Table 3.
Study | Topic | Patient population [n; age (yrs ± SD)] | Clinical presentation | Image analysis | Main results | Comments |
---|---|---|---|---|---|---|
(Dierksen et al., 2010)a | Microbleeds | Probable CAA (n = 16; 64.0 ± 11.8) | LICH (n = 9) | DVR (cerebellum) | Significant relationship between PiB retention and microbleeds location | 7 pathology-confirmed CAA patients |
(Ly et al., 2010a)a |
Post-thrombolysis ICH |
HC (n = 15; 74) ICH (n = 7; 77) No ICH (n = 8; 77) |
Ischemic stroke treated with rt.-PA within 3 h | DVR (cerebellum) | Higher PiB binding in patients with vs those without ICH and vs HCs | No symptomatic ICH studied. Topography of ICH (within or remote from infarct) not assessed. PiB not increased in simple haemorrhagic transformation. |
(Gurol et al., 2012) | Prediction of new ICH | Probable CAA (n = 11; 70.9 ± 8.6) | LICH (n = 5) Other (e.g., seizure, gait problems; n = 6) |
DVR (cerebellum) | New CAA-related haemorrhages (CMBs or ICH) occur preferentially at sites of increased amyloid deposition |
PiB uptake in a superior frontal/parasagittal aggregate ROI was predictive of the number of new haemorrhages. |
(Dhollander et al., 2011)a | cSS | Probable CAA (n = 1; 76); possible CAA (n = 1; 72) | cSS | DVR | PiB uptake significantly higher in the immediate vicinity of cSS | – |
(Na et al., 2015)a | cSS | Whole sample (n = 232; 72.2 ± 8.1) 1) AD (n = 90) 2) SVCI (n = 142) |
cSS (n = 12) No cSS (n = 220) |
SUVr | cSS present in both AD and SVCI, but never in PiB (−) patients, supporting the hypothesis that cSS reflects an amyloid rather than ischemic process |
|
(Ly et al., 2015)a | cSAH | Probable CAA, n = 7 (n = 2 with supporting pathology) | Non-aneurysmal cSAH | Visual analysis of summed 40-70 min images | 7/7 PiB + ‘consistent with CAA’ | Case series of 7 patients; no comparison to healthy controls or AD patients. PiB PET performed 3–36 months after cSAH. Three pts. had LICH at follow-up: no clear topographical relationship with PiB cortical burden. |
(Gurol et al., 2013)a | WMH |
|
LICH (n = 23) Other (n = 19) |
DVR (cerebellum) | Global PiB retention and WMH showed strong correlation (rho = 0.52, p < 0.001) in the CAA group but not in HC or AD | No significant PiB-WMH correlation in AD and HCs. |
(Charidimou et al., 2015a)a | CSO-PVS |
|
LICH | DVR |
PIB retention higher in high vs low CSO-PVS degree (p = 0.0007). |
Whole cortex PiB retention associated with CSO-PVS degree both as continuous (p = 0.040) and dichotomous variable p = 0.002). Finding present both in the whole sample (HC + CAA) and in CAA only. No significant relationship between PiB and basal ganglia PVS. |
(Carmona-Iragui et al., 2016)b | CAA-ri | Probable CAA-ri (n = 4); two patients only underwent PET | CAA-ri | SUVr (visual assessment) | Both patients PiB + | PET performed 13–19 months after corticosteroids. Pre-treatment PET not obtained. No comparison to HCs or AD. Lower PiB uptake in previously edematous areas. |
(Reijmer et al., 2015)a | Cognitive impairment | Probable CAA (n = 29) | LICH (n = 17); other (n = 21) | DVR (cerebellum) | Lower global network efficiency related to higher cortical PiB uptake (p = 0.004) | Structural brain network studied with MRI (DTI). CAA patients with predominantly posterior PiB retention showed lower connection strength in posterior nodes. |
CAA: cerebral amyloid angiopathy; HC: healthy control; ICH: intracerebral haemorrhage; L: lobar; rt.-PA: recombinant tissue-type plasminogen activator; WMH: white matter hyperintensities; CSO-PVS: centrum semiovale perivascular spaces; cSS: cortical superficial siderosis; AD = Alzheimer disease; SVCI: subcortical vascular cognitive impairment; CAA-ri: cerebral amyloid angiopathy-related inflammation; pts.: patients; PiB + and PiB −: PiB positive and PiB negative PET scan, respectively; cSAH: convexity subarachnoid haemorrhage; DTI: diffusion tensor imaging.
PiB.
Florbetapir.