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

Sleep disordered breathing is common in patients with tetraplegia. Nocturnal arterial hypoxemia and sleep fragmentation due to sleep apnoea may be associated with cognitive dysfunction. We therefore studied the influence of sleep disordered breathing on neuropsychological function in 37 representative tetraplegic patients (mean age 34 +/- 9.7 years). Thirty percent (11 of 37 patients) had clinically significant sleep disordered breathing, defined as apnoea plus hypopnoea index (AHI) greater than 15 per hour of sleep. Most apnoeas were obstructive in type. Seven patients (19%) desaturated to < 80% during the night. Neuropsychological variables were significantly correlated with measures of sleep hypoxia, but not with the AHI and the frequency of sleep arousals. The neuropsychological functions most affected by nocturnal desaturation were: verbal attention and concentration, immediate and short-term memory, cognitive flexibility, internal scanning and working memory. There appeared to be a weak association between the presence of severe sleep hypoxia and visual perception, attention and concentration but no association was found between sleep variables and depression scores. We concluded that sleep disordered breathing is common in patients with tetraplegia and may be accompanied with significant oxygen desaturation. The latter impairs daytime cognitive function in these patients, particularly attention, concentration, memory and learning skills. Cognitive disturbances resulting from sleep apnoea might adversely affect rehabilitation in patients with tetraplegia.
Spinal Cord 1998 Apr
PMID:Sleep apnoea related hypoxia is associated with cognitive disturbances in patients with tetraplegia. 1002 2

A 57-year-old man with obstructive sleep apnoea presented with acute progression of myelopathy into paraplegia resulting from cervical disc herniation at C4-C5 and C5-C6 levels. There was no associated history of trauma. Rapid progress to paraplegia from non-traumatic cervical disc herniation rarely occurs. Diagnostic and treatment modalities are discussed. The possible relationship between cervical myelopathy and sleep apnoea is also discussed.
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PMID:Non-traumatic acute paraplegia caused by cervical disc herniation in a patient with sleep apnoea. 1514 62

Achondroplasia is the most common of the heritable skeletal dysplasias. Compression at the cervicomedullary junction can result in myelopathy, hypotonia, sleep apnea, and even sudden death. However, most children with achondroplasia do not suffer from severe neurological symptoms and achieve normal motor and intellectual development without surgical intervention. At the authors' institution, magnetic resonance (MR) imaging and cerebrospinal fluid (CSF) flow studies have been incorporated in the assessment of children with achondroplasia for cervicomedullary junction compression. The authors recently identified four children with achondroplasia who had normal findings on MR imaging and flow studies obtained in the neutral position. On flexion studies, however, three had complete blockage of CSF flow, and more dramatic posterior cervicomedullary compression was demonstrated on extension studies. Some of these patients had severe neurological abnormalities and sleep apnea, while others just developed headaches and/or had apnea episodes when sleeping or in a car seat. Three children underwent decompressive surgery with dramatic improvement or resolution of signs and symptoms. The fourth patient had increased CSF pressure on MR images obtained in the flexed position, possibly due to venous outflow obstruction. Her condition improved dramatically after placement of a ventriculoperitoneal shunt. The increased risk of dynamic cord compression and alterations in CSF dynamics in patients with achondroplasia constitute indications for surgical intervention.
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PMID:Dynamic cervicomedullary cord compression and alterations in cerebrospinal fluid dynamics in children with achondroplasia. Report of four cases. 1815 22

Hunter disease (mucopolysaccharidosis type II, MPS II) is an X-linked lysosomal storage disease caused by deficiency of iduronate-2-sulfatase. Accumulation of chondroitin sulfate B and heparan sulfate in various tissues is the biochemical consequence of MPS II. Children with Hunter disease are normal at birth, and symptoms occur between 2 and 10 years of age. Typical symptoms include coarse facies with enlarged tongue and prominent forehead as well as a short, stocky built stature with short neck. The cardiovascular, respiratory and gastrointestinal systems may be affected, and oral, dermatological and psychiatric as well as neurological complications are described. Life expectancy is markedly reduced and may be limited to 12 years for severely affected patients. The most common causes of death are airway obstruction and cardiac failure. The most severe symptoms may result from neurological symptoms or complications including hydrocephalus, spinal cord compression, cervical myelopathy, optic nerve compression, and hearing impairment. Patients may also develop carpal tunnel syndrome, sleep apnoea, seizures or mental retardation. This review describes characteristic neurological manifestations in MPS II and its underlying pathophysiology. In addition, an appraisal is given whether or not enzyme replacement therapy may be able to improve in particular the neurological symptoms of Hunter disease.
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PMID:Neurological findings in Hunter disease: pathology and possible therapeutic effects reviewed. 1861 89

Since sleep apnea is a risk factor for high mortality of rheumatoid arthritis (RA) patients, this study examined the prevalence in RA patients with occipitocervical lesions, and the associated radiographic features. Twenty-nine RA patients requiring surgery for progressive myelopathy due to occipitocervical lesions (3 males, 26 females, average age 65 years) were preoperatively evaluated. Twenty-three (79%) had sleep apnea defined as apnea-hypopnea index >5 events per hour measured by a portable monitoring device, and all of them were classified as the obstructive type. Among gender, age, bone mass index (BMI), and radiographic parameters related to occipitocervical lesions: atlantodental interval (ADI), cervical angles (O/C1, C1/2, and C2/6), and cervical lengths (O-C2 and O-C6), the ADI and cervical lengths were shown to be significantly associated with the presence of sleep apnea by parametric statistical analysis. Since there were positive correlations between the ADI and cervical lengths by Pearson's test, we performed a multivariate logistic regression analysis after adjustment for confounding factors and found that small ADI was the principle parameter associated with sleep apnea. We therefore conclude that the prevalence of sleep apnea is higher than that in a general RA population that was reported previously, and believe that occipitocervical lesions are an independent risk factor for this condition. Small ADI and short neck, secondary to the vertical translocation by RA, may cause obstructive sleep apnea, probably through mechanical or neurological collapse of the upper airway.
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PMID:Sleep apnea in rheumatoid arthritis patients with occipitocervical lesions: the prevalence and associated radiographic features. 1936 41

Central sleep apnea is a breathing disorder that manifests as repetitive cessation of the breath during the sleep. The occurrence of breathing disorders after cervical laminectomy has been exceptionally described as a complication after cervical decompressive laminectomy for cervical stenotic myelopathy. In 1994, Naim-ur-Rahman reported the first case of postoperative central sleep apnea following C3-C6 laminectomy, occurring right after surgery and associated with spyncterial incontinence, that spontaneously recovered three weeks after onset. Recently we described a rare complication of cervical laminectomy for cervical stenotic myelopathy: the onset was delayed from surgery (nearly two weeks later) and cervical stenotic myelopathy was not associated to any other neurological sign of spinal cord damage as demonstrated by the neurophysiological assessment. Possible familiar predisposition can be matter of discussion. No definite interpretation of pathophysiological mechanisms can ultimately explain the occurrence of delayed and isolated central sleep apnea after laminectomy for the treatment of cervical stenotic myelopathy. Such a reversible and benign complication remain unpredictable in the best surgical hands.
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PMID:Transient breathing disorders after posterior cervical surgery for degenerative diseases: pathophysiological interpretation. 2482 50

Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of the lysosomal hydrolase a-L-Iduronidase leading to accumulation of the GAGs, dermatan sulfate, and heparan sulphate, The disease spectrum includes a disorder with severe involvement and CNS disease Hurler disease (HPS I H) a chronic disease without CNS disease Scheie disease (HPS I S5) and the intermediate Hurler/Scheie disease(HPS I HIS).The urine GAGs pattern. confirmed by Iduronidase enzyme assay is diagnostic. Over 200 mutations exist. Genotype / phenotype correlation is poor but two nonsense mutations results in Hurler disease.The skeletal disease dysostosis multiplex (DM) is seen in severe variants of MPS I. The hypoplastic odontoid putting these patients at high risk of cervical cord damage. MPS IH (Hurler Disease) affected infants develop a spinal 'gibbus' deformity, persistent nasal discharge, middle ear effusions and frequent upper respiratory infection. They have "coarse", facial features, and an enlarged tongue. . Progressive upper airway disease leads to obstructive sleep apnoea. Corneal clouding and cognitive impairment appears, growth ceases. Joint stiffness and contractures limit mobility. Cardiac disease is universal. Death occurs before 10 years. SCHEIE patients are diagnosed as teenagers with hepatomegaly, joint contractures, cardiac valve abnormalities and corneal clouding . Prolonged survival with considerable disability without cognitive impairment is usual. MPS IH/S Hurler/Scheie. is diagnosed by 6.5 years, with variable skeletal and visceral manifestations without cognitive involvement. Joint stiffness, corneal clouding, , umbilical hernia, abnormal facies, hepatomegaly, joint contractures, and cervical myelopathy occur. Patients die in their 20s .Haematopoietic stem cell transplantation (HSCT) the standard treatment of MPS IH for 30 years is unpredictable .When performed before 2 years it can stabilize cognitive impairment. Hepatosplenomegaly, urine GAGs excretion, upper airways obstruction and cardiomyopathy improve . The coarse hair and facial features soften and corneas partly clear,but dysostosis multiplex and cervical instability are not improved. Enzyme replacement therapy (ERT) in patients with MPS IH is associated with improved GAG excretion, left ventricular hypertrophy,sleep studies and liver size. The standard treatment of MPS IHIS and MIPS IS is ERT a-L-Iduronidase, laronidase, a life-long therapy. GAG excretion is reduced, respiratory function and physical endurance improve. Joint mobility improves but not dural thickening, cardiac valve lesions or eye changes. MPS I mice have been successfully treated with IDUA-expressing mesenchymaf stem cells . Gene therapy may be developed for MPS I, via an ex vivo approach demonstrated to improve even skeletal outcomes in animal models.
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PMID:Mucopolysaccharidosis type I. 2534 91

Ventral brainstem compression is an uncommon clinical diagnosis seen by pediatric neurosurgeons and associated with Chiari malformation, type I. Presenting clinical symptoms often include headaches, lower cranial neuropathies, myelopathy, central sleep apnea, ataxia, and nystagmus. When ventral decompression is required, both open and endoscopic transoral/transnasal approaches are highly effective.
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PMID:Ventral Decompression in Chiari Malformation, Basilar Invagination, and Related Disorders. 2640 67

We report the first case of ocular myasthenia gravis (OMG) in a patient with complete tetraplegia, highlighting diagnostic and management challenges. Spinal multidisciplinary rural clinic and specialised inpatient Spinal Cord Injury Unit, NSW, Australia. A 61-year-old man with established C5 AIS A tetraplegia, presented with sudden onset of diplopia and bilateral ptosis, later diagnosed as OMG, in context of other complex co-morbidities, including a cervical cord syrinx, obstructive sleep apnoea and labile blood pressure. Clinical findings were consistent with fluctuating bilateral partial third and sixth nerve palsies. Acetylcholine receptor antibodies were negative, but electromyography demonstrated muscle fatigue. The ocular signs responded well to pyridostigmine. Medications taken before diagnosis, including solifenacin for neurogenic bladder overactivity, were ceased to avoid attenuating the anti-cholinesterase effect. However, the unopposed anti-cholinesterase activity led to frequent and painful abdominal spasms, associated with uncontrolled detrusor hyperreflexia and worsening autonomic dysreflexia (AD). A trans-vesical phenol block to treat this provided only short-lasting benefit. Pyridostigmine was ceased to avoid provoking his abdominal spasms and his regular medications were recommenced. It was decided that the most appropriate treatment for his distressing diplopia was an eye patch. After discharge home, he continued to experience problems with recurrent urinary tract infections, abdominal spasms, episodic postural hypotension and AD. After 5 months, the patient died from an acute myocardial infarction. This case report contributes new knowledge about the rare presentation of OMG in a person with chronic tetraplegia.
Spinal Cord Ser Cases 2016
PMID:Ocular myasthenia gravis in a person with tetraplegia presenting challenges in diagnosis and management. 3126 10

In sleep-related breathing disorders, sleep apnea is a clinical symptom that can be categorized as obstructive sleep apnea (OSA) or mixed apnea by analysis using polysomnography. The occurrence of delayed central sleep apnea (CSA) is an extremely rare complication of cervical laminectomy for spondylotic myelopathy. So far only three studies concerning such an event have been reported in the literature. Naim-ur-Rahman, in 1994, reported a case of postoperative CSA following C3-C6 laminectomy, and Visocchi and colleagues, in 2014, in two studies, stressed the lack of association with any other neurological sign of spinal cord damage. No definitive mechanism has been recognized so far for delayed CSA after cervical laminectomy. A transient dysfunction of the reticulo-spinal fibers directed to the nucleus of the phrenic nerve can be speculated, although neither emi-diaphragm paralysis, nor any prominent nocturnal sleep-related disorders are associated with this delayed CSA.
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PMID:Focus on Functional Delayed Central Sleep Apnea Following Cervical Laminectomy. An Example of Respiratory Dysfunction in Restorative Neurosurgical Procedures. 2812 77


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