Traumatic brain injury

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]

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.

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 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.

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.

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.

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

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].

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

There is no racial predilection to TBI.

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

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]

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).

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).

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.

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.

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.

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.

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

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.

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.

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.

There are no ECG findings associated with traumatic brain injury.

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

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

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

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

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

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

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 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.

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)

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

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.

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.

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

Traumatic brain injury has been as ancient as prehistoric era. Human beings know about the effects traumatic brain injury since the inception of community. The understanding has only got better and with that the treatment. In modern times, TBI is thought to be a public health issue.

• Head injury and the immediate after effects has been known to humanity since the earliest civilizations and has been discussed in almost all civilizations.
• Head injuries were found in areas where weapons such as spears are more prevalent, suggesting war as primary reason for TBI just like modern times. There were biblical references about traumatic brain injury.
• The anatomy of head injuries and their treatment was discussed in the oldest known surgical literature of Egypt, the papyrus.
• Trephination is perhaps the oldest invasive procedure done for traumatic brain injury, and it was used to clear the blood from the skull after the injuries. Over the ages, the technique of craniotomy has only become more advanced.
• The effects of mild TBI such as concussion was first described in Greek text and, in 10th century, a Persian author differentiated concussion from other TBI.
• In modern medicine, the concept of concussion was widely spread during war times and most importantly in the recent times after a Hollywood movie actor will smith’s The concussion (2015). With more media attention, concussions are now being identified as a public health crisis associated with the famous national football league, NFL and the presence of sport in schools.

• Muhammad Ali
• James Brady
• Phineas Gage
• Lady Gaga
• Roald Dahl
• Jackie Chan
• Richard Hammond
• Gary Busey

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

There are several methods of classifying traumatic brain injury. One of the most widely used method is classification of TBI by severity of injury using clinical variables at the time of presentation into mild, moderate and severe. There are numerous other ways to classify TBI. Some of the most widely used classifications use the nature of the injury and the extent of the injury.

Traumatic brain injury may be classified according to clinical presentation, trauma mechanism (open vs closed) or severity:

• This type of classification predominantly uses Glasgow coma scale. The other variables that can be used here include
  • The damage from TBI can be focal, confined to one area of the brain, or diffuse, involving more than one area. Diffuse trauma to the brain is frequently associated with concussion (a shaking of the brain in response to sudden motion of the head), diffuse axonal injury, or coma. Localized injuries may be associated with neurobehavioral manifestations, hemiparesis or other focal neurologic deficits. Types of focal brain injury include bruising of brain tissue called a contusion and intracranial hemorrhage or hematoma, heavy bleeding in the skull. Hemorrhage, due to rupture of a blood vessel in the head, can be extra-axial, meaning it occurs within the skull but outside of the brain, or intra-axial, occurring within the brain. Extra-axial hemorrhages can be further divided into subdural hematoma, epidural hematoma, and subarachnoid hemorrhage. An epidural hematoma involves bleeding into the area between the skull and the dura. With a subdural hematoma, bleeding is confined to the area between the dura and the arachnoid membrane. A subarachnoid hemorrhage involves bleeding into the space between the surface of the brain and the arachnoid membrane that lies just above the surface of the brain, usually resulting from a tear in a blood vessel on the surface of the brain. Bleeding within the brain itself is called an intracerebral hematoma. Intra-axial bleeds are further divided into intraparenchymal hemorrhage which occurs within the brain tissue itself and intraventricular hemorrhage which occurs into the ventricular system.^[1]

• TBI can result from a closed or penetrating head injury. A closed injury occurs when the skull is not breached, while a penetrating injury occurs when an object pierces the skull and enters brain tissue. As the first line of defense, the skull is particularly vulnerable to injury. Skull fractures occur when a bone in the skull cracks or breaks. A depressed skull fracture occurs when pieces of the broken skull press into the tissue of the brain. A penetrating skull fracture occurs when something pierces the skull, such as a bullet, leaving a distinct and localized traumatic injury to brain tissue. Skull fractures can cause cerebral contusion.

• Head injuries can be subdivided into mild, moderate, and severe TBI to help predict outcome. One common classification system determines severity based on the Glasgow Coma Scale (GCS) and duration of post-traumatic amnesia (PTA) and loss of consciousness (LOC) according to the table at right. Other classification systems use GCS alone or PTA or LOC alone or together. Prognosis worsens with the severity of injury, but mild TBI is more poorly defined and prognosis is not as clear with it. Mild TBI is also commonly called concussion. Though prognosis for concussion is usually very good, a portion of people may suffer lasting problems associated with the injury, such as post-concussion syndrome. A patient who receives a second concussion before symptoms from another one have healed is at risk for developing a very rare but deadly condition called second-impact syndrome, in which the brain swells catastrophically after even a mild blow.^[2]

Levels of TBI severity

	GCS	PTA	LOC
Mild	13 to 15	<1 hour	<30 minutes
Moderate	9 to 12	30 minutes to 24 hours	1 to 24 hours
Severe	<8	>1 day	>24 hours

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-in-Chief : Deekshitha Manney, M. D[2]

The progression of traumatic brain injury usually involves the inflammatory response pathway.

• Unlike most forms of traumatic death, a large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event.^[1] Rather than improving after being hospitalized, some 40% of TBI patients deteriorate.^[2] 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^[3] and contribute a large amount to morbidity and mortality from TBI.^[4]

• Secondary injury events are poorly understood but are thought to include cerebral edema (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. Cerebral edema can eventually lead to herniation of brain leading to death.

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

Three most common causes of traumatic brain injury include falls, motor vehicle accidents and being struck by/against. Other etiologies include sports related injuries, assault, coup/counter coup injury.

• Common causes of traumatic brain injury may include:^[1][2]
  • Under age 75: Transportation accidents involving automobiles, motorcycles, bicycles, and pedestrians.
  • Aged 75 and older: Falls.

• Less common causes of traumatic brain injury include:
  • Firearm assaults
  • Child abuse
  • Sport injury

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Joanna Ekabua, M.D. [2]

Traumatic brain injury must be differentiated from other disease that causes headache, seizures and loss of consciousness such as subdural hemorrhage, meningitis, encephalitis, brain tumor, hemorrhagic stroke, neurosyphilis, migraine, hypertensive encephalopathy, wernicke’s encephalopathy, brain abscess, drug toxicity, conversion disorders, metabolic disturbance, multiple sclerosis, and seizure.

Traumatic brain injury must be differentiated from other disease that causes headache, seizures and loss of consciousness such as subdural hemorrhage, meningitis, encephalitis, brain tumor, hemorrhagic stroke, neurosyphilis, migraine, hypertensive encephalopathy, wernicke’s encephalopathy, brain abscess, drug toxicity, conversion disorders, metabolic disturbance, multiple sclerosis, and seizure.

Diseases	Symptoms				Physical Examination					Past medical history	Diagnostic tests			Other Findings
	Headache	↓LOC	Motor weakness	Abnormal sensory	Motor Deficit	Sensory deficit	Speech difficulty	Gait abnormality	Cranial nerves		CT /MRI	CSF Findings	Gold standard test
Traumatic brain injury	+	+/-	+/-	+/-	+/-	+/-	+/-	+/-		Alcoholic	+	Elevated serum albumin ratio	MRI	Headache Mental confusion Lightheadedness Dizziness
Subdural hemorrhage	+	+	+	+	+	–	–	–	+	Trauma, fall	+	Xanthochromia[1]	CT scan without contrast[2][3]	Confusion, dizziness, nausea, vomiting
Meningitis	+	–	–	–	–	+	+	–	–	History of fever and malaise	–	↑ Leukocytes, ↑ Protein ↓ Glucose	CSF analysis[4]	Fever, neck rigidity
Encephalitis	+	+	+/-	+/-	–	–	+	+/-	+	History of fever and malaise	+	↑ Leukocytes, ↓ Glucose	CSF PCR	Fever, seizures, focal neurologic abnormalities
Brain tumor[5]	+	–	–	–	+	+	+	–	+	Weight loss, fatigue	+	Cancer cells[6]	MRI	Cachexia, gradual progression of symptoms
Hemorrhagic stroke	+	+	+	+	+	+	+	+	–	Hypertension	+	–	CT scan without contrast[2][3]	Neck stiffness
Neurosyphilis[7][8]	+	–	+	+	+	+	–	+	–	STIs	+	↑ Leukocytes and protein	CSF VDRL-specifc CSF FTA-Ab -sensitive[9]	Blindness, confusion, depression, Abnormal gait
Complex or atypical migraine	+	–	+	+	–	–	+	–	–	Family history of migraine	–	–	Clinical assesment	Presence of aura, nausea, vomiting
Hypertensive encephalopathy	+	+	–	–	–	–	+	+	–	Hypertension	+	–	Clinical assesment	Delirium, cortical blindness, cerebral edema, seizure
Wernicke’s encephalopathy	–	+	–	–	–	+	+	+	+	History of alcohal abuse	–	–	Clinical assesment and lab findings	Ophthalmoplegia, confusion
CNS abscess	+	+	–	–	+	+	+	–	–	History of drug abuse, endocarditis, immunosupression	+	↑ leukocytes, ↓ glucose and ↑ protien	MRI is more sensitive and specific	High grade fever, fatigue,nausea, vomiting
Drug toxicity	–	+	–	+	+	+	–	+	–	–	–	–	Drug screen test	Lithium, Sedatives, phenytoin, carbamazepine
Conversion disorder	+	+	+	+	+	+	+	+		History of emotional stress	–	–	Diagnosis of exclusion	Tremors, blindness, difficulty swallowing
Metabolic disturbances (electrolyte imbalance, hypoglycemia)	–	+	+	+	+	+	–	–	+	–	–	Hypoglycemia, hypo and hypernatremia, hypo and hyperkalemia	Depends on the cause	Confusion, seizure, palpitations, sweating, dizziness, hypoglycemia
Multiple sclerosis exacerbation	–	–	+	+	–	+	+	+	+	History of relapses and remissions	+	↑ CSF IgG levels (monoclonal bands)	Clinical assesment and MRI [10]	Blurry vision, urinary incontinence, fatigue
Seizure	+	+	–	–	+	+	–	–	+	Previous history of seizures	–	Mass lesion	Clinical assesment and EEG [11]	Confusion, apathy, irritability,

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Joanna Ekabua, M.D. [2]

The incidence of traumatic brain injury varies by age, gender, region and other factors. The age groups most at risk for TBI are children ages five to nine and adults over age 80. There is no racial predilection to traumatic brain injury. Men are more commonly affected by traumatic brain injury than women with a ratio of 2:1.

• The incidence of traumatic brain injury varies by age, gender, region and other factors.^[1]
• The yearly incidence in the U.S. is estimated to be about 180 to 250 per 100,000 people, but the incidence is thought to be higher in Europe and South Africa.^[1]

• The age groups most at risk for traumatic brain injury are children ages five to nine and adults over age 80.^[2]
• Children age five and younger are also at high risk for TBI.
• Men suffer twice as many TBIs as women do and have a four-fold risk of fatal head injury.^[2]
• Males also account for two thirds of childhood and adolescent head trauma patients.^[3]

• There is no racial predilection to traumatic brain injury.

• Men are more commonly affected by traumatic brain injury than women with a ratio of 2:1.^[4]

Each year in the United States:

• About two million people suffer a traumatic brain injury^[2]
• About 500,000 people are hospitalized for TBI^[1]
• Approximately 270,000 people experience a moderate or severe TBI
• Approximately 60,000 new cases of epilepsy occur as a result of head trauma
• Approximately 50,000 people die from head injury
• Approximately 80,000 of these survivors live with chronic disabilities as a result of the injury.^[2]

• 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).^[5]

• 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).^[5]

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

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

Common risk factors for the development of traumatic brain injury include^[1][2]

• Male gender
• Certain occupations such as professional contact sports
• Age >65 and children under age 1
• Driving without helmet and seatbelts
• Driving under the influence of alcohol or other drugs
• Conduct disorder, depression, and anxiety
• Being on antiplatelet agents and/or anticoagulant medications

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Joanna Ekabua, M.D. [2]

There is insufficient evidence to recommend routine screening for traumatic brain injury.

There is insufficient evidence to recommend routine screening for traumatic brain injury.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-in-chief: Deekshitha Manney, M.D.[[2]]

The complications 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.

• If left untreated, 100% of patients with traumatic brain injury die.

• Generally, there are six abnormal states of consciousness that can result from a TBI: stupor, coma, persistent vegetative state, minimally conscious state, locked-in syndrome, and brain death.
• Stupor is a state in which the patient is unresponsive but can be aroused briefly by a strong stimulus, such as sharp pain.
• Coma is a state in which the patient is totally unconscious, unresponsive, unaware, and unarousable.
• Patients in a persistent vegetative state are unconscious and unaware of their surroundings, but they continue to have a sleep-wake cycle and can have periods of alertness.
• A vegetative state can result from diffuse injury to the cerebral hemispheres of the brain without damage to the lower brain and brainstem.
• Patients in a minimally conscious state have a reduced level of arousal and may appear, on the surface, to be in a persistent vegetative state but are capable of demonstrating the ability to actively process information.
• In the minimally conscious state a patient exhibits deliberate, or cognitively mediated, behavior often enough, or consistently enough, for clinicians to be able to distinguish it from the entirely unconscious, reflexive responses that are seen in the persistent vegetative state.
• Differentiating a patient in a persistent vegetative state from one in a minimally conscious state can be challenging but remains a critically important clinical task.
• Locked-in syndrome is a condition in which a patient is aware and awake, but cannot move or communicate due to complete paralysis of the body.
• Voluntary control of eye movements or blinking may be spared permitting the detection of conscious awareness and enabling the establishment of functional communication.
• Brain death is the lack of measurable brain function due to diffuse damage to the cerebral hemispheres and the brainstem, with loss of any integrated activity among distinct areas of the brain. Brain death is irreversible.
• Removal of assistive devices will result in immediate cardiac arrest and cessation of breathing.
• Recent studies have brought into question the nature of coma and consciousness in TBI.
• For example, a 23-year-old woman in a vegetative state after a severe brain injury due to a car accident was able to communicate with a team of British researchers at Cambridge University in England via functional magnetic resonance imaging.^[1]
• While cautious about accepting the study’s results, Nicholas Schiff, a neurologist at the Weill Cornell Medical College in New York, agrees that the research was groundbreaking. “It’s the first time we’ve ever seen something like this. It really is kind of shocking,” he said.^[2]

• Hydrocephalus or post-traumatic ventricular enlargement occurs when cerebrospinal fluid (CSF) accumulates in the brain resulting in dilation of the cerebral ventricles (cavities in the brain filled with CSF) and an increase in ICP.
• This condition can develop during the acute stage of TBI or may not appear until later.
• Generally, it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.
• The condition may develop as a result of meningitis, subarachnoid hemorrhage, intracranial hematoma, or other injuries.
• Treatment includes shunting and draining of CSF as well as any other appropriate treatment for the root cause of the condition.

• Skull fractures can tear the meninges, the membranes that cover the brain, leading to CSF leaks.
• A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma.

CSF can also leak from the nose and the ear. These tears that let CSF out of the brain cavity can also allow bacteria into the cavity, potentially causing infections such as meningitis. Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura mater, below the dura, below the arachnoid (meningitis), or within the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue. Meningitis may be especially dangerous, with the potential to spread to the rest of the brain and nervous system.

Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space.

Any damage to the head or brain usually results in some damage to the vascular system, which provides blood to the cells of the brain. The body can repair damage to small blood vessels, but damage to larger vessels can result in serious complications. Damage to one of the major arteries leading to the brain can cause a stroke, either through bleeding from the artery (hemorrhagic stroke) or through the formation of a clot at the site of injury, called a thrombus or thrombosis, blocking blood flow to the brain (ischemic stroke). Blood clots also can develop in other parts of the head. Symptoms such as headache, vomiting, seizures, paralysis on one side of the body, and semiconsciousness developing within several days of a head injury may be caused by a blood clot that forms in the tissue of one of the sinuses, or cavities, adjacent to the brain. Other types of vascular injuries include vasospasm and the formation of aneurysms.

Skull fractures, especially at the base of the skull, can cause cranial nerve injuries that result in compressive cranial neuropathies]]. All but three of the twelve cranial nerves project out from the brainstem to the head and face. Damage to the seventh cranial nerve, the most commonly injured cranial nerve in TBI can result in paralysis of facial muscles.

Pain, especially headache, is a common complication following a TBI.

Fluid and hormonal imbalances can complicate the treatment of hypermetabolism and high intracranial pressure (ICP). Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and hypothyroidism.

Trauma victims often develop hypermetabolism or an increased metabolic rate, which leads to an increase in the amount of heat the body produces. The body redirects into heat the energy needed to keep organ systems functioning, causing muscle wasting and the starvation of other tissues. The nutritional management of patients with TBI, including the provision of adequate calories, and protein through an available route of administration to balance consumption, is thus critically important in order to avoid complications related to hypermetabolism and resulting malnutrition. Provision of food through a feeding tube may be temporarily necessary to meet the nutritional needs of the patient with a severe TBI, until they are awake and able to eat and swallow safely without risking pulmonary aspiration and the development of aspiration pneumonia. Sometimes the use of parenteral feeding is necessary if the patient has associated injuries or complications that prevent direct access to the digestive system.

Disabilities resulting from a TBI depend upon the severity of the injury, the location of the injury, and the age and general health of the patient. Some common disabilities include problems with cognition (attention, calculation, memory, judgment, insight, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (language expression and understanding), social function (empathy, capacity for compassion, interpersonal social awareness and facility) and mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness).

Within days to weeks of the head injury, approximately 40% of TBI patients develop a host of troubling symptoms collectively called postconcussion syndrome (PCS). A patient need not have suffered a loss of consciousness to develop the syndrome. Symptoms include headache, dizziness, memory problems, trouble concentrating, sleeping problems, restlessness, irritability, apathy, clinical depression, and anxiety. These symptoms may last for a few weeks after the head injury. The syndrome is more prevalent in patients who had psychiatric symptoms, such as depression or anxiety, before the injury. Treatment involves treating symptoms, for example giving medicines for pain and psychiatric conditions, and psychotherapy and occupational therapy.

Most patients with severe TBI who recover consciousness suffer from cognitive disabilities, including the loss of many higher-level mental skills. The most common cognitive impairment among severely head-injured patients is memory loss, characterized by some loss of specific memories and the partial inability to form or store new ones. Some of these patients may experience post-traumatic amnesia (PTA), either anterograde or retrograde. Anterograde PTA is impaired memory of events that happened after the TBI, while retrograde PTA is impaired memory of events that happened before the TBI.

Many patients with mild to moderate head injuries who experience cognitive deficits become easily confused or distracted and have problems with concentration and attention. They also have problems with higher level, so-called executive functions, such as planning, organizing, abstract reasoning, problem-solving, and making judgments, which may make it difficult to resume pre-injury activities. Recovery from cognitive deficits is greatest within the first six months after the injury and more gradual after that.

Patients with moderate to severe TBI have more problems with cognitive deficits than patients with mild TBI, but a history of several mild TBIs may have an additive effect. Language and communication problems are common disabilities in TBI patients. Some may experience aphasia, defined as difficulty with understanding and producing spoken and written language; others may have difficulty with the more subtle aspects of communication, such as body language and emotional, non-verbal signals. TBI patients may have problems with spoken language if the part of the brain that controls speech muscles is damaged. In this disorder, called dysarthria, the patient can think of the appropriate language, but cannot easily speak the words because they are unable to use the muscles needed to form the words and produce the sounds. Speech is often slow, slurred, and garbled. Some may have problems with intonation or inflection, called prosodic dysfunction.

Alzheimer’s disease (AD) is a progressive, neurodegenerative disease characterized by dementia, memory loss, and deteriorating cognitive abilities. Research suggests an association between head injury in early adulthood and the development of AD later in life; the more severe the head injury, the greater the risk of developing AD. Some evidence indicates that a head injury may interact with other factors to trigger the disease and may hasten the onset of the disease in individuals already at risk. For example, people who have a particular form of the protein apolipoprotein E (apoE4) and suffer a head injury fall into this increased risk category. (ApoE4 is a naturally occurring protein that helps transport cholesterol through the bloodstream.)

Dementia pugilistica, also called chronic traumatic encephalopathy, primarily affects career boxers. The most common symptoms of the condition are dementia and parkinsonism caused by repetitive blows to the head over a long period of time. Symptoms begin anywhere between 6 and 40 years after the start of a boxing career, with an average onset of about 16 years.

Post-traumatic dementia is another potential long-term effect of TBI. The symptoms of post-traumatic dementia are very similar to those of dementia pugilistica, except that post-traumatic dementia is also characterized by long-term memory problems and is caused by a single, severe TBI that results in a coma.

Many TBI patients have sensory problems, especially problems with vision. Patients may not be able to register what they are seeing or may be slow to recognize objects. Also, TBI patients often have difficulty with hand-eye coordination. Because of this, TBI patients may seem clumsy or unsteady. Other sensory deficits may include problems with hearing, smell, taste, or touch. Some TBI patients develop tinnitus, a ringing or roaring in the ears. A person with damage to the part of the brain that processes taste or smell may develop a persistent bitter taste in the mouth or perceive a persistent noxious smell. Damage to the part of the brain that controls the sense of touch may cause a TBI patient to develop persistent skin tingling, itching, or pain. These conditions are rare and hard to treat.

Most TBI patients have emotional or behavioral problems that fit under the broad category of psychiatric health. Family members of TBI patients often find that personality changes and behavioral problems are the most difficult disabilities to handle. Psychiatric problems that may persist for one-half year to two years after the injury may include irritability, suicidal ideation, insomnia, and loss of the ability to experience pleasure from previously enjoyable experiences. Other problems include apathy, anxiety, anger, paranoia, confusion, frustration, agitation, and mood swings. About one-quarter of people with TBI suffer from clinical depression, and about 9% suffer mania. Problem behaviors may include aggression and violence, impulsivity, disinhibition, acting out, noncompliance, social inappropriateness, emotional outbursts, childish behavior, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, inappropriate sexual activity, and alcohol or drug abuse or addiction. Some patients’ personality problems may be so severe that they are diagnosed with an organic personality disorder, a psychiatric condition characterized by many of these problems. Sometimes TBI patients suffer from developmental stagnation, meaning that they fail to mature emotionally, socially, or psychologically after the trauma. This is a serious problem for children and young adults who suffer from a TBI, because attitudes and behaviors that are appropriate for a child or teenager become inappropriate in adulthood. TBI patients who show psychiatric or behavioral problems may be helped with medication and psychotherapy, although the effectiveness of psychotherapy may be limited by the residual neurocognitive impairment. Technological improvements and emergency care have diminished the incidence of devastating TBI while increasing the numbers of patients with mild or moderate TBI. Such patients are more adversely affected by their emotional problems than by their residual physical disabilities.

Parkinson’s disease and other motor problems as a result of TBI are rare but can occur. Parkinson’s disease may develop years after TBI as a result of damage to the basal ganglia. Symptoms of Parkinson’s disease include tremor or trembling, rigidity or stiffness, slow movement (bradykinesia), inability to move (akinesia), shuffling walk, and stooped posture. Despite many scientific advances in recent years, Parkinson’s disease remains a chronic and progressive disorder, meaning that it is incurable and will progress in severity until the end of life. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

About 25% of patients with brain contusions or hematomas and about 50% of patients with penetrating head injuries will develop immediate seizures, seizures that occur within the first 24 hours of the injury. These immediate seizures increase the risk of early seizures – defined as seizures occurring within 1 week after injury – but do not seem to be linked to the development of post-traumatic epilepsy (recurrent post-traumatic seizures occurring more than 1 week after the initial trauma). Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients only if the seizures persist.

The immediate effect after TBI is a cascade of molecular responses which includes ion imbalances. There will be an increased extracellular potassium and intracellular calcium, increase of glutamate and aspartate release from the neurons which results in blood-brain barrier compromise ultimately leading to inflammation and degeneration. Primary brain volume declines by 10% in the first 6 months after injury which equals to decades of ageing.^[3]

• 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.^[4][5]
• The outcome for patients with head injury depends heavily on the cause. For example, in the US, patients with TBIs from falls have an 89% survival rate, while only 9% of patients with firearm-related TBIs survive.^[6]

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