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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleepiness, a common complaint of epilepsy patients, is frequently attributed to antiepileptic medications. To determine predictors of subjective sleepiness in epilepsy patients, we gave self-administered, validated surveys of sleepiness [Epworth sleepiness scale (our major outcome measure)] and sleep apnea [sleep apnea scale of the sleep disorders questionnaire (SA/SDQ)] to 158 epilepsy patients and 68 neurology patients without epilepsy (controls). An elevated Epworth score (>10) was more likely in epilepsy patients compared to controls after controlling for age and gender (p < 0.05). When Epworth scores were adjusted for SA/SDQ scores and restless legs symptoms (RLS), however, epilepsy patients showed only a nonsignificant trend toward elevated Epworth scores compared to controls (p = 0.08). SA/SDQ scores (p < 0.005) and RLS (p < 0.007) were significant predictors of elevated Epworth score in both epilepsy patients and controls. Among the epilepsy patients, the number or type of antiepileptic medication, seizure frequency, epilepsy syndrome (partial vs. generalized), and the presence of sleep-related seizures were not significant predictors (p > 0.10) of elevated Epworth score. Before attributing sleepiness in epilepsy patients to antiepileptic medications or uncontrolled seizures, clinicians should consider the possibility of a coexisting sleep disorder.
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PMID:Predictors of sleepiness in epilepsy patients. 949 19

REM sleep behaviour disorder (RSBD) is a recently described parasomnia characterised by a history of excessive nocturnal motor activity and absence of muscle atonia during REM sleep. Only limited literature is available on this condition. The exact prevalence is unclear, but recent studies suggest it might not be an uncommon condition. The elderly are more often affected and there is a male preponderance. While transient RSBD can be seen after taking certain drugs or during drug withdrawal, the chronic type is usually idiopathic or associated with an underlying degenerative neurological condition. It can result in considerable distress and/or serious injury to the patients or their bed partners. Differential diagnoses include sleep-walking, night terrors, nightmares, nocturnal seizures, obstructive sleep apnoea, post-traumatic stress disorder, dissociative states and nocturnal confusional states. The dramatic response to clonazepam highlights the importance of recognition and appropriate treatment of this sleep disorder.
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PMID:REM sleep behaviour disorder: an overview. 953 85

Acute autonomic and sensory neuropathy (AASN) is a rare neuropathy characterized by acute autonomic dysfunction and objective sensory disturbances. A 26-year-old pregnant woman with severe autonomic and sensory dysfunction is reported. This patient suddenly developed marked nausea and vomitting in about 2 days after having a sore throat. She then developed signs of autonomic dysfunction including dilated non-reactive pupils, dryness of the eyes and oral mucous membranes, generalized anhidrosis, paralytic ileus, orthostatic hypotension, and continuous tachycardia. She also had severe generalized sensory impairments of all modalities, and all deep tendon reflexes were absent. Sensation was almost totally lost for all modalities below the neck. There was marked pseudoathetosis and sensory ataxia in all extremities. Motor examination was normal. She had inability to urinate. At this time she was 38 weeks pregnant, and when she showed signs of fetal distress, a Caesarean section was performed. Albumino-cytological dissociation was seen in the CSF. Serum noradrenaline was reduced, no sensory nerve action potentials could be elicited, and reduced coefficient of variation of the R-R interval on electrocardiography was observed. Plasma exchange was performed every other day for 3 days for about 3 weeks after the onset of the illness, but no favorable effects. Seven months after the onset, her autonomic dysfunction slightly improved, but there was no recovery from the sensory disturbances. Many symptoms and signs that characterize AASN occurred in this patient, and each was severe. The patient developed SIADH, sleep apnea, personality change, and amenorrhea in the course of the disease. We suggest that AASN patients might have both peripheral and central nervous system manifestations including seizures and personality changes.
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PMID:[A severe case of acute autonomic and sensory neuropathy]. 986 13

This self-directed learning module highlights new advances in the understanding of co-morbid conditions and medical complications of stroke. It is part of the chapter on stroke rehabilitation in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. This article covers co-morbid conditions of stroke patients, including cardiovascular disease, diabetes, and sleep apnea. It reviews recent information on complications of stroke, including deep venous thrombosis, dysphagia and aspiration, hospital-acquired infections, depression, falls, spasticity, shoulder pain, and seizures. Treatment advances in diabetes, depression, and spasticity are highlighted. Recent information is presented regarding exercise guidelines for the stroke patient with cardiovascular disease, the relationship between stroke and sleep apnea, prophylaxis of deep venous thrombosis, the changing spectrum of hospital-acquired infections, malnutrition in stroke patients, the problem of falls during rehabilitation, the evaluation and management of poststroke shoulder pain, and the risk of seizures after stroke.
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PMID:Stroke rehabilitation. 2. Co-morbidities and complications. 1032 98

Seizure disorder and sleep apnea are common chronic disorders in children, but the relationship between sleep apnea and seizure control has not been studied in the pediatric population. This retrospective review included nine children with neurodevelopmental disorders who had well-documented sleep apneic episodes and seizure disorders. Seizure frequency was reduced in five patients (56%) in the first 12 months after sleep apnea treatment without changes in their antiepileptic medications. Sleep apnea can be one of the seizure precipitants in children with epilepsy. This study indicates the importance of identifying sleep apnea when treating children with intractable epilepsy, particularly in those who are at high risk.
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PMID:Sleep apnea treatment improves seizure control in children with neurodevelopmental disorders. 1066 3

Over the past two to three decades, sleep medicine has emerged as an important discipline as it strives to meet the challenges of some of the most prevalent disorders among humans. Among the 110 disorders listed in the International Classification of Sleep Disorders, two of the most prevalent and treatable have only recently begun to receive significant attention: sleep apnea and restless legs syndrome with sleep-related periodic limb movements disorder. It is becoming clear that the sleep disruption caused by such disorders has ramifications beyond the usually associated daytime sleepiness, and may include: exacerbation of seizures, headaches, short-term memory deficits, and other cognitive problems. Sleep apnea has also been correlated with hypertension and cardiovascular/cerebrovascular disease. Animal studies have taken this one step further by demonstrating that total sleep deprivation is consistently fatal, usually within 1 month, although the precise mechanism remains to be discovered. The most compelling finding in the animal studies is that "rescuing" the animals with sleep, before the irreversible stage, is associated with rebound amounts of deep sleep and rapid eye movement (REM) sleep ("dream sleep"). This same response is seen after initiating treatment of sleep apnea with nasal continuous positive airway pressure (CPAP), and can also occur in patients with other sleep disorders in response to particular medications, such as valproate or gabapentin.
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PMID:Importance of sleep restoration in co-morbid disease: effect of anticonvulsants. 1071 82

Sleep disturbance in patients with epilepsy is frequently overlooked, but may contribute to decreased daytime functioning and increased seizure activity. Although complicated, the relationship between sleep and epilepsy is becoming clearer. Sleep, and particularly deep non-rapid-eye-movement sleep, increase interictal epileptiform activity. Sleep increases certain seizure types and the rate of generalization of partial seizures, however rapid-eye-movement sleep seems to suppress seizures. Sleep disorders, particularly sleep apnea, exacerbate seizures. Seizures, in turn, can disrupt sleep structure, particularly rapid-eye-movement sleep. An understanding of these relationships is important in seizure control and in maximizing the quality of life for patients with epilepsy.
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PMID:Sleep and epilepsy. 1098 75

A retrospective survey of consecutive 480 adult patients (394 men, 96 women, mean age 50.3, SD +/- 10.4 years) with sleep apnea syndrome (SAS) was made in attempt to find out among them the patients with epilepsy. In total 19 subjects (17 men, 2 women, average age 55.8 +/- 8.7 years) representing 4.0% experienced at least two seizures in adult age. The average age at the first seizure was 48.4 +/- 16.1 years. Ten subjects suffered from primarily generalized tonic-clonic seizures, seven from secondarily generalized tonic-clonic seizures, one had complex partial seizures and one simple partial seizures. In 15 subjects (78.9%) the seizures occurred exclusively during sleep. Two patients (11.1%) had seizures exclusively during vigilance and in remaining two subjects the seizures occurred during sleep and vigilance. The findings of high proportion of subjects with epilepsy among SAS subjects, of late seizure onset and of predominantly sleep occurrence of seizures suggest that sleep apnea and hypopnea can facilitate epileptic seizures.
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PMID:Seizures in sleep apnea patients: occurrence and time distribution. 1122 Jan 50

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age; 27 infants died from sudden infant death syndrome (SIDS), 5 from congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 with a prolonged seizure, and another with prolonged neonatal hypoxemia. The frequency and duration of sleep apneas recorded some 3-12 weeks prior to the infants' death were analyzed. Brainstem material was retrospectively collected from these 33 infants and studied in an attempt to elucidate the relationship between sleep apnea and hypoxic gliosis. The findings were compared between the SIDS victims and the control infants. Brainstem materials were immunohistochemically studied for quantitization of reactive astrocytes using an anti-glial fibrillary acidic protein (GFAP) antibody. The pathological materials were collected within 24h of death. This study focuses on the association between respiratory characteristics and pathology. Physiological and pathological data in the arousal pathway of the brainstem were linked for each infant and variant-covariant analyses were carried out using physiological data as dependent variables and pathological data and categorical data to evaluate the association with SIDS or non-SIDS as independent variables. The study failed to statistically support an association between hypoxic loads, reflected by the GFAP-positive reactive astrocytes in brainstems, the classification of being SIDS or non-SIDS infants, and the characteristics of sleep apnea.
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PMID:Association between sleep apnea and reactive astrocytes in brainstems of victims of SIDS and in control infants. 1235 Feb 98

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age (including 26 infant victims of sudden infant death syndrome (SIDS), 5 with congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 with a prolonged seizure, 1 from prolonged neonatal hypoxemia, 1 from meningitis and brain infarction). The frequency and duration of sleep apneas recorded some 3-12 weeks before the infants' death were analyzed. Brainstem material from these 38 infants was studied in an attempt to elucidate the relationship between sleep apnea and neuronal pathological changes in the arousal pathway. Immunohistochemical analyses included the evaluation of growth-associated phosphoprotein 43 (GAP43) as a marker for synaptic plasticity. The terminal-deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method was used to identify apoptosis. The positive pathological reactions were quantitatively analyzed. The pathological and physiological data were linked for each infant. Akaike Information Criterion (AIC) statistics was calculated to elucidate the relationship between the physiological and the pathological data in the SIDS victims. The findings illustrated the possibility of an organic fragility within the arousal pathway, particularly in the midbrain periaqueductal gray matter, which is associated with the "visceral alerting response". This autonomic response occurs within an acetylcholine afferent system and pedunculopontine tegmental nucleus (PPTN). The finding is, in future SIDS infants, associated with repetitive sleep apnea.
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PMID:From physiology to pathology: arousal deficiency theory in sudden infant death syndrome (SIDS)--with reference to apoptosis and neuronal plasticity. 1235 Feb 99


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