Objective. To identify clinical and non-hemorrhagic neuroimaging indicators of probable CAA in patients with acute non-traumatic lobar hematomas. Cerebral amyloid angiopathy (CAA) is a microangiopathy affecting the leptomeningial and cortical vessels of the brain due to the deposition of pathological b-amyloid in them. The most common clinical manifestation of CAA is lobar hematomas (LH) – spontaneous intracerebral hemorrhages localized between the cerebral cortex and basal ganglia. LH can also occur in hypertensive cerebral microangiopathy (hCMA) in patients with arterial hypertension. Since the tactics of managing patients with CAA and hCMA differ, it is important to determine the genesis of LH correctly.
Materials and methods. A comparative analysis of clinical and neuroimaging characteristics of acute non-traumatic hypertension in 32 patients with probable CAA and hCMA was carried out. Along with neurological examination and neuroimaging, all patients underwent a study using the Montreal Cognitive Assessment Scale and the Benson Complex Figure Test to reveal visuospatial impairments. The diagnosis of probable CAA was carried out in accordance with the updated Boston criteria of 2010, the diagnosis of hCMA was based on clinical data, anamnesis and results of neuroimaging of the brain.
Results. Probable CAA was diagnosed in 16 patients, and in all these cases it was combined with hCMA (1st subgroup). Isolated hCMA as a cause of LH was also observed in 16 patients (2nd subgroup). Patients of subgroup 1 were statistically significantly more likely to have clinically pronounced visual impairments, performed the MoCA subtest and the Benson Complex Figure Test worse, and the overall assessment of their cognitive functions according to Mo SA was lower than in patients of subgroup 2. According to neuroimaging data, in the 1st subgroup of patients, an expansion of perivascular spaces in the semi-oval center and a zero or negative value of the front-occipital gradient were more often detected. The application of the logistic regression method made it possible to integrate potential CAA indicators and create a prognostic model for revealing this pathology in patients with hypertension.
Conclusions. Clinically pronounced disorders of primary and higher visual functions, a negative front-occipital gradient and expansion of perivascular spaces in the semi-oval centers can serve as indicators of probable CAA in patients with acute lobar hematoma. On admission of such patients to the vascular center, it is advisable to include iron-sensitive pulse sequences in the neuroimaging screening protocol to verify the diagnosis of CAA.
