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2020, Number 1

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Rev Cubana Neurol Neurocir 2020; 10 (1)

Pathophysiological mechanisms involved in the relationship between sleep apnea-hypopnea and cerebral infarction

Guevara RM

Language: Spanish
References: 48
Page: 1-18
PDF size: 239.16 Kb.


ABSTRACT

Objective: To describe the pathophysiological mechanisms in the relationship between sleep apnea-hypopnea and cerebral infarction.
Evidence acquisition: A bibliographic search in Medline database was carried out, using the terms ischemic stroke prognosis or outcome; sleep apnea or sleep disordered breathing or apnea-hypopnea index, and pathophysiology mechanistic or endothelial dysfunction or inflammation. Forty-one original articles, 5 meta-analyzes and 4 systematic reviews, covering the topic from 2014 to 2019, were found.
Results: For each unit that increases the apnea-hypopnea index, the risk of cerebral infarction increases by 6%. Apnea episodes aggravate hypoperfusion in the injured brain area through a weak blood flow mechanism. After a first stroke, for each additional unit apnea-hypopnea index, the risk of mortality increases by 5%. The NIHSS scale increases by 17.6% in the group of apneic patients with cerebral infarction compared to 12.5% in non-apneic patients. Severe sleep apnea is self-sufficiently associated with Ranquin scale scores ≥2 6 months after stroke (OR: 9.7; 95% CI: 1.3-73.8; p = 0.03).
Conclusions: The main pathophysiological mechanisms involved in the relationship between sleep apnea-hypopnea and cerebral infarction were intermittent hypoxemia and hypercapnia, catecholaminergic discharge, autonomic dysfunction, oxidative stress, endothelial dysfunction, and systemic inflammation. Therefore, sleep apnea favors the development of vascular risk factors and predicts adverse outcomes after an ischemic stroke in terms of mortality, severity of the neurological deficit, complications, and functional recovery.


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