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Sleep apnoea

The primary symptom of sleep apnoea[2] is morning headache and general fatigue after waking up. People who suffer from this ailment often sleep restlessly, fidget while sleeping, can not find a suitable position for the duvet and the pillow. Another symptom of sleep apnoea is frequent waking up and rapid inhaling the air through mouth. Such restless sleeping instead of regenerating and adding vitality, unables proper rest. The lungs of the patient are not supplied with the adequte amount of the air and consequently, the blood is not properly oxygenated, which causes the whole range of disorders in the entire body.

OSA – Obstructive Sleep Apnea

Obstructive sleep apnoea (OSA) is a commonly registered disorder, whose association with the development of cardiovascular complications has been well documented[15]. Sleep apnoea (abnormal breathing during sleep) is a serious, potentially life-threatening syndrome. The rate of OSA occurance in population is estimated, depending on the source, at 2% at women and 4% at men[6], between 5 and 10%[7], 5.7% at females and 12.4% males[8]. The most common type of sleep apnoea, covering about 85% of cases, is called OSA – Obstructive sleep apnoea, caused by repeated stopping of the air flow in the upper airway (throat or nose) blocking breathing, despite more intensive activity of the lungs.

Symptoms of obstructive sleep apnoea

  • noticed by the partner: loud snoring and noticeable apnea periods
  • noticed by the patient: sudden awakening during the night, usually with the feeling of fear and confusion, at daytime signs of deteriorated  concentration and sleepiness, which in extreme cases can take the form of Pickwick syndrome with episodes of unwitting, short-term falling asleep in inadequate circumstances, eg. in the course of driving.

Sleep apnoea condition is often accompanied by other afflictions such as:

  • obesity,
  • cardiac arrhythmias[13]
  • hypertension,
  • decreased libido,
  • persistent migraine.

It was also proved that there is a connection between sleep apnoea and osteoporosis[9].

The causes of obstructive sleep apnoea – OSA?

Sleep apnoea (Obstructive Sleep Apnea Syndromes – OSAS) is often a consequence of abnormalities  in the structure of the upper respiratory tract, such as polyps[3], crooked nasal septum, post-infection hypertrophied tissue, abnormal structure of the jaw, overly flabby muscles of the palate, obesity,drinking alcohol, overeating before going to bed, smoking. It is usually one of the sources increasing oxidative stress[14]. Men due, to the throat structure, are more prone to this disease than women.

German organization ADAC[1] deals with analysing  the state of health of drivers, causing accidents. It turns out that more than 40% of the perpetrators suffer from sleep apnoea. The consequence of the disease is significantly impaired concentration while driving and overlong psychomotor reaction.

Plenty of scientific studies indicate that  people affected by sleep apnoea more often than others experience heart attacks and strokes[4], type 2 diabetes, hypertension, neurological disorders, declining libido.

Apnea can also have central roots, ie. disruption of brain function controlling breathing. At healthy individuals, the brain sends to muscles signals regulating breathing, and at ill people the  brain seems to have forgotten about this feature.

Types of sleep apnoea

The most common form of the disease (up to 99 per cent. of cases) is a peripheral apnea, which is caused by the existence of the obstacle blocking the airflow. The remaining 1 percent is mixed apnoea (provoked by the obstacle and neurological disorders) and central, which is the one caused by neurological disorders[5].

Prevention

  • At obese people – Absolute weight loss
  • abstinence from alcohol and nicotine
  • adoption of appropriate posture during sleeping (eg. the side, not on the back)[10][11]
  • the use of CPAP or continuous positive airway pressure[12]

Sources

  1. ADAC: Allgemeiner Deutscher Automobil-Club: https://www.adac.de/default.aspx
  2. Sleep apnea: https://en.wikipedia.org/wiki/Sleep_apnea
  3. Polipy rozwijają się jako reakcja błony śluzowej nosa na działające czynniki drażniące, takie jak alergeny czy infekcje. Charakteryzują się skłonnością do nawrotów, występują zwykle obustronnie. Drażniona błona śluzowa rozrasta się, tworząc „workowate” uwypuklenia. Występują częściej u mężczyzn w średnim wieku, nie są spotykane u dzieci poniżej 7 roku życia. http://www.emedica.pl/choroby/opis/170-polipy-nosa.html
  4. Strokes: https://en.wikipedia.org/wiki/Stroke
  5. Rodzaje bezdechu: http://www.poradnikzdrowie.pl/zdrowie/uklad-oddechowy/bezdech-senny-objawy-przyczyny-i-leczenie-bezdechu-nocnego_40441.html
  6. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The Occurrence of Sleep-Disordered Breathing among Middle-Aged Adults. „N Engl J Med”. 32, s. 1230–1235, 1993.
  7. David M. Hiestand, Pat Britz, Molly Goldman, and Barbara Phillips. Prevalence of Symptoms and Risk of Sleep Apnea in the US Population. „Chest”. 130, s. 780–786, 2006.
  8. Laila Simpson, David R. Hillman, Matthew N. Cooper. High prevalence of undiagnosed obstructive sleep apnoea in the general population and methods for screening for representative controls. „Sleep Breath”. 17, s. 967–973, 2013.
  9. YL. Chen, SF. Weng, YC. Shen, CW. Chou i inni. Obstructive sleep apnea and risk of osteoporosis: a population-based cohort study in Taiwan. „J Clin Endocrinol Metab”. 99 (7), s. 2441-2447, 2014.
  10. [10] Loord H., Hultcrantz E. Positioner–a method for preventing sleep apnea. „Acta Otolaryngol”. 8 (127), s. 861-868, 2007.
  11. Szollosi I., Roebuck T., Thompson B., Naughton MT. Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration. „Sleep”. 29 (8), s. 1045-1051, 2006.
  12. R. Nisha Aurora, Susmita Chowdhuri, Kannan Ramar et al.. The Treatment of Central Sleep Apnea Syndromes in Adults: Practice Parameters with an Evidence-Based Literature Review and Meta-Analyses.
  13. Główczyńska R., Kukwa W., Opolski G.: Choroby serca – powikłania u chorych na obturacyjny bezdech podczas snu. Pneumnol. Alergol. Pol. 2007; 75: suppl. 1, 50–56.
  14. Zespół obturacyjnego bezdechu sennego – ma złożoną patogenezę; ANN przewlekły może być jednym z jej elementów. Zwykle jest jednym ze źródeł nasilenia stresu oksydacyjnego – http://www.sciencedirect.com/science/article/pii/S2353385415001234.
  15. Obturacyjny bezdech senny (OBS)https://journals.viamedica.pl/choroby_serca_i_naczyn/article/view/38788.
  16. Povitz M, Bolo CE, Heitman SJ, Tsai WH, Wang J, James MT (2014) Effect of Treatment of Obstructive Sleep Apnea on Depressive Symptoms: Systematic Review and Meta-Analysis. PLoS Med 11(11).
  17. Hisanaga A, Saitoh O, Fukuda H, Kurokawa K, Okabe A, Tachibana H, Hagino H, Mita T, Yamashita I, Tsutsumi M, Kurachi M, Itoh T. “Treatment of obstructive sleep apnea syndrome with a Kampo-formula, San’o-shashin-to: a case report”, Psychiatry and Clinical Neurosciences (Volume 53, Issue 2, pages 303–305, April 1999).
  18. Guilleminault, Christian, Frederic L. Eldridge, and William C. Dement. “Insomnia with sleep apnea: a new syndrome.” Science 181.4102 (1973): 856-858.
  19. Brooks, Dina, et al. “Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model.” Journal of Clinical Investigation 99.1 (1997): 106.
  20. Logan, Alexander G., et al. “High prevalence of unrecognized sleep apnoea in drug-resistant hypertension.” Journal of hypertension 19.12 (2001): 2271-2277.
  21. Fung, Jeffrey WH, et al. “Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction.” CHEST Journal 121.2 (2002): 422-429.

Bibliography

  1. Akashiba T., Akahoshi T., Kawahara S., Majima T., Horie T.: Effects of long-term nasal continuous positive airway pressure on C-reactive protein in patients with obstructive sleep apnea syndrome. Intern. Med. 2005
  2. Alonso-Fernandez A., Garcia-Rio F., Arias M.A., Hernanz A., de la Pena M., Pierola J., Barcelo A., Lopez-Collazo E., Agusti A.: Effects of CPAP on oxidative stress and nitrate efficiency in sleep apnoea: a randomised trial. Thorax 2009
  3. Alzoghaibi M.A., Bahammam A.S.: Lipid peroxides, superoxide dismutase and circulating IL-8 and GCP-2 in patients with severe obstructive sleep apnea: a pilot study. Sleep Breath 2005
  4. American Academy of Sleep Medicine. International classification of sleep disorders, 2nd ed.: Diagnostic and coding manual. Westchester, Illinois: American Academy of Sleep Medicine 2005.
  5. American Academy of Sleep Medicine. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research: the report of an American Academy of Sleep Medicine Task Force. Sleep 1999
  6. Arnardottir E.S., Mackiewicz M., Gislason T., Teff K.L., Pack A.I.: Molecular signatures of obstructive sleep apnea in adults: a review and perspective. Sleep 2009
  7. Barcelo A., Barbe F., de la Pena M., Vila M., Perez G., Pierola J., Duran J., Agusti A.G.: Antioxidant status in patients with sleep apnoea and impact of continuous positive airway pressure treatment. Eur. Repir. J. 2006; 27: 756–760.
  8. Bonsignore M.R., Zito A.: Metabolic effects of the obstructive sleep apnea syndrome and cardiovascular risk. Arch. Physiol. Biochem. 2008
  9. Flemons W.W.: Clinical practice. Obstructive sleep apnea. N. Engl. J. Med. 2002; 347: 498–504.
  10. Jennum P., Riha R.L.: Epidemiology of sleep apnoea/hypopnoea syndrome and sleep-disordered breathing. Eur. Respir. J. 200
  11. Wysocka E., Cofta S., Piorunek T., Dzięgielewska-Gęsiak S., Bryl W., Torliński L.: Blood antioxidant status, dysglycemia and obstructive sleep apnea. Adv. Exp. Med. Biol. 2013

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