Multimodality evoked potentials and early prognosis in comatose patients

In 112 comatose patients somatosensory, visual and auditory evoked potentials were registered within 36 hours after the onset of coma or admission. Main causes of coma were head injury, and intracerebral and subarachnoid haemorrhage. The initial bilateral loss of any evoked potential was associated with a mortality of 98%. Normal somatosensory evoked potentials were associated with a survival rate of 74%, while normal visual and normal auditory evoked potentials had a survival rate of 60% and 66%, respectively. It is concluded that SEPs can be valuable for the prognosis of coma after primary brain lesions.     

Comparison of the APACHE III, APACHE II and Glasgow Coma Scale in acute head injury for prediction of mortality and functional outcome

Objectives: This study examines the efficacy of the predicting power for hospital mortality and functional outcome of three different scoring systems for head injury in a neurosurgical intensive care unit (NICU). Design: On the day of admission, data were collected from each patient to compute the Acute Physiology, Age, and Chronic Health Evaluation (APACHE) II and III, and Glasgow Coma Scale (GCS) scores. Hospital mortality was defined as the deaths of patients before discharge from hospital. Early mortality was defined as death before the 14th day after admission. Late mortality was defined as death after the 15th day from admission. Functional outcome was evaluated by Index of Independence in Activities of Daily Living (Index of ADL). Setting: An 8-bed NICU in a 1270-bed medical center in Taichung Veterans General Hospital. Patients and participants: Two hundred non-selected patients with acute head injury were included in our study in a consecutive period of 2 years. Patients less than 14 years old were not included. Interventions: None. Measurements and results: Sensitivity, specificity and correct prediction outcome were measured by the chi-square method in three scoring systems. The Youden index was also obtained. The best cut-off point in each scoring system was determined by the Youden index. The difference in Youden index was calculated by Z score. A difference was also considered if the probability value was less than 0.05. The area under Receiver Operating Characteristic (ROC) curve was computed. Then the area under ROC of each scoring system was compared by Z score. There was statistical significance if p was less than 0.05. For prediction of hospital mortality, the best cut-off points are 55 for APACHE III, 17 for APACHE II and 5 for GCS. The correct prediction outcome is 82.4% in APACHE III, 78.4% in APACHE II and 81.9% in the GCS. The Youden index has best cut-off points at 0.68 for APACHE III, 0.59 for APACHE II, and 0.56 for GCS. The area under Receiver Operating Characteristic (ROC) curve is 0.90 in the APACHE III, 0.84 in the APACHE II and 0.86 in the GCS. There are no statistical differences among APACHE III and II, and GCS in terms of correct prediction outcome, Youden Index and the area under the ROC curve. Other physiological variables excluding GCS in APACHE III and II (AP III-GCS, AP II-GCS) have less statistical value in the determination of mortality for acute head injury. For the prediction of late mortality, APACHE III and II yield significantly better results in the area under the ROC curve, correct prediction and Youden index than those of GCS. Other physiological variables (AP III-GCS and AP II-GCS) play an important role in the prediction of late mortality in APACHE scores. For prediction of the functional outcome of surviving patients with acute head injury, the APACHE III yields the best results of correct prediction outcome, Youden index and the area under the ROC curve. Conclusion: The APACHE III and II may not replace the role of GCS in cases of acute head injury for hospital or early mortality assessment. But for prediction of the late mortality, the APACHE III and II have better accuracy than GCS. Other physiological variables excluding GCS in the APACHE system play a crucial contribution for late mortality. GCS is simple, less time-consuming and economical for patients with acute head injury for the prediction of hospital and early mortality. The APACHE III provides better prediction for severe morbidity than GCS and APACHE II. Therefore, the APACHE III provides a good assessment not only for hospital and late mortality, but also for functional outcome. Received: 22 May 1995 Accepted: 2 September 1996     

格拉斯哥评分的纯数学意义及临床评估价值

总结１０２２例颅脑外伤进行格拉斯哥评分的实践实验，从纯数学意义上评价了评分在临床上的应用价值。指出格拉斯哥评分各参数之间只有１５种组合最常见且有临床价值。数学分析表明运动反应最有决定性意义；同时指出格拉斯可评分对患者预后判断有重要评估价值。评分的不足之处在于不能反映瞳孔改变和脑干症状。     

Reversible “locked-in” syndromes

Two young patients are described who made good recoveries from a locked-in syndrome presumed to be due to ventral pontine ischemia. The first patient recovered completely from quadriplegia and mutism. In the second patient the only permanent sequellae were slight dysarthria and mild spasticity. Since patients may recover nearly completely from a locked-in syndrome, aggressive supportive therapy seems justified during the initial weeks or months.     

Post-traumatic diffuse brain swelling: isolated or associated with cerebral axonal injury

Eighteen children with severe head injuries and diffuse brain swelling were studied. They were separated into two groups based on the computed tomography (CT) findings. Seven patients had small ventricles in the normal location and small or absent cisterns. Eleven had these signs plus small deep-seated intraparenchymal hemorrhagic foci and/or intraventricular hemorrhage. Patients in the first group were in relatively good neurological condition; their intracranial pressure was easily controlled and all had a favourable outcome. On contrast, children in the second group had a more severe clinical presentation, frequently had uncontrollable intracranial hypertension, and more than 50% died.     

Review of 1,000 consecutive cases of severe head injury treated before the advent of CT scanning

Summary This is a review of 1,000 consecutive cases of severe head injury admitted to our Neurosurgical Department between January 1973 and August 1976, before the advent of CT scanning. All patients were comatose following head injury (GCS8) and were treated homogeneously by the same neurosurgical team by a protocol that included immediate resuscitation on arrival, diagnosis of intracranial lesions by angiography, early surgery when needed, mechanical ventilation, steroids, and mannitol. Extracranial lesions, even if preponderant, were treated by various specialists in the Neurosurgical Department, which for all practical purposes operated as an Emergency Department. Admission criteria were very broad with no preadmission selection. The overall mortality for this series was 45%. A little less than half the patients made good recoveries or remained moderately disabled (47%); 6% were severely disabled, and 2% survived in a persistent vegetative state. More than two-thirds of the patients were brought to our Neurosurgical Department after a short stay at a general hospital; 72% were admitted within 6 hours of injury; 71% were traffic accident victims; and 34% had significant associated extracranial injuries. Carotid angiography was performed in 78% of the patients and indicated the presence of an intracranial haematoma requiring surgery in 36% of the whole series. Mortality was significantly higher in operated than in unoperated patients (56% versus 39%); those treated surgically, however, were older, in worse clinical condition, and showed a higher incidence of acute subdural haematomas associated with brain contusion. Carotid angiography proved very effective in revealing the presence of an expansive lesion but failed to reflect the severity of brain damage, since the group with negative angiograms showed a high mortality (52%). Patients with a lucid interval had a higher percentage of surgical lesions than those with immediate coma (58% versus 26%); but fully 42% of them did not require surgery, and 25% had negative angiograms. From the prognostic point of view the clinical data elicited after initial resuscitation were highly predictive of the outcome: some individual neurological signs, such as mydriasis, posturing and eye movements, were not inferior to the GCS score in that respect. Age also proved a strong predictor, since elderly patients are more likely to have severe subdural and parenchymal lesions and their clinical severity is accordingly greater.Our series amounts to a data bank of cases both contemporary to and in good agreement with that collected by Jennett and his associates in their 1977 multinational study; and it affords a useful reference in the assessment of epidemiological variations and alternative management in relation to outcome.     

Effect of acute ammonia intoxication on energy stores in the cerebral reticular activating system

Summary Ammonia intoxication causes loss of consciousness. One postulated mechanism for this stipulates impaired energy metabolism in critical brain sites. The ascending reticular activating system in the brainstem may modulate consciousness. Accordingly, the present study, using micromethods, assessed energy stores in cells from the reticular activating system of mice acutely intoxicated with ammonia. In the early coma period (3.5 min after ammonia) phosphocreatine, adenosine triphosphate and glucose fell significantly while glycogen decreased later. Subsequently during coma, the high energy phosphates returned to normal and supranormal. The maximal fall in these metabolites was not accompanied by a rise in lactate, implying lack of local hypoxia or acidosis. The cells of the posterior colliculus in the same animals failed to show a significant fall in energy stores. These data suggest a selective effect of ammonia on energy metabolism in the cells of the reticular activating system of the brainstem.Abbreviations NH Ammonia - ATP Adenosine Triphosphate - PC Phosphocreatine - RAS Reticular Activating System Presented at the Annual Meeting of the American Association of the Study of the Liver Disease, Chicago, 1980Supported in part by USPHS Grant N.S. 16621     

脑损害昏迷患者上消化道出血的预防

目的 探讨脑损害昏迷患者上消化道出血的发病因素和预防措施。方法 对274例脑损害昏迷患者,分析其并发上消化道出血的内环境因素和预防效果。结果 并发上消化道出血49例,占17.9%,而在ICU条件下早期鼻饲西沙必利、奥美拉唑及氢氧化铝凝胶预防组消化道出血的发生率为40%(2/50);伤后休克低血压、低氧血症、低钠血症、氮质血症、酸中毒、高血糖、高脂质过氧化水平均可增加上消化道出血的发生率。结论 ICU条件下维护内环境平衡、早期鼻饲、胃肠动力及抑酸药物应用,可显著关注脑损害昏迷患者上消化道出血的发生。