Impact of Wartime Stress on Multiple Sclerosis Relapse Risk

Stress is associated with increased relapse activity in multiple sclerosis (MS), and the relentless pressures of wartime conditions can intensify that stress. This relationship affects people globally and, for many, coincides with heightened symptom burden and healthcare disruptions during conflict.

The stress response, which is integral to immune regulation, has been associated with higher relapse activity in MS. Multiple sclerosis—a chronic disease characterized by immune-mediated damage to the central nervous system—may be particularly sensitive to environmental stressors. In conflict settings, those stressors can compound daily uncertainty and access-to-care barriers, which together are associated with increased inflammatory activity and symptom exacerbations, as suggested by observational reports such as this community-based analysis.

Wartime stress, with its chronic nature, is associated with increased inflammatory activity and symptom exacerbation. In a prospective cohort report, conflict-related stress coincided with increases in clinical symptoms and markers of disease activity, rather than definitive measures of neurodegeneration.

Against the backdrop of conflict, recent discussions of MS pathophysiology highlight how stress pathways intersect with immune activation and neurodegenerative processes. This framing helps explain why periods of chronic stress can coincide with increased inflammatory activity and fluctuating symptoms, even as the causal chain remains uncertain.

For people living with MS during conflict, the lived experience often reflects this biology. Displacement, disrupted routines, and limited access to disease-modifying therapies can magnify stress and complicate symptom monitoring. Interruptions in rehabilitation, sleep, and physical activity further strain coping strategies, while curfews and safety concerns can delay urgent care for relapses. These factors do not prove that stress alone drives disease activity, but they illustrate how stress and system-level barriers interact in ways that may worsen day-to-day functioning.

Biologically, stress can modulate immune responses relevant to MS. Activation of the hypothalamic–pituitary–adrenal axis and sympathetic nervous system can shift cytokine balance and influence blood–brain barrier permeability, aligning with observations of inflammatory flares during periods of chronic stress. In conflict zones, repeated alarms, loss of social support, and resource scarcity may sustain these physiologic responses beyond typical recovery windows, which could help explain why symptoms feel less predictable during prolonged instability.

Evidence appraisals remain cautious. While observational cohorts and clinical anecdotes describe temporal links between high-stress periods and increased disease activity, heterogeneity in exposure measurement, confounding by disrupted care, and limited randomized data prevent definitive conclusions about causality or effect size. MRI and biomarker endpoints, where available, often align with increased inflammatory activity, but results vary and long-term neurodegeneration effects are uncertain.

In clinical practice, stress management is best framed as an important adjunct to disease-modifying therapy rather than a stand-alone disease-control strategy. Structured interventions, including cognitive-behavioral approaches summarized in this meta-analysis, have shown improvements in mood, anxiety, fatigue, and quality of life—patient-centered outcomes that can support resilience during periods of heightened stress.

Practical planning can mitigate the impact of conflict-related stressors on MS care. Patients and clinicians can develop medication continuity plans (extra supplies when feasible, refrigeration workarounds, and alternative pharmacies), identify reliable communication channels for urgent concerns, and prearrange infusion or injection sites if relocation becomes necessary. Documenting relapse history and current therapies, and storing this information securely yet accessibly, can streamline care transitions.

Self-management strategies also matter. Maintaining consistent sleep routines when possible, prioritizing gentle physical activity, and scheduling brief relaxation practices can help dampen stress reactivity. Social connection—whether with family, peers, or support groups—can provide emotional buffering. During periods of acute disruption, setting realistic expectations and focusing on controllable actions can reduce distress.

For healthcare teams, clear triage pathways and remote check-ins may sustain monitoring when in-person visits are unsafe or impractical. Short, structured symptom checklists and shared decision-making around steroid use for suspected relapses can balance risks and benefits when diagnostics are limited. Where mental health resources are scarce, brief CBT-informed tools, psychoeducation, and peer-led support can extend reach.

Limitations of the current evidence deserve emphasis. Most studies rely on self-reported stress, have small sample sizes, or lack rigorous control for confounders such as care interruptions and comorbid anxiety or depression. Conflict settings add further complexity, making it hard to disentangle stress effects from environmental and healthcare-access factors. Future work should prioritize standardized stress measures, prospective designs, and integration of MRI or biomarker endpoints to clarify mechanisms and quantify risk.

Key Takeaways:

• Conflict-related stress may heighten inflammatory activity and symptom burden in MS, particularly when access to care is disrupted.
• Most evidence is observational; associations should be interpreted cautiously rather than as proof of causation.
• Adjunct stress-management strategies, including cognitive-behavioral tools, can improve mood, anxiety, fatigue, and quality of life.
• Clinicians can help patients plan for conflict-related challenges (medication continuity, communication, and support) to buffer stress impacts.