Acute Bilateral Lower Extremity Weakness Due to Spinal Cord Hematoma Secondary to Amyloid Angiopathy: A Case Report
Emina Dzafic1, Hesham Kelani2, Ahmed Abd Elazim3, Lauren Hatcher4, Srikanth Adidam Venkata5, Selvalakshmi Rathinavelu6, Nataly Mor6, Artem Sunik6, Amit Khaneja6, David Lerner6, Lisa Merlin7, Diana Greene-Chandos8
1Touro college of Osteopathic Medicine, 2Department of Neurology, SUNY Downstate Health Science University At One Brooklyn Health Downstate Health sciences UniversityAt One Brooklyn Health, 3Sanford USD Medical Center, 4UNMH, 5SUNY Downstate Health Science University At One Brooklyn Health, 6Department of Neurology, SUNY Downstate Health Science University At One Brooklyn Health, 7SUNY Downstate Medical Center, 8St. Louis University SOM/SSM Health, Dept of Neurology
Background:
Cerebral amyloid angiopathy (CAA), is an age-related neurological disease characterized by deposition of amyloid beta proteins in cerebral blood vessels walls, causing vessels fragility and increased risk of hemorrhagic events. Prevalence of CAA varies with age with 5-9% among individuals aged 60-69 years, 43-58% in patients above 90 years, and up to 90% in Alzheimer disease patients. However spinal cord amyloid angiopathy (SCAA) is extremely rare, with very few cases documented in the literature. Here we report a unique case of spinal cord hematoma secondary to amyloid angiopathy, presenting as acute onset of lower extremity weakness in an elderly patient.
Results:
78 Years old female with unremarkable past medical history, presented with acute onset of back pain, bilateral Lower extremities weakness more on the left side and gait imbalance, with no history of trauma or recent falls and otherwise neurologically intact. Brain MRI showed subacute 14 mm left frontal intraparenchymal hematoma, scattered cortically located chronic microhemorrhages in both cerebral hemispheres with no evidence of acute infarction. Radiological findings are consistent with CAA, but still not explaining patient’s clinical presentation. MRI thoracic and lumbar spine showed spinal cord hemorrhage at the level of T11 and T12 without underlying lesions or vascular malformation. Radiological findings of the brain and spinal cord in the absence of trauma or anticoagulation made spinal cord amyloid angiopathy (SCAA) the main cause of spinal cord hematoma. Conservative treatment with blood pressure control, physical therapy, and avoiding unnecessary blood thinners resulted in improvement of motor power to baseline over a period of six weeks.
Conclusions:
This case highlights the possibility that neurological deficits caused by spinal cord hematoma secondary to SCAA can be the first presentation in patient with cerebral amyloid angiopathy and underscores the need of further research for better understanding of this disease.
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