Electrocardiographic abnormalities secondary to acute central nervous system injury.

Most patients with acute central nervous system (CNS) lesions, including acute ischemic stroke, intracranial bleeding, traumatic brain or spinal cord injury, exhibit electrocardiographic (ECG) abnormalities. These are generally transient and considered secondary to the neurological condition. The most common neurogenic ECG alterations include ST-segment elevation or depression, T wave inversion, prominent U wave, prolonged QTc interval, sinus bradycardia and atrioventricular block. The primary mechanism involves autonomic nervous system alterations due to damage to the central autonomic network, causing regional changes in myocardial action potential duration, altered ventricular repolarization gradients, altered automaticity, or altered atrioventricular node conduction. These may promote arrhythmias including atrial fibrillation and ventricular arrhythmias. Sympathetic hyperactivation may additionally induce non-ischemic acute myocardial injury characterized by contraction band necrosis. The functional neuroanatomy of the central autonomic network determines the diverse cardiac manifestations observed with distinct CNS injuries. Insular cortex lesions typically result in sympathetic hyperactivation, whereas brain stem or spinal cord lesions above T6 can cause autonomic failure with reduced sympathetic tone and altered autonomic reflexes. While most patients exhibit asymptomatic ECG abnormalities, initial clinical evaluation should identify underlying cardiac conditions such as Takotsubo cardiomyopathy, myocardial infarction, or pre-existing chronic coronary syndromes. Serial ECG, cardiac biomarkers and echocardiography are key. Additional targeted work-up may be useful in selected patients. The implications of distinct ECG findings for neurological and cardiovascular prognosis should also be considered.