Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. Diagnosis of obstructive, central and mixed apneas, hypopneas, and hypoventilation is best made using polysomnography. Therapeutic options include noninvasive ventilation such as continuous positive airway pressure, bilevel positive airway pressure, intermittent positive pressure ventilation and, rarely, tracheostomy, oxygen, or protriptyline. Evaluation by a sleep specialist should be initiated in any neuromuscular patient with nocturnal symptoms such as air hunger, intermittent snoring or breathing, orthopnea, cyanosis, restlessness, and insomnia. Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.
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PMID:Nocturnal respiratory failure as an indication of noninvasive ventilation in the patient with neuromuscular disease. 967 Mar 10

Morvan's fibrillary chorea is a rare disease characterised by symptoms which include neuromyotonia, cramping, weakness, pruritus, hyperhidrosis, insomnia, and delirium. The first case of Morvan's fibrillary chorea to be associated with clinical manifestations of myasthenia gravis with thymoma, psoriasis, and atopic dermatitis is reported. Muscle histopathology disclosed chronic denervation and myopathic changes and in vitro electrophysiology demonstrated both presynaptic and postsynaptic defects in neuromuscular transmission. Serum antibodies to acetylcholine receptors, titin, N-type calcium channels, and voltage gated potassium channels were detected. Plasmapheresis, thymectomy, and long term immunosuppression induced a dramatic resolution of symptoms. The association of thymoma with other autoimmune disorders and autoantibodies, and prolonged and sustained remission with chronic immunosuppression, place Morvan's fibrillary chorea on the range of neurological diseases arising as a paraneoplastic complication of cortical thymomas.
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PMID:Morvan's fibrillary chorea: a paraneoplastic manifestation of thymoma. 985 61

My aim is to examine the relation between some sleep disorders and neurological diseases; to analyse their mutual interactions in order to achieve new practical data for clinical use. In the theoretical part I summarise some main points of sleep physiology concentrating on the associations of sleep regulation and neurological diseases. In my examinations, besides clinical methods, the most important tools used are sleep analyses performed by polysomnography and MESAM IV as well as brain imaging methods. To assess clinical state of my stroke patients I utilised NIH Stroke Scale. I found pathological sleep apnoea frequency in more than half of the patients in any type (bleeding/infarction) of acute stroke. In a prospective study, sleep apnoea parameters remain permanent during 3 months in the ischaemic group; on the other hand, sleep apnoea improves during follow up after brain haemorrhages. I showed pathological sleep apnoea frequency in myasthenia gravis among male patients without daytime respiration complaint. I looked for the link between the mechanism of the sleep disorder and the underlying organic lesion in two cases. In this analyses I took into account the function of the affected structure in sleep regulation. I found a basal forebrain tumour, affecting sleep regulating centres underlying severe insomnia and I suggest a neuro-vascular compression of the lateral preoptic area of the hypothalamus being the reason of sleep related painful erection, a parasomnia of unknown origin.
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PMID:Neurological aspects of some sleep disorders. 1513 14

Syndromes from antibodies to voltage-gated potassium channels include neuromyotonia (NMT), limbic encephalitis (LE) and Morvan syndrome (MVS). There are distinct clinical features for NMT (cramps, stiffness, fasciculations, myokymia, hyperhidrosis; afterdischarges and continuous motor activity on electromyogram), LE (encephalopathy with seizures, deficient recent memory; hyponatremia, temporal lobe magnetic resonance imaging and electroencephalographic abnormalities) and MVS (NMT plus hyperhidrosis, dysautonomia, encephalopathy, severe insomnia, and sleep disorders). There may be associated myasthenia gravis or thymoma, and rarely lung cancer (small cell or adenocarcinoma), mandating that chest imaging be part of the evaluation. Most cases respond favorably to immunosuppression with plasma exchange, intravenous immunoglobulin or pulse intravenous methylprednisolone, usually followed by oral steroids.
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PMID:Management of voltage-gated potassium channel antibody disorders. 2081 72

Myasthenia gravis (MG) is an autoimmune disorder generally mediated by antibodies against the acetylcholine receptors of the skeletal muscles. Depending on the disease burden, MG patients may experience chronic dysregulation of both the hormonal stress axis and the immune system, consequently, aggravating the disease itself but also leading to secondary psychopathological abnormalities. A long-term clinical course requires long-term glucocorticoid (GC) therapy, which may change the psychological state by affecting the pituitary-adrenocortical system in MG patients. In this study, we investigated the function of the pituitary-adrenocortical system in MG patients who were treated with prednisolone (PSL) and evaluated their quality of life by using the Medical Outcomes Study 36-item Short-Form Health Survey and the 28-item general health questionnaire (GHQ-28). ACTH and cortisol levels in the plasma of patients who were treated with PSL (PSL[+] group, n = 18) were lower than those in the plasma of patients who were treated without PSL (PSL[-] group, n = 29; P < 0.05 and P < 0.01, respectively). In the PSL(+) group, we confirmed that cortisol levels negatively correlated with daily PSL dosages (P < 0.05). The anxiety and depression scores from the GHQ-28 in the PSL(+) group were lower than those in the PSL(-) group (P < 0.05, respectively). There was no significant correlation between cortisol levels and corticotropin levels in plasma of the PSL(-) group. However, we confirmed that corticotropin levels positively correlated with cortisol levels in plasma (P < 0.01) and negatively correlated with anxiety/insomnia scores from the GHQ-28 (P < 0.05) in the PSL(+) group. In conclusion, low-dose GC treatment complemented the pituitary-adrenocortical system and improved the psychological state in MG patients.
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PMID:Low-dose glucocorticoid therapy complements the pituitary-adrenocortical system and reduces anxiety and insomnia in myasthenia gravis patients. 2224 Aug 58

Myasthenia gravis is a neuroimmunological disorder leading to skeletal muscle weakness. Common symptoms of the disease, such as anxiety, depression, and insomnia, can cause significant distress in patients. Unfortunately, selecting an appropriate medication for treatment of psychiatric comorbidities can prove to be challenging for providers given the unique pharmacologic constraints that myasthenia gravis presents. The authors present the following clinical vignette and accompanying discussion in an attempt to highlight the special considerations that must be taken into account when treating anxiety and insomnia in patients with myasthenia gravis, as well as to provide an overview of available medication options through the lens of existing constraints.
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PMID:Management of Insomnia and Anxiety in Myasthenia Gravis. 3117 4