Neurogenic Stunned Myocardium: A Review

Neurogenic stunned myocardium is a form of stress cardiomyopathy. The disorder is sometimes referred to as atypical Takotsubo cardiomyopathy. The pathophysiology of neurogenic stunned myocardium is hypothesized to involve significant overdrive of the sympathetic nervous system after a brain injury. Treatment options for a patient with a brain injury who has progressed to cardiogenic shock remain controversial, with no consistent guidelines. A patient with subarachnoid hemorrhage who progresses to cardiogenic shock with concurrent cerebral vasospasm presents a special treatment challenge. Neurogenic stunned myocardium is reversible; however, it must be recognized immediately to avoid or manage potential complications, such as cardiogenic shock and pulmonary edema. A multifaceted treatment approach is needed for the patient with cardiogenic shock and concurrent vasospasm.

P4136Neurogenic stunned myoacardium in multiple sclerosis patients

A wide spectrum of topics regarding Multiple Sclerosis (MS) have been thoroughly studied, like immunology, nature of demyelinating lesions (DL's), therapeutics, etc. However, little is known about the influence of MS DL's on the cardiovascular system and especially in the coronary vasculature although few reports mention coronary vasospasm due to autonomic nervous system (ANS) abnormalities. Aim of this study was the detection the presence of Neurogenic Stunned Myocardium (NSM) through perfusion test. Method We enrolled 50 asymptomatic fulfilling the criteria MS patients, aged 45±7 years old and disease in our study duration of 6±13 years with EDSS= 2,5. After echocardiography and clinical examination as primary screening, pharmacologic stress thallium 201 scintigraphy and/or coronary angiography were performed to identify the incidence of NSM. Clinical characteristics of MS, type of disease, treatments as well as localization of demyelinating plaques (DP) were noted. Results 13 patients (26%) had abnormal scintigraphy test although clinical profile was not indicative. Cardiac ultrasound showed that 2 patients from this group had a critical ejection fraction (around 50%). All positive patients that underwent for coronary angiogram were negative implying coronary artery spasm as a potential mechanism for the stress positive result. A common finding of all positive patients was the localization of DP which was in the lateral horn of the lower cervical part (C5–7) and upper thoracic part (Th1–4). No correlation seems to have the presence of CAD with disease duration, EDSS and treatment approaches. Discussion Our study shows a high incidence of NSM. This finding due to the location of the DP seems to correlate with ANS disturbance and might help to distinguish patients at higher risk.

Neurogenic Stunned Myocardium in Two Children with Neurological Injury

Neurogenic stunned myocardium is described as sudden and reversible cardiac dysfunction induced by an acute neurological event. This phenomenon has not been thoroughly investigated in infants, and is probably underdiagnosed. Here, we report the cases of two infants with neurogenic stunned myocardium in whom the clinical suspicion was relevant, with a brief discussion of this condition.

Hydrocephalus-induced neurogenic stunned myocardium and cardiac arrest in a child: completely reversed with CSF diversion

Neurogenic stunned myocardium (NSM) is a potentially fatal cause of sudden cardiogenic dysfunction due to an acute neurological event, most commonly aneurysmal subarachnoid hemorrhage in adults. Only two pediatric cases of hydrocephalus-induced NSM have been reported. Here the authors report a third case in a 14-year-old boy who presented with severe headache, decreased level of consciousness, and shock in the context of acute hydrocephalus secondary to fourth ventricular outlet obstruction 3 years after standard-risk medulloblastoma treatment. He was initially stabilized with the insertion of an external ventricular drain and vasopressor treatment. He had a profoundly reduced cardiac contractility and became asystolic for 1 minute, requiring cardiopulmonary resuscitation when vasopressors were inadvertently discontinued. Over 1 week, his ventricles decreased in size and his cardiac function returned to normal. All other causes of heart failure were ruled out, and his impressive response to CSF diversion clarified the diagnosis of NSM secondary to hydrocephalus. He was unable to be weaned from his drain during his time in the hospital, so he underwent an endoscopic third ventriculostomy and has remained well with normal cardiac function at more than 6 months’ follow-up. This case highlights the importance of prompt CSF diversion and cardiac support for acute hydrocephalus presenting with heart failure in the pediatric population.