Circumscribed cortical subarachnoid hemorrhages (SAHs) present with cephalgia, focal/generalized seizures, and focal neurological deficits. They are rarely of aneurysmal origin, and differential diagnosis is broad but should include ascorbic acid deficiency (AAD) when there is suspicion of nutritional deficiency. We report the case of a middle-aged woman with multiple comorbidities and malnutrition, evaluated for provoked seizure due to cortical SAHs with underlying AAD.

AAD causes a constellation of systemic signs and symptoms, including spontaneous bleeding that may affect the central nervous system. Ascorbic acid (AA) indirectly affects the transcription of various types of collagen and allows hydroxylation and crosslinking of pro-collagen, found in the blood vessel walls, and explain how AAD is a risk factor of spontaneous intracerebral hemorrhage (ICH).

Case report, literature review.

45-year-old woman with diabetes mellitus type 2 complicated with diabetic retinopathy, hypertension, end-stage renal disease on hemodialysis, and malnutrition (BMI 16.8), admitted for acute hypoxic/hypercapnic respiratory failure secondary to bilateral pleural effusions and Neurology consulted for transient neurologic deficit manifested by decreased level of consciousness followed by left hemiparesis with rapid improvement, likely secondary to focal seizure with impaired awareness. No history of fall or head trauma. Head CT revealed spontaneous cortical bi-frontoparietal SAHs. GRE/SWI brain MRI additionally showed numerous microbleeds. MR angiogram revealed intracranial atherosclerotic disease but no vascular malformations/aneurysms/arterial beading. Given malnutrition with suspected AAD due to spontaneous SAHs, patient was started on empiric AA replacement (500 mg IV BID) and levetiracetam (renally dose). Patient’s neurological examination remained non-focal, and workup confirmed AAD (<0.1, normal value: 0.4-2.0).

AAD should be included in the differential diagnosis of spontaneous SAHs. Patients with history of prolonged hospitalization, severe illnesses, and poor diet are at a higher risk. Immediate supplementation is critical, given that oral replacement is easy and deficiency is rapidly reversible.