Neurogenic Stunned Myocardium

By Published on October 5, 2025
[et_pb_section fb_built="1" specialty="on" _builder_version="4.9.3" _module_preset="default" custom_padding="0px|0px|0px|||"][et_pb_column type="3_4" specialty_columns="3" _builder_version="3.25" custom_padding="|||" custom_padding__hover="|||"][et_pb_row_inner _builder_version="4.9.3" _module_preset="default" custom_margin="|||-44px|false|false" custom_margin_tablet="|||0px|false|false" custom_margin_phone="" custom_margin_last_edited="on|tablet" custom_padding="28px|||||"][et_pb_column_inner saved_specialty_column_type="3_4" _builder_version="4.9.3" _module_preset="default"][et_pb_text _builder_version="4.9.3" _module_preset="default" hover_enabled="0" sticky_enabled="0"]
  1. QUESTION

     

     

    Neurogenic Stunned Myocardium    

     

    Patients with neurogenic stunned myocardium most often have no history of heart disease. Despite this, they present with wall motion abnormalities, ejection fraction is less than 40%, and troponin levels of less than 2.8ng/ml [1]. Atrial Fibrillation commonly develops, ushering in a tachycardia which eventually increases the oxygen-demand in the myocardium, further worsening myocardial ischemia [3]. Common ECG findings include T wave inversion, U wave inversion, and QT prolongation [1].
    Please answer the following questions: the incidence on NSM associated with seizure versus other causes as well as the incidence of cerebral T
    waves.

    As the insular cortex maintains autonomic control of the cardiovascular system [4], direct or indirect involvement of this area, whether by seizures, subarachnoid hemorrhage, or stroke, may precipitate cardiogenic shock secondary to neurogenic stunned myocardium.

[/et_pb_text][et_pb_text _builder_version="4.9.3" _module_preset="default" width_tablet="" width_phone="100%" width_last_edited="on|phone" max_width="100%"]

 

Subject Nursing Pages 4 Style APA
[/et_pb_text][/et_pb_column_inner][/et_pb_row_inner][et_pb_row_inner module_class="the_answer" _builder_version="4.9.3" _module_preset="default" custom_margin="|||-44px|false|false" custom_margin_tablet="|||0px|false|false" custom_margin_phone="" custom_margin_last_edited="on|tablet"][et_pb_column_inner saved_specialty_column_type="3_4" _builder_version="4.9.3" _module_preset="default"][et_pb_text _builder_version="4.9.3" _module_preset="default" width="100%" custom_margin="||||false|false" custom_margin_tablet="|0px|||false|false" custom_margin_phone="" custom_margin_last_edited="on|desktop"]

Answer

Neurogenic-stunned-myocardium is a condition where neurologic events result in sudden, but usually reversible cardiac abnormalities [1, 2].  Seizures, subarachnoid hemorrhage, and stroke are all examples of intense neurologic events that precipitate autonomic dysregulation, leading to a sympathetic storm.  This sympathetic storm induces myocardial injury and can manifest as ventricular dysfunction, arrhythmias, sudden cardiac death, and myocardial infarction [1]. The current report presents a case of a 72-year-old female with Cardiogenic Shock and subsequent respiratory failure, all secondary to Neurogenic-Stunned-Myocardium.

A 72-year-old female with a past medical history of grade IV glioblastoma multiforme status post craniectomy on Temozolomide and currently receiving radiation, with a history of seizures in the setting of GBM on Levetiracetam, presented as a stroke alert. Physical exam demonstrated left upper and lower extremity drift, leftward gaze deviation, global aphasia, and inattention. CT Scan of the head revealed postsurgical changes in the right posterior temporal lobe with some hyperdensity correlating with localized, well-contained hemorrhage along the inferior aspect of the surgical cavity.  CT perfusion did not reveal large vessel occlusion or ischemia, however significant hyperemia in the right temporal lobe surrounding the prior GBM was noted, correlating with seizure activity.  This hyperemia even extended into the right insular cortex (See Figure. 1). The patient was given a loading dose of Levetiracetam and admitted to the neuro intensive care unit. MRI brain GRE sequence confirmed hemorrhage localized to the prior surgical cavity. (See Figure. 2)

 

The patient was evaluated by the Neuro-Intensivist and was found to be in respiratory failure and cardiogenic shock. On initial assessment, the patient blood pressure by cuff was 90/70. Concern for cardiogenic shock was raised based on narrow pulse pressure. On further examination, the patient had elevated troponins of lactic acidosis and elevated troponins, increasing from 0.7 to 5.0. The central line and arterial line were placed emergently along with Flotrac, which demonstrated SVR 1615, CI 1.8, SVV 14. Bed and femoral lines were placed emergently. Bedside echo showed global hypokinesis with apical sparing (Fig. 3). The patient was started on Epinephrine drip, IVF fluids were stopped, and the patient was diuresed. After these changes were implemented, acidosis resolved, and lactate decreased to 2.0. Interventional cardiology was consulted.  Serial EKGs were repeated and there was a dynamic change in the precordial leads of ECG (cerebral T-waves) (Figure. 4).  With these findings, the patient was taken for coronary catherization, which confirmed non-occlusive neurogenic stunned myocardium.

 

 

The electrocardiographic features can also be used to properly differentiate NSM from other conditions and reach the correct diagnosis. Of all the patients suffering from cerebral infarction, about 60-90% also exhibited abnormal ECG findings [4]. Among the common ECG changes were longer QT interval, T-wave inversions, and the ST-depression. These changes are related to acute neurologic lesions. Various studies have revealed what the ECG means. Notably, the ST-segment change predicts early death and is among the key prognostic element in the long-term besides age. The history of the cardiac condition independently predicts mortality. The ECG changes are also mapped to the abnormalities in the brain locations. ECG pattern of cerebral T-waves with prolonged OT intervals is seen among 72% of the patients with SAH, while those with intraparenchymal hemorrhage are 57%.  Other causes of the T-waves are ischemic stroke, brain injury, and cerebral metastases. The second most common finding is a T-wave inversion. The highly prevalent abnormal rhythm is atrial fibrillation, just before sinus tachycardia [1]. Hence, approximately 8% of the cerebral infarction patients also showcased various instances of T-wave inversions [4], making it an important consideration when seeking the right diagnosis.

 

 

References

  1. Bisco, S., Wongrakpanich, S., Agrawal, A., Yadlapati, S., Kishlyansky, M., & Figueredo, V. (2017). A review of neurogenic stunned myocardium. Cardiovasc Psychiatry Neurol., 2017, 5842182. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5569748/#__ffn_sectitle
  2. Ruiz, L. D., Lorenzo, I. D., & Saez, O. O. (2019). Neuro stunned myocardium in two children with neurological injury. J Pediatric Intensive Care, 08(04), 238-241. https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0039-1693032
  3. Kosaraju, A., Pendela, V. S., & Hai, O. (2020). Cardiogenic shock. [Updated 2020 Jun 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482255/
  4. Ali, A., Ahmad, M. Q., Malik, M. B., Alvi, Z. Z., Iftikkhar, W., Kumar, D., Nasir, U., Ali, N. S., Sayyed, Z., Javaid, R., Waqas, N., Sami, S. A., & Cheema, A. M. (2018). Neurogenic stunned myocardium: a literature review. Cureus, 10(8), e3129.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6181249/
  1. Hawkes, M.A., & Hocker, S.E. (2018). Systemic Complications Following Status Epilepticus. Curr Neurol Neurosci Rep18,  https://doi.org/10.1007/s11910-018-0815-9
  2. Kenigsberg, B.B., Barnett, C.F., Mai, J.C. et al.(2019). Neurogenic Stunned Myocardium in Severe Neurological Injury. Curr Neurol Neurosci Rep 19,  https://doi.org/10.1007/s11910-019-0999-7
  3. Zahid, T., Eskander, N., Emamy, M., Ryad, R., & Jahan, N. (2020). Cardiac Troponin Elevation and Outcome in Subarachnoid Hemorrhage. Cureus12(8), e9792. https://doi.org/10.7759/cureus.9792

 

 

[/et_pb_text][/et_pb_column_inner][/et_pb_row_inner][et_pb_row_inner _builder_version="4.9.3" _module_preset="default" custom_margin="|||-44px|false|false" custom_margin_tablet="|||0px|false|false" custom_margin_phone="" custom_margin_last_edited="on|desktop" custom_padding="60px||6px|||"][et_pb_column_inner saved_specialty_column_type="3_4" _builder_version="4.9.3" _module_preset="default"][et_pb_text _builder_version="4.9.3" _module_preset="default" min_height="34px" custom_margin="||4px|1px||"]

Related Samples

[/et_pb_text][et_pb_divider color="#E02B20" divider_weight="2px" _builder_version="4.9.3" _module_preset="default" width="10%" module_alignment="center" custom_margin="|||349px||"][/et_pb_divider][/et_pb_column_inner][/et_pb_row_inner][et_pb_row_inner use_custom_gutter="on" _builder_version="4.9.3" _module_preset="default" custom_margin="|||-44px||" custom_margin_tablet="|||0px|false|false" custom_margin_phone="" custom_margin_last_edited="on|tablet" custom_padding="13px||16px|0px|false|false"][et_pb_column_inner saved_specialty_column_type="3_4" _builder_version="4.9.3" _module_preset="default"][et_pb_blog fullwidth="off" post_type="project" posts_number="5" excerpt_length="26" show_more="on" show_pagination="off" _builder_version="4.9.3" _module_preset="default" header_font="|600|||||||" read_more_font="|600|||||||" read_more_text_color="#e02b20" width="100%" custom_padding="|||0px|false|false" border_radii="on|5px|5px|5px|5px" border_width_all="2px" box_shadow_style="preset1"][/et_pb_blog][/et_pb_column_inner][/et_pb_row_inner][/et_pb_column][et_pb_column type="1_4" _builder_version="3.25" custom_padding="|||" custom_padding__hover="|||"][et_pb_sidebar orientation="right" area="sidebar-1" _builder_version="4.9.3" _module_preset="default" custom_margin="|-3px||||"][/et_pb_sidebar][/et_pb_column][/et_pb_section]