Head Injury

Introduction

Head injury can be defined as any alteration in mental or physical functioning related to a blow to the head. Loss of consciousness does not need to occur. The severity of head injuries most commonly is classified by the initial postresuscitation Glasgow Coma Scale (GCS) score, which generates a numerical summed score for eye, motor, and verbal abilities. A score of 13-15 indicates mild injury, a score of 9-12 indicates moderate injury, and a score of 8 or less indicates severe injury. Concussion and mild head injury are synonymous.

Research on head injury has advanced considerably in the past decade. As is typical of many endeavors, these efforts have exposed the complexity of this condition more deeply and have helped researchers and physicians to abandon crude simplifications. This review concentrates primarily on current developments in the diagnosis and management of closed head injuries in adults.

PATHOPHYSIOLOGY
Structural changes
Gross structural changes in head injury are common and often obvious both on autopsy and conventional neuroimaging. The skull can fracture in a simple linear fashion or in a more complicated depressed manner, in which bone fragments and pushes beneath the calvarial surface. In patients with mild head injury, skull fracture markedly increases the chance of significant intracranial injury.

Both direct impact and contrecoup injuries, in which the moving brain careens onto the distant skull opposite the point of impact, can result in focal bleeding beneath the calvaria. Such bleeding can result in an intracerebral focal contusion or hemorrhage as well as an extracerebral hemorrhage. Extracerebral hemorrhages are primarily subdural hemorrhages arising from tearing of bridging veins, but epidural hemorrhages from tearing of the middle meningeal artery or the diploic veins are also common. Occasionally, subdural hemorrhages can result from disruption of cortical arteries. This type of subdural hemorrhage is rapidly progressive and can occur after trivial head injury in elderly patients.

One study of CT images from 753 patients with severe head injury from the National Institute of Health Traumatic Coma Data Bank in the United States found evidence of intracranial hemorrhagic lesions in 27%. Traumatic subarachnoid hemorrhage was even more frequent and occurred in 39% of patients. Furthermore, diffuse cerebral edema also was present in 39%. Cerebral edema can be unilateral or diffuse and can occur even in the absence of intracranial bleeding. Severe brain edema probably occurs more commonly in children than in adults.
Neuronal loss is also important. A recent pathological study found that quantitative loss of neurons from the dorsal thalamus correlated with severe disability and vegetative state outcomes in patients with closed head injuries.
Finally, axonal injury increasingly has been recognized as a structural sequela of brain injury. The use of amyloid precursor protein staining has resulted in increased recognition of this form of injury. Using this technique, researchers have readily identified axonal injury in patients with mild head injury. Interestingly, a prominent locus of axonal damage has been the fornices, which are important for memory and cognition. More severe and diffuse axonal injury has been found to correlate with vegetative states and the acute onset of coma following injury.

Neurochemical changes
After traumatic brain injury, the brain is bathed with potentially toxic neurochemicals. Catecholamine surges have been documented in the plasma (higher catecholamine levels correlated with worse clinical outcomes) and in the cerebrospinal fluid (CSF) of patients with head injuries (higher CSF 5-hydroxyindole acetic acid (HIAA), the serotonin metabolite, correlated with worse outcomes). Head injury causes release of free radicals and breakdown of membrane lipids. These lipids fragment into mediators of inflammation. The excitotoxic amino acids (ie, glutamate, aspartate) initiate a cascade of processes culminating in an increase in intraneuronal calcium and cell death. Researchers using a microdialysis technique have correlated high CSF levels of excitotoxic amino acids with poor outcomes in head injury.

Although neuroprotective strategies employing antiexcitotoxic pharmacotherapies were effective in diminishing the effects of experimental brain injuries in laboratory animals, clinical trials in humans generally have been disappointing. These failures have prompted development of more complex models of neuronal injury and cell death. Recently, researchers have demonstrated that although certain types of glutamate antagonists may protect against acute cell death, they potentiate slowly progressive neuronal injury in experimental rodent models. Still others have found that low-dose glutamate administered before brain injury is somehow neuroprotective. Such dose and timing effects are only beginning to be understood.

Prostaglandins, inflammatory mediators produced by membrane lipid breakdown, are also elevated dramatically in the plasma of patients with moderate-to-severe head trauma during the first 2 weeks after injury. Patients with higher prostaglandin levels had significantly worse outcomes than those with more modest elevations. Furthermore, levels of a thromboxane metabolite, a potent vasoconstricting prostaglandin, were elevated disproportionately. Such a process may underlie posttraumatic vasospasm, which has been documented in some, but not all, transcranial Doppler studies of patients with closed head injuries, even in patients without traumatic subarachnoid bleeds.
Recently, an increase in T cells reactive against myelin antigens was found in 10 patients with severe head injuries. Although the sample size was limited, those patients with increased T-cell reactivity had improved outcomes compared with their nonreactive counterparts, and a beneficial autoimmune response was proposed.
In addition to structural and chemical changes, gene expression is altered following closed head injury. Genes involving growth factors, hormones, toxin-binders, apoptosis (programmed cell death), and inflammation have all been implicated in rodent models. For example, in mice, transthyretin mRNA levels increase for 2 hours to 2 weeks following a concussive impact. This protein binds amyloid protein and may offer neuroprotection after head injury.

Secondary insults
Hypotension and hypoxia cause the most prominent secondary trauma-induced brain insults. Both hypoxia and hypotension had adverse impacts on outcomes of 716 patients with severe head injuries from the Traumatic Coma Data Bank in the United States. Efforts to limit hypoxic injury with in-field intubation have been unsuccessful. Indeed, a multicenter study of 4098 patients with severe traumatic brain injury found that in-field intubation was associated with a dramatic increase in death and poor long-term neurologic outcome, even after controlling for injury severity.
In the Trauma Coma Data Bank study, hypotension was even more significant than hypoxia and, by itself, was associated with a 150% increase in mortality rate. Systemic hypotension is critical because brain perfusion diminishes with lower somatic blood pressures. Brain perfusion (ie, cerebral perfusion pressure) is the difference between the mean arterial pressure and intracranial pressure. The intracranial pressure is increased in head injury by intracranial bleeding, cell death, and secondary hypoxic and ischemic injuries. Accordingly, another recent study reported that death and increased disability outcomes correlated with the durations of both systemic hypotension and elevated intracranial pressures.

FREQUENCY
United States
In the United States, 1.5 million individuals per year incur a head injury. Of these injuries, 75% are classified as mild. Between 1998 and 2000, the incidence of mild traumatic brain injury was 503 cases per 100,000 persons, with a doubling of this incidence in Native Americans and children.
In 1995, hospitalization for brain injuries decreased 50% compared to 1980 data, primarily because of increased utilization of outpatient services for patients with minor head injuries.

International
European rates of hospitalization for head injury have ranged from 91 cases per 100,000 persons per year in Spain in 1988 to 313 cases per 100,000 persons per year in Scotland during the period 1974-1976. Using a door-to-door survey methodology, researchers have estimated that 56 cases per 100,000 persons per year in China sustained a brain injury in 1983.
Head injury data are difficult to compare internationally for various reasons, including inconsistencies and complexities of diagnostic coding and inclusion criteria, transfers to multiple care facilities (ie, patient admissions may be counted more than once), and regional medical practices, such as the aforementioned recent development in the United States of more outpatient, as opposed to inpatient, services for those with mild head injuries. Adding to this complexity is the finding that some individuals with cognitive and emotional sequelae from mild head injury may not establish the casual connection between their injury and its consequences. Such patients may not seek treatment and may not be expressed in official demographic data.

Mortality/Morbidity
In the United States each year, 50,000 individuals die from head injuries, and almost twice that number suffer permanent disability.

Race
An older study from the Chicago region documented that black residents experienced twice the risk of head injury as white residents. A more recent study of intentional head injury from Charlotte, North Carolina, found minority status was a major predictor of intentional head injury, even after controlling for other demographic factors. Furthermore, a study of moderate and severe head injury in 106 children reported that African Americans had worse functional outcomes 1 year after head injury than their white counterparts. This puzzling relationship existed even after considering the socioeconomic and educational levels of the parents.

Sex
Men in the United States are nearly twice as likely to be hospitalized with a brain injury than women. This male predominance is found worldwide.

Age
Approximately half of the patients admitted to a hospital for head injury are aged 24 years or younger.

Physical

Causes