episodic weakness (HyperPP or PMC) but remains intact for mutants studied so far that cause myotonia without weakness (PAM).

Action Potentials↗
PubMedDate not supplied

[A rare case of hypokalemic thyrotoxic periodic paralysis in a Caucasian patient with Basedow's disease].

Thyrotoxicosis periodic paralysis is a very rare complication of thyrotoxicosis in whites, but is more frequently reported in oriental and latin american populations and associates the clinical picture of hyperthyroidism with bouts of paralysis due to hypokalemia. The hypokalemia is due to a massive shift of potassium from the extra- to the intracellular compartment. In this paper the authors report a case of 34-years old white male with an history of hypokalemic periodic paralysis and hyperthyroidism, studied with potassium, thyroid hormone, TSH and thyroid antibodies sampling and thyroid ultrasonography with color-Doppler. The restoration of a euthyroid state with methimazole and propranolol was effective in preventing further episodes of paralysis. It is suggested that the mechanism for the development of the hypokalemic periodic paralysis is the intracellular blockade of potassium by the surplus of thyroid hormones.

Adult↗
PubMed2001

[Idiopathic facial paralysis (Bell's palsy): a study of 180 patients].

The objective of this study was to analyze some clinical and epidemiologic aspects, as well as the follow up of 180 patients with Bell's palsy. In the study population there was a predominance of female (66.7%). Two peaks of incidence in the age distribution were identified: third-fourth and sixth decades of life. In the group of 180 patients there were 198 events of facial paralysis, 17 recurrences and in one patient the paralysis was bilateral at the onset. In 15 patients (8.3%) there were recurrences of the facial paralysis, in 12 cases (70.6%) the recurrences were ipsilateral. The left side of the face was involved in 55.6% of the cases. In eight patients the paralysis occurred during pregnancy (n=5) or puerperium (n=3). As associated conditions we found: arterial hypertension (11.7%), diabetes mellitus (11.1%), pregnancy or puerperium (4.4%; 6.7% in the women), and neurocysticercosis (1.1%). In 72.8% of the cases no association with such conditions was found. In 22.8% of the patients some kind of sequelae were identified: hemifacial spasm (12.8%), partial recovery of the motor deficit (10.6%), syndrome of the crocodile tears (3.3%), sincinetic contraction (2.8%), and the Marcus Gunn inverse phenomenon (1.1%). In conclusion, this study shows that the idiopathic facial paralysis may lead to important sequelae in more than 20% of the patients.

Adolescent↗
PubMed2003

[Results of inferior oblique muscle surgery in superior oblique paralysis].

The aim of this study was to evaluate the results of inferior oblique muscle recession in certain cases of superior oblique paralysis. Twenty-three patients with moderate hyperaction of the inferior oblique muscle, secondary to paralysis of the superior oblique muscle, in whom a recession of the ipsilateral inferior oblique was applied were enrolled in this study. These cases were selected among those with congenital superior oblique paralysis and infantile nontraumatic paralysis and those of unknown origin. Isolated recession of the inferior oblique muscle achieved a mean decrease in 8.69 +/- 2.05 D in hypertropia in the primary position. In 19 cases out of 23 (82.6%) who received isolated recession of the inferior oblique muscle, a vertical deviation equal to or less than 4 PD was obtained, showing the efficacy of this method in the surgical treatment of the cases with superior oblique paralysis and a moderate inferior oblique hyperaction.

Adolescent↗
PubMed2005

The efficacy of steroids in idiopathic facial nerve paralysis: an open, randomized, prospective controlled study.

OBJECTIVES: Although corticosteroid therapy is widely used in idiopathic facial nerve paralysis, its efficacy has not been clearly demonstrated. This study was designed to evaluate the role of steroids in idiopathic facial nerve paralysis. PATIENTS AND METHODS: The study included 56 patients (29 males, 27 females; mean age, in men 44.1, in women 40.3 years) with a diagnosis of idiopathic facial nerve paralysis. Within the first three days after the onset of symptoms, the patients were randomly assigned to two groups to receive either steroids or other medications for the prevention of ocular complications or to provide pain relief. The severity of facial paralysis was evaluated using the House-Brackmann classification before and after three and six weeks of the treatment. Regression to stage 1 or 2 disease was regarded as a successful response. RESULTS: Although the initial response to steroid therapy seemed to be better, the results at the end of three and six weeks of the treatment were not statistically different from those of patients receiving other supportive treatments (p>0.05). CONCLUSION: Further studies with large patient series are needed to clarify the use of steroids in the treatment of idiopathic facial nerve paralysis.

Administration, Oral↗
PubMed1991

The effects of paralysis on skeletal development in the chick embryo. I. General effects.

In order to investigate further the effects of paralysis on skeletal development in the chick embryo, paralysis was induced at 6 days of incubation by dropping 0.2% solution of decamethonium bromide onto the chorioallantoic membrane and maintaining paralysis through to 20 days of incubation. General effects of paralysis included lower body weight, marked subcutaneous oedema, twisting of the neck to the right with marked rigidity, and protrusion of the lower beak beyond the upper. Skeletal abnormalities included cartilaginous and later bony fusion between cervical vertebrae and distortion of scapula and pubis. Long bones were normal in their general form but showed marked reductions in full length and in length of the calcified diaphysis. The patella occasionally underwent chondrification, unlike the tibial cartilage at the tarsus. Reduction in length of the bones of both jaws occurred but was substantially greater in the upper, resulting in the protrusion of the lower. Ossification times of most skeletal elements were little affected by paralysis but some centres appearing nearer the end of incubation showed slight delay in their times of appearance.

Animals↗