Traumatic Brain Injury - An Emphasis on "Mild"
Published: Friday, January 7, 2005 at 2:12 p.m.
Last Modified: Friday, January 7, 2005 at 2:12 p.m.
The Centers for Disease Control and Prevention has identified that approximately 5.3 million Americans live with the effects of traumatic brain injury (TBI) and that an estimated 2 million people sustain TBIs of all severities each year. Of these two million annual TBIs about half will incur at least short-term disability. The financial burden incurred by patients, employers, and managed care companies has been estimated at more than one billion dollars per year in the United States alone. Since more than 80% of all TBIs are considered mild, the health care and societal burden of mild traumatic brain injury (MTBI) is immense, especially if one considers that the true proportion of those living with the effects of MTBI has been underestimated. Hence, MTBI has been termed the silent epidemic of our times.
MTBI has both acute (immediate) and long-term complications associated with it. Acutely, there is a small but important risk for intracranial (brain) bleeding. Of adult patients evaluated in the emergency department anywhere from 3% to 13% will have an acute lesion on CT scan of the head and less than 1% of these patients will have a lesion requiring a neurosurgical intervention. MTBI is also associated with long-term problems such as impaired daily functioning. A significant minority of patients do not fully recover and do disproportionately worse than would have been predicted for months and even years after their injury. Most of the patients who develop problems begin experiencing neurological (e.g. headache, dizziness), cognitive (e.g. attention & memory problems), emotional (e.g. anxiety, depression), and functional (e.g. return to work) difficulties in the days or weeks after their injury. Some would refer to this constellation of complaints as the post-concussive syndrome.
MTBI has historically been referred to as having a "concussion." The definition of MTBI suffers from some variability and there exists no consensus regarding classification. Terms used have included: mild, minor, minimal, grade I, class I, and low risk. Even the terms head and brain have been used interchangeably. Head injury and traumatic brain injury (TBI) are two distinct entities that are often, but not necessarily, related. A head injury is best defined as an injury that is clinically evident on the physical exam and is recognized by the presence of bruising, lacerations, deformities, or cerebrospinal fluid (CSF) leakage. A traumatic brain injury refers specifically to an injury to the brain itself and is not always clinically evident; if unrecognized, it may result in an adverse outcome.
The formal definition of MTBI has been adopted from the American Congress of Rehabilitative Medicine. They delineated inclusion criteria for a diagnosis of MTBI of which at least one of the following must be met: 1) any period of loss of consciousness less than 30 minutes with a Glasgow Coma Scale (GCS) score of 13-15; 2) any loss of memory of the event immediately before or after the accident that lasts less than 24 hours; 3) any alteration in mental state at the time of the accident (e.g. feeling dazed, disoriented, or confused).
Historically, the system most often used for grading severity of brain injury is the Glasgow Coma Scale (GCS) score. The GCS is a 15-point scale that rates a patient's best eye opening, motor, and verbal responses. Created by Teasdale and Jennett in 1974, the GCS was developed as a standardized clinical scale to provide an easy-to-use assessment tool for serial evaluations by relatively inexperienced care providers, and to facilitate communication between them on rotating shifts. This was during a time when CT scanning was not readily available. Although MTBI refers to patients with a GCS score of 13 or greater, a single GCS score is of limited prognostic value and is insufficient to determine the degree of brain injury after trauma, but serial GCS scores are quite valuable. A low GCS score that remains low, or a high GCS that decreases, predicts a poorer outcome than a high GCS score that remains high or a low GCS score that progressively improves.
Brain injuries can be focal, diffuse, or a combination of focal and diffuse. The degree of brain injury depends on the primary mechanism/magnitude of injury, secondary insults, and the patient's genetic and molecular responses. Following the initial injury, cellular responses and neurochemical and metabolic cascades contribute to secondary injury. Some secondary insults are preventable through medical care and interventions and include the 7 H's: Hypoxia, Hypotension, Hyper/Hypocarbia, Hyperthermia, Hyponatremia, Hyper-excitability, Hyper/Hypoglycemia.
Focal brain injuries are usually from direct blows to the head and include epidural hematoma, subdural hematoma, subarachnoid bleeding, and contusions. These lesions can be diagnosed by CT scan of the head. An epidural hematoma is a blood clot that forms between the inner table of the skull and the dura and is often associated with skull fractures across the middle meningeal artery. It is usually unilateral, and up to 40% of patients have other intracranial lesions. A subdural hematoma is a blood clot that forms between the dura and the brain usually caused by acceleration-deceleration injuries with slow bleeding of venous structures. Traumatic subarachnoid hemorrhage is defined as blood within the cerebrospinal fluid (CSF) and meningeal intima and probably results from tears of small subarachnoid vessels. The most serious complication of subarachnoid hemorrhage is aggravation of cerebral vasospasm, which may be severe enough to induce cerebral ischemia. Cerebral contusions and intracerebral hematomas are formed deep within the brain tissue and are usually caused by shearing or tensile forces that mechanically tear deep small arterioles as the brain is propelled against irregular surfaces of the skull. Almost 85% are in the frontal and temporal lobes. Diffuse Axonal Injury (DAI) is one theory for the neuropathology of MTBI and may be a major factor influencing long-term neurological outcome. DAI results from shear or rotational forces in the brain created by sudden acceleration- deceleration forces. It produces microscopic lesions in the brain that are detectable at 15 hours after injury as a response to secondary neurochemical events in the brain.
Soon after the introduction of CT in 1974, clinical reports established head CT as the mainstay in the diagnosis of brain injury and neurotrauma. MRI is more sensitive for detecting neuronal lesions that may be responsible for long-term complications than CT scan but MRI is not indicated acutely at this time. Although acutely, most patients with suspected MTBI will not require any neurological treatment, a small proportion deteriorate and require neurosurgical intervention for intracranial bleeding. Neurosurgeons and emergency physicians alike are well aware of the phenomenon of patients who "talk and deteriorate." The key to salvaging these patients is early - diagnosis of intracranial bleeding with CT scan followed by early surgery. The question then becomes which patients with suspected MTBI should have a CT scan acutely?
This controversial question has lead to the development of two prospectively derived and validated clinical decision rules for adults sustaining a suspected MTBI to help clinicians decide who needs a CT scan: the New Orleans Criteria and the Canadian CT Head Rule. Based on a review of the literature the American College of Emergency Physicians (ACEP) evidence based guidelines have recommended that a head CT is not indicated in those patients with MTBI who do not have headache, vomiting, age over 60, drug or alcohol intoxication, deficits in short-term memory, physical evidence of trauma above the clavicle, or seizure.
Although there are no official evidenced-based guidelines on neuroimaging in children with MTBI yet, there is a considerable amount of ongoing research. In 1999 the American Academy of Pediatrics developed a practice guideline for the evaluation and management of MTBI in children. They recognized that the literature did not provide a sufficient scientific basis for evidence-based recommendations about most of the key issues in clinical management. The guidelines were for narrowly defined circumstances and were applicable only to children with isolated MTBI evaluated within 24 hours after trauma, with a normal mental status and neurological examination, and with a history of no more than a brief (less than 1 minute) LOC. It suggested that children with possible MTBI outside these parameters may require competent observation and/or a head CT scan. Since this guideline there have been two published prospective studies of indications for CT scan in children that still need validation.
Repeated MTBI occurring over an extended period (i.e. months or years) can result in cumulative neurological and cognitive deficits. Repeated MTBI occurring within a short period (i.e. hours, days, or weeks) can be catastrophic or fatal - a phenomenon termed "second impact syndrome." Although it is rare, this is a particularly important phenomenon in athletes. The risk of this occurring is increased in those with a prolonged loss of consciousness or post-traumatic amnesia, and persistent neuropsychological deficits following their MTBI. When to return a concussed athlete or worker to participation is a highly controversial topic and there are several sets of guidelines available.
Although some patients with MTBI may be admitted to the hospital overnight, most patients with MTBI are treated and released from the emergency department with basic discharge instructions and little or no follow-up care. Neurological and psychosocial sequelae of MTBI are more subtle and difficult to assess than moderate and severe TBI and many MTBI patients initially appear unimpaired. Unfortunately, a significant number of patients have difficulty recovering from their MTBI and their disabilities remain undiagnosed. Subsequently, patients and families become frustrated because of the failure to understand the nature of the difficulties they encounter daily. Post-concussive symptoms have been documented in as many as 50% of patients having sustained a MTBI and may surface a few days or even weeks following the head trauma with great variability in both the degree and duration of symptoms. Depending on how disability is defined, anywhere from 7% to 30% of patients with MTBI will continue to have compromised function one year after their injury that may result in lifelong impairments of physical, cognitive, and psychosocial functioning and may adversely affect the patient's personal, financial and social life.
Treatment protocols for MTBI have only slowly begun to emerge and are still experimental because therapies typically afforded moderate or severe TBI have been assumed to be inappropriate for patients with presumptively "mild" injury. Although no formal standards of care have been developed, preliminary data suggest that verbal and written explanations about why symptoms may persist, access to community resources, neuropsychological assessment, cognitive-behavioral therapy, and other rehabilitation strategies may be efficacious in reducing post-injury difficulties and improve functional outcome.
Clearly, there is a great need for research in MTBI. A major problem in MTBI has been the lack of sensitive diagnostic and prognostic tools available to assess these patients. Future research must address early identification of those at risk for impairment in the early stages of injury using clinical decision tools, neuroimaging and serum biochemical markers. NewMRI imaging technologies such as Diffusion Tensor Imaging and Magnetic Transfer Imaging are more sensitive to structural changes of the brain following a MTBI. Biochemical markers that detect severity of injury through blood tests are being developed that could offer essential information about diagnosis and prognosis. At the University of Florida's McKnight Brain Institute, a multi-disciplinary team of researchers are hard at work to find scientific evidence that will optimize care and functional recovery in patients with MTBI.
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