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Studies that investigate the performance of prognostic and predictive biomarkers are commonplace in medicine. Evaluating the performance of biomarkers is challenging in traumatic brain injury (TBI) and other conditions when both the time factor (i.e. time from injury to biomarker measurement) and different levels or doses of treatments are in play. Such factors need to be accounted for when assessing the biomarker's performance in relation to a clinical outcome. The Hyperbaric Oxygen in Brain Injury Treatment (HOBIT) trial, a phase II randomized control clinical trial seeks to determine the dose of hyperbaric oxygen therapy (HBOT) for treating severe TBI that has the highest likelihood of demonstrating efficacy in a phase III trial. Hyperbaric Oxygen in Brain Injury Treatment will study up to 200 participants with severe TBI. This paper discusses the statistical approaches to assess the prognostic and predictive performance of the biomarkers studied in this trial, where prognosis refers to the association between a biomarker and the clinical outcome while the predictiveness refers to the ability of the biomarker to identify patient subgroups that benefit from therapy. Analyses based on initial biomarker levels accounting for different levels of HBOT and other baseline clinical characteristics, and analyses of longitudinal changes in biomarker levels are discussed from a statistical point of view. Methods for combining biomarkers that are of complementary nature are also considered and the relevant algorithms are illustrated in detail along with an extensive simulation study that assesses the performance of the statistical methods. Even though the discussed approaches are motivated by the HOBIT trial, their applications are broader. They can be applied in studies assessing the predictiveness and prognostic ability of biomarkers in relation to a well-defined therapeutic intervention and clinical outcome., Competing Interests: Declaration of conflicting interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

There has been no major advancement in a quarter of a century for the treatment of acute severe traumatic brain injury (TBI). This review summarizes 40 years of clinical and pre-clinical research on the treatment of acute TBI with hyperbaric oxygen therapy (HBO 2 ) in the context of an impending National Institute of Neurologic Disorders and Stroke-funded, multi-center, randomized, adaptive Phase II clinical trial -the Hyperbaric Oxygen Brain Injury Treatment (HOBIT) trial. Thirty studies (eight clinical and 22 pre-clinical) that administered HBO 2 within 30 days of a TBI were identified from PubMed searches. The pre-clinical studies consistently reported positive treatment effects across a variety of outcome measures with almost no safety concerns, thus providing strong proof-of-concept evidence for treating severe TBI in the acute setting. Of the eight clinical studies reviewed, four were based on the senior author's (GR) investigation of HBO 2 as a treatment for acute severe TBI. These studies provided evidence that HBO 2 significantly improves physiologic measures without causing cerebral or pulmonary toxicity and can potentially improve clinical outcome. These results were consistent across the other four reviewed clinical studies, thus providing preliminary clinical data supporting the HOBIT trial. This comprehensive review demonstrates that HBO 2 has the potential to be the first significant treatment in the acute phase of severe TBI.

Background: The presence of osmotic gradients in the development of cerebral edema and the effectiveness of osmotherapy are well recognized. A modification of ventriculostomy catheters described in this article provides a method of osmotherapy that is not currently available. The reductive ventricular osmotherapy (RVOT) catheter removes free water from ventricular cerebrospinal fluid (CSF) by incorporating hollow fibers that remove water vapor, thereby providing osmotherapy without increasing osmotic load., Objective: To increase osmolarity in the ventricular CSF through use of RVOT in vivo., Methods: Twelve Yorkshire swine with contusional injury were randomized to external ventricular drainage (EVD) or RVOT for 12 hours. MR imaging was obtained. Serum, CSF, and brain ultrafiltrate were analyzed. Histology was compared using Fluor-Jade B and hematoxylin and eosin (H & E) stains., Results: With RVOT, CSF osmolality increased from 292 ± 2.7 to 345 ± 8.0 mOsmol/kg (mean ± SE, P = 0.0006), and the apparent diffusion coefficient (ADC) in the injury region increased from 0.735 ± 0.047 to 1.135 ± .063 (P = 0.004) over 24 hours. With EVD controls, CSF osmolarity and ADC were not significantly changed. Histologically, all RVOT pigs showed no evidence of neuronal degeneration (Grade 1/4) compared to moderate degeneration (Grade 2.6 ± .4/4) seen in EVD treated animals (P = 0.02). The difference in intracranial pressure (ICP) by area under the curve approached significance at P = .065 by Mann Whitney test., Conclusion: RVOT can increase CSF osmolarity in vivo after experimental traumatic brain injury (TBI). In anticipated clinical use, only a slight increase in CSF osmolarity may be required to reduce cerebral edema.

This report describes how 27 patients with severe traumatic brain injury were safely treated, monitored and managed in a monoplace chamber that was compressed with air to 1.5 atmospheres absolute (152 kPa). A total of 75 hyperbaric oxygen treatments were delivered using the monoplace system described, with all patients receiving 100% oxygen via mechanical ventilation. Specific pieces of equipment, components and features were selected, and modifications were interfaced to safely and effectively treat these critically ill patients in a monoplace chamber. Patient monitoring included cardiovascular and ventilatory parameters as well as intracranial pressure, brain tissue oxygen levels, brain temperature and cerebral microdialysis. The chamber and all the supporting equipment for ventilating, monitoring and managing the patient functioned well.

Object: Hyperbaric oxygenation (HBO) therapy has been shown to reduce mortality by 50% in a prospective randomized trial of severely brain injured patients conducted at the authors' institution. The purpose of the present study was to determine the effects of HBO on cerebral blood flow (CBF), cerebral metabolism, and intracranial pressure (ICP), and to determine the optimal HBO treatment paradigm., Methods: Oxygen (100% O2, 1.5 atm absolute) was delivered to 37 patients in a hyperbaric chamber for 60 minutes every 24 hours (maximum of seven treatments/patient). Cerebral blood flow, arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), ventricular cerebrospinal fluid (CSF) lactate, and ICP values were obtained 1 hour before and 1 hour and 6 hours after a session in an HBO chamber. Patients were assigned to one of three categories according to whether they had reduced, normal, or raised CBF before HBO. In patients in whom CBF levels were reduced before HBO sessions, both CBF and CMRO2 levels were raised 1 hour and 6 hours after HBO (p < 0.05). In patients in whom CBF levels were normal before HBO sessions, both CBF and CMRO2 levels were increased at 1 hour (p < 0.05), but were decreased by 6 hours after HBO. Cerebral blood flow was reduced 1 hour and 6 hours after HBO (p < 0.05), but CMRO2 was unchanged in patients who had exhibited a raised CBF before an HBO session. In all patients AVDO2 remained constant both before and after HBO. Levels of CSF lactate were consistently decreased 1 hour and 6 hours after HBO, regardless of the patient's CBF category before undergoing HBO (p < 0.05). Intracranial pressure values higher than 15 mm Hg before HBO were decreased 1 hour and 6 hours after HBO (p < 0.05). The effects of each HBO treatment did not last until the next session in the hyperbaric chamber., Conclusions: The increased CMRO2 and decreased CSF lactate levels after treatment indicate that HBO may improve aerobic metabolism in severely brain injured patients. This is the first study to demonstrate a prolonged effect of HBO treatment on CBF and cerebral metabolism. On the basis of their data the authors assert that shorter, more frequent exposure to HBO may optimize treatment.

Objective: Recent studies suggest that in some circumstances, alcohol intoxication at the time of severe head injury may be neuroprotective. The objective of this study was to determine the effect of acute and chronic alcohol ingestion on outcome in rodents sustaining multiple episodes of mild traumatic brain injury while intoxicated., Method: For two weeks before experimentation, adult male Sprague-Dawley rats received intoxicating levels of 95% ethanol (3 g/kg) or normal saline (NS) every other day by orogastric instillation. On the day of experimentation, the animals were randomized to receive alcohol or NS. Two hours later, the animals received either mild (1.2 +/- 0.4 ATA) fluid percussion injury (FPI) or no injury. The injured animals received a total of three episodes of FPI (once every four days). Mean reflex recovery time (RRT) was determined (seconds +/- SEM) immediately after each episode. Mean latency time (seconds +/- SEM) for Morris Water Maze (MWM) performance was assessed at post-trauma days 11-19., Results: The chronic alcohol-exposed (CA) and the non-alcohol-exposed (NA) animals intoxicated when injured had prolonged escape, righting, and corneal RRTs after each FPI compared with the nonintoxicated injured animals and the non-injured shams. However, the CA animals had significantly shorter RRTs when compared with the NA rats. All the injured animals had MWM deficits on testing days 1-6 compared with the noninjured controls. On the last two MWM testing days, the injured NA animals had significantly better MWM performance than the injured CA rats., Conclusions: The injured intoxicated CA animals had a more rapid recovery of reflexes compared with the injured intoxicated NA animals. Despite initial MWM deficits, the injured NA rodents eventually began to learn the MWM. The injured CA rats never learned the maze. Under the conditions of this study, acute alcohol intoxication at the time of multiple episodes of minor head trauma did not provide neuroprotection for NA or CA rodents.

Background: Light deprivation significantly accelerates recovery from attention deficits (neglect) after cortical ablation in rats. We hypothesized that light deprivation would improve recovery after traumatic contusive brain injury (TBI) and do so by enhancing dopaminergic function in the ipsilateral basal ganglia., Methods: Adult rats received left frontal contusion injury and were placed into darkness or standard light/dark cycling for 48 hours. Neurologic evaluation included attentional and sensorimotor tasks. Amphetamine-induced production of the immediate early gene protein product Fos was quantified to determine neuronal dopaminergic response in caudate-putamen (striatum)., Results: Unilateral frontal TBI produced severe contralateral deficits in all tasks. Postoperative light deprivation resulted in improved recovery from attentional but not sensorimotor deficits. Five days after injury, ipsilateral striatal Fos expression was reduced by 51% in TBI rats experiencing normal light cycling (p < 0.006). In contrast, postoperative light deprivation normalized striatal Fos expression. By 6 weeks, all TBI rats demonstrated nearly full recovery and striatal Fos expression was symmetrical between the two striata., Conclusion: Postoperative light deprivation may improve recovery from TBI-induced attention deficits by normalizing basal ganglia function.

Using human fetal microglial cell cultures, we found that the gram-negative bacterial cell wall component lipopolysaccharide (LPS) stimulated RANTES (regulated upon activation of normal T cell expressed and secreted) production through the protein kinase C signaling pathway and that activation of transcription nuclear factor (NF)-kappaB was required for this effect. Similarly, the proinflammatory cytokines interleukin (IL)-1beta and tumor necrosis factor-alpha dose-dependently stimulated microglial cell RANTES production via NF-kappaB activation. Anti-inflammatory cytokines, IL-10, and transforming growth factor (TGF)-beta sequentially inhibited LPS- and cytokine-induced microglial cell NF-kappaB activation, RANTES mRNA expression, and protein release. Proinflammatory cytokines but not LPS also stimulated RANTES production by human astrocytes. These findings demonstrate that human microglia synthesize RANTES in response to proinflammatory stimuli, and that the anti-inflammatory cytokines IL-10 and TGF-beta down-regulate the production of this beta-chemokine. These results may have important therapeutic implications for inflammatory diseases of the brain.

Background: It has been suggested that early fixation of a fracture is deleterious to eventual neurologic outcome. We undertook this study to determine whether the timing of fracture fixation is correlated to neurologic outcome., Methods: We retrospectively reviewed patients with severe head and orthopedic injuries requiring fracture fixation. Patients were divided into two groups: early fracture fixation (< 24 hours after injury) and late fracture fixation (> 24 hours after injury)., Results: One hundred twenty-three patients met entry criteria. During fracture fixation, the early group had a significant 2-, 3-, and 2-fold increase in crystalloid, blood infusion, and blood loss, respectively. There was no difference in oxygen saturation and systolic blood pressure or episodes of cranial hypertension or hypoperfusion. There was no difference in outcomes as measured by in-hospital complications, stay in the intensive care unit or hospital, mortality rates, hospital discharge or follow-up Glasgow Coma Scores, or long-term orthopedic or neurologic results., Conclusions: Patients undergoing fracture fixation with severe head injury mandate monitoring of intracranial pressure and perfusion and tailored fluid resuscitation to meet specific organ end points. Integrating end organ perfusion and pressure with meticulous fluid status during the definitive repair phase may reduce the exposure to secondary brain injury in patients undergoing early fracture fixation.

IL-8 involvement in neutrophil activation and chemotaxis may be important in inflammatory responses within the central nervous system, secondary to meningitis, encephalitis, and traumatic injury. The source of IL-8 within the brain during these inflammatory processes, however, is unknown. To explore the role of microglia in the production of IL-8, human fetal microglia, which are the resident macrophages of the brain, were treated with LPS and pro- and anti-inflammatory cytokines to determine their effects on IL-8 production. We found that IL-8 protein levels increased in response to LPS or IL-1 beta, or to TNF-alpha, which also corresponded to elevated IL-8 mRNA levels by RT-PCR. Pretreatment with IL-4, IL-10, or TGF-beta 1 potently inhibited the stimulatory effects of these proinflammatory agents. These findings indicate that human microglia synthesize IL-8 in response to proinflammatory stimuli, and that anti-inflammatory cytokines down-regulate the production of this chemokine. These results may have important therapeutic implications for certain central nervous system insults involving inflammation.

Palmar hyperhidrosis is a disabling condition that manifests itself as excessive sweating of the hands. Although the exact cause is unknown, several medical and surgical therapies are available to treat it. Recent developments in surgical technique have made the less invasive thoracoscopic sympathectomy a viable alternative to the open sympathectomy for medically refractory cases. We believe that thoracoscopic sympathectomy is a safe and effective treatment for palmar hyperhidrosis.

The authors reviewed 29 cases of spinal tuberculosis treated from 1973 to 1993 with an average follow-up time of 7.4 years. Clinical findings included back pain, paraparesis, kyphosis, fever, sensory disturbance, and bowel and bladder dysfunction. Twenty-two patients (76%) presented with neurological deficit; 12 (41%) were initially misdiagnosed. Sixteen patients (55%) had predominant vertebral body involvement; nine had marked bone collapse with neurological compromise. Eleven individuals (39%) had intraspinal granulomatous tissue causing neurological dysfunction in the absence of bone destruction, and two (7%) had intramedullary tuberculomas. All patients received antituberculous medications: 13 were initially treated with bracing alone, eight underwent laminectomy and debridement of extra- or intradural granulomatous tissue, and eight underwent anterior, posterior, or combined fusion procedures. No patient with neurological deficit recovered or stabilized with nonoperative management. Thirteen patients were readmitted with progression of inadequately treated osteomyelitis; 12 (92%) of these required new or more radical fusion procedures. Anterior fusion failure was associated with marked preoperative kyphosis and multilevel disease requiring a graft that spanned more than two disc spaces. Courses of antibiotic medications shorter than 6 months were invariably associated with disease recurrence. It was concluded that 1) patients should receive at least 12 months of appropriate antituberculous therapy; 2) individuals with neurological deficit should undergo surgical decompression; 3) laminectomy and debridement are adequate for intraspinal granulomatous tissue in the absence of significant bone destruction; 4) when vertebral body involvement has produced wedging and kyphosis, aggressive debridement and fusion are indicated to prevent delayed instability and progression of disease.

This study was designed to evaluate the production of cerebral edema [as measured by tissue specific gravity (SpG)] following moderate fluid percussion (FP) and cortical impact (CI) injury in rodents. To determine the effects of a secondary systemic insult, hypoxia (13% oxygen for 30 min) was added to some experimental groups immediately after head injury. To determine the effects of hyperbaric oxygen (HBO) on injured cortical tissue, additional animal groups were exposed to HBO (1.5 atm, for 60 min), beginning 4 h after head trauma. Both injury models produced equal amounts of tissue edema at the site of injury (mean SpG +/- SEM = 1.035 +/- 0.001), when measured 6 h posttrauma. There was no significant edema at the tissue sites immediately adjacent to the trauma sites. The addition of hypoxia to either injury system did not increase edema formation beyond that produced by injury alone. HBO reduced the water content of the trauma site in animals that had received FP, but not in animals receiving CI. We conclude that with the injury parameters used in this protocol, both FP and CI appear to produce focal cerebral edema at the site of trauma. Hypoxia does not worsen edema. HBO appears to reduce edema produced by FP, but not by CI.

Patients who "talk and deteriorate" are defined as those who utter recognizable words at some time after head injury and then deteriorate to a severe head-injured condition (Glasgow Coma Scale score of 8 or less) within 48 hours of injury. They represent a very small but important subgroup of patients with brain injury. In approximately 75% of these patients, the cause of this deterioration is intracranial hematoma. Despite the fact that talking indicates nonlethal impact brain injury, deterioration is a marker of poor prognosis. Outcome depends on early recognition of deterioration and rapid removal of mass lesions. The challenge for emergency physicians is to distinguish patients at risk for deterioration from the many patients evaluated after head injury.

The authors enrolled 168 patients with closed-head trauma into a prospective trial to evaluate the effect of hyperbaric oxygen in the treatment of brain injury. Patients were included if they had a total Glasgow Coma Scale (GCS) score of 9 or less for at least 6 hours. After the GCS score was established and consent obtained, the patient was randomly assigned, stratified by GCS score and age, to either a treatment or a control group. Hyperbaric oxygen was administered to the treatment group in a monoplace chamber every 8 hours for 1 hour at 1.5 atm absolute; this treatment course continued for 2 weeks or until the patient was either brain dead or awake. An average of 21 treatments per patient was given. Outcome was assessed by blinded independent examiners. The entire group of 168 patients was followed for 12 months, with two patients lost to follow-up study. The mortality rate was 17% for the 84 hyperbaric oxygen-treated patients and 32% for the 82 control patients (chi-squared test, 1 df, p = 0.037). Among the 80 patients with an initial GCS score of 4, 5, or 6, the mortality rate was 17% for the hyperbaric oxygen-treated group and 42% for the controls (chi-squared test, 1 df, p = 0.04). Analysis of the 87 patients with peak intracranial pressures (ICP) greater than 20 mm Hg revealed a 21% mortality rate for the hyperbaric oxygen-treated patients, as opposed to 48% for the control group (chi-squared test, 1 df, p = 0.02). Myringotomy to reduce pain during hyperbaric oxygen treatment helped to reduce ICP. Analysis of the outcome of survivors reveals that hyperbaric oxygen treatment did not increase the number of patients in the favorable outcome categories (good recovery and moderate disability). The possibility that a different hyperbaric oxygen treatment paradigm or the addition of other agents, such as a 21-aminosteroid, may improve quality of survival is being explored.

In the management of cervical spine injuries, it is not always clear when to use halo immobilization alone, surgical fusion alone, or a combination of the two. To investigate the relative effectiveness of each of these approaches, we reviewed the medical records of 140 patients with cervical spine injuries treated with either halo immobilization or surgical fusion, or both. Seventy (50%) of the patients were neurologically intact on admission (two of these were paraplegic from previous injuries). Halo immobilization was used as the primary treatment in 99 patients, and yielded a successful fusion rate of 78%. Within this group, the 26 patients with hyperflexion-anterior subluxation injuries had only a 54% successful fusion rate, while the rate for the 73 with non-flexion injuries was 87% (Chi-square = 11.36; p = 0.0008). Surgical fusion was used as the primary treatment in 41 patients and as a subsequent treatment in the 22 for whom halo immobilization did not bring about fusion. Of these 63 patients treated with surgical fusion, six remained unstable after the surgery; five of these six had sustained a hyperflexion-anterior subluxation. One patient experienced neurologic deterioration after surgical fusion. There were three deaths in the entire series. Excluding fusion failure, complications with halo immobilization were frequent (25%) but usually minor; with surgical fusion, less frequent (6%) but usually more severe. We draw the following conclusions. 1) Halo immobilization brings about satisfactory healing for most fracture types. 2) Both halo immobilization and surgical fusion have relatively high failure rates in the treatment of hyperflexion-anterior subluxation injury, with or without bilaterally locked facets.(ABSTRACT TRUNCATED AT 250 WORDS)

Nine cases of delayed posttraumatic intracerebral hematomas (DTICH) were found retrospectively among 656 patients with closed head injuries admitted to the Hennepin County Medical Center in a 12-month period. All cases had severe head injuries sustained with the head in motion. The interval from cranial injury to diagnosis of DTICH by computerized tomography (CT) varied from 8 hours to 13 days. Eight patients were comatose on admission, three had focal seizures, and three had focal findings. The diagnosis was made on repeat CT scans obtained because of the development of focal findings in four cases, lack of improvement in four cases, and general neurological deterioration in one case. Four patients had initially negative CT scans. Four demonstrated only extracerebral hematomas on initial CT scan. One patient showed intracerebral hematoma on the initial scan followed by new hematomas on repeat study. The cases presented are discussed in light of pertinent literature.

Stimulating electrodes were placed on the terminal branches of the pelvic nerves to the urinary bladder and the pudendal nerve to the sphincters in seven Rhesus monkeys and two chimpanzees. The proximity of the electrodes to these structures assured organ specificity. Evoked responses produced by stimulation of these terminal nerve branches were recorded in the fascicles and rootlets of the lower thoracic, lumbar, and sacral nerve roots. During identical stimulating and recording conditions, the amplitude as well as presence or absence of the evoked responses recorded was variable within the various roots. The amplitude of the evoked responses or their absence depended on the number of fibers within a particular fascicle which conducted impulses to the urinary bladder or the urethral and anal sphincters. By this method, it was determined that there was segregation or compartmentalization of the nervous innervation to the urinary bladder and sphincters within the spinal roots. In addition, the segmental spinal cord origin of the innervation of the urinary bladder was determined for the Rhesus monkey and chimpanzee. In the Rhesus monkey, the pelvic nerves to the urinary bladder arose from the first and second sacral segments and to a much lesser extent from the seventh lumbar segment. In the chimpanzee, the sacral segments one to four gave rise to innervation of the urinary bladder.

Subependymomas are extremely rare tumors in the pediatric population and, when they occur, they are usually of a mixed type with elements of subependymoma and ependymoma. This report is of a 2 1/2-year-old male infant with a pure subependymoma of the fourth ventricle.

A case of accidental inhalation of liquid nitrogen vapor is reported. The patient, a 29-year-old man, developed acute burns of his lips and oropharynx and presented with signs and symptoms of acute upper airway distress within an hour of the injury. The patient underwent emergency tracheostomy and was placed on intravenous dexamethasone and ampicillin. Large mucosal ulcers developed in the posterior hypopharynx and hard palate but the patient was discharged four days post operatively and had no permanent sequelae.

A newborn infant with a massive left to right shunt secondary to a cerebral arteriovenous malformation required continuous oxygen therapy in high concentrations. Despite high PO2, the infant maintained low to normal PaO2 concentrations. Light and ultrastructural studies of the lungs demonstrated typical changes of acute pulmonary oxygen toxicity, including degeneration of capillary endothelium and type I pneumonocytes, interstitial edema, and alveolar exudation. These observations confirm earlier experimental animal studies that demonstrated that the alveolar Po2 concentration and not the Pao2 is the major factor contributing to pulmonary oxygen toxic effect.

The authors describe long-term follow-up results (4 to 6 years) in 13 patients who underwent differential sacral rhizotomy for urgency incontinence. Six patients were originally presented in a preliminary report in 1973. In the last seven patients, a highly selective rhizotomy of sacral fascicles innervating only the urinary bladder was performed. Results in the original six patients appear to be superior to those in patients who underwent a more refined rhizotomy. Possible explanations for this as well as alternative approaches to the treatment of urgency incontinence are briefly discussed.

A case of subarachnoid hematoma after a difficult lumbar puncture and anticoagulation is presented. Subarachnoid adhesions preventing the free flow of spinal fluid at the T-6 level served to limit the cranial progression of the hemorrhage and produced a transverse myelopathy at that level. The underlying pathology, clinical course, and myelographic findings are reviewed. Pertinent literature is presented.

A 5-year retrospective review was done to evaluate C-7 and C7-T1 cervical spine injuries and to assess the advanced trauma life support guidelines for cervical spine evaluation. Eighteen fractures of C-7 and four fracture-dislocation at C7-T1 were identified. Nineteen of the patients had neck pain, tenderness, or neurologic findings on initial examination. Three patients were awake and asymptomatic. The initial diagnosis could be made from lateral cervical spine x-ray film in only three of the 22 patients. In the remaining patients, the diagnosis was made by either swimmer's view (7 of 8 positive), oblique views (1 of 1 positive), flexion-extension views (2 of 3 positive), or computed tomography (CT) scan (7 of 7 positive). In two patients, the diagnosis was not made in the first 24 hours. Follow-up x-ray films were positive in 3 of 22 lateral cervical spine films, 10 of 14 swimmer's views, 2 of 3 oblique views, 2 of 3 flexion-extension views, and 14 of 20 CT scans. The data support the advanced trauma life support recommendation for liberal use of cervical spine radiologic screening. We recommend that the screening examination consist of a lateral cervical spine film, and a swimmer's view, if necessary, to visualize C-7 and the C7-T1 interspace. We further recommend that strong consideration be given to the use of a five-view trauma series. CT scan should be viewed as complementary to conventional film techniques.

During the years 1974 of 1976, 514 patients with prehospital cardiopulmonary arrest were brought to the Hennepin County Medical Center (HCMC) Emergency Department. Of these, 344 patients (67%) were either dead on arrival or died in the emergency department despite efforts at resuscitation. The remaining 170 patients were admitted to the coronary care unit. Eighty-seven patients (51%) died in the coronary care unit, primarily from uncontrolled rhythm disturbances and/or cardiogenic shock. The remaining 83 patients (16% of the total group, 49% of those admitted to the hospital) were discharged alive from HCMC. In this group, 49 patients of the 83 long-term survivors were ambulatory with full mental function when discharged. The remaining 34 patients were trnasferred to chronic care facilities for medical treatment of on-going problems. Of the 49 ambulatory patients, satisfactory data for follow-up was obtained on 47. Their mortality rate was 15% in the first year and 50% in the second, primarily from sudden death syndrome.

Seven months following severe crushing closed-head trauma with initial excellent recovery, neurologic deficits referable to the right mesencephalon abruptly developed in a 28-year-old man. Computed tomography demonstrated a cystic midbrain lesion with apparent communication with the aqueduct (later confirmed at autopsy). Brain-stem auditory evoked potentials after the clinical deterioration showed depression of amplitude of wave V, compared with predeficit records, only when the ear contralateral to the brain-stem lesion was stimulated.

The authors describe the use of evoked electromyographic responses recorded in the anal sphincter induced by stimulation of the bladder wall and urethra in evaluating lesions of the conus medullaris and cauda equina in 110 patients. This reflex response took effect by way of the pelvic nerves and cauda equina to the sacral cord where the pudendal nerve nucleus was activated, resulting in a contraction of the external anal sphincter. Various lesions along this pathway have been shown to produce either increased latencies and depressed responses or complete loss of response depending on the extent of the lesion. The correlation of results of this technique with clinical, myelographic, and operative findings indicate it to be a useful clinical tool.

An electrophysiologic technique to evaluate the anatomic integrity of the peripheral pathways to the bladder and sphincters is described. Evoked electromyographic responses of the anal sphincter are produced by stimulating the bladder wall and urethra. Impulses travel via the pelvic nerves and cauda equina to the conus medullaris, activating the pudendal nerve nucleus and resulting in contraction of the external anal sphincter. Lesions along this pathway produce either prolonged latencies and depressed responses or complete loss of response. Correlation of the results of this technique in 110 patients with clinical myelographic and operative findings indicates that the technique is a useful clinical tool.

A case of impressive neurologic recovery after a complete cervical spinal cord injury is presented. The importance of prehospital recognition and immobilization and prompt management of cervical spine injuries is emphasized. Full reduction of the fracture-dislocation of C3 on C4 was accomplished 90 minutes postinjury.