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Traumatic Brain Injury

TBI


Presentation

The immediate effects of traumatic brain injury include cell injury or death, neurovascular disruption, neurotransmitter dysfunction, and biochemical imbalance [10].

The most common neurological finding in traumatic brain injury is loss of consciousness. The Glasgow Coma Scale (GCS) is used to assess consciousness and the severity of injury [5].

Symptoms in severe traumatic brain injury include [5]:

Other symptoms with all levels of traumatic brain injury include [5]:

Worsening neurologic signs appearing after the time of injury indicate complications: Progressive brain edema, intracranial hemorrhage or thrombosis. This can occur even with mild injuries and needs further evaluation [5].

Traumatic brain injury in children increases the risk of adverse behavioral disabilities, including attention deficit disorder, hyperactivity, aggression, anxiety, depression, and psychiatric disorders [12].

Approximately 75% of traumatic brain injuries are classified as mild, with only brief loss of consciousness and transient symptoms. Most patients recover completely [10].

Some individuals, however, have persistent or worsening cognitive, behavioral, or somatic symptoms. These symptoms suggest more severe brain dysfunction [10].

Headaches often occur post-traumatic brain injury and some studies have reported them more often after mild injuries than after those that are more severe [10]. Post-trauma headaches vary in type and intensity and may become chronic [10].

Emotional, social, or behavioral problems and changes in personality can occur after a traumatic brain injury. Studies indicate that these patients are also at higher risk of psychiatric disorders [1] [2] [13].

Epilepsy
  • Copyright 2018 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.[ncbi.nlm.nih.gov]
  • Glucocorticoid administration early after head injury also has not been found to reduce the risk of posttraumatic epilepsy.[doi.org]
  • A review of selected articles dealing with epilepsy after brain trauma was undertaken.[ncbi.nlm.nih.gov]
  • Asadi-Pooya, Prognosis after late relapse following epilepsy surgery, Epilepsy Research, 78, 1, (77), (2008).[doi.org]
Anosmia
  • We then provide our recommendation for an orbit magnetic resonance imaging (MRI) to evaluate the inferior frontal lobes and olfactory bulbs in patients with unexplained anosmia.[ncbi.nlm.nih.gov]
  • […] diplopia) Blurred vision Problems judging distance Involuntary eye movements (nystagmus) Intolerance of light (photophobia) Decreased or loss of hearing Ringing in the ears (tinnitus) Increased sensitivity to sounds Loss or diminished sense of smell (anosmia[northeastern.edu]
  • Posttraumatic anosmia secondary to central nervous system injury. Am J Rhinol. Nov-Dec/2008. 22:606-7. Bhatoe HS. Primary brainstem injury: benign course and improved survival. Acta Neurochir (Wien). 1999. 141(5):515-9. [Medline].[emedicine.medscape.com]
Stroke
  • Ischemic stroke was the most frequent (8296 events). Hemorrhagic stroke (1706 events) and seizures (1841) were least often observed.[ncbi.nlm.nih.gov]
  • The volume of brain swelling measured in all patients in the stroke series would be accommodated by a 5-mm offset plate.[ncbi.nlm.nih.gov]
  • Pathological laughing and crying, or pseudobulbar affect (PBA), has been described in patients with neurological disorders such as multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease, stroke, and traumatic brain injury (TBI) since the[ncbi.nlm.nih.gov]
  • Stroke 2004;35:2059–2063. CrossRef PubMed Google Scholar 27. Ikawa F, Ohbayashi N, Imada Y, Matsushige T, Kajihara Y, Inagawa T, Kobayashi S.[doi.org]
Amnesia
  • Participants showing poorer outcome on the GOSE had significantly longer posttraumatic amnesia duration; less education; performed more poorly on cognitive measures of information processing speed, attention, memory, and executive function; and showed[ncbi.nlm.nih.gov]
  • The patient did not experience loss of consciousness or post-traumatic amnesia and the patient's Glasgow Coma Scale score was 15. She had begun to feel pain in her left hand and foot at 7 days after onset.[ncbi.nlm.nih.gov]
  • The patient lost consciousness and experienced post-traumatic amnesia for 1minute from the time of the car-accident. The patient's Glasgow Coma Scale score was 15. No specific lesion was observed on brain MRI.[ncbi.nlm.nih.gov]
  • The patient lost consciousness for approximately 10 minutes and experienced posttraumatic amnesia approximately 30 minutes from the time of the accident. Her Glasgow Coma Scale score was 15.[ncbi.nlm.nih.gov]
  • She lost consciousness and experienced post-traumatic amnesia for approximately ten minutes.[ncbi.nlm.nih.gov]
Dizziness
  • BACKGROUND: Case reports are presented on four Veterans, aged 29-46 years, who complained of chronic dizziness and/or postural instability following blast exposures.[ncbi.nlm.nih.gov]
  • Symptoms can be wide-ranging, from physical effects such as balance problems, headaches and dizziness to cognitive, emotional and behavioural effects such as memory problems and anger.[headway.org.uk]
  • dizzy patient may include audiological testing, electronystagmography, a fistula test, and posturography. 55 Patients with ongoing posttraumatic dizziness should be referred for neuro-otolaryngology evaluations.[dx.doi.org]
  • It can cause a headache or neck pain, nausea, ringing in the ears, dizziness, and tiredness.[medlineplus.gov]
Intracranial Hemorrhage
  • INTRODUCTION: Current literature estimates the risk of delayed intracranial hemorrhage as between 0.6 and 6% after mild head injury for patients on warfarin.[ncbi.nlm.nih.gov]
  • She developed an intracranial hemorrhage while systemically heparinized that required emergent decannulation and bedside craniectomy for hematoma extraction. She survived with an excellent neurologic outcome.[ncbi.nlm.nih.gov]
  • Intracranial Hemorrhage Epidural, subdural, subarachnoid, or intracerebral hemorrhages may complicate MTBI. Intracranial hemorrhages occur less often with MTBI than with other types of brain injury.[web.archive.org]
  • Intracranial hemorrhages occur less often with MTBI than with other types of brain injury. However, anticoagulant therapy or coagulopathies increase risk.[dx.doi.org]
Aphasia
  • He showed severe aphasia and brain MRI showed leukomalactic lesion in the left frontal lobe. The result WAB for the patient showed severe aphasia, with an aphasia quotient of 45.3 percentile.[ncbi.nlm.nih.gov]
  • […] of auditory functions as well as cognition and language functions important for accurate diagnosis and appropriate treatment, because the verbal auditory agnosia tends to be easily misdiagnosed as hearing impairment, cognitive dysfunction and sensory aphasia[ncbi.nlm.nih.gov]
  • Conditions and Other Information anoxia and hypoxia aphasia biomechanics of brain injury cognitive and communication disorders coma concussion epidemiology of traumatic brain injury sexual dysfunction stroke traumatic brain injury recovery traumatic brain[neuroskills.com]
  • Factors identified as determinant for the third verdict in head injuries are depressed skull fragments, dura laceration with exposed brain, infected cranial wounds/tetanus, major craniofacial fractures, deep skull–penetrating stab wounds, and aphasia.[doi.org]
  • Aphasia. Howard S. Kirshner, MD 12B. Motor Speech Disorders: Dysarthria and Apraxia of Speech, Howard S. Kirshner, MD 13. Neurogenic dysphagia, Ronald Pfeiffer, MD 14. Vision loss, Robert Tomsak, MD PhD 15.[worldcat.org]

Workup

Neuroimaging is an important part of the diagnostic work up for traumatic brain injury [4]. Neuroimaging should be done if any of the following occur [4]:

Neuroimaging techniques include [4] [5]:

  • Computed tomography, more available and cost effective, is the initial imaging technique used in the first 24 hours.
  • Magnetic resonance imaging is more sensitive and accurate and may reveal defects in patients with normal computed tomography scan findings[14].
  • Positron emission tomography (PET) and single-photon emission computed tomography (SPECT) imaging are not used routinely because they have limited availability [14].

Computer tomography (CT) and magnetic resonance imaging
(MRI) have improved diagnosis, management, and treatment of traumatic brain injury [5]. However, studies reveal even with a normal computed tomography scans a significant number of patents experience poor long-term cognitive outcomes after traumatic brain injury [3].

Laboratory tests have not yet been widely used for evaluation after traumatic brain injury. Glucose and hemoglobin levels have been shown to be prognostic [8]. Coagulation studies are very relevant for outcome prediction, as well [8]. Any abnormal laboratory findings need follow-up and treated. For example, hyperglycemia management has been shown to reduce mortality [8].

Epileptiform Activity
  • Ling, Spontaneous Epileptiform Activity in Rat Neocortex after Controlled Cortical Impact Injury, Journal of Neurotrauma, 27, 8, (1541), (2010).[doi.org]

Treatment

Rapid and complete resuscitation at the time of traumatic brain injury using the "ABCs" of resuscitation is the initial intervention needed [15]. The goal is to optimize cerebral perfusion and prevent secondary damage due to cerebral ischemia [15].
Emergency treatment should be started as soon as possible after injury to optimize outcomes [1] [2]. In the initial phase the aim of treatment is to stabilize the patient and prevent further injury.

During the acute stage the goals are to maintain oxygen supply, ensure adequate cerebral circulation, and control increasing intracranial pressure (ICP). Preventing seizures is also a major concern [1] [2]. Intraventricular monitoring of intracranial pressure is important during the acute phase in individuals with severe traumatic head injury [2].

With an unconscious patient airway and oxygen supply may be maintained with endotracheal intubation and mechanical ventilation [2].

Treatment of increased intracranial pressure is an important measure in preventing further injury after head injuries. Some useful techniques include [2] [15]:

  • Raising the head of the bed
  • Keeping head and neck in a neutral position to maximize blood flow
  • Sedatives, analgesics and paralytic agents
  • Intravenous hypertonic saline solutions should be used with caution
  • Mannitol, an osmotic diuretic
  • Diuretics, to increase urine output, but may cause hypovolemia
  • Hyperventilation reduces carbon dioxide levels and causes constriction of blood vessels but can cause ischemia 
  • Corticosteroids should not be given routinely as they may be associated with an increased risk of death.

Signs and symptoms that suggest a severe injury and indicate aggressive treatment include [2] [4]:

Monitoring and preventing hypotension, which can be a complication of traumatic brain injury, is important. It can be prevented with intravenous fluids to maintain a normal blood pressure [1]. Norepinephrine and similar medications help to maintain cerebral perfusion by maintaining blood pressure [2].

Maintaining a normal or lower body temperature reduces the brain's metabolic needs [2].

Seizures are common with traumatic brain injury. They may be treated with benzodiazepines and anticonvulsants [2] [13].

Neurosurgical interventions are used to reduce vascular compression, remove hematomas, and repair lacerations. Hemorrhage or edema can directly compress vasculature causing ischemia and infarct [4]. Therefore, these hematomas need immediate evacuation.

Decompressive craniectomy, temporary removal of part of the skull, is used routinely in to control high intracranial pressures [2]. Treatment of vascular damage may involve open surgical or endovascular approaches [4].

During the chronic phase the goal is optimal rehabilitation [13].
Goals of rehabilitation are to optimize motor, speech, and social functioning [1]. A multidisciplinary approach is needed and should include: physicians, nurses, physiotherapists, speech therapists, cognitive rehabilitation therapists, and occupational therapists [1][2].

Psychiatric and psychological services should also be involved with patients post-traumatic brain injury. These specialties can evaluate and manage cognitive deficits [1].

Prognosis

The best indicators of patient prognosis from traumatic brain injury are age, Glasgow Coma Scale, and pupillary reactivity on admission [8].

Predictors of poor outcomes are [2] [8]:

  • Age > 65 years.
  • Decreased motor response
  • Fixed, unequal, or diminished pupil reaction

If compression on brain tissue is relieved in time, full recovery will be more likely [8]. The incidence of disability after a head injury is estimated in recent studies to be 100 to ­150 per 100,000 population per year. This is significantly higher than previous estimates [9] [10].

Etiology

Traumatic brain injury is a leading cause of morbidity and
mortality in children and adults worldwide [5]. It is responsible for significant long-term neurologic, physical, and psychosocial disability in the United States [3].

Brain injury occurring as a result of trauma occurs in two phases. Primary injury occurs at the time of insult and is a result of the direct force or to penetration of the skull. Secondary injury occurs after the initial phase and is due to primarily to inflammation [3]. Neurologic dysfunction and complications of traumatic brain injury during both stages are a result of brain ischemia due to altered cerebral profusion, tissue compression, and increased intracranial pressure [3].

The severity of a traumatic brain injury is determined by using the Glasgow Coma Scale (GCS) during the first 48 hours after injury [3][5]. The Glasgow Coma Scale evaluates eye movement, verbal response, and motor response on a scale of 1 to 5/6, with 1 as no response and 5/6 as spontaneous resposes.

The severity of traumatic brain injury according to the Glasgow Coma Scale is as follows [5] [6]:

  • Severe = score of 3-8
  • Moderate = score of 9-12
  • Mild = score of 13-15

Epidemiology

It is difficult to assess the incidence rate of traumatic brain injury because the definition and criteria used for diagnosis vary widely [4]. This is further confused because incidence rates are calculated only from the number of hospitalized cases or fatalities. Numbers do not include individuals not seeking care or without access to care [7]. The incidence of traumatic brain injury may actually be 3 to 4 times greater than estimated [7].

It is estimated that there are nearly 1.6 million head injuries in the United States every year and over 50,000 deaths [8]. In Europe an incidence rate is estimated to be 235 per 100,000 populations. Less data is available from other regions of the world, but is believed to be a significant problem worldwide [7].

The incidence rates of traumatic brain injury are highest in young adults, 20 to 40 years of age. The second highest rate is in the elderly, usually from falls [7]. Males are more likely to suffer a traumatic brain injury than females [7].

The mortality rate for traumatic brain injury is estimated to be 6-17 per 100,000 people. The mortality rate for severe traumatic brain injury is about 33% [4].

Research studies estimate that some 70,000 individuals are living with permanent neurological deficits due to head trauma [4] [9] and nearly 2 million with other related disabilities [10].

The incidence of traumatic brain injury in children is estimated to be about 475,000 each year [5] [11]. Ninety percent of children suffer only mild trauma and are released from the emergency department [5]. Approximately 8% of children with traumatic brain injury need hospitalization and 0.6% die [5]. The incidence is highest in children aged 0 to 4 years and in adolescents older than 14 years [11] [12]. For children, rates of both death and hospitalization are significantly higher for blacks than whites [11].

Traumatic brain injury is responsible for approximately 40% of all acute injury deaths in the United States and 200,000 hospitalizations. As a result it accounts for approximately 10% of the health care budget in the United States [4]. The cost of traumatic brain injury is estimated to be $4 billion yearly [4].

Sex distribution
Age distribution

Pathophysiology

Typically traumatic brain injury involves a combination of primary injury, injury occurring at time of insult, and secondary injury, which happens over time [7].

The signs, symptoms, and complications of traumatic brain injury are due to the development of cerebral edema and a rise in intracranial pressure (ICP) secondary to inflammation [5]. Inflammation reduces cerebral blood flow, decreases cerebral perfusion, and increases cerebral ischemia [5].

In response to traumatic brain injury, cell death and injury, cytokine production by activated glia cells is increased [10]. This inflammatory response is initially protective and reparative. However, when it persists it can lead to secondary damage due to cerebral ischemia [10]. Progressive inflammation accounts for neurological symptoms seen after traumatic brain injury, especially headaches [10].

Brain contusions, subsequent inflammation and cerebral edema are relatively common with traumatic brain injury, occurring in approximately 43% of patients. They can occur with blunt force trauma or coup-contra-coup injuries (deceleration/acceleration trauma) [4]. The process of injury affects the pattern of injury. The more diffuse the initial injury the more wide-spread the neural damage [10]. Prompt neurosurgical intervention is needed to prevent further injury [4].

Traumatic brain injury in children differs from injuries in adults. The pediatric skull and brain are undergoing anatomical and functional development. Therefore, the type of injury, complications, and neurological and functional disability vary with each age group [5]. In infancy open sutures prevent early and rapid increase in intracranial pressure. This can limit or prevent secondary brain injuries, but may also interfere with early detection of problems [5].

Injuries occurring with or following traumatic brain injury include [4] [5]:

  • Subdural hematomas are common in traumatic brain injuries occurring in about 10 to 20% of patients. They are linked to mortality rates of up to 50 to 85% [2] [4].
  • Epidural hematomas are uncommon, occurring in only 1 to 4% of patients usually those with skull fractures
  • Intraventricular hemorrhages occur in about 3% of patients and have high morbidity and mortality rates. 
  • Increased intracranial pressure is a frequent complication of traumatic brain injury and accounts for further cerebral ischemia and dysfunction. 
  • Cerebral herniation is life-threatening and can lead to compression of vital structures resulting significant neurological deficits.
  • Vascular dissections and aneurysms can occur due to trauma to the vessels. 

All complications of traumatic head injury can cause cerebral ischemia. If untreated this may cause increased morbidity and mortality. The primary consequence of all complications of traumatic brain injury is a decrease in cerebral perfusion [4].

Prevention

Preventive measures include use of technology to protect those involved in motor vehicle accidents, such as seat belts and air bags, and better sports or motorcycle helmets. The most effective measures are those that reduce the number of automobile accidents and education programs aimed at increasing the use of seat belts and helmets [5] [7].

Traumatic brain injury is a serious public health problem affecting nearly half a million children every year. Variations in incidence by race suggest socioeconomic factors might contribute to its occurrence [11]. Further study in this area is needed to develop preventive strategies.

Summary

Traumatic brain injury (TBI) is defined as an insult to the brain due to an external mechanical force [1]. It is associated with diminished or altered consciousness and can lead to permanent or temporary impairment of cognitive, physical, and/or psychosocial function [2].

There is increasing evidence that even mild traumatic brain injuries, often referred to as concussions, can result in significant neurologic injury and long-term brain dysfunction [2] [3]. Early identification and appropriate management of traumatic brain injury and its complications can alter the course and outcome especially in the first 48 hours of the injury [2] [3] [4].

Patient Information

What is traumatic brain injury?

Traumatic brain injury refers to neurological injury resulting from a blow to the head. The usual causes are motor vehicle accidents, sports injuries, and falls. They are classified as mild, moderate, and severe depending on the level and duration of loss of consciousness, verbal and motor dysfunction. Most individuals experiencing mild injury recover without further incident. Approximately 25% of those with severe traumatic brain injury die of their injuries.

What are the symptoms of traumatic brain injury?

Symptoms in severe traumatic brain injury include:

  • Loss of consciousness for longer than 5 minutes
  • Absent, diminished, or unbalanced pupil reaction
  • Paralysis
  • Slow heart rate
  • Apnea, no or slow respirations
  • Worsening level of consciousness
  • Neurological deficits, loss of sensation
  • Seizures
  • Failure of the mental status to improve over time

Other symptoms with all levels of traumatic brain injury include:


What causes traumatic brain injury?

The symptoms and complications of traumatic brain injury are the result of swelling and inflammation of the brain due to a blow to the head. Swelling and inflammation cause an increase in the intracranial pressure, pressure within the skull. The increased pressure decreases the flow of blood to the brain and causes ischemia of brain tissue resulting in brain cell death.

Who gets traumatic brain injury?

Anyone who sustains a blow to the head is at risk of developing a traumatic brain injury.

How is it diagnosed?

Traumatic brain injury is diagnosed using computed tomography (CT) scans or magnetic resonance imaging (MRI). However, some individuals have neurological symptoms after a traumatic injury with normal imaging findings.

How is traumatic brain injury treated?

The goal of treatment for traumatic brain injury is to maintain the oxygen supply to the brain and prevent further injury due to inflammation and ischemia of brain tissue. Treatment of severe trauma usually requires hospitalization in an intensive care unit. Patients may also need intubation and mechanical ventilation, medication for seizure prevention, and possible surgery to decrease intracranial pressure.

What are the complications?

Traumatic brain injury can result in temporary, long-term, or permanent neurological disabilities. These may include motor dysfunction (paralysis, balance or gait abnormalities), cognitive impairment (amnesia, disorientation, confusion), speech defects (aphasia, dysphasia), and psychiatric disorders (depression, ADHD, psychoses).

How can traumatic brain injury be prevented?

Preventive measures include use of technology to protect those involved in motor vehicle accidents, such as seat belts and air bags, and better sports or motorcycle helmets. The most effective measures are those that reduce the number of automobile accidents and education programs aimed at increasing the use of seat belts and helmets.

References

Article

  1. Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurology. 2008;7 (8): 728–41. 
  2. Kushner D. Mild traumatic brain injury: Toward understanding manifestations and treatment. Archives of Inter Med.1998;158 (15): 1617–24.
  3. Bazarian JJ, Blyth B, Cimpello L. Bench to Bedside: Evidence for Brain Injury after Concussion—Looking beyond the Computed Tomography. Scan. Medicine. 2006; 13:199–214.
  4. Lee B, Newberg A. Neuroimaging in traumatic brain imaging. Neoro Rx. 2005;2(2):372-383.
  5. Pinto PS, Poretti A, Meoded A, Tekes A, Huisman T. The Unique Features of Traumatic Brain Injury in Children. Review of the Characteristics of the Pediatric Skull and Brain, Mechanisms of Trauma, Patterns of Injury, Complications and Their Imaging Findings—Part 1. Journal of Neuroimaging. 2012;22(2): e1-e17.
  6. Thompson DO, Hurtado TR, Liao MM, Byyny RL, Gravitz C, Haukoos JS. Validation of the Simplified Motor Score in the Out-of-Hospital Setting for the Prediction of Outcomes After Traumatic Brain Injury. Ann Emerg Med. 2011;58(5):417-25.
  7. Mcallister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry. 2008;7:3-10.
  8. Steyerberg EW, Mushkudiani N, Perel P, Butcher I, Lu J, McHugh GS. et al. Predicting outcome after traumatic brain injury: development and international validation of prognostic scores based on admission characteristics. PLoS Med. 2008;5(8):1251-62.
  9. Thornhill S, Teasdale GM, Murray GD, McEwen J, Roy Cw, Penny KI. Disability in young people and adults one year after head injury: prospective cohort study. BMJ. 2000;320(7250):1631-5.
  10. Mayer CL, Huber BR, Peskind E. Traumatic Brain Injury, Neuroinflammation and Post-Traumatic Headaches. Headache. Oct,2013:1524- 32.
  11. Langlois JA, Rutland-Brown W, Thomas KE. The incidence of traumatic brain injury among children in the United States: differences by race. J Head Trauma Rehabil. 2005;20(3):229-38.
  12. Li L, Liu J. The effect of pediatric traumatic brain injury on behavioral outcomes: a systematic review. Developmental Medicine & Child Neurology. 2013; 55: 37–45.
  13. Parikh S, Koch M, Narayan RK. Traumatic brain injury. International Anesthesiology Clinics. 2007; 45 (3): 119–35.
  14. Topal NB, Hakyemez B, Erdogan C, et al. MR imaging in the detection of diffuse axonal injury with mild traumatic brain injury. Neurol Res. 2008; 30(9):974-8.
  15. Chesnut RM. The management of severe traumatic brain injury. Emerg Med Clin North Am. 1997;15(3):581-604.

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Last updated: 2019-06-28 10:37