Seeking Tau in Head Injury

The aim of this study was to determine if heart rate, blood pressure (diastolic, systolic, and mean), intracranial pressure, and cerebral perfusion pressure of patients with head injury have circadian rhythm. We studied data of 13 patients with severe head injury using the Iterative Cosinor method. We detected a circadian rhythm for at least one of the parameters in 11 (85%) of the 13 patients. The period of the rhythms (tau) was often not equal to 24 hours. Also, taus within and between patients were different. The results of our study showed that in these patients, when parameters are recorded hourly, tau can be estimated reasonably accurately (average error 0.7 hours). The distribution of taus suggests that the patients in our sample had free-running circadian rhythm. We used the surrogate data technique to validate the results of our study. Possible reasons for uncertainty in tau-estimation and proposed changes in data collection protocols and inclusion criteria are discussed.     

Dizziness and Head Injury

Dizziness, whether vague or specifically rotational, is a common sequel to head injury, and is often postural. One hundred and sixty-five patients with this symptom were examined. The simple posture tests employed to detect positional nystagmus are described. This physical finding was present in one-quarter of the entire group, and in nearly one-half of cases of longitudinal fracture of temporal bone. In such cases, it is an objective finding that corresponds precisely to the patient''s complaint of vertigo.Transverse fracture of temporal bone destroys the inner ear in both cochlear and vestibular parts. Longitudinal fracture is commoner and causes bleeding from the ear; inner-ear damage is usually minor.In the rare cases where persisting postural vertigo and positional nystagmus are disabling, relief of the symptom may be achieved by vestibular denervation of the affected side.     

Hypothermia in the Treatment of Critical Head Injury

Because of the beneficial effect on the character and mortality of experimental brain injury, 21 patients with critical brain injury (thought to be incompatible with life using standard methods of treatment) were subjected to artificial hypothermia (28°-36° C.) for two to 10 days. Nine died and 12 survived, but six of the survivors are permanent invalids with dementia. The hazards are staphylococcal pneumonia, which occurred in eight cases and contributed to all the deaths, and gastrointestinal ulceration with bleeding and perforation, which was fatal in another. The results in patients with clots did not differ from those without. Youth was the only common factor in the successful cases. Prognosis was hopeless in the presence of large fixed pupils. About one in four of these critical cases will fare well, but it is evident that a large proportion have such gross or microscopic tearing of deep cerebral structures that in the event of survival there will be severe mental and physical handicaps.     

Brain Hydroxyl Radical Generation in Acute Experimental Head Injury

Abstract: The time course and intensity of brain hydroxyl radical (^?OH) generation were examined in male CF-1 mice during the first hour after moderate or severe concussive head injury. Hydroxyl radical production was measured using the salicylate trapping method in which the production of 2,3- and/or 2,5-dihydroxybenzoic acid (DHBA) in brain 15 min after salicylate administration was used as an index of ^?OH formation. In mice injured with a concussion of moderate severity as defined by the 1-h posttraumatic neurologic recovery (grip score), a 60% increase in 2,5-DHBA formation was observed by 1 min after injury compared with that observed in uninjured mice. The peak in DHBA formation occurred at 15 min after injury (+67.5%; p < 0.02, compared with uninjured). At 30 min, the increase in DHBA lost significance, indicating that the posttraumatic increase in brain ^?OH formation is a transient phenomenon. In severely injured mice, the peak increase in DHBA (both 2,3- and 2,5-) was observed at 30 min after injury, but also fell off thereafter as with the moderate injury severity. Preinjury dosing of the mice with SKF-525A (50 mg/kg i.p.), an inhibitor of microsomal drug oxidations, did not blunt the posttraumatic increase in salicylate-derived 2,5-DHBA, thus showing that it is not due to increased metabolic hydroxylation. Neither injury nor SKF-525A administration affected the DHBA plasma levels. However, saline perfusion of the injured mice to remove the intravascular blood before brain removal eliminated the injury-induced increase in 2,5-DHBA, but did not affect the baseline levels seen in uninjured mice. This implies that the source of the increased DHBA in the injured mice is the microvasculature, probably the endothelium. The administration of the 21-aminosteroid lipid antioxidant, tirilazad mesylate, which possesses ^?OH scavenging properties, also attenuated the posttraumatic increase in DHBA, further supporting that it reflects an increase in ^?OH radical formation. These results are the first direct demonstration of the occurrence and time course of increased ^?OH production in injured brain.     

Advances in the Understanding and Treatment of Head Injury

The author describes his personal involvement in head injury prevention and management over the past 40 years. He reviews the evolution of knowledge concerning the role of increased intracranial pressure, and considers the importance of cerebral vasoparalysis in the production of signs and symptoms following head injury, and the development of methods of recording intracranial pressure continuously, over hours and days.The development of an experimental compression model has led to a fuller understanding of edema of the brain and has provided a means of studying, by light and electron microscopy, the histological changes that result from edema. More recently, analyses of biochemical changes and disturbed membrane function have opened up a new avenue of potential treatment. Moreover, it is now clear that cerebral vascular dilatation and abrupt pressure increase can be produced in the monkey, in over 50% of cases, by lesions in the dorsomedial nucleus of the hypothalamus. Similar lesions may occur in the human and this suggests other therapeutic approaches. There is, then, a genuine hope of a breakthrough in the management of head injuries.     

重度颅脑损伤的气道监测护理干预

目的:探讨气道监测护理干预对重症颅脑外伤患者预后的影响。方法:回顾分析2010年1月-2012年1月重症颅脑外伤入住我院ICU病房均行气管切开机械通气的患者189例,随机分为两组,对照组和干预组,其中对照组采用常规护理方法进行护理,干预组在常规护理的基础上加强气道监测护理干预,观察比较两组患者ICU治疗时间、肺部感染情况、呼吸机使用时间、ICU花费等情况。结果:两组患者比较:干预组肺部感染控制情况明显优于对照组(x2=4.006,P<0.05),考虑差异有统计学意义。干预组患者呼吸机使用时间及ICU治疗时间均较对照组时间缩短(t=12.9,3.82,3.95 P<0.05),有统计学差异。结论:合理的的气道监测护理能有效减少患者肺部疾病感染等并发症发生率,促进患者病情恢复,临床上值得推广。