Traumatic brain injury overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Deekshitha Manney, M.D.[[2]] Joanna Ekabua, M.D. [3]

Overview[edit | edit source]

Traumatic brain injury (TBI) occurs when physical trauma causes brain damage. TBI can result from a blunt head trauma or a penetrating head injury and is one of two subsets of acquired brain injury (ABI). The other subset is non-traumatic brain injury, or injuries that do not involve external mechanical force (e.g. stroke, meningitis, anoxia). Parts of the brain that can be damaged include the cerebral hemispheres, cerebellum, and brain stem.

TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain^{[1] [2]}. TBI can cause a host of physical, cognitive, emotional^[3], and social effects. Outcome can be anything from complete recovery to permanent disability or death. Long term sequelae however, can be difficult to assess because of co-existing neurologic issues such as a stroke or degeneration as well as the different interpretation of questions in scoring models by patients and scales may not capture the complete clinical picture.

Historical perspective[edit | edit source]

Historically TBI was differentiated from concussion, sports related chronic traumatic encephalopathy^[4] and extra-axial hematomas but, now they all are being characterized under a broad umbrella of the disease spectrum.

Classification[edit | edit source]

Classification of TBI is challenging because of the heterogeneity of the trauma and different pathophysiologic mechanisms involved. The most common method of classifying TBI is through GCS. Traumatic brain injury may be classified as mild, moderate or severe^[5] using GCS.

Pathophysiology[edit | edit source]

The pathophysiology of traumatic brain injury is unclear. The increased public awareness of TBI and recognition of TBI as a public health problem is bringing in more attention to study pathophysiolog. The advantage of studying pathophysiology is that it can identify therapeutic targets.

Primary injury (the damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed, and torn) is not adequate to explain this degeneration. Rather, the deterioration is caused by secondary injury, a complex set of biochemical cascades that occur in the minutes to days following the trauma and contribute a large amount to morbidity and mortality from TBI. Secondary injury events are poorly understood but are thought to include brain swelling, alterations in cerebral blood flow, a decrease in the tissues' pH, free radical overload, and excitotoxicity. These secondary processes damage neurons that were not directly harmed by the primary injury.

Causes[edit | edit source]

The causes of TBI can be divided into impact and non-impact^[6] These include head strike from an object, falls in elderly patients and penetration by a foreign body ^[7] ,rapid acceleration/deceleration injuries.

Differentiating Traumatic Brain Injury from other Diseases[edit | edit source]

Traumatic brain injury must be differentiated from concussion, chronic traumatic encephalopathy, extra-axial hematomas, contusions, traumatic subarachnoid hemorrhage and diffuse axonal injury.

Epidemiology and Demographics[edit | edit source]

Incidence[edit | edit source]

The true incidence of TBI is unknown as many patient's with mild TBI, especially children and younger population, often doesn't seek medical attention^[8]. In 2019, CDC published a surveillance report and according to that, there were 2.87 million TBI related emergency department visits, hospitalizations and deaths in 2014 in the US^[9].

Age[edit | edit source]

TBI carries a bimodal distribution with the age groups most at risk are children ages five to nine and adults over age 80.

Race[edit | edit source]

There is no racial predilection to TBI.

Gender[edit | edit source]

Younger men and elderly women are more commonly affected by TBI. Usually males>females with a ratio of 2.5:1^[10]

Region[edit | edit source]

Each year in the United States:

• About two million people suffer a TBI^[11]
• About 500,000 people are hospitalized for TBI^[12]
• Approximately 270,000 people experience a moderate or severe TBI^[13]
• Approximately 60,000 new cases of epilepsy occur as a result of head trauma^[14]
• Approximately 50,000 people die from head injury^[15]
• Approximately 80,000 of these survivors live with chronic disabilities as a result of the injury.^[16]

Developed countries[edit | edit source]

About sixty-nine million (95% CI 64–74 million) people worldwide sustain a TBI/year. The percentage of TBIs resulting from motor vehicle accident was minimal in North America (25%). The universal incidence of TBI per 100,000 people was significant in North America (1299 cases, 95% CI 650–1947) and Europe (1012 cases, 95% CI 911–1113).

Developing countries[edit | edit source]

About sixty-nine million (95% CI 64–74 million) people worldwide sustain a TBI/year. The percentage of TBIs resulting from motor vehicle accident was significant in Africa and Southeast Asia (both 56%). The universal incidence of TBI per 100,000 people was minimal in Africa (801 cases, 95% CI 732–871) and the Eastern Mediterranean (897 cases, 95% CI 771–1023).

Risk factors[edit | edit source]

Common risk factors for traumatic brain injury include male gender, age >55, driving without helmet and seatbelts, driving under the influence, conduct disorder, depression, and anxiety.

Natural History, Complications and Prognosis[edit | edit source]

Natural history[edit | edit source]

The natural history of TBI is widely varied and depends on the severity and recurrence of the trauma. People with mild TBI such as concussion can lead a normal life. More recent knowledge suggests that recurrent concussions can lead to neurodegenerative diseases such as early onset dementia and Parkinson's disease. Severe TBI such as penetrating injuries can lead to instant death and blunt trauma leading to extra-axial hematomas may not have neurological symptoms immediately after impact, but they are at risk for cerebral edema and herniation leading to neurological symptoms and/or death.

Complications[edit | edit source]

The results of traumatic brain injury vary widely in type and duration. A head-injured patient may experience physical effects of the trauma such as headaches, movement disorders (e.g. Parkinsonism), seizures, difficulty walking, sexual dysfunction, lethargy, or coma. Cognitive symptoms include changes in judgment or ability to reason or plan, memory problems, and loss of mathematical ability. Emotional problems include mood swings, poor impulse control, agitation, low frustration threshold, self-centeredness, clinical depression, and psychotic symptoms such as hallucinations and delusions.

Prognosis[edit | edit source]

Traumatic brain injury is a frequent cause of major long-term disability in individuals surviving head injuries sustained in war zones. This is becoming an issue of growing concern in modern warfare, in which rapid deployment of acute interventions is effective in saving the lives of combatants with significant head injuries. Traumatic brain injury has been identified as the "signature injury" among wounded soldiers of the current military engagement in Iraq.

Diagnosis[edit | edit source]

Diagnostic study of choice[edit | edit source]

MRI is the gold standard test for the diagnosis of traumatic brain injury.

History and Symptoms[edit | edit source]

The hallmark of traumatic brain injury is finding a positive history of headache, mental confusion, lightheadedness, dizziness, double vision, repeated vomiting or nausea, seizures, inability to awaken, dilation (widening) of one or both pupils, slurred speech.

Physical Examination[edit | edit source]

Common physical examination findings of traumatic brain injury include Neurologic deficit Motor and sensory skills Hearing and speech Coordination and balance Mental status Mood or behavior changes Normal to abnormal Glasgow Coma Scale (GCS). Head injured people with signs of moderate or severe TBI should receive immediate emergency medical attention.

Laboratory Findings[edit | edit source]

An elevated concentration of CSF sceptrin breakdown product (SBDP)120 and SBDP145, ubiquitin C-terminal hydrolase-L1 (UCH-L1), and glial fibrillary acidic protein (GFAP) is diagnostic of traumatic brain injury.

Electrocardiogram[edit | edit source]

There are no ECG findings associated with traumatic brain injury.

X Ray[edit | edit source]

There are no x-ray findings associated with traumatic brain injury.

Echocardiography and Ultrasound[edit | edit source]

There are no echocardiography/ultrasound findings associated with traumatic brain injury.

CT[edit | edit source]

Head CT scan may be helpful in the diagnosis of traumatic brain injury. Findings include Midline shift Cerebral contusion Brain herniation Hydrocephalus Skull fracture Hematomas Subarachnoid hemorrhage Intraventricular hemorrhage

MRI[edit | edit source]

Brain MRI may be helpful in the diagnosis of traumatic brain injury. Findings on MRI suggestive of/diagnostic of traumatic brain injury. Encephalomalacia - softening or loss of brain tissue in previous areas of contusion or hemorrhage. Diffuse axonal injury

Other Imaging Findings[edit | edit source]

There are no other imaging findings associated with traumatic brain injury.

Other Diagnostic Studies[edit | edit source]

There are no other imaging findings associated with traumatic brain injury.

Treatment[edit | edit source]

Medical Therapy[edit | edit source]

Traumatic brain injury is a medical emergency and requires prompt treatment. Hyperventilation, Seizure prophylaxis, Hyperosmolar therapy, Medically induced coma, Therapeutic hypothermia,and ICP Monitoring. Primary concerns include insuring proper oxygen supply, maintaining adequate blood flow, and controlling blood pressure. Since many head-injured patients may also have spinal cord injuries, the patient is placed on a back-board and in a neck restraint to prevent further injury to the head and spinal cord. Medical personnel assess the patient's condition by measuring vital signs and reflexes and by performing a neurological examination. They assess the patient's level of consciousness and neurological functioning using the Glasgow Coma Scale. Barbiturates can be used to decrease ICP; mannitol was thought to be useful, but it appears likely that the studies suggesting that it was of use may have been falsified.

Surgery[edit | edit source]

Surgery is not a first-line treatment option for patients with traumatic brain injury. Surgery is usually reserved for patients with either: Subdural/epidural hematoma >10mm in thickness. Midline shift >5mm Cerebral edema Syncope Decompressive craniectomy is a last-resort surgical procedure in which part of the skull is removed in an attempt to reduce severely high ICP.

Primary prevention[edit | edit source]

Effective measures for the primary prevention of traumatic brain injury include Wearing a seat belt. Buckling children into a child safety seat, booster seat, or seat belt (depending on the child's age) every time the child rides in a car. Wearing a helmet and making sure children wear helmets when undertaking high-risk activities. Keeping firearms and bullets stored in a locked cabinet when not in use Avoiding falls by using a support Using only playgrounds with surfaces made of shock-absorbing material (e.g. mulch, sand)

Secondary prevention[edit | edit source]

Effective measures for the secondary prevention of traumatic brain injury includes Early removal of intracranial hematoma,Reduction of hypoxia,Reduction of hypotension and Calcium homeostasis

Cost-Effectiveness of Therapy[edit | edit source]

Management of traumatic brain injury patients in hospital is expensive. It has been estimated that the total global annual burden of traumatic brain injury US$ 400 billion. The in-hospital cost ranged from $$2,130 - $401,808, which was determined by the patient's length of stay and surgical procedure underwent. The cost was also directly proportional to the severity of traumatic brain injury. Aggressive care is notably better across all age groups and is recommended for the management of traumatic brain injury patients. Cost of aggressive management is less than routine management until age 80 where it is more costly than routine management. Comfort care has been associated with poor outcomes in all age groups and costs more for all groups except 80-year-olds.

Future or Investigational Therapies[edit | edit source]

In spite of robust experiments on the efficacy of neuroprotective drugs tested in animal models of traumatic brain injury, all Phase III clinical trials of neuroprotection have failed in patients with traumatic brain injury.

References[edit | edit source]

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