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  • Title: [Changes in regional CNS perfusion in obstructive sleep apnea syndrome: initial SPECT studies with injected nocturnal 99mTc-HMPAO].
    Author: Ficker JH, Feistel H, Möller C, Merkl M, Dertinger S, Siegfried W, Hahn EG.
    Journal: Pneumologie; 1997 Sep; 51(9):926-30. PubMed ID: 9411446.
    Abstract:
    Some of the clinical features of obstructive sleep apnoea syndrome (OSA) are suggestive of impaired cerebral blood flow. Cerebral blood flow alterations might, for example, be responsible for headaches, which are frequent complaints in patients with OSA. Even the high frequency of ischaemic cerebral complications in patients with OSA might be caused in part by sleep apnoea-associated impairment of cerebral perfusion. Previous studies have demonstrated reduced total cerebral blood flow in patients with OSA, but regional changes of cerebral perfusion have not been studied up to now. We performed SPECT studies using 99mTc-(d,l)-hexamethyl-propylenaminoxim (HMPAO) as a tracer in 14 adult patients with moderate to severe OSA (AHI > 30/h; mean AHI 59.2 +/- 4.3). The injection of the tracer took place between 2:00 and 4:00 a.m. while repeated episodes of obstructive apnoea were detected by polysomnography during stage II sleep. Data acquisition took place at 7:30 a.m. All measurements were repeated some nights later under effective treatment with nCPAP. Visual analysis showed marked frontal hyperperfusion in 5 patients. When regional perfusion indices were calculated for 32 regions of interest statistical analysis showed reduced perfusion of the left parietal region. These changes were completely reversed by effective nCPAP therapy. These data suggest that OSA is associated with reversible changes of regional cerebral perfusion. The underlying pathophysiologic mechanisms are matter of speculation so far. There might be an apnoea-associated effect of local vascular autoregulation mechanisms acting to compensate systemic blood flow alterations or blood gas changes in OSA. The observed frontal hyperperfusion might be caused by activation of the frontal lobe by repetitive cortical arousals.
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