Neurogenic stunned myocardium

Neurogenic stunned myocardium may be defined as myocardial injury and dysfunction occurring after diverse types of acute brain injury as a result of imbalance of the autonomic nervous system. The spectrum of observed cardiac abnormalities includes electrocardiographic changes, arrhythmia, myocardial necrosis, release of B-type natriuretic peptide, and both systolic and diastolic dysfunction of the left ventricle. These are reversible abnormalities, and although management should include careful cardiac monitoring, treatments should generally focus on the underlying neurologic process to maximize neurologic recovery.     

Postictal neurogenic stunned myocardium

Neurogenic left ventricular dysfunction is a recognized complication of subarachnoid hemorrhage, but this condition has not been reported after seizure activity. The authors present two cases of neurogenic stunned myocardium after convulsive seizures, suggesting that ictal activity can lead to sympathetically mediated cardiac injury.     

脑挫裂伤出血进展的危险因素分析

目的 探讨影响脑挫裂伤出血进展（HPC）的危险因素。方法 回顾性分析2015年12月至2019年3月收治的216例脑挫裂伤的临床资料。采用多因素logistic回归分析检验HPC的危险因素。结果 216例脑挫裂伤中,84例发生HPC,发生率为38.89%。多因素logistic回归分析结果显示,长期吸烟、入院血清离子钙水平<1.12 mmol/L、合并蛛网膜下腔出血、初始血肿体积>4.0 ml为HPC的独立危险因素（P<0.05）。结论 对于脑挫裂伤病人,如果存在长期吸烟史、血清离子钙<1.12 mmol/L、蛛网膜下腔出血以及初始血肿体积>4.0 ml,应注意采取针对性措施防治HPC。     

Glial swelling following human cerebral contusion: an ultrastructural study.

The ultrastructural features of cerebral contusion seen three hours to 11 days after head injury were studied in 18 patients undergoing surgery. Massive astrocytic swelling ("cytotoxic" oedema) was seen three hours to three days after injury, maximal in perivascular foot processes, and compressing some of the underlying capillaries. The tight junctions were not disrupted. Neuronal damage was most marked three to 11 days after injury. The pathophysiological mechanisms leading to oedema formation and neuronal degeneration are discussed.     

Intraventricular colloid cyst, hydrocephalus and neurogenic stunned myocardium

OBJECTIVE: To report the occurrence of neurogenic stunned myocardium in the context of a hydrocephalus due to a third ventricle colloid cyst. DESIGN: Case report. SETTING: Neurocritical care unit of a university hospital. PATIENT: The case of a 33-year-old woman with an intraventricular cerebral colloid cyst who developed hydrocephalus, cardiac arrest and survived is presented. Workup was consistent with neurogenic stunned myocardium in the context of acute hydrocephalus due to an intraventricular colloid cyst. RESULTS: The patient had decreased left ventricular ejection fraction, apex-sparing areas of hypokinesis and akinesis, wall motion abnormalities not matching a particular vascular territories, the peak troponin T level of 0.09 ng/ml and had normal coronary arteries at angiography. Seven days after the initial event the cardiac function recovered. Tumor resection was successfully performed. At 10 months after discharge, the only complaint was mild memory disturbance, she was completely functional with no evidence of seizures or of cardiac dysfunction. CONCLUSION: The sudden elevation of intracranial pressure, with the subsequent decreased cerebral perfusion pressure induces a vigorous cerebro-protective neuroendocrine system activation that can lead to the neurogenic stunned myocardium. Sudden death in patients with colloid cysts may be related to acute neurogenic cardiac dysfunction, and not necessarily cerebral herniation(s), as previously thought.     

Acute myelitis with neurogenic stunned myocardium in a boy

Neurogenic stunned myocardium is characterized by reversible left ventricular dysfunction, which occurs after severe central nervous system injury in patients without coronary artery disease. It has been described in association with subarachnoid hemorrhage, Guillain-Barré syndrome, and metastatic brain tumors in adults, but has been rarely reported in association with acute myelitis. Described here is a novel case of acute myelitis in a child associated with neurogenic stunned myocardium. This case demonstrates that patients with acute myelitis may harbor a risk of sympathetic dysregulation, leading to neurogenic myocardial dysfunction.     

Multiple cerebral white matter lesions following head trauma with eyeball contusion]

We reported a 36-year-old man with multiple cerebral white matter lesions following head trauma with eyeball contusion. He had suffered from optic neuritis on non-injured side after one and half months from the head trauma. Brain MRI revealed multiple cerebral white matter lesions and lumbar puncture disclosed an elevated level of protein of the cerebrospinal fluid after two and half months from the head trauma. He was treated with steroid pulse therapy and resulted in an improvement of his visual acuity and a remarkable decrease of multiple cerebral white matter lesions. There has been a controversy concerning the causal relationship between trauma and multiple sclerosis (MS). In this case, MS-like multiple cerebral white matter lesions are considered to be relevant to the head trauma.     

Aquaporin 4 expression and ultrastructure of the blood-brain barrier following cerebral contusion injury

This study aimed to investigate aquaporin 4 expression and the ultrastructure of the blood-brain barrier at 2–72 hours following cerebral contusion injury, and correlate these changes to the formation of brain edema. Results revealed that at 2 hours after cerebral contusion and laceration injury, aquaporin 4 expression significantly increased, brain water content and blood-brain barrier permeability increased, and the number of pinocytotic vesicles in cerebral microvascular endothelial cells increased. In addition, the mitochondrial accumulation was observed. As contusion and laceration injury became aggravated, aquaporin 4 expression continued to increase, brain water content and blood-brain barrier permeability gradually increased, brain capillary endothelial cells and astrocytes swelled, and capillary basement membrane injury gradually increased. The above changes were most apparent at 12 hours after injury, after which they gradually attenuated. Aquaporin 4 expression positively correlated with brain water content and the blood-brain barrier index. Our experimental findings indicate that increasing aquaporin 4 expression and blood-brain barrier permeability after cerebral contusion and laceration injury in humans is involved in the formation of brain edema.     

脑梗死静脉溶栓治疗后出血性转化临床分析

目的探讨急性脑梗死患者溶栓治疗后出血性转化(hemorrhagic transformation,HT)的危险因素以及继发HT患者的溶栓后并发症。方法回顾性分析62例经静脉溶栓治疗的急性脑梗死患者的临床资料,结合文献选择溶栓后继发HT的危险因素,包括年龄、性别、高血压、糖尿病、心功能不全史、脑卒中史、有无早期CT缺血改变、是否大面积脑梗死、是否心源性脑栓塞、发病至溶栓时间、溶栓药物、溶栓前NIHSS评分、溶栓前血糖水平、溶栓后3d内最低纤维蛋白原水平、血小板计数、肌酐水平等进行分析,对单因素分析法发现有统计学差异的危险因素进一步行Logistic回归分析。结果单因素分析发现,与无HT组相比,继发HT组年龄较大(P<0.01),溶栓前血糖水平(P<0.05)、溶栓后6h和12h的收缩压和舒张压较高(均P<0.05),大面积脑梗死发病至溶栓时间>3h、有早期CT缺血改变的患者比例高(均P<0.05)。Logistic多因素回归分析发现高龄(OR:1.129,P<0.05)、溶栓时间>3h(OR:2.592,P<0.05)、早期CT有缺血改变(OR:1.728,P<0.05)是继发HT的危险因素。继发HT组出现颅外出血并发症(52.2%vs 20.5%,χ2=6.637,P<0.05)、重度脑水肿(30.4%vs 5.1%,χ2=5.567,P<0.05)和脑疝形成(26.1%vs 2.6%,P<0.05)的比例更高。结论急性脑梗死患者静脉溶栓后HT的发生率高,高龄、发病至溶栓时间>3h和早期CT缺血改变是HT的危险因素。     

Temporally changing patterns of hippocampal cerebral glucose utilization following sensorimotor cortical contusion in rats

Unilateral sensorimotor cortical contusion significantly decreased ipsilateral hippocampal cerebral metabolic rates of glucose utilization (CMRE_glu) compared to sham controls at 2 and 16 days post injury. In contrast, hippocampal CMR_glu was transiently increased at 6 days post injury. Both the increased and decreased CMR_glu were predominantly localized to the hippocampal CA3 subfield ipsilateral to injury and were significantly different from sham controls in the dorsal but not ventral hippocampal formation.     

Neurogenic control of cerebral blood flow

In experiments on 15 isolated dog brains, cerebral blood flow could be influenced by short (20 sec) supramaximal, unilateral electrical stimulation of the vagoysympathetic trunk, the trigeminal nerve and the medulla oblongata. The changes in cerebral vascular resistance and cerebral oxygen consumption developed 2 sec after onset of the stimulation, reaching their peak 30 sec later and lasted up to 3 min. During sympathetic stimulation cerebral blood flow decreased from 47.2 ml to $\text{42.0 ml}\text{100 g}$ tissue/min and cerebral vascular resistance increased about 18%. This constrictor effect was completely blocked by phentolamine. During vagal stimulation no effect could be observed. During trigeminal stimulation cerebral blood flow increased from 44.0 ml to $\text{48.9 ml}\text{100 g}$ tissue/min, cerebral vascular resistance decreased about 19%, and cerebral oxygen consumption increased about 12%. Reliable inhibition of this dilating response was not achieved with either propranolol or atropine and it is assumed that there are no vasodilator fibers in the trigeminal nerve. During medullary stimulation cerebral blood flow increased from 42.0 ml to $\text{54.7 ml}\text{100 g}$ tissue/min, cerebral vascular resistance decreased about 45% and cerebral oxygen consumption increased about 23%. The diminishing effects of propranolol and atropine on this dilating response was not statistically significant. A restricted region in the medulla is presented from which changes in cerebral blood flow produced by electrical stimulation were not associated with changes in the electrical pattern of the brain. Observations that the vascular and functional reactions of the brain can be dissociated point to a role of the medulla in regulating cerebral blood flow, but do not elucidate the mechanism. In general, the results support evidence that a double—metabolic and neurogenic—mechanism is involved in the control of cerebral blood flow. It is suggested that the effects during vagosympathetic stimulation are completely neurogenic, the effects during trigeminal stimulation mainly metabolic, and the effects during medullary stimulation both metabolic and neurogenic in origin.     

Neurogenic vesico-urethral dysfunction in children with cerebral palsy

20 children with severe cerebral palsy and history of urinary incontinence and recurrent urinary infection underwent radio- and neuro-urologic evaluation. Vesico-ureteral reflux was found in 7 patients. In 9, who had presented episodes of urine sub-retention, a urodynamic study demonstrated detrusor muscle hyperreflexia in all, deficit of vesicourethral sensation in 5 and detrusor-sphincter dyssynergia in 2. These functional findings are compatible with an upper motor neuron lesion, and may be the cause of episodes of altered bladder emptying, and consequently, urinary infection.

---

Sommario Allo scopo di valutare la presenza di disfunzione vescico-uretrale nei bambini affetti da grave paralisi cerebrale infantile, nella cui anamnesi sono documentate incontinenza urinaria e infezione urinaria recidivante, 20 pazienti sono stati sottoposti ad una valutazione radio e neuro-urologica. Reflusso vescico-ureterale era presente in 7 pazienti. In 9, che avevano presentato episodi di subritenzione urinaria, è stato eseguito uno studio urodinamico che ha evidenziato iperreflessia detrusoriale in tutti, deficit delle sensibilità vescico-uretrale in 5 e dissinergia sfintero-detrusoriale in 2. Tali reperti funzionali sono compatibili con un danno a livello del 1° motoneurone e possono essere causa degli episodi di alterato svuotamento vescicale e quindi di infezione urinaria.

     

双侧额叶脑挫裂伤的手术指征探讨

探讨双侧额叶脑挫裂伤的手术指征的研究进展。通过查阅国内外近年来大量文献著作,对双侧额叶脑挫裂伤的手术指征进行分析和总结。双额叶脑挫裂伤患者的手术指征目前尚无统一的标准,大多数学者认为因为双侧额叶脑挫裂伤极易形成中央型脑疝,其中间脑期为抢救中央型脑疝成功的关键期,开颅手术指征要适当放宽,早期识别并积极进行手术,可降低患者病死率和致残率,提高抢救成功率。     

Central necrosis following contusion to the sheep's spinal cord

This paper presents the results of a study on the pathological changes associated with post traumatic central spinal cord necrosis.     

Uncoupling of cerebral blood flow and metabolism after cerebral contusion in the rat.

Positron emission tomography scans of patients with head injuries often show discrete areas of increased 18F-fluorodeoxyglucose uptake ("hot spots") when performed hours to days after the initial ictus. Using quantitative autoradiographic methods, the authors have investigated whether cerebral blood flow and glucose metabolism are uncoupled 2 hours after controlled head injury in an animal model, and whether any "hot spots" are accompanied by changes in cerebral glucose concentration. Experiments were performed on 18 anesthetized, ventilated (1.5% halothane in 2:1 nitrous oxide:oxygen) Sprague-Dawley rats weighing 300 to 330 g. A burr hole was made over the left parietal cortex, and all animals received a piston impact on the intact dura (2 mm in diameter, 2.0 m/sec, 2 mm in depth). All animals remained anesthetized and ventilated for a further 2 hours, after which quantitative autoradiography was used to determine either (1) local cerebral blood flow (LCBF) using 14C-iodoantipyrine, (2) local cerebral glucose utilization (LCGU) using 14C-deoxyglucose, or (3) local cerebral glucose content (LCGC) using 14C-methylglucose. Local CBF, LCGU, and LCGC were measured in five regions adjacent to the contusion, and values then were normalized on the contralateral cortex. Normalized LCBF, LCGU, or LCGC varied in parallel in ipsilateral cortex (no change) and in the ischemic core of the contusion (reduced). However, there were marked changes in the patterns observed in the boundary zone (within 1 mm of the contusion). In all six rats used for LCGU measurement, there were discrete areas of high metabolism, whereas in all six rats used for LCBF measurement, flow was universally depressed in the boundary zone. Of the six rats used for LCGC determination, there was a discrete area of high signal in only one. The authors conclude that there are discrete areas of uncoupling of cerebral blood flow and metabolism after head injury within 2 hours of cerebral contusion in the rat that cannot be explained by changes in cerebral glucose content in the majority of animals.