Persistent Cognitive Dysfunction in Postural Orthostatic Tachycardia Syndrome: A Scoping Review of Neural Mechanisms, Interventions, and Critical Research Gaps.

Authors

Ananya Rao Prassanna

Published in

Cureus. Volume 18. Issue 7. Pages e112862. Epub Jul 17, 2026.

Abstract

Postural orthostatic tachycardia syndrome (POTS) is widely treated as a cardiovascular-autonomic syndrome, but cognitive dysfunction is a disabling and poorly treated clinical phenomenon. This scoping review discusses why brain fog, impaired attention, slowed processing speed, memory difficulties, word-finding issues, and executive dysfunction may persist despite conventional pharmacological and non-pharmacological POTS treatments. The study uses a structured scoping review design to synthesize 18 peer-reviewed sources that meet the inclusion criteria, with publication dates between 2013 and 2025, across the domains of mechanistic, clinical, treatment, rehabilitation, and interventional studies. The evidence can be grouped into three principal mechanistic pathways: cerebral hypoperfusion and hemodynamic dysfunction; autonomic dysregulation and sympathetic overactivation; and neuroinflammation, autoimmune responses, mast cell activation, and microclot formation. The review found that abnormal cerebral blood flow (CBF) was reported in 61% of 56 POTS patients with cognitive dysfunction, and that sustained cognitive stress induced a greater reduction in CBF velocity in POTS patients than in controls, at approximately 7.8% and 1.8%, respectively. Current therapies, including beta-blockers, ivabradine, midodrine, exercise, salt and fluid loading, compression garments, cognitive behavioral therapy (CBT), and sleep management, rarely use cognition as a primary endpoint. Findings suggest that persistent cognitive dysfunction in POTS may reflect incomplete alignment between neurological mechanisms and cardiovascular-centered care, requiring validated cognitive outcomes and multimodal trials combining biological, autonomic, and rehabilitative interventions.

PMID:
42605371
Bibliographic data and abstract were imported from PubMed on 17 Aug 2026.

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