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PubMed2002

Obstructive sleep apnea syndrome and snoring in patients with bilateral vocal cord paralysis.

The analysis of the correlation between bilateral vocal cord paralysis and the occurrence of obstructive sleep apnea syndrome and snoring is presented. The aim of the study was to establish whether the decrease of the air flow in the upper airway in patients with bilateral vocal cord paralysis involves OSAS and/or snoring occurrence and whether arytenoidectomy affects an improvement of breathing parameters measured during sleep. Fourteen patients with bilateral vocal cord paralysis underwent Poly-MESAM examination before and 3 months after arytenoidectomy. They had never complained of snoring before. The Epworth sleepiness scale was used to quantify excessive daytime somnolence. The RDI, DI, mean saturation and percentage of snoring, loud snoring and sleep without snoring were estimated and compared pre- and postoperatively. The results were compared by the Student's t-test for dependent values. No significant differences were shown between the Epworth scores before and after the treatment. The RDI, DI and mean saturation were normal before and after the operation. The percentage of loud snoring decreased and the percentage of sleep without snoring increased significantly after arytenoidectomy in both cases. The mechanism of snoring in patients with vocal cord paralysis seems to be similar to OSAS. The difference consists in the level of flow limitation. On the basis of the results there is no reason to diagnose OSAS and UARS in patients with bilateral vocal cord paralysis. On the other hand, the intensive snoring that occurs after paralysis was significantly reduced as a result of arytenoidectomy.

Adult↗
PubMed2003

Obstructive sleep apnea caused by bilateral vocal fold paralysis.

We describe the case of a woman who had been referred to us with a history of breathing difficulties and snoring and a suspicion of obstructive sleep apnea (OSA). Our investigation revealed that she did indeed have severe OSA in addition to undiagnosed bilateral vocal fold paralysis of unknown origin. Nocturnal polysomnography found that her apnea/hypopnea index was 120 and her minimum arterial oxygen saturation level was 63%. She was treated with laterofixation of the right vocal fold, and her OSA resolved immediately. During 10 years of follow-up with nocturnal polysomnogrpahy, no recurrence of apnea or low oxygen saturation levels was noted. However, she did experience a recurrence of her snoring 4 years postoperatively, along with the onset of progressively worsening daytime fatigue. When these conditions persisted, we performed a repeat laterofixation of the same vocal fold. Following the repeat surgery, subjectively and objectively assessed results were good.

Female↗
PubMed2003

Drug treatment of REM sleep behavior disorders in dementia with Lewy bodies.

BACKGROUND: Dementia with Lewy bodies (DLB) is often associated with REM sleep behavior disorders (RBD) characterized, in contrast to the usual paralysis of REM sleep, by violent motor and verbal activity. PATIENTS AND METHODS: The pharmacological management of RBD was investigated in three DLB patients treated with clonazepam, a benzodiazepine used as an antiepileptic, or donepezil, a cholinesterase inhibitor. RESULTS: All three patients had marked improvement. The pharmacodynamic mechanisms underlying the efficacy of the two drugs might be due to facilitator effect on the pedunculopontine nucleus, a key structure in the physiology of REM sleep.

Aged↗
PubMed1980

Effects of endotoxin-tolerance on in vivo drug metabolism in mice.

Acute doses of endotoxin and the induction of endotoxin-tolerance lowered the apparent in vivo rates of hexobarbital and zoxazolamine metabolism in mice. Acute doses of endotoxin increased the duration of narcosis induced by these two compounds to a greater extent than did induction of the endotoxin-tolerant state. In endotoxin-tolerant mice, however, acute endotoxin treatment did not extend hexobarbital sleeping or zoxazolamine paralysis times beyond those noted in endotoxin-tolerant mice given no acute endotoxin.

Animals↗
PubMed2000

Physiological basis: how NREM sleep components can promote and REM sleep components can suppress seizure discharge propagation.

OBJECTIVES: To describe how the neural generators of different sleep components can provoke seizure discharge propagation during NREM sleep and can suppress it during REM sleep. METHODS: Experimental manipulations of discrete physiological components were conducted in feline epilepsy models (n=64), mostly in the systemic penicillin epilepsy model of primary generalized epilepsy and the amygdala kindling model of the localization-related seizure disorder, temporal lobe epilepsy. Procedures included seizure induction as well as quantifying norepinephrine concentrations (microdialysis) and the sleep-waking state distribution of seizures before and after lesions, systemic and localized drug administration and/or photic stimulation. RESULTS: (1) Neural generators of synchronous EEG oscillations, including tonic background slow waves and phasic 'arousal' events (sleep EEG transients such as sleep spindles, k-complexes), can combine to promote electrographic seizure propagation during NREM and drowsiness; anti-gravity muscle tone permits seizure-related movement. (2) Neural generators of asynchronous neuronal discharge patterns can reduce electrographic seizures during alert waking and REM sleep; skeletal motor paralysis blocks seizure-related movement during REM. (3) Etiology of the seizure disorder can interact with sleep and arousal mechanisms to determine sleep-waking state distribution of interictal and ictal events. CONCLUSIONS: Differential effects of NREM versus REM sleep components on seizure discharge propagation are to some extent non-specific and in other ways specific to seizure etiology.

Animals↗
PubMed2004

Changes of sleep-disordered breathing after laryngeal surgery in patients with bilateral vocal fold paralysis.

Snoring is the most obvious symptom of sleep-disordered breathing (SDB). Vibratory sound usually originates from the pharynx; however, in some circumstances, the narrowing of glottic structures can also cause nighttime breathing noise. This clinical study investigated the role of laryngeal obstruction in patients with SDB. Nine female patients with paralysis of bilateral vocal folds were enrolled in this study. All the patients received unilateral laser arytenoidectomy as the only treatment. Nocturnal polysomnography (PSG) was performed at baseline and 6 months after the operation. Parameters of PSG including the respiratory disturbance index (RDI) and snoring index (SI) were recorded, as well as the subjective Epworth Sleepiness Scale (ESS). Before surgery, six patients (66.6%) were identified as having obstructive sleep apnea (OSA, RDI>5). After the operation, the SI improved significantly (P=0.02). The RDI (P=0.07) and ESS (P=0.11) showed no significant improvement. The success rate of surgery in OSA patients was 66% (4/6) according to the criteria of a greater than 50% reduction of the preoperative RDI and less than 20 events per hour. The mechanism, outcomes and causes of failure are discussed in this unusual larynx-related SDB.

Adult↗
PubMed1987

Effects of lipid A content, hydrocortisone and polymyxin B on endotoxin-induced decreases in in vivo drug metabolism.

Using hexobarbital sleeping and zoxazolamine paralysis time as indices of in vivo hepatic drug metabolism, the effects of endotoxin on drug action appear to be time- and dose-dependent and the lipid A moiety of endotoxin appears to be responsible for its inhibitory effects. These studies have also demonstrated that polymyxin B can ameliorate the adverse effects of endotoxin on drug metabolism. Since hydrocortisone protects mice from endotoxin lethality, but does not alter the prolongation of hexobarbital sleeping time caused by endotoxin, it is possible to separate the lethal effects of endotoxin from its effects on drug metabolism.

Animals↗
PubMed1976

A survey of the response of different strains of mice to substances metabolised by microsomal oxidation; hexobarbitone, zoxazolamine and warfarin.

Sixteen strains of mice were compared with respect to their hexobarbitone sleeping time and their zoxazolamine paralysis time. The strains were A2G, CBA, CE, C3H, C57BL, C57L, DBA, F/st, ICFW, NMRI, NZB, Schneider, Simpson, SM, TO and 129/rr. All the strains except 129 Rr were also tested for survival on a diet containing 0.05% racemic Warfarin. There was highly significant interstrain correlation between hexobarbitone sleeping time and zoxazolamine paralysis time (r = 0.72) and between hexobarbitone sleeping time Warfarin survival (r = 0.68). There was a significant correlation between zoxazolamine paralysis time and Warfarin survival (r = 0.56). The correlations can be explained if: (1) there is a genetically determined interstrain variable which is some common component of the microsomal mixed-function oxidase systems involved in the hydroxylation of the three substances; (2) the anticoagulant action of Warfarin is caused more by a hydroxylated metabolite of Warfarin than by Warfarin itself. Phenobarbitone pretreatment shortened hexobarbitone sleeping times and zoxazolamine paralysis times, but its effect was greater in those strains with longer initial hexobarbitone sleeping times and zoxazolamine paralysis times. Piperonyl butoxide pretreatment lengthened hexobarbitone sleeping times, but had no effect on zoxazolamine paralysis times. Warfarin survival was unaltered by pretreatment with either phenobarbital or piperonyl butoxide.

Animals↗
PubMed1982

Protective effect of diethyldithiocarbamate and carbon disulfide against liver injury induced by various hepatotoxic agents.

Diethyldithiocarbamate (DTC) and carbon disulfide (CS2), at nearly equimolar oral dose levels, protected mice against liver damage induced by carbon tetrachloride, chloroform, bromotrichloromethane, thioacetamide, bromobenzene, furosemide, acetaminophen, dimethylnitrosamine and trichloroethylene, as evidenced by the suppression of elevations in plasma GPT activity and liver calcium content, and of histopathological alterations. Both agents also prolonged hexobarbital sleeping time and zoxazolamine paralysis time in mice. DTC and SC, alone, given orally, decreased microsomal metabolism of several substrates (aniline, p-nitroanisole, hexobarbital, zoxazolamine, aminopyrine and 3,4-benzopyrene), CC14-induced lipid peroxidation, and cytochrome P-450 content. The loss of microsomal drug-metabolizing enzyme activity was also observed in the experiments in vitro using liver slices and isolated microsomes. Since a characteristic common to such diverse hepatotoxins is that they require metabolic activation before exhibiting hepatotoxicity, the protective mechanisms of DTC and CS2 may involve their interference with the process of metabolic activation of these hepatotoxins. The protective action of DTC may be mediated almost entirely through CS2 when administered orally and at least partly with parenteral administration, since, in CCl4-induced liver injury, DTC was most effective when given orally, while the action of CS2 was less dependent on the route of administration. Thus CS2 and CS2-producing agents in vivo such as dithiocarbamate derivatives and disulfiram may modify toxicological and pharmacological effects of foreign compounds by inhibiting microsomal drug-metabolizing enzyme activity in the liver.

Animals↗
PubMed1983

Sleep apnea following bilateral excision of carotid body tumors.

A patient is described who developed apnea, hypertention, and tachycardia following the excision of bilateral carotid body tumors. Hypertension and tachycardia resulted, most probably, from bilateral ablation of the carotid sinus and/or the nerve of Hering. These phenomena have been described in the literature. The pathogenesis of the apneic attacks may be related to the ablation of the peripheral sensory organs (both carotid bodies), interference with the function of the respiratory automatic control system, and impaired control of ventilation during non-REM sleep. Temporary unilateral paralysis of the hypoglossal nerve with partial airway obstruction possibly represented a mechanical trigger. The apneic attacks subsided but bouts of hypertention and tachycardia persist.

Adult↗
PubMed1991

[Radial nerve paralysis--causes, site and diagnosis. Analysis of 103 cases].

The results of a retrospective analysis of 103 patients presenting with a radial nerve palsy are reported. Among the traumatic injuries of peripheral nerves the radial nerve is the one most frequently affected due to its exposed anatomic site with close neighbourhood to the long bones of the arm. Fractures of the shaft of the humerus (18%) and proximal radius (12%) are the main causes of traumatic lesions (55%). Among the non-traumatic peripheral nerve injuries the radial nerve is less frequently affected than the median and the ulnar nerves. The most frequent site of radial nerve lesions in these cases is the upper arm (22%), the most frequent cause is pressure palsy (21%) during unphysiological deep sleep ("Saturday night paralysis").

Arm↗
PubMed1991

Sleep-disordered breathing in Möbius syndrome.

Möbius syndrome is a complex neurologic disorder characterized by congenital bilateral facial paralysis associated with lateral gaze paralysis. The syndrome has variable manifestations and several variants, some with somatic stigmata. In 1990, Möbius syndrome is conceptualized as a spectrum of clinical caudal brain-stem signs. Some deficits are manifested by laryngeal paralysis and aspiration. Sleep-disordered breathing syndromes have not been previously reported in association with Möbius syndrome. We report two children with Möbius syndrome and sleep-disordered breathing. Based on known pathologic findings and clinical manifestations, we believe that sleep-disordered breathing may be a common complication of Möbius syndrome and should be sought, since potential outcomes of such complications include serious morbidity.

Child↗
PubMed2006

Respiratory insufficiency as the primary presenting symptom of multiple-system atrophy.

BACKGROUND: Respiratory stridor, sleep-disordered breathing, and respiratory insufficiency are part of the clinical spectrum of multiple-system atrophy (MSA). We have encountered cases where these were presenting symptoms, with the diagnosis of MSA being initially unrecognized. OBJECTIVE: To describe cases in which breathing difficulties were the initial and primary manifestation of MSA. DESIGN: Database review from January 1, 1996, through October 31, 2005. SETTING: Mayo Clinic, Rochester, Minn. PATIENTS: All patients diagnosed as having MSA, cross-referenced for apnea, hypopnea, or hypoventilation. On review, we included only cases in which respiratory dysfunction was the primary initial clinical event in MSA, excluding equivocal cases. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Characteristics and clinical course of patients. RESULTS: Six cases were identified in which substantial respiratory insufficiency occurred as an early, presenting symptom of MSA. Three patients had been examined emergently for acute respiratory distress before the ultimate diagnosis of MSA; the other 3 patients were diagnosed as having obstructive sleep apnea unresponsive to therapy, with bilateral vocal cord paralysis found on ear, nose, and throat examination. Stridor was noted early in the course in all. All patients required tracheostomy, and all eventually developed features consistent with probable MSA. CONCLUSIONS: Multiple-system atrophy may occasionally present as primary respiratory failure or dysfunction, with initially mild motor and autonomic symptoms. Otherwise unexplained central respiratory failure, bilateral vocal cord paralysis, stridor, or refractory central sleep apnea should prompt consideration of MSA.

Aged↗
PubMed1989

The neurology in Shakespeare.

William Shakespeare's 37 plays and poetry contain many references of interest for almost all of the medical specialties. To support that the Bard could be considered a Renaissance neurologist, the following important neurological phenomena have been selected from his repertoire for discussion: tremors, paralysis and stroke, sleep disturbances, epilepsy, dementia, encephalopathies, and the neurology of syphilis.

Drama↗
PubMed1997

3,4,5-Trihydroxy benzoic acid (gallic acid), the hepatoprotective principle in the fruits of Terminalia belerica-bioassay guided activity.

Compound I isolated from fraction TB5 of Terminalia belerica and finally identified as 3,4,5-trihydroxy benzoic acid (gallic acid) was evaluated for its hepatoprotective activity against carbon tetrachloride (CCl4)-induced physiological and biochemical alterations in the liver. The main parameters studied were hexobarbitone-induced sleep, zoxazolamine induced paralysis, serum levels of transaminases and bilirubin. The hepatic markers assessed were lipid peroxidation, drug metabolising enzymes, glucose-6-phosphatase and triglycerides. Administration of Compound I led to significant reversal of majority of the altered parameters. Our results confirm the presence of hepatoprotective activity in altered parameters. Our results confirm the presence of hepatoprotective activity in Compound I.

Animals↗
PubMed2001

Sleep and brain lesions: a critical review of the literature and additional new cases.

We present a comprehensive review of sleep studies performed in patients with brain lesions complemented by 16 additional personal selected cases and by discussion of the corresponding animal data. The reader is cautioned about the risk of establishing an erroneous correlation between abnormal sleep and a given disorder due to the important inter and intra variability of sleep parameters among individuals. Salient points are stressed: the high frequency of post-stroke sleep breathing disorders is becoming increasingly recognised and may, in the near future, change the way this condition is managed. Meso-diencephalic bilateral infarcts induce a variable degree of damage to both waking and non-REM sleep networks producing and abnormal waking and sometimes a stage 1 hypersomnia reduced by modafinil or bromocriptine, which can be considered as a syndrome of cathecholaminergic deficiency. Central pontine lesions induce REM and non-REM sleep insomnia with bilateral lateral gaze paralysis. Bulbar stroke leads to frequent sleep breathing disorders. Polysomnography can help define the extent of involvement of various degenerative diseases. Fragmented sleep in Parkinson's disease may be preceded by REM sleep behavioural disorders. Multiple system atrophies are characterised by important sleep disorganization. Sleep waking disorganization and a specific ocular REM pattern are often seen in supra-nuclear ophtalmoplegia. In Alzheimer patients, sleep perturbations parallel the mental deterioration and are possibly related to cholinergic deficiency. Fronto-temporal dementia may be associated with an important decrease in REM sleep. Few narcoleptic syndromes are reported to be associated with a tumour of the third ventricle or a multiple sclerosis or to follow a brain trauma; all these cases raise the question whether this is a simple coincidence, a revelation of a latent narcolepsy or, as in non-DR16/DQ5 patients, a genuine symptomatic narcolepsy. Trypanosomiasis and the abnormal prion protein precociously after sleep patterns. Polysomnography is a precious tool for evaluating brain function provided it is realised under optimal conditions in stable patients and interpreted with caution. Several unpublished cases are presented: one case of pseudohypersomnia due to a bilateral thalamic infarct and corrected by modafinil, four probable late-onset autosomal recessive cerebellar ataxias without sleep pattern anomalies, six cases of fronto-temporal dementia with strong reduction in total sleep time and REMS percentage on the first polysomnographic night, one case of periodic hypersomnia associated with a Rathke's cleft cyst and four cases of suspected symptomatic narcolepsy with a DR16-DQ5 haplotype, three of which were post-traumatic without MRI anomalies, and one associated with multiple sclerosis exhibiting pontine hyper signals on MRI.

Animals↗
PubMed2001

In vivo hepatoprotective activity of active fraction from ethanolic extract of Eclipta alba leaves.

The alcoholic extract of fresh leaves of the plant Eclipta alba (Ea), previously reported for is hepatoprotective activity was fractionated into three parts to chemically identify the most potent bioactive fraction. The hepatoprotective potential of the fraction prepared from extract was studied in vivo in rats and mice against carbon tetrachloride induced hepatotoxicity. The hepatoprotective activity was determined on the basis of their effects on parameters like hexobarbitone sleep time, zoxazolamine paralysis time, bromosulphaline clearance, serum transaminases and serum bilirubin. Fraction EaII (10-80 mg/kg, p.o.) containing coumestan wedelolactone and desmethylwedelolactone as major components with apigenin, luteolin, 4-hydroxybenzoic acid and protocateuic acid as minor constituents exhibited maximum hepatoprotective activity and is the active fraction for hepatoprotective activity of Eclipta alba leave. The acute toxicity studies have shown that like Ea, Fraction EaII also high safety margin.

Animals↗