Seizures in Patients with Cerebral Amyloid Angiopathy: A Preliminary Report
Abstract number :
2.432
Submission category :
4. Clinical Epilepsy / 4B. Clinical Diagnosis
Year :
2022
Submission ID :
2232972
Source :
www.aesnet.org
Presentation date :
12/4/2022 12:00:00 PM
Published date :
Nov 22, 2022, 05:29 AM
Authors :
Aafreen Khan, MBBS – Mayo Clinic College of Medicine and Science; Brin Freund, MD – Neurology – Mayo Clinic College of Medicine; Sofia Sánchez-Boluarte, MD – Neurology – Instituto Nacional de Ciencias Neurologicas, Peru.; Karen Blackmon, Ph.D – Psychiatry – Mayo Clinic College of Medicine; Michelle Lin, MD – Neurology – Mayo Clinic College of Medicine; Anteneh Feyissa, MD – Epilepsy – Mayo Clinic College of Medicine; Erik Middlebrooks, MD – Radiology – Mayo Clinic College of Medicine; William Tatum, DO – Director of Epilepsy, Epilepsy, Mayo Clinic College of Medicine
This is a Late Breaking abstract
Rationale: Cerebral amyloid angiopathy (CAA) is characterized by the accumulation of amyloid-β deposits within the small to medium-sized cortical and leptomeningeal blood vessels with a prevalence of 7% in cognitively normal elderly patients and 22% to 48% in those with Alzheimer’s disease. A common acute presentation of CAA is lobar intracerebral hemorrhage (ICH).There are limited data on seizures and their association with CAA. Therefore, we performed a study to identify the prevalence and predictors of seizures in patients with CAA.
Methods: We performed a retrospective study of patients with CAA seen at Mayo Clinic Florida from January 1, 2015, to January 1, 2021. Diagnostic codes were used as EHR search criteria, and CAA diagnosis was confirmed by reviewing neuroimaging using the modified Boston criteria. Demographic, clinical and neuroimaging characteristics were compared between patients with and without seizure.
Results: A total of 364 patients were identified in the initial screening using ICD10 codes. Ongoing analysis confirmed CAA in 194 of these patients (53%), with an average follow-up duration of 23.1 months (IQR: 6.9-47.2). Mean age was 75.16 and 93 (47.94%) were women. Thirty-six (18.56%) had presenting symptoms of ICH. 85 (43.81%) manifested cognitive impairment. Forty-four (22%) developed seizures at onset or following a diagnosis of CAA. Focal to bilateral tonic-clonic seizures were seen in majority of patients. Superficial siderosis (SS) was observed on neuroimaging in 17 (38.6%) patients with seizures and 43 (28.6%) patients without seizures (p= 0.248). At least one macrohemorrhage was seen in 13 (29.5%) patients with seizures and 33 (22%) without seizures (p=0.516). Abnormal EEG was present in 33 patients (82.5%) with ten (30.3%) correlating with the location on neuroimaging findings. At the time of a seizure diagnosis, mild cognitive impairment (MCI) was present in 29 (65.9%) and dementia (of varying severity) in 9 (20.45%) patients. The median duration of follow up was 37.85 months (IQR: 15.1-65.6), during which 55/194 (28.3%) died, and 11/55 (20%) of these patients had seizures.
Conclusions: Seizures are not an uncommon clinical manifestation of CAA. Overall, 22% of patients developed epilepsy and 25% presented with seizures leading to the diagnosis of CAA. SS and macrohemorrhages were a risk factor for seizures in our population. Further studies should expand upon risk factors for epilepsy in patients with CAA and the relationship to neuroimaging and cognition.
Funding: No targeted funding reported
Clinical Epilepsy