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WGA Rescources

Editors Selection IGR 22-4

Clinical Examination Methods: Noninvasive Analysis of the Cerebrovascular Autoregulation

Alon Harris

Comment by Alon Harris on:

98779 Prospective Pilot Clinical Study of Noninvasive Cerebrovascular Autoregulation Monitoring in Open-Angle Glaucoma Patients and Healthy Subjects, Hamarat Y; Deimantavicius M; Dambrauskas V et al., Translational vision science & technology, 2022; 11: 17


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Glaucoma has long been associated with alterations in ocular and systemic hemodynamic factors, including faulty autoregulation of the retinal circulation during known vasoactive stimulus.1-3 Similarities in cerebrovascular and ocular tissues and blood vessel autoregulation pathways suggest the potential for shared mechanisms of disease through impairment of local tissue autoregulation. Diseases such as Alzheimer's and glaucoma both involve changes to microvascular tissues and subsequent neurodegeneration, and these shared pathways may be even more significant in patients of African descent.4 In the current article, Hamarat and colleagues present novel findings highlighting compromised cerebral autoregulation in patients with normal tension (NTG) based on a novel non-invasive ultrasonic technique utilizing intracranial blood volume slowwave measurements. The authors specifically found the volumetric reactivity index (VRx) and the duration and doses of longest cerebral autoregulation impairment (LCAI) were significantly lower (P < 0.05) in healthy subjects than in patients with NTG and high tension (HTG) glaucoma during a Valsalva maneuver (forceful breathing test). No statically significant differences were identified between healthy and HTG, or NTG and HTG subjects. Previously in my laboratories, we have used transcranial Doppler to identify an absence of vasoreactivity in the middle cerebral artery (MCA) during hyperoxia in glaucoma patients.5 These data compliment this finding, with a significant strength of the current approach being the inclusion of cerebrovascular autoregulation assessment over the entire cranium.

The non-invasive ultrasonic approach is highly translatable to a clinical setting

The non-invasive ultrasonic approach is highly translatable to a clinical setting, and may provide diagnostic enhancements for other brain diseases involving the microvasculature including traumatic brain injury (TBI) and patients with cardiac procedures. One limitation is the small patient sample and study power (ten NTG, eight HTG, and ten healthy) while the cross-sectional study design and lack of comparison to a Gold standard for cerebrovascular autoregulation suggest need for confirmation in larger prospective controlled trials. Future studies should also account for potential influence of race, age, gender, and diurnal fluctuation of autoregulation. In summary, the novel findings presented by Hamarat et al. are highly impactful in demonstrating the ability to non-invasively identify cerebrovascular autoregulatory deficits in patients with NTG in a clinical setting. These data highlight the potential shared relationship of cerebrovascular and retinal vascular tissues, especially patients with NTG, and suggest a potential utility in the diagnosis of other vascular brain impairments.

References

  1. Harris A, Guidoboni G, Siesky B, et al. Ocular blood flow as a clinical observation: Value, limitations and data analysis. J Prog Retin Eye Res. 2020:100841. PMID: 31987983
  2. Harris A, Martin BJ, Shoemaker JA. Regulation of retinal blood flow during blood gas perturbation. J Glaucoma. 1994;3 Suppl 1:S82-90.PMID: 19920593.
  3. Hosking SL, Harris A, Chung HS, et al. Ocular haemodynamic responses to induced hypercapnia and hyperoxia in glaucoma. Br J Ophthalmol. 2004;88(3):406-411.
  4. Hutchins K, Harris A, Thomas J, et al. Alzheimer's disease and primary open-angle glaucoma associated with vascular health in patients of African descent. Acta Ophthalmol. 2018;96(8):e1031.
  5. Harris A, Zarfati D, Zalish M, et al. Reduced cerebrovascular blood flow velocities and vasoreactivity in open-angle glaucoma. Am J Ophthalmol. 2003;135(2):144- 147.PMID: 12566016.


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