Mania as a Symptom of Hypertensive Emergency in Cerebral Amyloid Angiopathy

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, defines a manic episode, hallmark of bipolar 1 disorder, as 7 days of symptoms including grandiosity, decreased need for sleep, rapid and excessive speech, flight of ideas, racing thoughts, distractibility, increased goal-directed activity, and excessive involvement in dangerous or risky behaviors.¹ Cerebrovascular insults such as strokes and hemorrhages have been associated with the development of various neuropsychiatric symptoms. One systematic review estimated roughly 1.6% of stroke patients met criteria for mania.² There is scarce literature examining neuropathologic trends in patients exhibiting mania beyond the acute poststroke period. This report describes a case in which a patient presented with mania in the setting of cerebral amyloid angiopathy and hypertension that did not abate until treatment with antihypertensives.

Case Report

A 52-year-old man presented with 2 weeks of personality change, emotional lability, sleeplessness, and hypertensive urgency. He had no history of psychiatric disease. His wife noted that he exhibited similar symptoms 3 years earlier prior to having a right thalamic hemorrhagic stroke; at that time, magnetic resonance imaging (MRI) showed multiple bleeds consistent with amyloid angiopathy. On this presentation to the emergency department, the patient’s blood pressure reached 188/110 mm Hg. Head computed tomography ruled out acute abnormality, and an MRI of the brain showed “extensive foci of hemosiderin staining consistent with changes of amyloid angiopathy” without new strokes, masses, or bleeds. The patient was admitted to the hospital and started on quetiapine 100 mg. The patient denied psychotic symptoms, was oriented, and showed no evidence of dementia or any new neurologic deficit. As blood pressures normalized, mania persisted despite increase of quetiapine to 100 mg twice daily. The neurology department was consulted, and the patient was started on intravenous immunoglobulin (IVIG) for potential autoimmune encephalitis. However, lumbar puncture was ordered and was unremarkable aside from elevated protein. Autoimmune workup did reveal a positive antinuclear antibody; however, other autoimmune markers, including antibodies against voltage-gated potassium and calcium channels, were within normal limits. On day 3, the patient was started on a loading dose of divalproex 1,000 mg twice daily, which resulted in mild improvement of euphoria, though sleeplessness continued. He was started on temazepam 15 mg nightly. The patient became somnolent, but distractibility and euphoria persisted, prompting an increase of quetiapine to 300 mg. Divalproex dosing was adjusted to 1,500 mg nightly. Once the IVIG course was completed, the patient was transferred to the inpatient psychiatry unit. Upon transfer, his blood pressure remained elevated, with an initial blood pressure of 162/106 mm Hg with maximum systolic pressure of 183 and diastolic pressure of 107 during his week-long stay. While there, antihypertensives were titrated until his blood pressures stabilized below 140/90 mm Hg, which is when his mania symptoms also subsided 2 days before his discharge date. His final regimen of antihypertensives included hydralazine 100 mg twice daily, lisinopril 40 mg daily, nifedipine 90 mg daily, and hydrochlorothiazide 25 mg daily; his final blood pressure before discharge was 131/90 mm Hg. Divalproex sodium 1,500 mg nightly and quetiapine 300 mg nightly were continued throughout his inpatient psychiatric stay. The aforementioned medications were continued, and follow-up was arranged with primary care and psychiatry prior to discharge.

Discussion

Poststroke psychiatric changes are common, with 1 study indicating that 52.9% of patients develop this complication. While there is no definitive way to predict which patients will develop manic symptoms in the poststroke period, some factors show an association. Poststroke manic symptoms are more often seen in patients with right hemispheric lesions causing a dysfunction in the ventral limbic circuit that involves the right orbitofrontal and basotemporal cortices, dorsomedial thalamic nucleus, and head of the caudate nucleus.² Patients with poststroke mania are typically male, with no personal or family history of psychiatric disorder and no subcortical atrophy, but with at least 1 vascular risk factor. Prior to diagnosing poststroke mania, providers should rule out drug interactions, infections, metabolic derangements, neoplasm, or toxic exposure. Especially in the elderly, mania with organic etiology may be confused with delirium and cognitive impairment.³ Significant improvement in mania was seen when treated with atypical antipsychotics; benzodiazepines have also shown success as adjunct treatment, though efficacy can vary with stroke location. Mood stabilizers have also been efficacious, although lithium is controversial when used for cerebral lesions.² While there is no specific period of treatment for patients with poststroke mania, as with most psychiatric disorders, treatment is recommended until symptoms resolve and patients are stable. The exact neuropathological mechanism of why hypertension appeared to provoke manic symptoms in this patient is unclear, but neurovascular changes were likely involved. Further research is needed to assess the relationship between affective disorders and stroke and other vascular pathology.

Article Information

Published Online: March 19, 2026. https://doi.org/10.4088/PCC.25cr04097
© 2026 Physicians Postgraduate Press, Inc.
Prim Care Companion CNS Disord 2026;28(2):25cr04097
Submitted: October 1, 2025; accepted December 22, 2025.
To Cite: Becker E, Dharla VK, Chowdhury I, et al. Mania as a symptom of hypertensive emergency in cerebral amyloid angiopathy. Prim Care Companion CNS Disord 2026; 28(2):25cr04097.
Author Affiliations: Behavioral Health Department, Community Health Network, Indianapolis, Indiana (Becker, Dharla, Chowdhury, Karalis); Department of Family Medicine, Community Health Network, Indianapolis, Indiana (Budd).
Corresponding Author: Vijai Kumar Dharla, MD, Community Health Network, 6950 Hillsdale Court, Indianapolis, IN 46250 ([email protected]).
Financial Disclosure: None.
Funding/Support: None.
Previous Presentation: Previously presented as a poster at the Multidisciplinary Scholarly Activity Symposium at Community Health Network; May 14, 2024; Indianapolis, Indiana.
Additional Information: This case was reviewed by the Institutional Review Board at Community Health Network to ensure all patient-identifying information was removed to protect anonymity.
ORCID: Vijai Kumar Dharla: https://orcid.org/0000-0003-0942-1314