ArticleCureus2026
The Heart-Brain Connection: Acute Intracranial Pressure Elevation as a Cause of Isolated Bradycardia.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Paradoxical reflex bradycardia in paroxysmal sympathetic hyperactivity following traumatic brain injury: a case report.Frontiers in neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bradyarrhythmias are commonly attributed to intrinsic conduction disease, ischemia, or medication effects; however, not all etiologies are cardiac in origin. Acute elevation in intracranial pressure (ICP) can provoke clinically significant bradycardia, sometimes without the complete Cushing triad. We describe a 50-year-old nonverbal man with marginal zone lymphoma on rituximab, prior cerebrovascular accident, seizure disorder, and chronic hydrocephalus managed with a ventriculoperitoneal (VP) shunt who presented with lethargy and hypotension during rituximab infusion and was found to have pneumonia with acute hypoxemic respiratory failure (AHRF). During hospitalization, he developed recurrent profound bradycardia with sinus pauses on telemetry. Standard reversible cardiac causes were addressed and ruled out; however, given his history of hydrocephalus and concern for intermittent ICP elevation, a lumbar puncture was performed, which demonstrated an opening pressure of 22 cm H₂O. Therapeutic drainage of 28 cc of cerebrospinal fluid (CSF) resulted in immediate and durable resolution of bradycardia with stable telemetry thereafter. This case highlights acute ICP elevation as a reversible and underrecognized cause of clinically significant bradyarrhythmia and underscores the importance of considering central drivers of bradycardia in patients with neurologic comorbidity to avoid unnecessary permanent device implantation.
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Registered trials
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