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At least 1,225 records · Page 68Linked to original sources
PubMed2001

Sodium channel inactivation defects are associated with acetazolamide-exacerbated hypokalemic periodic paralysis.

A novel mutation in a family with hypokalemic periodic paralysis is described. The mutation R672S is located in the voltage sensor segment S4 of domain II in the SCN4A gene encoding the human skeletal muscle voltage-gated sodium channel. Functional expression of the R672S channels in human embryonic kidney 293 cells revealed a small but significant hyperpolarizing shift in the steady-state fast inactivation, and a dramatic enhancement in channel slow inactivation. These two defects are mainly due to a slow recovery of the mutant channels from fast and/or slow inactivation. Our data may help explain the mechanism underlying hypokalemic periodic paralysis and the patient's worsening from acetazolamide.

Acetazolamide↗
PubMed2006

Recovery from paralysis in adult rats using embryonic stem cells.

OBJECTIVE: We explored the potential of embryonic stem cell-derived motor neurons to functionally replace those cells destroyed in paralyzed adult rats. METHODS: We administered a phosphodiesterase type 4 inhibitor and dibutyryl cyclic adenosine monophosphate to overcome myelin-mediated repulsion and provided glial cell-derived neurotrophic factor within the sciatic nerve to attract transplanted embryonic stem cell-derived axons toward skeletal muscle targets. RESULTS: We found that these strategies significantly increased the success of transplanted axons extending out of the spinal cord into ventral roots. Furthermore, transplant-derived axons reached muscle, formed neuromuscular junctions, were physiologically active, and mediated partial recovery from paralysis. INTERPRETATION: We conclude that restoration of functional motor units by embryonic stem cells is possible and represents a potential therapeutic strategy for patients with paralysis. To our knowledge, this is the first report of the anatomical and functional replacement of a motor neuron circuit within the adult mammalian host.

Age Factors↗
PubMed1989

Hyperkalemic periodic paralysis in Gordon's syndrome: a possible defect in atrial natriuretic peptide function.

We present the case of a 14-year-old boy who had secondary hyperkalemic periodic paralysis caused by Gordon's syndrome. This syndrome consists of hypertension, tubular acidosis, and hyperkalemia with normal glomerular filtration rate. The pathophysiological mechanism is still unknown. Pathophysiological studies suggest that in this disorder the kidney lacks sensitivity to atrial natriuretic peptide. After treatment with hydrochlorothiazide, serum potassium and plasma aldosterone values, plasma renin activity, and blood pressure became normal and the attacks of periodic paralysis disappeared.

Adolescent↗
PubMed1993

Acute motor axonal neuropathy: a frequent cause of acute flaccid paralysis in China.

In northern China, annual epidemics of acute-onset flaccid paralysis diagnosed clinically as Guillain-Barré syndrome have been recognized for at least 20 years. On the basis of an historical analysis of more than 3,200 patients, distinctive features include most cases occurring during the summer months among children and young adults, most of whom reside in rural areas. Of 90 patients with acute flaccid paralysis, 88 had a distinctive pattern that shares clinical and cerebrospinal fluid findings with demyelinating Guillain-Barré syndrome, but that differs from Guillain-Barré syndrome physiologically and pathologically. The clinical course is marked by rapidly progressive ascending tetraparesis, often with respiratory failure, but without fever, systemic illness, or sensory involvement. Cerebrospinal fluid is acellular, and elevations of protein content occur in the second or third week of illness. Electrodiagnostic studies show normal motor distal latencies and limb conduction velocities, but reduced compound muscle action potential amplitudes. Sensory nerve action potentials and, when elicitable, F waves are within the range of normal. Recovery is usually good. Autopsy studies have shown Wallerian-like degeneration of motor fibers. These studies establish that this is a distinctive syndrome, distinguishable from poliomyelitis and demyelinating Guillain-Barré syndrome.

Acute Disease↗
PubMedDate not supplied

Early gold weight lid implant for rehabilitation of faulty eyelid closure with facial paralysis: an alternative to tarsorrhaphy.

Although tarsorrhaphy has been the mainstay of treatment for lagophthalmus associated with facial paralysis, it has many drawbacks which make it a less than ideal procedure. Gold weight implantation is a functionally and cosmetically superior alternative in many patients. Eighteen patients with both reversible and irreversible facial (eyelid) paralysis underwent early gold weight implantation for rehabilitation of faulty eyelid closure with satisfactory results. The advantages and disadvantages of this technique, when compared with other methods of correcting paralytic lagophthalmus, are discussed.

Blinking↗
PubMed1990

Bone blood flow after spinal paralysis in the rat.

The goal of this study was to investigate the acute and chronic effects of paralysis induced by spinal cord section or sciatic neurotomy on bone blood flow in the rat. Regional bone blood flow was measured in the early stage with the hydrogen washout technique and the change of whole bone blood flow was measured in the early and the late stages with the radioactive microsphere technique. Four to 6 h after cordotomy at the level of the 13th thoracic vertebra, the regional bone blood flow in the denervated tibia increased significantly (p less than 0.01). After hemicordotomy with rhizotomy at the same level, the regional bone blood flow in the denervated tibia increased significantly (p less than 0.05) 6 h postoperatively. The whole bone blood flow in the denervated tibia had also increased significantly (p less than 0.05) at 6 h and at 4 and 12 weeks postoperatively. After sciatic neurotomy, the regional and the whole bone blood flow in the paralytic tibia did not change significantly. The present study demonstrated that monoplegic paralysis caused an increase in bone blood flow in the denervated hind limb from a very early stage. It was suggested that the spinal nervous system contributed to the control of bone blood flow.

Animals↗
PubMed1991

Variables affecting disc size in the lumbar spine of rabbits: anesthesia, paralysis, and disc injury.

Methods have been developed that permit repetitive radiographic measurement of the lumbar intervertebral disc space in a rostral-caudal direction (width) in the anesthetized laboratory rabbit. Using isolated control discs and injured discs in which narrowing has been induced for chronic and acute periods, the widths of the lumbar intervertebral disc spaces determined ratio-graphically correlate with widths determined histologically (p less than 0.000, r = 0.75). Both an increase (widening) and a decrease (narrowing) in disc width were observed using radiography after different experimental treatments. Anesthesia and lower-body paralysis (an experimentally induced inability to bear weight on and to perceive a pinch stimulus in hind limbs) caused widening of the discs: anesthesia causing a general widening throughout the lumbar spine and lower-body paralysis causing a specific widening low in the lumbar spine. Both disc injection and piercing the disc with needles to recover nucleus pulposus material caused narrowing of the discs. Acridine-orange injection induced a narrowing accompanied by osteophytosis. Experimentally induced narrowing at L4-5 (the result of injury to the disc) resulted in narrowing also at L2-3. These findings are consistent with the hypothesis that in vivo disc-width size in the young rabbit depends on both the quantity of nucleus pulposus material and the force-generating activities of the adjacent spinal muscles, and that disc injury at one level stimulates narrowing at other levels.

Acepromazine↗
PubMed1983

Phrenic nerve graft for bilateral vocal cord paralysis.

For bilateral vocal cord paralysis, the phrenic nerve graft procedure has been used in five patients. Data from four of these patients suggest that the technique may in some way improve the glottic airway without long-term diaphragmatic paralysis. No patient to date has demonstrated visible inspiratory vocal cord abduction however. The mechanism of action, if any, is unclear at this time, and we have no electromyographic nor other physiologic data to confirm that true posterior cricoarytenoid muscle reinnervation has taken place.

Adult↗
PubMed1983

Recurrent alternobaric facial paralysis resulting from scuba diving.

Only one detailed case of alternobaric (referring to alternating pressure changes) facial paralysis resulting from scuba diving has been reported in the world literature. This article describes the dive profile and clinical course of a commercial diver who developed facial paralysis after scuba diving on three different occasions. Probable pathophysiologies, identification of the diver at risk, treatment and prophylactic measures are reviewed. Additional cases from the literature due to scuba diving and flying are cited.

Acoustic Impedance Tests↗
PubMed1983

Transient paralysis of the diaphragm following radical neck surgery.

We have observed transient diaphragmatic paralysis with high alveolar to arterial oxygen partial pressure difference following radical neck surgery. Patients required supplemental oxygen for maintenance of arterial oxygenation. Patients following radical and neck surgery should be followed with chest roentgenograph to exclude pneumothorax and diaphragmatic paralysis and arterial blood gases in the immediate postoperative period.

Aged↗
PubMed1991

Update: ansa cervicalis to recurrent laryngeal nerve anastomosis for unilateral laryngeal paralysis.

Twenty cases of unilateral laryngeal paralysis are reported. Satisfactory follow-up intervals and data (videostroboscopy and glottographic analysis) were available on 12 patients. The excellent to normal phonatory quality achieved in many of these patients indicates that the ansa cervicalis to recurrent laryngeal nerve anastomosis is the procedure of choice in selected patients with unilateral vocal cord paralysis. Excellent medialization of the paralyzed cord, as well as correction of arytenoid malposition and thyroarytenoid muscle atrophy appear to explain the technique's success, since the reinnervated cord neither abducts nor adducts. We feel that this technique is the procedure of choice in younger patients, or those who use their voices professionally, since the phonatory quality achieved is superior to Teflon injection or Isshiki thyroplasty, and the technique is reversible.

Humans↗
PubMed1979

Lip transposition in patients with facial paralysis.

Since facial reanimation is not always possible in patients with facial paralysis, one must have alternate methods of reconstruction available. Satisfactory static reconstruction of the face may be accomplished with the use of a brow lift, tarsorrhaphy, and correction of the paralyzed mouth. Transposition of the corner of the mouth utilizing the Z-plasty technique has proven to be an effective method to correct the drooling and garbled speech associated with facial paralysis. When combined with a brow lift and tarsorrhaphy, symmetry of the facial appearance while at rest has also been obtained.

Aged↗
PubMed2002

Hypokalemic periodic paralysis associated with malignant hyperthermia.

Hypokalemic periodic paralysis is in most cases related to mutations within the dihydropyridine receptor gene. Susceptibility to malignant hyperthermia has been linked to a different part of the same gene, but is more frequently caused by mutations within the ryanodine receptor gene. We report the association of the two disorders in a patient for whom the most frequent mutations for hypokalemic periodic paralysis were not found. This suggests further genetic heterogeneity of this condition, the interest of this case residing in the known coupling between dihydropyridine and ryanodine receptors.

Adult↗
PubMed2006

Adaptive response of human tendon to paralysis.

To gain insight into the adaptive response of human tendon to paralysis, we compared the mechanical properties of the in vivo patellar tendon in six men who were spinal cord-injured (SCI) and eight age-matched, able-bodied men. Measurements were taken by combining dynamometry, electrical stimulation, and ultrasonography. Tendon stiffness and Young's modulus, calculated from force-elongation and stress-strain curves, respectively, were lower by 77% (P < 0.01) and 59% (P < 0.05) in the SCI than able-bodied subjects. The cross-sectional area (CSA) of the tendon was 17% smaller (P < 0.05) in the SCI subjects, but there was no difference in tendon length between the two groups. Our results indicate that paralysis causes substantial deterioration of the structural and material properties of tendon. This needs to be taken into consideration in the design of electrical stimulation protocols for rehabilitation and experimental purposes, and when interpreting changes in the contractile speed of paralyzed muscle.

Adaptation, Physiological↗
PubMed1992

Improvement of the exercise test after therapy in thyrotoxic periodic paralysis.

The diagnosis of periodic paralysis (PP) can be aided by demonstrating a decrease in compound motor action potential (CMAP) amplitude after several minutes of exercise. We report a case of secondary hypokalemic PP due to thyrotoxicosis in which the decrease in the CMAP amplitude after exercise dramatically improved after treatment, when a euthyroid state was achieved. The exercise test is a useful electrophysiologic means of monitoring the neuromuscular status of patients with thyrotoxic periodic paralysis prior to, and after treatment of the thyrotoxicosis.

Action Potentials↗
PubMed1993

Vocal cord paralysis: clinical and electrophysiologic features.

Vocal cord paralysis may occur in isolation or as part of a constellation of findings in neurological disease. We investigated the pathophysiology of these disorders with laryngeal electromyography (LEMG). We studied 44 patients with idiopathic vocal cord paralysis, confirmed by laryngoscopy. The major LEMG finding, present in 29 vocal cords, was evidence of active or chronic denervation in the thyroarytenoid (TA), indicating recurrent laryngeal neuropathy. Denervation of the cricothyroid (CT) in 5 patients indicated superior laryngeal neuropathy. TA and CT involvement in 1 patient indicated proximal laryngeal or vagus nerve damage. LEMG was performed in 48 patients with other laryngeal disorders. LEMG proved to be a safe and effective procedure in the diagnosis of laryngeal neuropathy as distinguished from supranuclear and mechanical disorders of the larynx.

Electromyography↗
PubMed1994

Elimination of superfluous neuromuscular junctions in rat calf muscles recovering from botulinum toxin-induced paralysis.

In order to determine the fate of the superfluous neuromuscular junctions (NMJs) formed during the course of botulinum toxin (BoTx)-induced paralysis, we have quantified the change in the total length of the nerve muscle contact area(s) following BoTx injection into rat calf muscles. The results indicate that: (1) at least some of the superfluous NMJs are eliminated following muscle recovery; (2) synapse elimination is a slow process, as 4 months after recovery it was not yet complete; (3) muscles with different content of type I and II fibers follow a different time course during synapse formation and elimination. We further investigated the possibility that the neural cell adhesion molecule (NCAM) would be the element whose loss from the NMJ might play a role in synapse elimination. Using immunofluorescence and immunoelectron microscopy we show that NCAM is exclusively localized between nerve terminals and Schwann cells and not between nerve terminals and muscle. This localization was maintained throughout paralysis and following recovery, suggesting that NCAM does not play a role in synapse elimination.

Animals↗
PubMed2001

Digger wasp versus cricket: mechanisms underlying the total paralysis caused by the predator's venom.

The data presented here describe neurophysiological experiments addressing the question of cellular mechanisms underlying the total paralysis of locomotor behavior in crickets occurring after being stung by females of the digger wasp species Liris niger. The Liris venom effects have been studied by both in vivo recordings from identified neurons of the well-described giant fiber pathway and in vitro recordings from cultured neurons isolated from the terminal ganglion of crickets. The total paralysis of the prey is characterized by a general block of action potential generation as well as by a block of synaptic transmission. Intracellular recordings from neurons in intact ganglia under single electrode voltage-clamp conditions, as well as whole-cell patch-clamp recordings from cultured cricket neurons consistently show that the block of action potential generation by the Liris venom is due to a block of voltage-gated sodium inward currents in neurons of the stung ganglia. Furthermore, our data provide evidence that the Liris venom also blocks calcium currents in identified neurosecretory neurons. On the other hand, outward currents are not affected by the Liris venom. The in vitro recordings suggest that the Liris venom contains active venom components, which, at least for the observed block of inward currents, do not require a metabolic modification. Because venom application does not affect the ACh-induced EPSPs in giant interneurons, the Liris venom does not seem to influence the postsynaptic ACh receptors. The possible pre- and postsynaptic sites of venom action and the functional consequences on synaptic transmission within the giant fiber system are discussed.

Animals↗