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Results for “Sleep Paralysis”

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At least 271 records · Page 15Linked to original sources
PubMed1980

Determinants of hypoventilation during wakefulness and sleep in diaphragmatic paralysis.

A 45-yr-old man with limb girdle muscular dystrophy, bilateral diaphragmatic paralysis, chronic carbon dioxide retention, and hypersomnolence was studied to determine the causes of hypoventilation during wakefulness and during sleep. Awake hypoventilation was associated with an insufficient inspiratory effort in the presence of inefficient respiratory muscles and a shortened inspiratory time. During sleep, severe hypoventilation and oxygen desaturation occurred only during REM-induced intercostal and accessory muscle inhibition.

Diaphragm↗
PubMed1999

Hyperkalemic periodic paralysis associated with multiple sleep onset REM periods.

A 24-year-old man with sporadic hyperkalemic periodic paralysis (HPP) presented with moderate excessive daytime sleepiness and transitory episodes of weakness which occurred during and after sleep. Multiple sleep latency test (MSLT) demonstrated the presence of five sleep onset REM periods (SOREMPs) and a sleep latency of five minutes. Treatment with a diuretic which decreases serum potassium resolved all the clinical symtomps and a new MSLT showed the absence of SOREMPs and a sleep latency of 13.5 minutes. To our knowledge, the patient herein reported is the first case that associates sleep abnormalities and multiple SOREMPs with HPP. Furthermore, the present case suggests that SOREMPs may be explained by an increased extracellular potassium conductance related to HPP.

Adult↗
PubMed2004

Respiratory muscle activity during REM sleep in patients with diaphragm paralysis.

The diaphragm is the main inspiratory muscle during REM sleep. It was hypothesized that patients with isolated bilateral diaphragm paralysis (BDP) might not be able to sustain REM sleep. Polysomnography with EMG recordings was undertaken from accessory respiratory muscles in patients with BDP and normal subjects. Patients with BDP had a normal quantity of REM sleep (mean +/- SD, 18.6 +/- 7.5% of total sleep time) achieved by inspiratory recruitment of extradiaphragmatic muscles in both tonic and phasic REM, suggesting brainstem reorganization.

Adult↗
PubMedDate not supplied

[Changes in the monosynaptic reflex during wakefulness and sleep of children with cerebral paralysis].

Changes of the H reflex during sleep were studied in 13 children with cerebral palsy (8 with spastic tetraplegia, 2 with a mixed form of cerebral palsy without spasticity, 3 with hypotonic diplegia or tetraplegia). These modifications were compared with those of 5 normal children of the same age. During repeated night recordings, responses in the calf muscle elicited by electrical stimuli to the posterior tibial nerve were studied at the same time as the EEG, EOG and EMG of the mental muscles. The results show that:--in normal children the max H reflex progressively decreases in amplitude from wakefulness to REM sleep; -- in spastic patients there is only a slight decrease in the H reflex in NREM sleep and no significant change in REM sleep; the amplitude of the H reflex is always greater than that in the control group; -- in the dystonic and hypotonic group the results obtained are similar to those of the control group. From these results one may draw the conclusion that in spastic patients as opposed to the control, dystonic and hypotonic groups, normal balance between the function of supraspinal systems regulating the amplitude of the spinal reflexes is alterated probably through the scarce functionality of the supraspinal inhibitory structures.

Cerebral Palsy↗
PubMed1987

Sleep apnea and vocal cord paralysis secondary to type I Chiari malformation.

A previously healthy 13-year-old boy without myelodysplasia who had mild scoliosis was seen with complaints of nasal congestion, noisy nighttime breathing, and difficulty sleeping. Flattening of the inspiratory loop on the flow-volume curve was found on pulmonary function testing, suggesting a variable extrathoracic obstruction due to a laryngeal lesion. Bilateral abductor vocal cord paralysis and sleep apnea developed precipitously following general anesthesia. Further workup demonstrated a type-I Chiari malformation with syringomyelia. Brainstem abnormalities such as Chiari malformation with secondary tenth cranial nerve deficits should be considered in previously healthy children and adolescents with signs and symptoms of upper airway obstruction and apnea.

Adolescent↗
PubMed1998

[A case of central sleep-apnea syndrome accompanied by bilateral paralysis of the diaphragma after pediatric cardiac surgery].

Sleep-apnea syndrome is a serious problem in respiratory care. Considerable attention has been paid to it, because it sometimes produces severe hypoxia and hypercapnia, and can cause death. We present a case of a six-year-old girl who showed sleep-apnea syndrome. She suffered from bilateral paralysis of the diaphragm after cardiac surgery and had to be managed under mechanical ventilation for three months. When weaning was tried from mechanical ventilation, she frequently showed apnea lasting over 15 seconds at night, and she was diagnosed as having sleep apnea. She was medicated with theophylline to stimulate the so-called respiratory center. Next day she was successfully weaned from mechanical ventilation. After she had been weaned from mechanical ventilation, hypoxia, hypercapnia, and tachycardia were detected by respiratory monitor at night. The respiratory monitor enabled us to identify the clinical appearance of sleep-apnea, and theophylline may have contributed to its improvement.

Cardiac Surgical Procedures↗
PubMed2005

Characterization of the spontaneous and gripping-induced immobility episodes on taiep rats.

In 1989, we described a new autosomic-recessive myelin-mutant rat that develops a progressive motor syndrome characterized by tremor, ataxia, immobility episodes (IEs), epilepsy, and paralysis. taiep is the acronym of these symptoms. The rat developed a hypomyelination, followed by demyelination. At an age of 7-8 months, taiep rats developed IEs, characterized electroencephalographically by REM sleep-like cortical activity. In our study, we analyzed the ontogeny of gripping-induced IEs between 5 and 18 months, their dependence to light-dark changes, sexual dimorphism, and susceptibility to mild stress. Our results showed that IEs start at an age of 6.5 months, with a peak frequency between 8.5 and 9.5 months. IEs have two peaks, one in the morning (0800-1000 h) and a second peak in the middle of the night (2300-0100 h). Spontaneous IEs showed an even distribution with a mean of 3 IEs every 2 h. IEs are sexually dimorphic being more common in male rats. The IEs can be induced by gripping the rat by the tail or the thorax, but most of the IEs were produced by gripping the tail. Mild stress produced by i.p. injection of physiological saline significantly decreased IEs. These results suggested that IEs are dependent on several biological variables, which are caused by hypomyelination, followed by demyelization, which causes alterations in the brainstem and hypothalamic mechanisms responsible for the sleep-wake cycle regulation, producing emergence of REM sleep-like behavior during awake periods.

Age Factors↗
PubMed2002

[A case of brachial plexus neuropathy who presented with acute paralysis of the hand after sleep].

We report a 46-year-old woman who presented with acute paresis of the right hand and arm. She was well until when she noted a paresis and dysesthesia in her right hand in the morning. Neurological examination revealed weakness in the muscles which were supplied by lower cervical segments, with increased deep tendon reflexes in the right arm. Allen's test and Wright's test were positive. The nerve conduction studies disclosed a reduced CMAPs more severely by right median than ulnar nerve stimulation. The frequency and amplitude of the F waves was also reduced. Needle electromyogram showed a mild neurogenic pattern in the right hand muscles. Digital subtraction angiography revealed a tapering of the subclavian artery when the right arm was abducted. She underwent decompression surgery. A remarkable improvement of the symptoms was observed after surgery. Our patient suggests that brachial plexus neuropathy should be considered in the acute paresis of the hand after sleep, and that surgical procedure would lead to a successful outcome.

Acute Disease↗
PubMed1980

[Sleep study of progressive supranuclear paralysis].

From a group of 9 patients suffering from progressive supranuclear palsy 11 polygraphic records and 6 tests with probenecid have been made. The changes in sleep can be correlated with the severity of the clinical picture and the stage of evolution of the disease. They support the hypothesis of a systematic progression of the lesions in the hypnogenic structures of the brain stem.

Aged↗
PubMed2003

REM sleep behavior disorder and vocal cord paralysis in Machado-Joseph disease.

We evaluated the occurrence of REM sleep behaviour disorder (RBD) and vocal cord abductor paralysis (VCAP) in a group of 9 Machado-Joseph disease (MJD) patients. RBD was diagnosed by clinical history plus audiovisual polysomnography in 4 men and 1 woman (55%). While dreaming, 4 fell out of the bed and the other injured his arms. Laryngoscopy detected bilateral VCAP in 1 patient with stridor who required emergency tracheotomy, and partial vocal cord abductor restriction in 2. RBD and VCAP are two potentially injurious conditions that should be considered part of the clinical spectrum of MJD.

Adult↗
PubMed1987

Effect of acute diaphragm paralysis on ventilation in awake and sleeping dogs.

The mechanisms responsible for hypoventilation during rapid-eye-movement (REM) sleep in patients with diaphragmatic weakness are not clear. Therefore, we studied the effects of unilateral (UDP) and bilateral (BDP) diaphragmatic paralysis on ventilation during wakefulness (W), slow-wave sleep (SWS), and REM sleep. Studies were performed in 3 trained dogs in which small silicone cuffs had been implanted surgically around the phrenic nerves. Reversible diaphragmatic paralysis was induced during wakefulness or sleep by bathing the phrenic nerves in local anesthetic injected through a catheter attached to the phrenic cuffs. The UDP reduced abdominal expansion and increased rib cage expansion, but had no effect on minute volume of ventilation (VI) or end-tidal PCO2 (PACO2). The BDP produced marked abdominal paradox, but did not reduce VI during W or SWS and had no effect on tidal volume or respiratory frequency. In contrast, during REM sleep, VI was decreased by an average of 21% mainly because of a fall in tidal volume, and PACO2 increased by 2.4 mm Hg compared with that during the intact state. Furthermore, addition of extra dead space to the breathing circuit, which was well tolerated in intact dogs, led to a progressive increase in PACO2 during BDP and to arousal from sleep. The findings indicate that acute BDP does not impair ventilation during quiet W or SWS, but reduces ventilation during REM sleep, supporting the concept that during REM sleep maintenance of ventilation is critically dependent on diaphragmatic compensation for intercostal and accessory muscle inhibition.

Animals↗