Cerebrocardiac syndrome (CCS), including myocardial injury, arrhythmia or heart failure is one of serious complications of traumatic brain injury (TBI), mostly occurs within seven days after TBI, which directly aggravates the brain damage and affects the prognosis of TBI patients. Accumulative evidences suggest that autonomic nervous system disorder is a key initiation point for CCS, but how TBI affects the specific action patterns is not yet clear. Therefore, elucidating the neural mechanisms of TBI-induced CCS, maintaining the central sympathetic-parasympathetic balance through novel interventions such as noninvasive brain stimulation, may fundamentally block the downstream peripheral mechanism, thus achieving effective prevention and treatment for CCS. Based on the current emerging research in brain connectomics and lesion-symptom mapping, we speculate that cerebral contusions can cause structural or functional disconnection of key nodes in the central autonomic nervous system regulatory network, thereby mediating the occurrence of TBI-induced CCS. In this study, magnetic resonance imaging (MRI) or functional MRI (fMRI) examinations were performed in patients with mild or moderate TBI with aim to explore the association between structural and functional disconnection caused by cerebral contusion and TBI-induced CCS, and to screen out the neural anatomical structures to predict CCS following TBI, providing therapy targets for prevention and treatment of CCS.
Study Type
OBSERVATIONAL
Enrollment
90
Shanghai 6th People's Hospital
Shanghai, China
RECRUITINGShanghai Sixth People's Hospital
Shanghai, China
RECRUITINGBrain network evaluation by MRI
MRI data of all participants are acquired within 3 days after enrollment, and the MRI scans include one or more of the following contents： 1. 3D T1-weighted images, which were acquired with a magnetization prepared rapid-acquisition gradient-echo sequence. 2. The resting state-fMRI data, acquired with an interleaved T2-weighted axial gradient-echo echoplanar imaging sequence. 3. DTI datasets, acquired using a fully-sampled spin-echo EPI sequence.
Time frame: Within 3 days after enrollment
Cardiac evaluation by ECG
ECG data of all participants are acquired within 3 days after enrollment, and include resting and ambulatory ECG to detect arrhythmias, heart rate variability or myocardial ischemia. Specifically, arrhythmias include atrial fibrillation (irregular R-R intervals, absent P waves, fibrillatory waves), ventricular tachycardia (QRS \>120 ms, rapid rate, often no discernible P waves), heart blocks (1st degree: PR interval \>200 ms; 2nd degree: progressive PR prolongation until a QRS drops; 3rd degree: complete AV dissociation and atrial rate \> ventricular rate) and premature contractions (early beats with wide or narrow QRS). Heart rate variability is analyzed via R-R interval variability over time (24-hour Holter), and the indicators include Time-Domain (SDNN and RMSSD) and Frequency-Domain (LF/HF ratio). Myocardial ischemia indicators include ST segment depression ≥0.5 mm in ≥2 contiguous leads, ST elevation ≥1 mm in ≥2 contiguous leads, and inversion or hyperacute T waves.
Time frame: Within 3 days after enrollment
Cardiac evaluation by echocardiography
Echocardiography data of all participants are acquired within 3 days after enrollment, in order to assess heart pumping function. Specifically, the key parameters assessed include ventricular function (ejection fraction: % of blood ejected per beat) and cardiac output quantification. The decline in the above indicators suggests heart ischemia or heart failure.
Time frame: Within 3 days after enrollment
Cardiac evaluation by blood testing-1
Blood testing data of all participants are acquired within 3 days after enrollment and include several key cardiac biomarkers: myoglobin (normal: 14.3-65.8 μg/L), cardiac troponin I (cTnI, normal: 0-0.03 μg/L), cardiac troponin T (cTnT, normal: 0-0.1 μg/L), B-type natriuretic peptide (BNP, normal: 0-0.1 μg/L) and NT-proBNP (normal: \<0.3 μg/L). Specifically, elevated myoglobin is useful for early detection of myocardial infarction (MI); elevated cTnI and cTnT, especially with a rising/falling pattern, are gold standard for diagnosing MI; elevated BNP and NT-proBNP suggest heart failure (HF), especially BNP \>0.4 μg/L indicates severe HF.
Time frame: Within 3 days after enrollment
Cardiac evaluation by blood testing-2
Blood testing data of all participants are acquired within 3 days after enrollment and include the following cardiac biomarkers: creatine kinase (CK, normal: 21-190 U/L ), CK-MB (normal: 0-25 U/L) and lactate dehydrogenase (LDH, normal: 114-240 U/L). Specifically, elevated CK and CK-MB suggest cardiac muscle injury; elevated LDH are useful for early detection of MI.
Time frame: Within 3 days after enrollment
Clinical prognosis assessed by GOS score
Glasgow Outcome Scale (GOS) score (1 = death; 2 = persistent vegetative state; 3 = severe disability; 4 = moderate disability; 5 = good but not necessarily complete recovery; unfavorable outcome was defined as score of ≤3, and favorable outcome was defined as a score of \>3)
Time frame: One month, three and six months after trauma
Neurological function assessed by mRS score
Modified Rankin Scale (mRS) score (0 = no symptoms; 1 = no significant disability; 2 = slight disability; 3 = moderate disability; 4 = moderately severe disability; 5 = severe disability; 6 = dead; favorable outcome was defined as score of 0-2, and unfavorable outcome was defined as score of 3-6)
Time frame: One month, three and six months after trauma
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