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PubMed1998

Sleep paralysis and hallucinosis.

Background: Sleep paralysis is one of the many conditions of which visual hallucinations can be a part but has received relatively little attention. It can be associated with other dramatic symptoms of a psychotic nature likely to cause diagnostic uncertainty. Methods and results: These points are illustrated by the case of a young man with a severe bipolar affective disorder who independently developed terrifying visual, auditory and somatic hallucinatory episodes at sleep onset, associated with a sense of evil influence and presence. The episodes were not obviously related to his psychiatric disorder. Past diagnoses included nightmares and night terrors. Review provided no convincing evidence of various other sleep disorders nor physical conditions in which hallucinatory experiences can occur. A diagnosis of predormital isolated sleep paralysis was made and appropriate treatment recommended. Conclusions: Sleep paralysis, common in the general population, can be associated with dramatic auxiliary symptoms suggestive of a psychotic state. Less common forms are either part of the narcolepsy syndrome or (rarely) they are familial in type. Interestingly, sleep paralysis (especially breathing difficulty) features prominently in the folklore of various countries.

Journal Article↗

PubMed1986

Computer-controlled muscle paralysis with atracurium in the sheep.

Paralysis was maintained in sheep by computer-controlled infusion of atracurium, using the integrated electromyogram as a measure of neuromuscular transmission. A number of experiments were conducted to ascertain the average infusion rate required to achieve a given level of paralysis for one hour. Each experiment yielded a point on a plot of paralysis versus infusion rate. A dose-response curve based upon a simple model of drug receptor interaction at the neuromuscular junction was fitted to the experimental points by least squares and is able to provide a useful explanation of clinically observed behaviour. The recovery time was also measured in each experiment and plotted against both prior level of paralysis and prior average infusion rate.

Animals↗

PubMed1994

Omeprazole potentiates atracurium and succinylcholine paralysis in vivo in rats.

We examined the effect of proton pump inhibitor omeprazole on neuromuscular paralysis induced with either nondepolarizing or depolarizing neuromuscular blocking drugs in anesthetized and mechanically ventilated rats. Neuromuscular paralysis, as judged by tibialis anterior muscle twitch tension in response to sciatic nerve stimulation, was maintained at about 50% with intravenous (i.v.) bolus and infusion regimens of either atracurium or succinylcholine. Omeprazole, 0.5, 1, and 10 mg/kg i.v., was then administered at 10-min intervals while the infusion of the neuromuscular blocker was continued. Omeprazole at all three doses increased the steady-state neuromuscular paralysis produced with either atracurium (pre-omeprazole versus final post-omeprazole paralysis; mean +/- SE, n = 6, 53.0% +/- 2.3% vs 80.0% +/- 5.3%) or succinylcholine (50.8% +/- 1.5% vs 86.4% +/- 5.1%). Omeprazole, 0.5, 1.0, and 10 mg/kg i.v., given directly and without any neuromuscular blocker, produced approximately 5% depression of the muscle twitch response. Omeprazole, i.v. at human therapeutic doses, alters neuromuscular function and enhances the action of both atracurium and succinylcholine in vivo in rats.

Animals↗

PubMed2003

Acute flaccid paralysis and West Nile virus infection.

Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a peripheral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic features of this paralysis syndrome, we evaluated acute flaccid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hospitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnormalities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropriate treatment and diagnostic testing.

Adult↗

PubMed1999

Activation and inactivation of the voltage-gated sodium channel: role of segment S5 revealed by a novel hyperkalaemic periodic paralysis mutation.

Hyperkalaemic periodic paralysis, paramyotonia congenita, and potassium-aggravated myotonia are three autosomal dominant skeletal muscle disorders linked to the SCN4A gene encoding the alpha-subunit of the human voltage-sensitive sodium channel. To date, approximately 20 point mutations causing these disorders have been described. We have identified a new point mutation, in the SCN4A gene, in a family with a hyperkalaemic periodic paralysis phenotype. This mutation predicts an isoleucine-to-phenylalanine substitution at position 1495 located in the transmembrane segment S5 in the fourth homologous domain of the human alpha-subunit sodium channel. Introduction of the I1495F mutation into the wild-type channels disrupted the macroscopic current inactivation decay and shifted both steady-state activation and inactivation to the hyperpolarizing direction. The recovery from fast inactivation was slowed, and there was no effect on channel deactivation. Additionally, a significant enhancement of slow inactivation was observed in the I1495F mutation. In contrast, the T704M mutation, a hyperkalaemic periodic paralysis mutation located in the cytoplasmic interface of the S5 segment of the second domain, also shifted activation in the hyperpolarizing direction but had little effect on fast inactivation and dramatically impaired slow inactivation. These results, showing that the I1495F and T704M hyperkalaemic periodic paralysis mutations both have profound effects on channel activation and fast-slow inactivation, suggest that the S5 segment maybe in a location where fast and slow inactivation converge.

Cells, Cultured↗

PubMed1999

[Thyrotoxic periodic paralysis].

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism mainly seen in patients of Oriental origin and is rarely encountered in Western countries. TPP clinically resembles familial periodic paralysis with recurrent episodes of weakness or flaccid paralysis of especially the legs. Transient hypokalaemia is regularly observed during attacks and remission can be achieved by administration of potassium salts. The definitive treatment of TPP is to restore euthyroidism. This case describes a thyrotoxic patient who initially presented with periodic paralysis.

Adult↗

PubMed2001

Acute flaccid paralysis associated with circulating vaccine-derived poliovirus--Philippines, 2001.

Three cases of acute flaccid paralysis (AFP) associated with circulating vaccine-derived poliovirus (cVDPV) isolates were reported in the Philippines during March 15-July 26, 2001. The first case-patient, a child aged 8 years from northern Mindanao island (500 miles south of Manila) who had received 3 doses of oral polio vaccine (OPV), had onset of paralysis on March 15. A second child, aged 3 years from Laguna province on Luzon island (60 miles south of Manila) who had received 3 OPV doses, presented with signs of meningitis but no paralysis on July 23. A third child, aged 14 months from Cavite province (25 miles from Manila and 45 miles north of Laguna province) who had received 2 OPV doses, had onset of paralysis on July 26. No patients had traveled outside of their province of residence since birth. Characterization of isolates from the three patients revealed type 1 polioviruses derived from Sabin vaccine strain type 1, with a 3% genetic sequence difference between Sabin 1 vaccine and vaccine-derived poliovirus (VDPV) isolates. The three polioviruses are not identical but are closely related (>99% sequence homology); they also appear to share an identical recombination site with a nonpolio enterovirus in the noncapsid region of the genome.

Child↗

PubMed2002

Clinical profile of acute flaccid paralysis.

This study was done to determine the clinical course, cause and outcome of Acute Flaccid Paralysis (AFP) in children. All AFP cases (< 15 years) in the children's ward of Khulna Medical College Hospital (Bangladesh) were recorded, investigated and followed up to sixty days as a part of passive surveillance. Main outcome variables were vulnerable age group, vaccine status, predominant limb involvement, clinical variants, virus isolation and residual paralysis. Thirty-four children with AFP were admitted in hospital in the last three years with the highest number (14) in 1998. The majority of children belonged to the age group 5-9 years with a male female ratio of 1.3:1. Nearly one third of the cases were either partially vaccinated or not vaccinated at all. The lower limbs bore the brunt of paralysis excepting a few (14.7%). Clinically, Guillain Barre Syndrome was the commonest (47.1%) followed by encephalomyelitis. No poliovirus was isolated from these cases. Residual paralysis was observed in four out of ten cases who returned for follow up. AFP will continue to occur even after eradication of poliomyelitis and Guillain Barre Syndrome is the most important clinical entity for this.

Acute Disease↗

PubMed2003

[Isolated unilateral hypoglossal nerve paralysis: a report of two cases].

Two cases of unilateral isolated hypoglossal nerve paralysis are presented. One patient (aged 56 years, male) had a history of intubation during open cardiac surgery. Spontaneous clinical improvement was observed about 3.5 months after the onset of paralysis. In the other patient (aged 42 years, female), the onset of paralysis dated back 23 years before. Since no etiologic cause could be determined to be associated with hypoglossal nerve paralysis either at the time of onset or on final examinations, the case was thought to be idiopathic. No clinical improvement was observed during a six-month follow-up period.

Adult↗

PubMed2006

[Experimental study of the facial nerve paralysis induced by herpes simplex virus type 1 infection in mice].

OBJECTIVE: To establish an animal model of Bell palsy induced by type I herpes simplex virus (HSV-1) infection and to assess the role and site of HSV-1 in the pathogenesis of facial paralysis. METHODS: Fifty-three female Balb/c mice four-week-old weighted 16-18 g were studied. After scratching the surface of bilateral auricles with a 26-gauge needle, 25 microL HSV-1 with a titer of 6. 7 x 10(7) PFU/ml was inoculated into the right auricle, and the same volume of PBS was placed in the left. As a control, PBS was placed on the bilateral auricles of 4 mice. The HSV-1 DNA in bilateral facial nerve, bilateral brainstem, bilateral trigeminal carrier ganglion, bilateral brain, and blood at different stage was examined with polymerase chain reaction analysis. RESULTS: Thirty-seven animals (75.51%) appeared different degree facial paralysis among the 49 inoculated animals. Fourteen facial paralysis (37.84%) were on the right, 3 (8.11%) on the left, and 20 (54.05%) on the bilateral side. Six animals with facial palsy were recovered during 3-13 days, the average recovery time was 7.83 days. CONCLUSIONS: The existence of HSV-1 in the brainstem and the cerebral cortex is significant for facial paralysis.

Animals↗

PubMed1991

[Association of HLA antigens with thyrotoxic periodic paralysis].

Periodic paralysis is a rare and peculiar complication of thyrotoxicosis, especially in Chinese and Japanese patients. The susceptibility to autoimmune thyroid disease has recently been reported to be strongly linked with certain immunogenetic factors. The objective of this study was to seek a genetic marker by HLA typing in Chinese patients with thyrotoxic periodic paralysis (TPP). The distribution of HLA-A, B, C, DR and DQ antigens in 20 thyrotoxic patients with periodic paralysis and 51 thyrotoxic patients without periodic paralysis was compared with that in 100 controls. The results showed that among the patients with TPP, these was a highly significantly increase of HLA-B51 frequency and B51 appeared to be linked with Cw3 in a state of dysequilibrium.

Adult↗

PubMed1991

[Thyrotoxic periodic paralysis].

Thyrotoxic Periodic Paralysis associates the clinical picture of hyperthyroidism with bouts of paralysis due to hypokalaemia. The hypokalaemia is due to a massive shift of potassium from the extra- to the intracellular compartment. This entity is found almost exclusively in Asian males. The onset of bouts of paralysis is favoured by carbohydrate-rich meals and by strenuous exercise. The bouts cease after correction of the hyperthyroidism. They may be prevented by propranolol. Although the clinical manifestations and treatment of this condition are now well known, the physiopathology remains unclear. This paper presents two cases of thyrotoxic periodic paralysis in young Chinese and Philippine males with hypokalaemia at 1.5 and 2.1 mmol/l respectively. Different hypotheses concerning the physiopathology of the association are discussed.

Adult↗

PubMed1987

Intratracheal suctioning in sick preterm infants: prevention of intracranial hypertension and cerebral hypoperfusion by muscle paralysis.

In a prospective nonrandomized study, using each baby as his or her own control, we compared intracranial pressure (anterior fontanel pressure as measured with the Digilab pneumotonometer), cerebral perfusion pressure, BP, heart rate, transcutaneous Po2, and transcutaneous Pco2 before, during, and after endotracheal suctioning, with and without muscle paralysis, in 28 critically ill preterm infants with respiratory distress syndrome. With suctioning, there was a small but significant increase in intracranial pressure in paralyzed patients (from 13.7 [mean] +/- 4.4 mm Hg [SD] to 15.8 +/- 5.2 mm Hg) but a significantly larger (P less than .001) increase when they were not paralyzed (from 12.5 +/- 3.6 to 28.5 +/- 8.3 mm Hg). Suctioning led to a slight increase in BP with (from 45.3 +/- 9.1 to 48.0 +/- 8.7 mm Hg) and without muscle paralysis (from 45.1 +/- 9.4 to 50.0 +/- 11.7 mm Hg); but there was no significant difference between the two groups. The cerebral perfusion pressure in paralyzed infants did not show any significant change before, during, and after suctioning (31.5 +/- 9.1 mm Hg before v 32.0 +/- 8.7 mm Hg during suctioning), but without muscle paralysis cerebral perfusion pressure decreased (P less than .001) from 32.8 +/- 9.7 to 21.3 +/- 13.1 mm Hg. Suctioning induced a slight decrease in mean heart rate and transcutaneous Po2, but pancuronium did not alter these changes. There was no statistical difference in transcutaneous Pco2 before, during, and after suctioning with and without muscle paralysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Monitoring, Transcutaneous↗

PubMed1995

[Hypokalemic periodic paralysis as the sole manifestation of hyperthyroidism].

Hypopotassaemic periodic paralysis as the sole manifestation of hyperthyroidism. Hypopotassaemic periodic paralysis is a rare disorder that is found in certain families, sporadically or in association with certain diseases. The association with hyperthyroidism is almost wholly restricted to south-east Asian males. It is characterized by attacks of subacute paralysis, starting most often early in the morning and lasting some hours to a few days. We present a 42-year-old patient of Indonesian origin, who experienced four attacks of paralysis before underlying hyperthyroidism was diagnosed. The mechanism is based on potassium shift into the muscle cell due to higher activity of the Na-K-ATP-ase pump, under the influence of beta-adrenergic stimulation and thyroid hormone. Treatment with antithyroidal medication and beta-blockers led to the complete abolition of attacks.

Adult↗

PubMed1993

Thyrotoxic hypokalemic periodic paralysis following second-trimester prostaglandin-induced abortion.

BACKGROUND: Hypokalemic periodic paralysis with thyrotoxicosis has never been described in pregnancy or the puerperium. CASE: A 31-year-old Hispanic woman underwent three prostaglandin inductions for a second-trimester missed abortion. Her management was complicated by hyperthermia, nausea, vomiting, and diarrhea. She developed isolated proximal muscle paralysis and sensory loss on the first post-abortion day. Her serum potassium was 1.5 mEq/L. The serum free thyroxine index exceeded 25 and TSH was below 0.03 microIU/mL, leading to a diagnosis of thyrotoxic hypokalemic periodic paralysis. Oral and parenteral potassium repletion restored full neurologic function, and propylthiouracil treatment was initiated until thyroid ablation could be performed. CONCLUSION: Gastrointestinal potassium loss during prostaglandin-induced abortion may unmask previously undiagnosed periodic paralysis.

Abortion, Induced↗

PubMed1995

[Thyrotoxic periodic paralysis: an exceptional case report in Spanish population].

Thyrotoxic periodic paralysis is a rare clinical manifestation of thyrotoxicosis in spanish population. Patients show weakness and frecuently, paralysis and low levels of potassium in serum. The episode can be triggered by eating high carbohydrate diet, exercise, stress and some drugs. We present a new case of thyrotoxic periodic paralysis in a Grave's disease patient. Only four cases have been reported in the spanish literature. We conclude that a functional evaluation of thyroid gland is necessary in thyrotoxic periodic paralysis patients.

Adolescent↗

PubMed1997

[A case of potassium-sensitive periodic paralysis with cardiac dysrhythmia].

The authors reported a case of potassium-sensitive periodic paralysis with cardiac dysrhythmia. The patient was a 21-year-old male and had periodic paralysis and asymptomatic cardiac dysrhythmia since the age of 12. His attacks worsened in frequency and intensity which brought him to our hospital at the age of 21. Physical examination on admission revealed slight dysmorphic features such as hypoplastic mandible and high-arched palate. He had slight proximal muscle atrophy with no myotonia. Electrocardiogram showed multifocal ventricular arrhythmia. The serum potassium levels during his paralytic attacks were normal or slightly decreased (3.6-4.2 mEq/l). Both potassium and glucose tolerance tests provoked paralytic attacks. Glucose tolerance test also aggravated his cardiac dysrhythmia. Acetazoramide administration improved his paralytic attack. Potassium-sensitive periodic paralysis with cardiac dysrhythmia can not be defined by the classification of periodic paralysis based on the serum potassium concentration. Provocative tests should be done to make a definite diagnosis and treatment should be done taking into consideration both paralytic attack and cardiac dysrhythmia.

Abnormalities, Multiple↗

PubMed1997

Lansoprazole potentiates vecuronium paralysis.

The effect of lansoprazole, a newer second generation proton pump inhibitor, on vecuronium induced muscle paralysis was evaluated. Fifty adult patients comprising grade I (normal healthy patient) and grade II (patient with a mild systemic disease) as classified by the American Society of Anesthesiologists were randomly allocated into two different groups each consisting of 25 patients. Group I (control) did not receive lansoprazole and group II (study) received 30 mg lansoprazole in the night before operation. There was no statistically significant difference (p > 0.05) in the time required for complete paralysis between group I (215.7 +/- 15.19 seconds) and group II (197.5 +/- 14.13 seconds). However, the duration of paralysis was significantly different (p < 0.05) between group I (32.7 +/- 8.7 minutes) and group II (43.9 +/- 9.3 minutes). It was concluded that there is a potential for interactions and one should carefully and closely monitor the patients to prevent prolonged paralysis in patients receiving lansoprazole, as a pre-anaesthetic medication.

2-Pyridinylmethylsulfinylbenzimidazoles↗