Neurogenic stunned myocardium after acute hydrocephalus

Abstract

<jats:p>Neurogenic stunned myocardium (NSM) is a syndrome of cardiac stunning after a neurological insult. It is commonly observed after aneurysmal subarachnoid hemorrhage but is increasingly being reported after other neurological events. The underlying mechanism of NSM is believed to be a hypothalamic-mediated sympathetic surge causing weakened cardiac contractility and even direct cardiac myocyte damage. The authors report 2 cases of NSM in pediatric patients after acute hydrocephalus. Both patients experienced severe cardiac dysfunction in the acute phase but ultimately had a good neurological outcome and a full cardiac recovery. The identification, treatment, and outcome in 2 rare pediatric cases of NSM are discussed, and the history of the brain-cardiac connection is reviewed.</jats:p>

Ogłuszone serce neurogenne — czy uwzględniamy to rozpoznanie u chorych z ostrym uszkodzeniem ośrodkowego układu nerwowego i niewydolnością serca?

“…According to monkey experimental model findings, myocardial sympathetic denervation, as opposed to vagotomy or bilateral adrenalectomy, completely eliminates the phenomenon of subendocardial necrosis [3], which confirms the role of local release of catecholamines from nerve endings. Moreover, animal studies demonstrate a correlation between concentrations of troponin I, CK-MB and catecholamines in plasma [13]. The theory described above seems to be confirmed by a small-scale study involving patients with subarachnoid haemorrhage in whom the administration of propranolol and phentolamine had cardioprotective effects [13].…”

“…The theory described above seems to be confirmed by a small-scale study involving patients with subarachnoid haemorrhage in whom the administration of propranolol and phentolamine had cardioprotective effects [13]. Likewise, another randomized study of 114 patients with acute CNS damage has demonstrated that the immediate initiation of atenolol treatment reduced the severity of myocardial necrosis determined by increased CK-MB concentrations [13]. The question arises whether catecholamines commonly used in such cases can exert iatrogenic effects.…”

“…NSM has also been observed in individuals with ischaemic stroke [4], craniocerebral trauma [5,6], encephalitis [7], myelitis [8], Guillain-Barre syndrome [9,10], following neurosurgical procedures [11], as well as in those with acute hydrocephalus [12,13], status epilepticus [14] and other acute CNS injuries. Although any acute pathology of CNS is likely to induce NSM syndrome, one's individual predisposition seems crucial.…”

“…Moreover, animal studies demonstrate a correlation between concentrations of troponin I, CK-MB and catecholamines in plasma [13]. The theory described above seems to be confirmed by a small-scale study involving patients with subarachnoid haemorrhage in whom the administration of propranolol and phentolamine had cardioprotective effects [13]. Likewise, another randomized study of 114 patients with acute CNS damage has demonstrated that the immediate initiation of atenolol treatment reduced the severity of myocardial necrosis determined by increased CK-MB concentrations [13].…”

Subarachnoid Hemorrhage Complicated With Neurogenic Pulmonary Edema and Takotsubo-Like Cardiomyopathy

“…4,11,15) However, TCM occurs more frequently than NPE in the absence of a posterior fossa lesion, 18,19) and the relationship between aneurysm location and TCM has been studied less frequently. The possible anatomical difference in a causative brain lesion between NPE and TCM suggests that a sudden rise in serum catecholamine level induces TCM, whereas both rise in the serum catecholamine level and mechanical compression of the medulla are required for induction of NPE.…”