Brain Injury Can Stun the Heart in Children, Pooled Analysis Shows

When a child suffers a devastating brain injury, the damage is not always confined to the skull. In a striking example of how intimately the brain and heart are connected, acute neurological insults can trigger a sudden, often dramatic form of heart failure known as neurogenic stunned myocardium. The condition has been well documented in adults, particularly after subarachnoid hemorrhage, but in children it has remained a shadowy entity known mostly through scattered case reports. Now, a systematic review and pooled individual-level analysis published in Neurocritical Care has brought together nearly every documented pediatric case to date, offering the clearest picture yet of how this reversible cardiac syndrome behaves in young patients and which signs point toward recovery or catastrophe.

The research team, led by Cédérick Montplaisir and senior author Alexander G. Weil of the University of Montreal and Sainte-Justine University Hospital Centre, conducted the review according to the Meta-analysis Of Observational Studies in Epidemiology, or MOOSE, guidelines. The investigators searched PubMed, Web of Science, and the Cumulative Index to Nursing and Allied Health Literature from their inception through November 2025, looking for studies reporting patients aged 18 years or younger with neurogenic stunned myocardium and available outcome data. From the literature they identified 29 studies encompassing just 38 children, a small number that underscores how rare and under-recognized the condition is in pediatrics. Yet by pooling individual patient data rather than merely counting studies, the team was able to extract patterns that no single case report could reveal.

The children in the pooled cohort had a mean age of 7.7 years, and their cardiac dysfunction emerged on average 60.8 hours after the neurological injury, a delay that clinicians may find counterintuitive. Rather than striking at the moment of brain insult, the heart often falters a day or more later, when attention may already be fixed on the primary neurological problem. Ventricular dysfunction was present in 94.7 percent of the children, and the pattern of wall-motion abnormalities frequently involved the basal segments of the heart, a distribution that overlaps with, but is not identical to, the classic apical ballooning seen in adult Takotsubo cardiomyopathy. This basal hypokinesis suggests that the pediatric version of the syndrome may have its own distinct fingerprint on echocardiography.

The underlying neurological triggers were heterogeneous. Reported causes included subarachnoid hemorrhage, traumatic brain injury, hydrocephalus, brain tumors and their surgical treatment, intracranial infections, acute myelitis, ruptured arteriovenous malformations, and even nonaccidental head trauma. In several reported cases, the cardiac crisis was the first and most alarming manifestation of the brain pathology, forcing clinicians to look upward from the bedside monitor to the head. Some children required advanced mechanical support, including extracorporeal membrane oxygenation, when the stunned heart could no longer sustain circulation. The diversity of triggers reinforces the idea that any acute central nervous system injury, whether hemorrhagic, traumatic, infectious, or surgical in origin, can potentially unleash the autonomic storm that stuns the myocardium.

The proposed mechanism centers on a massive, unregulated surge of catecholamines and autonomic dysregulation. Acute brain injury, particularly when it involves the insula, hypothalamus, or brainstem, can generate a torrent of sympathetic nervous activity that floods the heart with norepinephrine released from cardiac nerve endings. This catecholamine excess is thought to cause direct myocyte injury, microvascular dysfunction, and metabolic derangement within heart muscle cells, producing transient contractile failure without obstructed coronary arteries. Elevated levels of cardiac biomarkers such as troponin, along with electrocardiographic changes and echocardiographic wall-motion abnormalities, typically accompany the syndrome. Because the injury to the myocardium is functional rather than structural, the heart often recovers completely within days to weeks if the child survives the acute phase, which is precisely why the condition is described as stunned rather than infarcted.

The outcomes in the pooled cohort were a study in contrasts. On the encouraging side, 71.1 percent of the children achieved a favorable neurological outcome, defined as a modified Rankin Scale score of 0 to 2, indicating little or no disability. This proportion is remarkably high given the severity of the brain injuries involved and supports the notion that pediatric neurogenic stunned myocardium is usually reversible. On the sobering side, cardiac arrest occurred in 26.3 percent of the children and mortality reached 23.7 percent. In other words, roughly one in four children with the condition suffered a cardiac arrest, and nearly one in four died, figures that make the syndrome far more than a benign curiosity. The dual message, that recovery is common but the acute phase is genuinely dangerous, is the central clinical takeaway of the analysis.

The individual-level data also yielded prognostic signals that could help clinicians stratify risk at the bedside. Subarachnoid hemorrhage was associated with a worse neurological outcome compared with other neurological insults, marking it as the most ominous trigger in the pediatric population. Conversely, two neurological findings predicted a favorable course: the absence of pupil abnormalities and the preservation of reflexes. These are simple, rapidly assessable signs available in any intensive care unit, and their association with good outcomes suggests that intact brainstem function at presentation may be a key determinant of recovery. The authors emphasize that early recognition of the cardiac syndrome, combined with multidisciplinary management involving neurocritical care, cardiology, and intensive care teams, may improve outcomes, although the observational nature of the evidence cannot prove causation.

The study’s methodology deserves attention because it represents an increasingly popular middle path between narrative reviews and large randomized trials. By pooling individual patient data from 29 studies, the investigators could standardize variable definitions, analyze outcomes at the level of the child rather than the study, and apply the modified Rankin Scale as a common functional outcome measure. The team assessed risk of bias using established tools for prognostic studies and followed the JBI Manual for Evidence Synthesis for the review process. Still, the authors are candid about the limitations. Thirty-eight patients is a very small sample, the evidence consists almost entirely of case reports and case series subject to publication bias, and the absence of prospective pediatric cohorts means that the true incidence of the condition remains unknown. Many children with mild cardiac dysfunction after brain injury may never be diagnosed, meaning the pooled cohort likely captures only the most severe end of the spectrum.

What the analysis makes unmistakably clear is that pediatric neurocritical care teams should keep the heart on their radar whenever a child sustains an acute brain injury. Unexplained hypotension, pulmonary edema, arrhythmias, or a sudden drop in cardiac output hours to days after neurological deterioration should prompt urgent echocardiography and consideration of neurogenic stunned myocardium. Treatment is largely supportive, focusing on hemodynamic support with inotropes or mechanical circulatory assistance when needed while avoiding excessive catecholamine loading, and simultaneously treating the primary brain pathology. The authors call for larger prospective studies to refine prognostic stratification and establish evidence-based management protocols. Until such studies exist, this pooled analysis of nearly four decades of pediatric cases provides the best available map of a rare but treacherous syndrome in which a broken brain can, at least temporarily, break the heart.

Subject of Research: Pediatric neurogenic stunned myocardium, a reversible cardiac dysfunction triggered by acute neurological injury in children

Article Title: Pediatric Neurogenic Stunned Myocardium: A Systematic Review and Pooled Individual-Level Analysis

Article References: Montplaisir, C., Packirisamy, S., Lee, N., Niazi, F., Han, A., Korman, C., Phaneuf-Garand, N., Brunette-Clément, T., Lahlou, K. S., Carmona, X., Pellan-Sayegh, A., Venne, D., Dupont-Thibodeau, G., Bojanowski, M. W., Hadjinicolaou, A., & Weil, A. G. (2026). Pediatric Neurogenic Stunned Myocardium: A Systematic Review and Pooled Individual-Level Analysis. Neurocritical Care. https://doi.org/10.1007/s12028-026-02652-7

Image Credits: AI Generated

DOI: 10.1007/s12028-026-02652-7

Keywords: neurogenic stunned myocardium, pediatrics, neurocritical care, Takotsubo cardiomyopathy, subarachnoid hemorrhage, traumatic brain injury, systematic review, ventricular dysfunction, catecholamines, cardiac arrest, modified Rankin Scale, autonomic dysregulation