Elsevier

Brain Research

Volume 1717, 15 August 2019, Pages 60-65
Brain Research

Research report
Impaired dynamic cerebral autoregulation in patients with cerebral amyloid angiopathy

https://doi.org/10.1016/j.brainres.2019.04.014Get rights and content

Highlights

Abstract

Cerebral amyloid angiopathy (CAA) might disturb the sensitive mechanism of cerebral pressure autoregulation. This study examines whether dynamic cerebral autoregulation (CA) is impaired in the posterior or anterior circulation of CAA patients. Fifteen patients with known CAA on magnetic resonance imaging (MRI) and 14 age-matched controls were examined with transcranial Doppler. Dynamic CA was assessed in the middle (MCA) and posterior cerebral artery (PCA) via transfer function phase and gain during respiratory-induced 0.1 Hz oscillations of arterial pressure. Within the patient group, 4 patients showed additional microbleeds in the basal ganglia on the MRI performed within the study (pure CAA vs mixed microbleeds). PCA phase was significantly lower in patients compared with controls (p = 0.018), particularly in patients with pure CAA (p = 0.0034). MCA values showed a similar but non-significant trend towards lower phase in patients with pure CAA. Poorer phase was associated with a higher number of microbleeds on MRI (MCA r = −0.57, p = 0.027; PCA r = −0.52, p = 0.098) and superficial cortical siderosis (PCA: p = 0.0025). In conclusion, dynamic cerebral autoregulation is impaired in patients with CAA. The degree of impairment is associated with the extent of cerebral microbleeds.

Section snippets

Introduction:

Cerebral amyloid angiopathy (CAA) is a major cause of intracerebral hemorrhage in the elderly (Banerjee et al., 2017). Accumulation of Amyloid β in cerebral arterioles characterizes the histopathology of the disease (Gahr et al., 2013). The pathophysiological link to the increased risk of cerebral hemorrhage, starting from micro- to macrovascular and subarachnoid sulcal hemorrhages, seems to be degradation of small vessels but perhaps also impairment of vasoregulation. Of interest, the risk of

Results

We included 15 patients and 14 controls in the final analysis. One control person had to be excluded because of previously-unknown severe cerebral small vessel disease (SVD) on brain MRI performed within the study.

Analysis of MRI scans performed within the study showed typical lobar microbleeds in all patients and in none of the control group. Within the patient group, 4 of 15 patients also showed multiple microbleeds in the basal ganglia, resulting in classification as mixed microbleeds.

Discussion

In this study we found that dynamic characteristics of cerebral autoregulation are impaired in patients with CAA and that the extent of autoregulatory impairment associates with the degree of microbleeds.

There are no previous studies on autoregulation of cerebral blood flow in CAA. The mechanism of neurovascular coupling was impaired in the PCA in patients with CAA, while cerebrovascular reactivity to hypercapnia was unaltered in the MCA in patients with CAA (Dumas et al., 2012, Smith et al.,

Methods and materials

Within a prospective observational study we included 15 patients according to the following inclusion criteria: 1. At least “probable” CAA according to Boston criteria (≥2 hemorrhages – including microbleeds on brain MRI, age ≥ 55 yrs, absence of other causes of hemorrhage, typical history) (van Rooden et al., 2009). 2. Absent history of non-lacunar ischemic stroke 3. No recent cerebral hemorrhage or any other neurological event within the previous 90 days. 4. Absence of stenosis >50% of brain

Disclosure

None of the authors received any financial compensation for their contribution to this study. There are no conflicts of interest.

References (25)

  • R.V. Immink et al.

    Impaired cerebral autoregulation in patients with malignant hypertension

    Circulation

    (2004)
  • A. Koller et al.

    Contribution of flow-dependent vasomotor mechanisms to the autoregulation of cerebral blood flow

    J. Vasc. Res.

    (2012)
  • View full text