Victims should be aware of brain injury symptoms so they can promptly seek medical attention. The symptoms of brain injury are varied and can be easy to miss.
There are two types of brain injury: acquired brain injury and in-born brain injury. In-born brain injuries occur before birth. They may be due to genetic brain disorders, fetal alcohol syndrome, or neurological damage from maternal drug abuse. These factors constitute only a limited list of possible causes of in-born brain injury. Doctors and parents are most likely to notice the symptoms of brain injury in children.
An acquired brain injury occurs after birth and can either be traumatic or non-traumatic. A non-traumatic injury can be caused by stroke, infections, hypoxia, or medical errors, among other possibilities. External, physical impacts cause traumatic brain injuries, such as motor vehicle accidents, falls, assaults, and other sudden events are the most common causes of traumatic brain injuries. Any sudden incident that causes the brain to hit the inside of the skull can cause a traumatic brain injury.
People can suffer a wide range of severity in brain injuries typically classified as mild, moderate, or severe. A mild injury might cause brief changes in consciousness, whereas a severe one might result in unconsciousness, coma, or even death. Disruption of normal brain function is the main characteristic of all brain injuries.
People can often recognize the cognitive symptoms of brain injury more easily than sensory ones because the media often portrays them in connection with brain injuries. Such symptoms include:
Traumatic Brain Injury: According to the U.S. Department of Health and Human Services and the Centers for Disease Control and Prevention, “[t]raumatic brain injury (TBI) is an important public health problem in the United States. TBI is frequently referred to as the ‘silent epidemic’ because the complications from TBI, such as changes affecting thinking, sensation, language, or emotions, may not be readily apparent.” TBI is defined as an alteration in brain function, or other evidence of brain pathology, caused by an external force. TBI typically results from inertial forces on the brain and cause immediate structural damage from compression, tensile strains, shearing of neurons and diffuse axonal injury. Damage most frequently occurs to the orbital surface of the frontal lobes, the poles of the frontal and temporal lobes, and the brain stem structures, increasing to other areas with increased severity. Functional changes may also occur in cerebral blood flow, intracranial pressure, cortical activity, and biochemistry. Since neuroanatomy of memory is incompletely understood, it is difficult to explain the high frequency of subsequent memory deficits.
More than two million people sustain a traumatic brain injury in the United States each year. “It is well-recognized that mild brain injury patients often have persisting difficulties with concentration and memory.” The “onset of symptoms may occur days, weeks, or months after the initial injury.” “Many [TBI-injured people] are acutely aware that they are mentally inefficient—easily confused, disoriented, overwhelmed, or distracted. These patients may try to compensate for their deficiencies with obsessive-compulsive strategies and tend to avoid stressful (i.e., highly stimulating) situations—such as cocktail parties, the local pub, big family gatherings, and shopping malls—thus becoming somewhat socially withdrawn.” At the same time, “[s]ome patients may not become aware of, or admit, the extent of their symptoms until they attempt to return to normal functioning.” Even following a “mild” TBI, “some patients suffer from physical, cognitive or psychological impairments even years after the trauma, which may hamper their reintegration into social, familial and professional life. … [T]he notion of complete recovery after mTBI is not supported.” Indeed, estimates indicate that up to “50% of persons with a mild TBI experience long-term health issues such as persistent headache, difficulty with memory or concentration, or mood changes.” Additionally, persistent post-concussive symptoms are often responsible for social distress, while the failure to regain working activities after a TBI has devastating consequences with loss of financial independence, difficulties in psychosocial adjustment and deterioration in quality of life.
Worse yet, a TBI increases long-term mortality and reduces life expectancy, is associated with an increased incident of seizures, sleep disorders, neurodegenerative diseases, neuroendocrine dysregulation and psychiatric diseases, as well as non-neurological disorders such as sexual dysfunction, bladder and bowel incontinence, and systemic metabolic dysregulation that may arise and/or persist for months to years post-injury. Indeed, even a mild TBI places a person at increased risk of developing long-term complications. For instance, one study of over 350,000 veterans found that even a mild TBI without loss of consciousness more than doubles the risk of a subsequent dementia diagnosis. Other studies have linked mild TBIs with an increased risk of developing Alzheimer’s disease, epilepsy, PTSD and depression, Multiple Sclerosis, Parkinson’s Disease, and numerous neuroendocrine disorders (including hypopituitarism, growth hormone deficiency, hypothyroidism, and gonadotropin deficiency).
According to a study published in the New England Journal of Medicine in 2014, by David Wright, MD et all (Emory University), more than 2.4 million ER visits, hospitalization and deaths are attributable to Traumatic Brain Injury (TBI) annually in the United States, with 5.3 million individuals suffering from the after effects of TBI at any given time. TBI is responsible for 12% of hospitalization, and 76 billion dollars in total costs to American society every year, and afflicted individuals typically require 5 to 10 years of intensive therapy. Traumatic brain injury, also called acquired brain injury or head injury, occurs when a sudden trauma causes damage to the brain. The damage can be focal or diffuse. Click the following link for a video simulation showing a Diffuse Axonal Injury: https://www.youtube.com/watch?v=UbGDFT6cVNG The definition of Diffuse Axonal Injury (DAI) in TBI is a potentially severe form of TBI, and is the underlying cause of injury in 50% of TBI patients requiring hospitalization. Diffuse Axonal Injury results from sudden changes in velocity of the head. Motor Vehicle Accidents are a frequent example of such situations. Severe TBI seen in MVAs arise as a result of acceleration/deceleration events of the brain within the skull, without skull fracture (closed-head trauma). This event usually occurs as vehicle occupants are thrown forward or sideways, resulting in collisions between the head and windshields/dashboards/steering wheels. While the majority of severe brain injuries in acceleration-deceleration events results from DAI, other forms of traumatic brain injury such as contusion, anoxia, hemorrhage, and penetration may occur at the same time, complicating cognitive deficits and prognosis. While many such injuries involve physical impact of the head with some portion of the vehicle, it is the sudden acceleration/deceleration of the head, apart from impact, that results in diffuse axonal injury. Some degree of diffuse axonal injury is considered to be present in any individual involved in an MVA who is rendered unconscious by head injury.
Many researchers now believe that long-term neurological deficits in football players, hockey players, and soccer players who have received multiple concussions is more closely related to diffuse axonal injury, rather than the concussive effects suffered on collision, as the symptom complex and course seen in these individuals is similar to patients involved in MVAs.
Diffuse Axonal Injury Mechanism
DAI involves massive loss of neuronal function toward the central area of the brain, well away from any area of direct trauma with the skull. Researchers were initially puzzled as to why such extensive damage occurred without direct trauma. The mechanism of DAI was subsequently discovered to occur as a result of rotational movement of the brain during acceleration-deceleration events. The key to understanding the injury lies in the varying densities of the brain tissue. Gray matter, primarily the cerebral brain structures, is less dense than white matter (brainstem and central brain structures). Due to different inertial characteristics based on these densities, as the brain rotates during acceleration-deceleration events, lower density tissues move more rapidly than those of greater density. This velocity difference causes shearing of the neuronal axons which traverse the junction of gray and white matter, and explains why DAI lesions are seen most frequently in the areas of the brain where gray and white matter meet (see video link). The term shear injury may be used interchangeably with DAI. The magnitude of axonal injury in DAI is dependent on three factors: 1) the distance from the center of rotation; 2)the arc of the rotation; and 3) the duration and intensity of the force.
There appears to be two phases to the axonal injury in DAI. The primary injury is where axons undergo shear forces and stretch at the moment of impact. The secondary, or delayed phase, is where the stretched axons undergo swelling and rupture as a result of biochemical changes related to primary injury. Initial abnormal changes in stretched axons, known as the bulb formation, is generally seen within a day or two of injury, but completion of the degenerative process may take up to two years. Clinical symptoms may take two years to fully develop in individuals who are not rendered unconscious at the moment of injury. It is now widely held that the greatest injury to neurons with DAI occurs as a result of primary strain, followed by delayed secondary rupture due to metabolic disturbances within the neuronal axon, rather than tearing of axons at injury. Jay Meythaler, MD, et. al. Describes this process in their review of DAI in a 2001 article in The Achieves of Physical Medicine and Rehabilitation. In a paper published March 1, 2013, in the Journal of Neurotrauma, Douglas Smith, MD, et. al. describes the pathological process of axonal injury in detail. In this paper, Dr. Smith describes the formation of axonal bulbs – swelling at the ends of axons that eventually result in disconnection, as well as a process known as “beading” in which swellings, or “axonal varicosities”, occur along the length of a single axon, resulting in multiple points of interruption to neurotransmitter flow.
Diffuse Axonal Injury Effects on Neurological Function
The Adams classification categorizes DAI based on the degree and location of injury-related lesions in the white matter. In this classification, mild (grade 1) is characterized by micro-scopic changes in the white matter of cerebral cortex, corpus callosum, brainstem, and occasionally the cerebellum. Moderate DAI (grade 2) is defined by grossly evident focal lesions isolated to the corpus callosum. In severe DAI (grade 3), there are additional focal lesions in the dorsolateral quadrants of the rostrals brainstem (commonalty in the superior cerebellar peduncle).
Severe DAI results in an immediate loss of consciousness, and most individuals with a severe DAI injury (>90%) remain in a persistent vegetative state. Essential cardiac and respiratory brain function required for life are typically not affected by DAI, as these functions are located deep in the brainstem, away from the gray-white matter interface. As a result, DAI rarely causes death. The prognosis worsens in direct relationship to the number of lesions present.
A diffuse axonal injury is a type of severe traumatic brain injury that affects patients and their families. Patients with diffuse axonal injury have a range of multiple neurological deficits that affect the physical and mental status of the patient. These changes usually compromise social reintegration, return to productivity, and quality of life of patients and their families. For most patients and families, the clinical status of patients with diffuse axonal injury will continue to persist for a minimum of two years. Then, most patients and families will achieve and accept a new baseline. Recent epidemiological studies indicate that the outcomes of patients with diffuse axonal injury are associated with the number of lesions identified through imaging. There are emerging studies suggesting that during the acute phase of diffuse axonal injury, hypoxia, and hypotension are associated with increased mortality. Therefore, it is important to continue investigating the clinical, pathophysiological, and radiographic studies to advance the management of patients with diffuse axonal injury.
Patients with DAI often have a severe brain injury and are best managed by an interprofessional team that includes a neurologist, neurosurgeon, physical and occupational therapist, speech therapist, intensivist, internist, ICU nurses, neuroscience nurses, and rehabilitation nurses. Pharmacists review prescribed medications including anticonvulsants and check for drug-drug interactions. Nurses monitor patients and inform the team about changes in status. Patients with diffuse axonal injury have a range of multiple neurological deficits that affect the physical and mental status of the patient. These changes usually compromise social reintegration, return to productivity, and quality of life of patients and their families. For most patients and families, the clinical status of patients with diffuse axonal injury will continue to persist for a minimum of two years.
The outcome for patients with DAI is generally poor. The recovery is long, and complete recovery is usually not possible in cases of severe injury. For many, there is life long disability with a poor quality of life. Because DAI can affect virtually every higher brain function, deficits can consist of a broad range of cognitive problems, including thinking, reasoning, problem solving, information processing, and memory. The most common cognitive impairment is memory loss. Many patients with DAI suffer from cognitive disabilities, including the loss of may higher-level mental skills, most commonly, memory loss. Many patients with mild to moderate head injuries who experience cognitive deficits become easily confused or distracted and have problems with concentration, attention, planning, organizing, abstract reasoning, problem solving, and making judgments, which make it difficult to resume pre-injury work-related activities. Many DAI patients have sensory problems, especially with vision. Patients may not be able to register what they are seeing or may be slow to recognize objects or with hand-eye coordination. Because of the sensory issues, DAI patients may be prone to bumping into things, dropping objects, or unsteadiness. DAI patients may have difficulty with driving a car, working complex machinery, playing sports, and issues with hearing, smell, taste or touch. Other issues faced with a DAI are speech, emotional, behavioral, sleep and psychiatric problems.
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 Lezak, Muriel, et al., Neuropsychological Assessment (5th ed) at 180; McPeak, LA, et al. Disability evaluation following traumatic brain injury. Phys Med Rehab Clin N. Am., Aug. 2001; 12(3): 587–601.
 Reeder, KP and Logue, PE. The effects of traumatic brain injuries on information processing. Arch Clin Neuropsych. 1994; 9(6): 491–500.
 See Silver, J.M., et al., The Association Between Head Injuries and Psychiatric Disorders: Findings from the New Haven NIMH Epidemiologic Catchment Area Study, Brain Injury (2001); 15(11): 935–45); World Health Organization, Neurological disorders: public health challenges § 3.10 traumatic brain injuries (“Many years of productive life are lost, and many people have to suffer years of disability after brain injury.”) available at https://www.who.int/mental_health/neurology/neurodiso/en/).
 Smith, Douglas, et al, Diffuse Axonal Injury in Head Trauma, J. Head Trauma Rehabil. 2003 18(4).
 See U.S. Dept. of Health and Human Srvcs, Centers for Disease Control and Prevention, Heads Up Facts for Physicians About Mild Traumatic Brain Injuries (MTBI) at 4 (citing Moore E, Terryberry-Spohr L, Hope D. mild traumatic brain injury and anxiety sequelae: A review of the literature. Brain Injury 2006; 20(2):117-32) available at https://stacks.cdc.gov/view/cdc/12340.
 Lezak, Muriel, et al., Neuropsychological Assessment (4th ed. 2004) at 168–69; id. (5th ed) at 201.
 Definition of mild traumatic brain injury, developed by the Mild Traumatic Brain Injury Committee of the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine, J. Head Trauma Rehabil. 1993; 8(3):86–87 available at https://acrm.org/wp-content/uploads/pdf/TBIDef_English_10-10.pdf.
 Konrad, et al., Long-term cognitive and emotional consequences of mild traumatic brain injury, Psychological Medicine (Cambridge 2010) pp. 1–2, 12.
 The CDC, NIH, DoD, and VA Leadership Panel. Report to Congress on Traumatic Brain Injury in the United States: Understanding the Public Health Problem among Current and Former Military Personnel. Centers for Disease Control and Prevention (CDC), the National Institutes of Health (NIH), the Department of Defense (DoD), and the Department of Veterans Affairs (VA) at 33 (June 2013) available at https://www.cdc.gov/traumaticbraininjury/pdf/Report_to_Congress_on_Traumatic_Brain_Injury_2013-a.pdf.
 Chamelian, L., et al, Outcome After Mild to Moderate Traumatic Brain Injury: the Role of Dizziness, Arch Phys. Med. Rehabil., Oct. 2004; 85:1662–66.
 See, e.g., McMillan, TM, et al, Death after head injury: the 13 year outcome of a case control study. J. of Neurology, Neurosurgery & Psychiatry, Aug. 2011, 82(8): 931–35 (finding that the death rate was elevated for those who’d previously suffered a TBI, including a seven-fold increase in younger adults after a mild head injury); C. Harrison Felix, et al, Causes of death following 1 year postinjury among individuals with traumatic brain injury, J Head Trauma Rehabil. Jan. 2006, 21(1): 22–33 (finding a statistically significant reduction in long-term survival for those with a mild traumatic brain injury); McMillan, TM, et al, Mortality and morbidity 15 years after hospital admission with mild head injury: a prospective case-controlled population study. J. of Neurology, Neurosurgery & Psychiatry, Nov. 2014, 85(11): 1214–20 (finding that younger adults with a mild head injury had a 4.2-fold greater risk of death).
 Masel, BE and DeWitt, DS. Traumatic brain injury: a disease process, not an event. J. Neurotrauma. Aug. 2010, 27(8): 1529–40; Masel, BE. Conceptualizing Brain Injury as a Chronic Disease, A position paper of the Brain Injury Assoc. of Am. Mar. 2009 available at https://www.biausa.org/public-affairs/media/conceptualizing-brain-injury-as-a-chronic-disease.
 Deborah E. Barnes, et al, Association of Mild Traumatic Brain Injury With and Without Loss of Consciousness With Dementia in US Military Veterans, JAMA Neurol., Sept. 2018; 75(9): 1055–61 available at https://jamanetwork.com/journals/jamaneurology/fullarticle/2679879; see also Deborah E. Barnes, et al, Traumatic brain injury and risk of dementia in older veterans, Neurology, July 2014; 83(4): 312–19; Fann, JR, et al, Long-term risk of dementia among people with traumatic brain injury in Denmark: a population-based observational cohort study, Lancet, May 2018 5(5):424–31; Anna Nordstrom and Peter Nordstrom, Traumatic brain injury and the risk of dementia diagnosis: A nationwide cohort study. PLoS Med. Jan. 2018, 15(1) available at https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002496.
 Plassman, BL, et al, Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias, Neurology, Oct. 200, 55(8): 1158–66; Schofield, PW, et al, Alzheimer’s disease after remote head injury: an incidence study. J. Neurology, Neurosurgery & Psychiatry, Feb. 1997, 62(2): 119–24.
 Christensen, J., et al, Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study. Lancet, Mar. 2009, 373 (9669): 1105–10 (finding risk of epilepsy ten years after suffering a traumatic brain injury was 4.3 times greater for those with a severe TBI and 1.5 times greater for those who sustained a mild TBI).
 Stein, MB, et al, Risk of Posttraumatic Stress Disorder and Major Depression in Civilian Patients After Mild Traumatic Brain Injury: a Track-TBI Study. JAMA Psychiatry. Mar. 2019, 76(3): 249–58.
 Kang, JH, et al, Increased Risk of Multiple Sclerosis after Traumatic Brain Injury: A Nationwide Population-Based Study. J. Neurotrauma, Jan. 2012, 29(1): 90–95; Montgomery, S., et al. Concussion in adolescence and risk of multiple sclerosis. Annals of Neurology. Oct. 2017, 82(4): 554–61.
 Gardner, RC, et al, Mild TBI and risk of Parkinson disease: A Chronic Effects of Neurotrauma Consortium Study, Neurology, May 2018, 90(20): e1771–79.
 Schneider, HJ, et al, Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systemic review. JAMA. Sept. 2007, 298(12): 1429–38; Agha, A. et al, Anterior pituitary dysfunction following traumatic brain injury. Clinical Endocrinology. Apr. 2006, 64(5): 481–88.