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At least 451 records · Page 25Linked to original sources
PubMed1992

[HTLV-I associated myelopathy with bilateral abductor vocal cord paralysis--case report].

We have reported a 50-year-old woman with HTLV-I associated myelopathy (HAM) who had bilateral abductor vocal cord paralysis. The symptoms and signs were slowly progressive spastic paraplegia, dysuria, inspiratory stridor, and snoring during sleep. She had no hoarseness. Titers of anti-HTLV-I antibody were elevated in both the serum and cerebrospinal fluid. FEV1.0% on the spirogram was reduced to 66%. The fiberscopic examination demonstrated the abductor limitation of the vocal cords during the inspiratory phase. During induced sleep after the intravenous administration of thiopental sodium, this abductor paralysis was worsened, producing a high pitched inspiratory stridor. The adduction was not disturbed at all. Needle electromyogram of the posterior crico-arytenoid muscle which is a sole abductor muscle revealed the high amplitude up to approximately 1.0 mV (normal less than 0.8 mV) with poor interference pattern, indicating neurogenic changes. After 2 months course of prednisolone (60 mg/alternative day), FEV1.0% was recovered to be 92% with the improvement of the gait disturbance, which suggests the abductor vocal cord paralysis is related to HAM. The abductor vocal cord paralysis in HAM would require a careful follow-up observation to protect the respiratory failure in the advanced stage.

Electromyography↗
PubMed2001

[Pathology of craniocervical junction and sleep disorders].

Sleep apnea is a manifestation which has recently been recognized in anomalies of craniovertebral junction. The main reported cases involve Arnold-Chiari malformation, and clinical manifestation is a central sleep apnea syndrome. The pathophysiological mechanisms of such a sleep apnea are a blunted bulbar chemical drive (in hypercapnic patients) or an increased bulbar chemical drive which destabilizes the breathing pattern during sleep (in normo/hypocapnic patients). As this sleep apnea can be the initial manifestation of a Arnold-Chiari malformation, craniocervical magnetic resonance imaging is recommended when a central sleep apnea without evident aetiology is discovered in a young patient. Other anomalies, such as bone malformations (platybasia for example) or syryngobulbomyelia can be involved. Other respiratory manifestations can be observed such as obstructive sleep apnea syndrome, diaphragmatic or vocal cord paralysis. These manifestations may be life-threatening and may lead to decompressive surgery.

Arnold-Chiari Malformation↗
PubMed1984

Selectivity of cholestyramine treatment on hepatic mixed function oxidase activity.

The possibility that oral cholestyramine treatment might indirectly increase hepatic drug oxidations was investigated in rats using pentobarbital, antipyrine, zoxazolamine, and aminopyrine as probes of the hepatic mixed function oxidase system and in humans using amobarbital and antipyrine as probes. Cholestyramine pretreatment of rats for 5 days (87.5 mg/kg twice daily by stomach tube) shortened pentobarbital sleep times, decreased antipyrine-induced hypothermia, but did not influence either zoxazolamine paralysis times or the in vitro N-demethylation of aminopyrine. Neither pentobarbital nor antipyrine pharmacokinetics in rats were affected by the cholestyramine pretreatment. Similarly, in two-way crossover studies with human subjects, a 5-day oral cholestyramine pretreatment (4 g 3 times daily) had no demonstrable effect on the pharmacokinetics of single doses of amobarbital (200 mg i.v.) or antipyrine (500 mg per os). After cholestyramine pretreatment, a trend toward diminished CNS depression produced by amobarbital was observed, but the effect was not statistically significant. The results suggest that hepatic mixed function oxidases in rats for which aminopyrine, antipyrine, pentobarbital, and zoxazolamine are substrates and that hepatic mixed function oxidases in humans for which amobarbital and antipyrine are substrates are not significantly affected by cholestyramine pretreatment.

Adult↗
PubMed1977

Alteration of Hepatic microsomal enzyme systems and the lethal action of non-steroidal anti-arthritic drugs in acute and chronic models of inflammation.

Depression of the hepatic microsomal enzyme system(s) in adjuvant-induced polyarthritis (AIP), a chronic inflammation model, has been confirmed indirectly by the enhancement of hexobarbital Na-induced sleeping time and extended for the first time to zoxazolamine-induced paralysis. In addition, barbital Na-induced anesthesia was increased during the course of AIP development, indicating that the CNS of these rats appears to be more sensitive to drug effects, since this barbiturate is excreted virtually unmetabolized. Most likely because of these effects, LD50 values for acetylsalicylic acid, phenylbutazone and indomethacin in AIP rats decreased in terms of mg/kg (increased toxicity) as the disease became more severe (Day 21) since they are known ultimately to be metabolized by the liver. On the other hand, the toxicity of a new non-steroidal anti-inflammatory agent, meseclazone, was not altered significantly in AIP. This is most likely due to the fact that its near total conversion to 5-chlorosalicylic acid has been shown to occur by hydrolytic cleavage as it pases through the intestinal wall with litter hepatic involvement. Finally, carrageenan edema, a model of acute inflammation, did not affect barbiturate sleeping times of zoxazolamine paralysis, nor were any of these drugs studied more lethal in this disease state.

Acute Disease↗
PubMed1995

[Fear paralysis--still a possible cause of crib death].

There is overwhelming evidence that prone sleeping entails more risk of sudden infant death than supine sleeping does. However, no generally accepted biological explanation of this phenomenon has been found. In a viewpoint article in Acta Paediatrica in 1994 the author has re-emphasized that the fear paralysis reflex (tonic immobility) could be a cause of sudden infant death. The response consists of immobility, apnea, profound bradycardia and vasoconstriction. The bradycardia may proceed to irreversible asystole and silent death within a few minutes. In infant monkeys, this innate, atavistic reflex, which is prompted by aversive environmental fear-producing events, has the same age distribution as sudden infant death syndrome between the 2nd and 5th month of life. Main triggering stimuli are: restraint of movement (preventing flight) and sudden exposure to unfamiliar environments and persons, events for which the organism appears to be unprepared. Movements of the extremities are more restrained in the prone than in the supine position with greater chance of eliciting fear paralysis responses and death in prone sleepers. This biological mechanism presumably also applies to the winter peak (restraint due to overwrapping), sleeping outdoors (overwrapping) and co-sleeping in the same bed as another (parent).

Animals↗
PubMed1987

Diaphragm paralysis causing ventilatory failure in an adult with the rigid spine syndrome.

A syndrome consisting of a rigid spine and myopathy predominantly affecting proximal limb muscles has been previously described in children, and as with most neuromuscular disorders, the respiratory muscles appear to be affected only at an advanced stage in the disease. We describe an adult male with this syndrome who presented with ventilatory failure caused by severe respiratory muscle weakness and who demonstrated profound nocturnal arterial oxygen desaturation, particularly during rapid eye movement sleep. Treatment with negative pressure ventilation initially resulted in only modest improvements in symptoms, blood gas tensions, and nocturnal desaturation. The cause of this only partial improvement was upper airway obstruction provoked by the mode of ventilatory support used. After tracheostomy there was a dramatic and sustained improvement in symptoms and blood gas tensions and complete abolition of nocturnal arterial oxygen desaturation. This is the first report of an adult with the rigid spine syndrome presenting with ventilatory failure and cor pulmonale due to severe respiratory muscle weakness.

Adult↗
PubMed1987

Respiration during sleep in kyphoscoliosis.

Eleven subjects with non-paralytic and 10 with paralytic kyphoscoliosis and nine normal control subjects were studied during sleep. The Cobb angle of those with kyphoscoliosis varied from 60 degrees to 140 degrees (median 100 degrees) and the vital capacity varied from 17% to 56% (median 28%) of the value predicted on the basis of span. Recordings made during sleep included expired carbon dioxide tension at the nose, gas flow at the mouth, arterial oxygen saturation, chest wall movement, and the electroencephalogram, electro-oculogram, and electrocardiogram. In three subjects transcutaneous carbon dioxide tension was measured simultaneously. Patients with kyphoscoliosis hypoventilated during sleep, particularly in rapid eye movement sleep, resulting in a rise in end tidal and transcutaneous carbon dioxide tension, and a reduction in oxygen saturation to a degree not observed in normal subjects. Reduced chest wall movement was the major cause of these episodes, which were more frequent and occupied a greater proportion of sleep time in those with kyphoscoliosis than in normal subjects. Serious cardiac arrhythmias were rarely associated. It is concluded that disturbances of respiration during sleep occur in patients with kyphoscoliosis and that these may be important in the pathogenesis of cardiorespiratory failure.

Adolescent↗
PubMed1976

Sleep abnormalities in patients with brain stem lesions.

Seven patients with "locked-in" syndrome were studied by prolonged polygraphic recordings. Severe alterations in the sleep pattern were observed in five patients who had bilateral extensive pontine lesions resulting in tetraplegia, facial and pseudobulbar paralysis, and absence of conjugate horizontal gaze. Rapid eye movement (REM) sleep was entirely absent while non-rapid eye movement (NREM) sleep was absent, reduced, or altered. The remaining two patients, both of whom had relative sparing of horizontal gaze and apparently either no or minimal pontine tegmental involvement, showed both REM and NREM sleep with only a minimal alteration in the sleep pattern. The study suggests that, in human beings as in animals, pontine structures near the midline are essential for control of sleep states.

Akinetic Mutism↗
PubMed1990

Nocturnal stridor in olivopontocerebellar atrophy.

We describe a patient with olivopontocerebellar atrophy (OPCA) who was referred for alleged "snoring." Polysomnogram with video and audio monitoring revealed that the patient actually had nocturnal stridor causing repetitive oxygen desaturations. Direct laryngoscopy while awake showed a unilateral vocal cord paralysis. The nocturnal stridor persisted after unilateral vocal cord pinning, suggesting that the patient had probably been experiencing bilateral vocal cord paresis while asleep. We conclude that state-dependent vocal cord dysfunction may be severe in OPCA and related multiple system atrophy. Nocturnal stridor has many causes and may mimic snoring and obstructive sleep apnea syndrome. Polysomnography with audio and video recordings are necessary to make the diagnosis.

Arousal↗
PubMedDate not supplied

The effect of a single treatment with cigarette smoke on the blood levels and hemodynamic effects of propranolol in rats.

The effect of a single treatment with cigarette smoke on the blood levels and hemodynamic effects of propranolol in rats was studied. Pentobarbital sleep time was not affected whereas zoxazolamine paralysis time was shortened 72% in rats, 24 h after the cigarette smoke exposure. The beta-adrenoceptor blocking effect of propranolol observed at 10 and 20 min time intervals was abolished in rats exposed to cigarette smoke 24 h after the exposure. The blood propranolol concentrations were decreased in rats pretreated with phenobarbital, 3,4-benzpyrene and ethanol as well as in cigarette smoke exposed rats. Among several factors that could influence propranolol metabolism, in this study, enzyme induction is suggested to be dominant.

Anesthesia↗
PubMed1980

Respiratory activity and sleep--wakefulness in the deafferented, paralyzed cat.

The purpose of this study was to assess the role, if any, that peripheral feedback plays in the distinct respiratory patterns which are characteristic of the various states of consciousness. Those states include wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. Eight adult cats, implanted with electrodes and skull bolts for sleep recordings and head restraint, sustained extensive deafferentations (bilateral vagotomy and pneumothorax, spinal transection at T-1 level, bilateral section of the phrenic nerves), were paralyzed with gallamine, artificially ventilated (ensuring stable blood gases), and held at a constant temperature. Central respiratory activity was determined by phrenic nerve recordings. During NREM sleep, respiratory activity slowed as in intact cats. During REM sleep without phasic events, phrenic activity did not differ from that in NREM sleep. During REM sleep with phasic phenomena, fast and irregular "breathing" was observed. It is concluded that states of consciousness have a direct effect on central respiratory activity. Possible mechanisms for this effect are discussed.

Animals↗