Biomechanics and neuropathology of adult and paediatric head injury.

The objective of this study was to understand the biomechanics in age-related primary traumatic brain injuries (TBI) causing initial severity and secondary progressive damage and to develop strategy reducing TBI outcome variability using biomechanical reconstruction to identify types of causal mechanisms prior to clinical trials of neuro-protective treatment. The methods included the explanation of TBI biomechanics and physiopathological mechanisms from dual perspectives of neurosurgery and biomechanical engineering. Scaling of tolerances for skull failure and brain injuries in infants, children and adults are developed. Diagnostic assumptions without biomechanical considerations are critiqued. Methods for retrospective TBI reconstruction for prevention are summarized. Mechanisms of TBI are based on the differences between the mechanical properties of the head and neck related to age. Skull fracture levels correlate with increasing cranial bone thickness and in the development of the cranial sutures in infants and in adults. Head injury tolerance levels at three age categories for cerebral concussion, skull fracture and three grades of diffuse axonal injuries (DAI) are presented. Brain mass correlates inversely for TBI caused by angular head motions and locations of injurious stresses are predictable by centripetal theory. Improved quantitative diagnosis of TBI type and severity levels depend primarily on age and biomechanical mechanisms. Reconstruction of the biomechanics is feasible and enables quantitative stratification of TBI severity. Experimental treatment has succeeded in preventing progressive damage in animal TBI models. In humans this has failed, because the animal model received biomechanically controlled TBI and humans did not. Clinical similarities of human TBI patients do not necessarily predict equivalent biomechanics because such trauma can be produced in various ways. We recommend 'reverse engineering' for in-depth reconstruction of the TBI injury mechanism for qualitative diagnoses and reduction of outcome variability.

More on assessing outcomes of emergency care.

New methods of assessing the outcomes of emergency department care are needed to provide information to purchasers, plans, providers, and patients to prove improvements in EMS system organization, quality, efficiency, and patient satisfaction. This commentary expands on the important components of an outcomes research agenda for ED care.

Motivation for traumatic brain injury rehabilitation questionnaire (MOT-Q): reliability, factor analysis, and relationship to MMPI-2 variables.

A Likert scale questionnaire was developed to assess motivation for postacute rehabilitation by traumatic brain injury patients. Items were designed to reflect head-injured individuals' statements about their attitudes toward head injury rehabilitation. Factors such as denial of illness, anger, compliance with treatment, and medical information seeking behavior were used to assess unfavorable and favorable components of motivation. Reliability was assessed using Cronbach's Alpha, which was found to be 0.91 for the total scale. Four factor analysis derived subscales were identified: Lack of Denial, Interest in Rehabilitation, Lack of Anger, and Reliance on Professional Help. Correlation and multiple regression analyses demonstrated moderate relationships between MOT-Q and several MMPI-2 variables largely related to indicators of somatic distress, depression and capacity for self-sufficiency. Lack of Denial subscale showed the strongest relationship to MMPI-2 of all MOT-Q variables, while Interest in Rehabilitation showed the best correlation to the MOT-Q total.

Outcome after traumatic brain injury in the U.S. military medical system.

Personality and behavioral change after traumatic brain injury (TBI) are often the most significant concerns for the families of TBI patients. This report examines discharge from military service after TBI for medical and behavioral criteria. When compared with the total discharge population (n = 1,879,724), the relative risk for behavioral discharge was 1.8 times greater for those with mild TBI (n = 1,778), and no difference for those with moderate (n = 174) or severe TBI (n = 274). Discharge for alcoholism or drug use was 2.6 times for mild TBI, 5.4 times for moderate TBI, and no difference for severe TBI compared with the total discharge population. Discharge for criminal conviction was 2.7 times for those with mild head injury, and no difference for those with moderate or severe TBI when compared with the total discharge population. Discharge for medical disability ranged from 7.5 times to 40.4 times, and mortality ranged from 11.6 to 142.4 times the total discharge population. Total sick days defined as the time from admission to return to duty or separation from service increased with head injury severity. Mean Injury Severity Score for mild TBI was 5.5, and 20.9 for severe TBI. Patients who sustain TBI should be monitored after injury for development of behavioral problems. The most effective way to reduce the cost of TBI is primary prevention of these injuries and examining military practices to reduce exposure to risk of TBI. Secondary and tertiary prevention measures such as evaluation and rehabilitation, where indicated, should be undertaken on a routine basis after TBI.

Causation, incidence, and costs of traumatic brain injury in the U.S. military medical system.

Hospital discharge records from military facilities and private facilities reimbursed by Civilian Health and Medical Program of the Uniformed Services for fiscal year 1992 were reviewed to identify head injury admissions. Incidence rates, case fatality rates, causes of head injuries, and direct cost for hospital admissions were computed in this well-defined population. For fiscal year 1992, there were 5,568 hospitalized cases of noncombat head injury in the military medical system. The age-adjusted head injury rates for ages 15-44 years are higher in active-duty individuals compared with other beneficiaries (1.6 times greater for men and 2.5 times greater for women). The total cost for hospitalization in this population was $43 million. Private facility rehabilitation accounted for 26% of all private facility costs but only 6% of head injury cases. Firearms and motor vehicle crashes caused the most severe injuries for cases admitted to military facilities. Motor vehicle crashes, falls, and fighting accounted for 80% of the total military facility cost for head injuries. Military active-duty individuals are at increased risk for noncombat head injury. Prevention of head injury in military settings should focus on motor vehicle crashes, fist fights (assault), and falls.

Head injury mechanisms and the concept of preventive management: a review and critical synthesis.

Recent advances in head injury research have produced a plethora of useful data coupled with a paucity of conceptual integration across the four ways in which this research is pursued. These research orientations are the epidemiological, biomechanical, basic neuroscientific, and clinicopathologic/therapeutic (including rehabilitation). This overview of the history and current state of the art assumes that biomechanics is the basic science of causation in head injury research and when fully integrated with its counterparts, physiology and pathology, it can serve to overcome our conceptual handicaps. A paradigm integrating biomechanics; into the sequence of preventive, protective, acute therapeutic, and rehabilitative interventions will be described as the concept of preventive management. From this we derive the hypothesized claim that the exact biomechanics and the physiopathologic response at the time of injury (at the macroscopic and microscopic levels) determine the sequence of so-called secondary effects that are conceived as the inexorable delayed manifestations of the primary events and concomitant boundary conditions. Knowledge of these events will enable accurate predictions of the natural history and outcome of head injuries from observations carried out in the early acute phase. Examples to test this claim will be given with particular reference to the two types of traumatic brain injury (TBI) phenomenologically associated with disturbances of consciousness, the onset of which can be either immediate or delayed. The current economics and availability of computational power provide a significant opportunity for the development of selected experimental, physical, and simulated models of head injury on the basis of which the complex neurovascular and nonneural cellular and fluid elements of the nervous system may be accurately modeled. This approach will significantly improve the efficiency and quality of the essential biological and clinical observations and model experiments required to validate the theoretical methods and their predictions.

Massive cortical reorganization after sensory deafferentation in adult macaques.

After limited sensory deafferentations in adult primates, somatosensory cortical maps reorganize over a distance of 1 to 2 millimeters mediolaterally, that is, in the dimension along which different body parts are represented. This amount of reorganization was considered to be an upper limit imposed by the size of the projection zones of individual thalamocortical axons, which typically also extend a mediolateral distance of 1 to 2 millimeters. However, after extensive long-term deafferentations in adult primates, changes in cortical maps were found to be an order of magnitude greater than those previously described. These results show the need for a reevaluation of both the upper limit of cortical reorganization in adult primates and the mechanisms responsible for it.

Implantable devices for chronic access and drug delivery to the central nervous system.

This is a review of implantable devices for chronic access and drug delivery to the central nervous system (CNS) via the cerebrospinal fluid, extracellular fluid, and vascular pathways. The current applications of such devices in the management of mycotic meningitis, meningeal leukemia and carcinomatosis, solid malignant tumors of the CNS, intractable cancer-associated pain, unresectable cystic tumors and in cytologic, pharmacologic, and experimental studies on the cerebrospinal fluid (CSF) are assessed. Specific attention is paid to the applications of the most commonly used device, a subcutaneous reservoir and pump (SRP), including its major uses and complications. A new system for local chemotherapy of malignant gliomas, the tumor cyst device (TCD), is also described.

Cerebral abscesses produced by bacterial implantation and septic embolisation in primates.

The degree of brain abscess encapsulation is positively related to surgical mortality and methods to enhance capsule wall formation, therefore, have therapeutic relevance. Two primate models are described which may be useful in the investigation of encapsulation of traumatic and metastatic brain abscesses. Direct intracerebral inoculation induces abscesses displaying more prominent inflammatory responses and encapsulation than does septic embolisation, despite similar abscess age and size. Cerebral ischaemia surrounding metastatic suppurative foci may retard capsule wall formation.

Role of vascular proliferation on angiographic appearance and encapsulation of experimental traumatic and metastatic brain abscesses.

Experimental traumatic abscesses were produced in rhesus monkeys by intracerebral injection of nutrient agar contaminated with Staphylococcus epidermidis, and metastatic abscesses were induced by intracarotid embolization of silicone cylinders contaminated with Staphylococcus epidermidis. All monkeys underwent preoperative and serial postoperative carotid angiography. Traumatic abscesses produced early capsular blushes and progressive anterior cerebral artery displacements. Metastatic abscesses induced transient midline shifts but no capsular stains. Postmortem studies on the monkeys showed that mean capsular thickness and segmental wall vascularity of the traumatic and metastatic abscesses were significantly different (p less than 0.001), despite equal abscess ages and similar abscess volumes. In comparison to traumatic abscesses, metastatic abscesses demonstrated reduced inflammatory cell infiltration and retarded collagen formation around proliferating capsular vessels. Brain surrounding the metastatic abscesses demonstrated ischemic changes. The results suggest that 1) capsular blushes during cerebral angiography are secondary to vascular proliferation within the capsule and not to compression of surrounding brain, 2) vascular staining reflects capsular thickness, 3) capsular vascularity contributes to collagen formation, 4) encapsulation is dependent upon the integrity of surrounding brain, and 5) adjacent cerebral ischemia may impede inflammatory responses involved in capsule formation.

Chronic ventricular cerebrospinal fluid sampling, drug injections, and pressure monitoring using subcutaneous reservoirs in monkeys.

Animal models enabling reliable access to ventricular cerebrospinal fluid (CSF) are crucial to the study of neuropharmacological and neurotoxicological effects of cytotoxic agents used to treat central nervous system neoplasms. This investigation concludes that 4th ventricular catheterization using subcutaneous CSF reservoirs in rhesus monkeys: (a) provides chronic access to sterile CSF without chronic immobilization, (b) enables mixing of injected drugs with lateral ventricular CSF, (c) permits sensitive monitoring of intraventricular pressure and (d) does not produce tissue damage during cannula implantation or breakdown of the blood-brain barrier.

A primate model for study of methotrexate pharmacokinetics in the central nervous system.

A new technique enabling repetitive sampling of cerebrospinal fluid (CSF) in unanesthetized rhesus monkeys was developed to study the pharmacokinetics of methotrexate (MTX) in the CSF. CSF and plasma MTX levels were monitored following intraventricular and intravenous MTX administration. CSF and plasma MTX disappearance curves in the monkey were virtually identical to curves generated in humans, suggesting that the mechanisms of transport between the CSF and plasma compartments are similar in both species. These observations validate this experimental primate model and indicate its potential application to the pharmacological study of CNS chemotherapeutic agents in man.