What peer‑reviewed studies exist on long‑term neurological outcomes after alleged 'Havana Syndrome' incidents?

Checked on January 26, 2026
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Executive summary

Peer‑reviewed literature on long‑term neurological outcomes after alleged “Havana Syndrome” or anomalous health incidents (AHIs) is small, heterogeneous and divided: several larger, more recent cohort studies led by U.S. government researchers report no MRI‑detectable brain injuries while earlier case series and mechanistic papers posit concussion‑like or neuroimmune disruption; systematic reviews emphasize weak evidence and unresolved causation [1] [2] [3] [4].

1. The peer‑reviewed landscape: few large cohorts, many case reports

The published record includes early case series and retrospective reports that described acute auditory‑vestibular and cognitive complaints in diplomats and intelligence officers (notably Swanson et al. in JAMA and similar retrospective studies), computational and mechanistic modeling papers, a 2022 scoping review that found only a handful of original studies with low levels of evidence, and larger multicenter NIH studies that applied advanced MRI and clinical batteries [5] [3] [4] [1].

2. Cohort studies and clinical outcomes: NIH’s multi‑year work

A nearly five‑year NIH program examined federal employees with AHIs using advanced imaging and in‑depth clinical assessments and reported no significant MRI‑detectable brain injury or biological abnormalities compared with controls, while documenting real, sometimes severe symptoms including dizziness, cognitive complaints and a high proportion meeting criteria for functional neurological disorders or persistent postural‑perceptual dizziness (PPPD) [1] [6] [7] [2].

3. Earlier case series that suggested structural injury or concussive‑like syndromes

Initial observational reports and smaller series—frequently retrospective and without matched controls—described patterns of sudden onset auditory phenomena followed by symptoms some investigators likened to mild traumatic brain injury (mTBI) or inner‑ear dysfunction; these reports fueled early concern about structural brain damage but were limited by sample size and methodology [8] [5] [4].

4. Mechanistic and modeling studies: neuroimmune, neurotransmission, or recovery trajectories

Peer‑reviewed mechanistic work includes computational regulatory‑pathway models that argue AHI symptoms could reflect dysregulation of neuroimmune and neurotransmission networks similar to patterns seen in mTBI, and which predict some biomarker differences and a slow recovery trajectory in small groups of subjects; these studies are hypothesis‑generating but not definitive proof of a specific injurious agent [3] [9].

5. Reviews, critiques and scientific reactions: persistent uncertainty and competing interpretations

A 2022 scoping review concluded the evidence base is weak and nonspecific, noting an acute auditory‑vestibular phase and a chronic neurobehavioral phase but no consensus on cause, while critical commentaries warn that framing the syndrome as novel brain injury risks nocebo effects and call for rigorously controlled studies; independent science media reactions to later larger studies highlighted that symptom differences (fatigue, PTSD, depression, imbalance) were found even where MRI abnormalities were absent [4] [5] [10].

6. What the peer‑reviewed record actually shows—and where it stops

In sum, peer‑reviewed work spans small retrospective case series, mechanistic modeling, a scoping review that found limited high‑quality evidence, and larger NIH investigations reporting no MRI‑detectable lesions but continuing symptom burden and frequent diagnoses such as FND or PPPD; none of the peer‑reviewed studies provides conclusive, universally accepted evidence linking a single external physical agent to persistent structural brain injury, and key gaps remain—particularly prospective, controlled long‑term outcome studies and reproducible biomarker signatures [1] [4] [3] [5] [10].

Want to dive deeper?
What prospective, controlled study designs would best test for long‑term neurological injury after anomalous health incidents?
Which biomarkers or imaging modalities have the greatest promise for detecting subtle brain injury and have they been applied to Havana Syndrome cohorts?
How have diagnostic labels like functional neurological disorder and PPPD been applied in other post‑acute syndromes and what does that imply for treatment and prognosis?