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J. Jaap van der Sande, Jan J. Veltkamp, Ria J. Boekhout-Mussert and Marijke L. Bouwhuis-Hoogerwerf

defibrination were observed. Defibrination, which is sometimes called “consumption coagulopathy,” results from excessive disseminated intravascular coagulation (DIC) which can be triggered by several mechanisms, such as widespread denudation of the endothelium, or infusion of thrombin-like or thromboplastic substances, which explains the wide variety of diseases in which DIC occurs. 1, 5, 7, 8, 18, 22, 31, 33 Additional cases of DIC or defibrination have been reported after head injury from missiles 10, 17 and from non-missile causes. 9, 23, 25 Although some prospective

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Marius Maxwell, Dimitris Karacostas, Richard G. Ellenbogen, Amnon Brzezinski, Nicholas T. Zervas and Peter McL. Black

S exual precocity may be defined as the onset of secondary sexual characteristics before the age of 8 years in girls or 9 years in boys. It may be the result of hypothalamic involvement by tumor or infection, but it is an exceedingly rare sequela of head injury. Only four case reports establishing a causal relationship between trauma and sexual precocity have been published in the last two decades. 22, 29, 30 Reproductive function, manifested by the secretion of gonadotrophins and gonadal steroids, is active during fetal life but regresses during early

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Head injury in the chimpanzee

Part 1: Biodynamics of traumatic unconsciousness

Ayub K. Ommaya, Paul Corrao and Frank S. Letcher

A n understanding of head injury mechanisms requires correlation of the mechanical input (biodynamics) with the physiopathological responses. 6, 12 An earlier report from this laboratory 7 has shown how rotational components of the violently moving head in experimental “whiplash” (indirect impact) can be correlated with the onset of cerebral concussion (traumatic unconsciousness) and visible brain lesions in the monkey. It has also been shown that such head rotations measured in three primate species (squirrel monkey, rhesus monkey, and chimpanzee) can be

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Head injury in the champanzee

Part 2: Spontaneous and evoked epidural potentials as indices of injury severity

Frank S. Letcher, Paul G. Corrao and Ayub K. Ommaya

, and diminished EEG activity).” An earlier study in lightly anesthetized monkeys by one of us 14, 15 showed that early onset of large amplitude slow waves might be related to the onset of unconsciousness after occipital impact. There have been no previous studies of electrophysiological correlates of head injury in the chimpanzee. Thus, in conjunction with an investigation into the biomechanics of head injury, we are reporting the effect of a controlled occipital blow on the EEG and epidural somatic evoked response (SER) of alert, drug-free chimpanzees and

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Dexamethasone and severe head injury

A prospective double-blind study

Paul R. Cooper, Sarah Moody, W. Kemp Clark, Joel Kirkpatrick, Kenneth Maravilla, A. Lawrence Gould and Wanzer Drane

T he efficacy of corticosteroid administration in the management of the edema associated with primary and metastatic brain tumors is well established. 4, 12, 24, 26 The results of studies to investigate the effects of corticosteroids on experimental brain injury are, however, contradictory. 5, 16, 20, 21, 25, 28, 29, 31, 35 Similarly, the usefulness of corticosteroids in the management of severe head injury in humans remains controversial. Sparacio, et al., 32 Gobiet, et al., 13 Faupel, et al., 9 and Ransohoff 30 believe that corticosteroids are

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Marek Czosnyka, Piotr Smielewski, Stefan Piechnik, Luzius A. Steiner and John D. Pickard

C erebral autoregulation is one of the major mechanisms responsible for brain protection in circumstances in which CPP may become unstable. 15, 26, 32 Maintaining CPP above 70 mm Hg by using CPP-oriented therapy is a realistic target, 35 but changes in CPP often may be too rapid for timely intervention to prevent temporary falls in pressure. Elevations of ICP, variations in ABP, and other factors may lead to ischemic insults when autoregulation is defective. Disturbed autoregulation has been demonstrated to occur after head injury. 5–7, 15, 28, 34 In

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Cerebral circulation after head injury

Part 3: Does reduced regional cerebral blood flow determine recovery of brain function after blunt head injury?

Jørn Overgaard, Claus Mosdal and William A. Tweed

I n the last decade, many studies have shown that during the acute stage following severe head injury a reduction of cerebral blood flow (CBF) is found in most patients, but, in some, hyperemia is encountered. 9, 11, 20, 25, 29, 30, 33 A consistent and reproducible relationship between mean hemispheric CBF and patient outcome has not been established, although recovery of integrative cortical function generally does not occur in patients with mean hemispheric CBF lower than 20 ml/100 gm/min. 29, 31 Less is known about recovery after severe head injury when

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Thomas W. Langfitt

I n clinical medicine, outcome, which is the end result of a disease process, is measured in terms of morbidity and mortality. It is well recognized that the morbidity and mortality from severe head injuries are heavy, but until the past few years there were surprisingly few reports that presented outcome in terms of the patients' neurological status at the time of admission and other characteristics of the injury. In the early decades of this century there were a few reports of mortality rates, followed by a gap of many decades during which time there was

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Cerebral circulation after head injury

Part 4: Functional anatomy and boundary-zone flow deprivation in the first week of traumatic coma

Jørn Overgaard and William A. Tweed

S evere head injury is generally associated with decreased cerebral blood flow (CBF), 23 and a marked heterogeneity in the regional distribution of CBF, both at the gross and microscopic levels. 25 We have previously demonstrated a significant relationship between an ischemic regional cerebral blood flow (rCBF) of less than 17 ml/100 gm/min and nonrecovery of brain function. 23 Other authors have reported ischemic neuronal infarction in the arterial boundary regions of patients dying after head injury. 8 Although we have speculated that ischemic rCBF

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Cerebral circulation after head injury

Part 1: Cerebral blood flow and its regulation after closed head injury with emphasis on clinical correlations

Jørn Overgaard and William A. Tweed

) changes after closed head injury in a group of relatively young, healthy patients. Other investigations included intraventricular pressure measurement, functional tests of cerebrovascular autoregulation and CO 2 reactivity, and ventricular CSF acid-base determination. The objectives of this study were to: 1. Determine the time course of rCBF changes after head injury, particularly in relation to the development of “secondary injury” due to brain edema and increased intracranial pressure 2. Establish the prognostic value of rCBF studies and functional