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Head injury

A head injury is any trauma to the scalp, skull, or brain, which can be classified as closed (without skin breakage or penetration) or open (penetrating, involving a break in the skull or penetration by an object).^[1] Traumatic brain injury (TBI), often resulting from such trauma, is defined as a disruption in the brain's normal function caused by an external force, such as a bump, blow, or jolt to the head or body, or by a penetrating object.^[2] TBIs are categorized by severity as mild, moderate, or severe and represent a leading cause of death and disability worldwide, with an estimated 64–74 million cases annually,^[3] over 69,000 TBI-related deaths in the United States alone in 2021 and approximately 214,000 hospitalizations in 2020.^[4]^[5] Common causes of head injuries include falls, which account for the majority of cases especially among young children and adults over 65; motor vehicle crashes; assaults or violence; and sports or recreational activities.^[2]^[6] Risk factors encompass age extremes (children under 4 and adults over 65), male gender (with men nearly three times more likely to die from TBI than women), alcohol or substance use, and involvement in high-risk occupations or sports.^[2]^[7] Symptoms vary widely depending on the injury's severity and location but commonly include physical effects like headache, nausea, dizziness, seizures, or loss of consciousness; cognitive issues such as confusion, memory loss, or difficulty concentrating; and sensory or emotional changes like blurred vision, irritability, or mood swings.^[7] In children, signs may manifest as increased crying, refusal to eat, or altered sleep patterns.^[7] Complications can include brain swelling, bleeding, infections, long-term cognitive impairments, or degenerative conditions like Alzheimer's disease.^[7] Diagnosis typically involves a physical and neurological examination, imaging such as CT scans or MRIs, and sometimes neuropsychological testing to assess brain function.^[2] Treatment ranges from rest, pain management, and monitoring for mild cases to emergency surgery, medications to reduce swelling, and extensive rehabilitation for severe TBIs.^[8] Prognosis depends on injury severity, with many mild cases recovering fully within weeks, while severe injuries may lead to permanent disability or death; prevention through helmets, seatbelts, fall-proofing environments, and avoiding risky behaviors is essential to mitigate risks.^[2]^[8]

Overview

Definition and scope

A head injury refers to any trauma to the scalp, skull, or brain, encompassing both closed injuries, where the skin remains intact, and open (penetrating) injuries, where there is a breach in the scalp or skull. This definition highlights the potential involvement of multiple anatomical structures beyond the brain itself, distinguishing head injury as a broader category than traumatic brain injury (TBI).^[9] While TBI specifically denotes damage to the brain parenchyma resulting from an external force, such as a bump, blow, or jolt to the head that disrupts normal brain function, head injury includes extracranial elements like scalp lacerations or skull fractures without necessarily affecting brain tissue.^[10]^[2] Thus, all TBIs are head injuries, but not all head injuries qualify as TBIs.^[9] The scope of head injuries ranges from mild cases, such as superficial scalp lacerations or minor contusions, to severe instances involving life-threatening intracranial hemorrhages or widespread brain damage.^[11] This spectrum underscores the condition's variability in presentation and potential outcomes, affecting individuals across all ages and demographics.^[12] Relevant head anatomy includes the scalp, a multilayered soft tissue structure covering the cranium, consisting of skin, dense connective tissue, aponeurosis, loose areolar tissue, and pericranium.^[13] Beneath lies the skull, or cranium, formed by 22 bones that protect the brain, divided into the neurocranium (enclosing the brain) and viscerocranium (forming the facial skeleton).^[14] The meninges—three protective membranes (dura mater, arachnoid mater, and pia mater)—encase the brain, providing cushioning and containing cerebrospinal fluid, while the brain itself comprises delicate neural tissue vulnerable to mechanical disruption.^[15]^[16]

Global impact

Traumatic brain injury (TBI), a primary consequence of head injuries, results in approximately 20.8 million incident cases globally each year, with prevalence reaching 37.9 million cases as of 2021, representing a major public health challenge.^[17] According to the Global Burden of Disease Study 2021, these figures highlight a significant burden, particularly in low- and middle-income countries where incidence and mortality rates are higher.^[18] Mortality from TBI is significant, contributing to 30–40% of all injury-related deaths globally, though exact annual figures vary; in the United States alone, over 69,000 TBI-related deaths occurred in 2021.^[4] The economic burden of head injuries, particularly TBIs, is substantial, encompassing direct medical costs, rehabilitation, and indirect losses from reduced productivity and long-term care. Globally, the annual economic cost of TBI is estimated at around US$400 billion as of 2017.^[19] In the United States, the lifetime economic impact of TBI, including medical expenses and lost productivity, totals approximately $76.5 billion annually as of 2010.^[20] Head injuries rank as a leading cause of death and disability worldwide, especially among children, adolescents, and young adults, where TBI accounts for a significant portion of years lived with disability.^[21] This burden is particularly pronounced in vulnerable age groups, contributing to long-term neurological impairments, cognitive deficits, and reduced quality of life.^[22] Recent trends indicate fluctuations in head injury incidence post-2020, influenced by the COVID-19 pandemic's initial reductions in traffic-related incidents due to lockdowns, followed by rebounds in motor vehicle accidents and increases in falls among aging populations.^[19] Sports-related head injuries have also risen with the resumption of activities, exacerbating the overall global burden.^[23]

Classification

By severity

Head injuries are classified by severity primarily using the Glasgow Coma Scale (GCS), a standardized tool that evaluates a patient's level of consciousness through three components: eye opening (scored 1-4), verbal response (scored 1-5), and motor response (scored 1-6), yielding a total score ranging from 3 to 15.^[24]^[25] Mild head injuries are defined by a GCS score of 13-15, moderate by 9-12, and severe by 3-8, with lower scores indicating greater impairment in responsiveness.^[11]^[26] The eye opening component assesses spontaneous opening (4 points), response to verbal stimuli (3 points), response to pain (2 points), or no response (1 point). Verbal response evaluates orientation (5 points), confused conversation (4 points), inappropriate words (3 points), incomprehensible sounds (2 points), or no response (1 point). Motor response measures obeys commands (6 points), localizes pain (5 points), withdraws from pain (4 points), flexes abnormally (3 points), extends abnormally (2 points), or no response (1 point).^[27]^[28] Severity is further indicated by the duration of unconsciousness (loss of consciousness, or LOC) and post-traumatic amnesia (PTA), the period following injury during which new memories cannot be formed. For mild injuries, LOC typically lasts less than 30 minutes and PTA less than 24 hours; moderate injuries involve LOC from 30 minutes to 24 hours and PTA from 1 to 7 days; severe injuries feature LOC exceeding 24 hours and PTA longer than 7 days.^[11] Clinically, mild head injuries often resolve quickly with conservative management such as rest and monitoring, while moderate cases may require hospitalization for observation, and severe cases necessitate intensive care unit admission, mechanical ventilation, and multidisciplinary intervention to address life-threatening complications.^[11]^[29] Despite its widespread use, the GCS has limitations, including subjectivity in scoring due to inter-rater variability and the influence of factors like intoxication or sedation, necessitating integration with neuroimaging such as CT scans for a comprehensive assessment.^[30]^[31]

By type

Head injuries are broadly classified into closed and open (penetrating) types based on whether the skull and dura mater remain intact. A closed head injury occurs without violation of the skull or the dura mater, typically resulting from blunt force that causes the brain to move within the skull, leading to examples such as coup-contrecoup injuries where damage happens both at the impact site (coup) and the opposite side (contrecoup) due to rebound against the skull.^[11]^[32] In contrast, an open or penetrating head injury involves breach of the skull and dura by an external object, such as a bullet or shrapnel, allowing direct intrusion into brain tissue and increasing infection risk.^[11]^[2] Specific types of head injuries include concussion, which represents a functional disruption of brain activity without detectable structural damage, often manifesting as transient alterations in mental status following a blow to the head.^[11]^[33] Intracranial hemorrhages, accumulations of blood within the cranial cavity, vary by location: epidural hematomas collect between the skull and dura mater, usually from arterial rupture associated with skull fractures; subdural hematomas form between the dura and arachnoid mater, commonly from venous tears in bridging veins; and subarachnoid hemorrhages involve bleeding into the space surrounding the brain, often traumatic in origin from vessel disruption.^[11]^[34] Cerebral contusion refers to localized bruising of brain tissue, typically with associated edema and hemorrhage at the site of impact or opposite side.^[11]^[35] Diffuse axonal injury involves widespread shearing of white matter tracts due to rotational forces, leading to microscopic damage across the brain without large focal lesions.^[11]^[36] Skull fractures, breaks in the cranial bone, are categorized as linear (simple cracks without displacement, the most common type), depressed (inward displacement of bone fragments potentially compressing brain tissue), or basilar (involving the skull base, often with cerebrospinal fluid leakage).^[11]^[37]^[38] Compound injuries combine multiple elements, such as a scalp laceration overlying a skull fracture that extends to underlying brain damage, classifying the fracture as open and elevating risks of contamination and infection.^[11]^[39] Emerging recognition includes chronic traumatic encephalopathy (CTE), a neurodegenerative condition arising from repetitive mild head injuries, such as those in contact sports, characterized by tau protein accumulation in the brain. As of 2025, CTE diagnosis remains postmortem via neuropathological examination, but advances in in-vivo criteria for traumatic encephalopathy syndrome (TES)—including behavioral, cognitive, mixed, and dementia variants—continue to evolve through NIH-funded research to enable antemortem identification using biomarkers and imaging.^[40]^[41]^[42]

Pathophysiology

Primary injury mechanisms

Primary injury mechanisms in head trauma refer to the immediate physical damage inflicted on brain tissue at the moment of impact, resulting from biomechanical forces that disrupt the structural integrity of the skull, meninges, and parenchyma. These mechanisms are distinct from subsequent biochemical cascades and encompass direct mechanical insults that initiate tissue deformation and disruption. Understanding these processes is crucial for injury prevention and modeling, as they determine the initial extent of damage in traumatic brain injury (TBI).^[43] The primary forces involved include linear acceleration and deceleration, rotational acceleration, and penetrating trauma. Linear forces occur when the head undergoes rapid forward or backward motion, causing the brain to shift relative to the skull due to inertial effects; this is common in vehicular collisions or falls. Rotational forces, arising from angular accelerations such as those in rotational impacts or blasts, generate shear strains throughout the brain, particularly at interfaces between gray and white matter. Penetrating trauma involves direct intrusion by foreign objects, like bullets or fragments, breaching the skull and lacerating underlying tissue.^[43]^[44]^[45] Biomechanically, these forces lead to skull deformation and brain displacement within the rigid cranial vault. Upon impact, the skull may flex or fracture, transmitting compressive waves inward, while the brain's softer consistency allows it to lag behind or rebound, creating pressure gradients. A classic example is the coup-contrecoup dynamic, where the brain impacts the skull at the coup site (directly under the blow) and then rebounds to strike the opposite contrecoup site, resulting in contusions at both locations due to focal compression and tension. This shifting exacerbates injury through relative motion between the brain and skull, amplified by cerebrospinal fluid dynamics.^[43]^[32]^[46] At the tissue level, these biomechanics produce shearing, compression, and cavitation. Shearing strains stretch and tear axons and blood vessels, particularly in white matter tracts, leading to diffuse axonal injury (DAI) from rotational forces that impose differential velocities across tissue layers. Compression deforms neurons and glia under high pressure, causing localized necrosis in contusions from focal impacts. Cavitation arises in fluid-filled regions or under blast-like conditions, where negative pressures form vapor bubbles that collapse and rupture nearby cells.^[47] These effects are scale-dependent, with higher strain rates increasing damage severity, as strains exceeding 10-15% often correlate with axonal disruption.^[48]^[49]^[44]^[50]

Secondary injury processes

Secondary injury processes in head injury refer to the delayed pathophysiological cascades that follow the initial mechanical trauma, amplifying neuronal damage and contributing to long-term neurological deficits. These processes begin shortly after the primary injury and involve a complex interplay of biochemical and cellular events that propagate harm throughout the brain. Unlike the immediate structural damage from impact, secondary injuries are potentially modifiable through timely intervention, though they remain a major determinant of outcome in traumatic brain injury (TBI). The key secondary injury processes include excitotoxicity driven by a surge in glutamate release, cerebral ischemia, inflammation, cerebral edema, and disruption of the blood-brain barrier (BBB). Excitotoxicity occurs when excessive glutamate activates N-methyl-D-aspartate (NMDA) receptors, leading to calcium influx and neuronal death; this process initiates within minutes of injury and can persist for hours. Cerebral ischemia arises from vascular compression or hypoperfusion, reducing oxygen delivery and exacerbating energy failure in brain tissue. Inflammation involves the activation of microglia and astrocytes, releasing pro-inflammatory cytokines such as interleukin-1β and tumor necrosis factor-α, which further recruit peripheral immune cells and amplify tissue damage. Cerebral edema, manifesting as cytotoxic (intracellular swelling) or vasogenic (extracellular fluid accumulation) types, increases intracranial pressure and compromises cerebral perfusion. BBB disruption allows plasma proteins and immune cells to infiltrate the brain parenchyma, promoting edema and oxidative stress. These processes unfold over a timeline starting within minutes to hours post-injury, with many peaking in the first 24–72 hours, though some effects like inflammation can extend into weeks. For instance, glutamate-mediated excitotoxicity and ischemia onset rapidly due to membrane depolarization and blood flow dysregulation immediately following trauma. Inflammation and BBB breakdown intensify over hours to days, driven by initial ischemic signals, while edema can evolve dynamically, often requiring monitoring in acute care settings. At the cellular level, secondary injuries trigger apoptosis, oxidative stress, and mitochondrial dysfunction. Apoptosis, or programmed cell death, is induced by caspase activation in response to excitotoxic calcium overload and inflammatory signals, affecting neurons and glia alike. Oxidative stress results from reactive oxygen species (ROS) generation, overwhelming antioxidant defenses and damaging lipids, proteins, and DNA in vulnerable brain regions. Mitochondrial dysfunction impairs ATP production, further fueling calcium dysregulation and necrotic cell death pathways. Recent research as of 2025 highlights the pivotal role of neuroinflammation in linking acute secondary injuries to chronic outcomes, such as neurodegeneration in conditions like chronic traumatic encephalopathy (CTE). Sustained microglial activation and cytokine release post-TBI promote tau pathology and amyloid-beta accumulation, contributing to long-term cognitive decline; studies using advanced neuroimaging and biomarkers have underscored this progression in both animal models and human cohorts.^[51]

Causes and Risk Factors

Common mechanisms

Head injuries, particularly traumatic brain injuries (TBIs), arise from a variety of external events that impart mechanical forces to the head. The most prevalent mechanisms include falls, motor vehicle accidents, firearm-related injuries (including suicides and assaults), assaults, sports-related impacts, and blast exposures in military settings. These events often result in direct or indirect forces such as acceleration, deceleration, or penetration, leading to primary brain tissue disruption.^[4] Falls represent the leading cause of nonfatal TBIs, accounting for nearly half (about 50%) of TBI-related hospitalizations across all ages in the United States as of 2021. In adults aged 65 years and older, falls are even more dominant, contributing to nearly half (49%) of TBI-related hospitalizations. This mechanism is particularly associated with environmental hazards like slippery surfaces or uneven terrain, often exacerbated by age-related balance issues.^[52]^[4] Motor vehicle accidents, including crashes involving cars, motorcycles, and pedestrians, account for about 17% of nonfatal TBIs and a significant portion of TBI-related deaths, though not the primary cause overall. These incidents typically involve high-speed collisions that generate rapid head accelerations, resulting in diffuse axonal injuries. Firearm-related injuries are the primary cause of TBI-related deaths as of 2021, accounting for around 35%, often through suicides or assaults.^[53]^[4]^[12] Assaults and being struck by or against an object contribute to roughly 16-21% of nonfatal TBIs, often through blunt force trauma from weapons, fists, or falling objects. Sports impacts, such as those in contact sports like football or boxing, form a subset of these strikes, leading to concussions in up to 21% of TBIs among children and adolescents. In military contexts, blast exposures from improvised explosive devices have been a significant mechanism, with studies indicating that up to 70% of screened service members in certain conflicts sustained blast-related mild TBIs between 2006 and 2011.^[53]^[53]^[54] Alcohol intoxication is a key environmental factor implicated in 30-50% of TBI cases presenting for treatment, often impairing judgment and coordination to heighten the risk during falls or assaults. Emerging trends post-2020, driven by increased urban mobility during the COVID-19 pandemic, have seen a surge in e-bike accidents, with head trauma incidence rising approximately 49-fold from 2017 to 2022 in the United States. This reflects broader growth in micromobility, where collisions with vehicles or infrastructure frequently cause unprotected head impacts.^[55]^[56]

Vulnerable populations

Certain age groups exhibit heightened vulnerability to head injuries due to developmental, behavioral, and physiological factors. Infants and young children under the age of four are particularly susceptible, with falls being a leading cause alongside abusive head trauma, which often involves shaking or direct impact.^[57] The thinner, more pliable skulls in infants increase the risk of fractures and underlying brain damage from even minor forces.^[58] Adolescents and young adults, especially those aged 15 to 19, face elevated risks from participation in contact sports such as football and from interpersonal violence, including assaults.^[59] These activities expose them to high-impact collisions or blows that can result in concussions or more severe traumatic brain injuries.^[60] Older adults aged 65 and above, with those 75 and older showing the highest hospitalization and mortality rates, are prone to head injuries primarily from falls linked to frailty, reduced balance, and comorbidities.^[61] Frailty exacerbates the impact of ground-level falls, often leading to intracranial injuries, while widespread use of anticoagulants or antiplatelet medications in this population increases the risk of hemorrhagic complications following blunt head trauma.^[62]^[63] Beyond age-related vulnerabilities, specific occupational and recreational groups are at greater risk. Athletes in contact sports endure repeated head impacts, elevating the likelihood of cumulative brain injury over time.^[64] Military personnel experience heightened exposure through combat, training blasts, and explosive devices, which can cause mild to severe traumatic brain injuries via direct or pressure wave mechanisms.^[65] Workers in high-risk occupations like construction face dangers from falls, struck-by incidents, and unstable environments, making head protection essential.^[66]^[67] Socioeconomic disparities further amplify head injury risks, with higher incidence in low-income communities due to inadequate road safety infrastructure, such as poor lighting, unpaved roads, and limited vehicle safety features.^[61] Globally, low- and middle-income countries bear over 90% of road traffic fatalities and injuries, perpetuating inequities as of 2025, where financing shortfalls hinder safety improvements.^[68]^[69]

Signs and Symptoms

In adults

Head injuries in adults often present with a range of immediate signs that can indicate the initial impact on brain function. Loss of consciousness, which may last from seconds to several minutes or longer depending on injury severity, is a frequent early indicator of traumatic brain injury (TBI).^[7] Headaches, typically developing shortly after the injury, are reported in the majority of cases and can vary from mild to severe throbbing pain.^[70] Nausea and vomiting frequently accompany these symptoms, particularly in the acute phase, and may signal increased intracranial pressure.^[71] Seizures can also occur immediately post-injury, manifesting as convulsions or twitching, and affect approximately 10-20% of severe TBI patients in the first week.^[72] Neurological symptoms in adults with head injuries often reflect disruption to cognitive and motor processes. Confusion or disorientation is common, with patients exhibiting difficulty maintaining attention or following conversations shortly after the event.^[2] Amnesia, including retrograde loss of memory for events before the injury or anterograde impairment for new information, is a hallmark of moderate to severe cases.^[7] Focal neurological deficits, such as weakness or paralysis in limbs due to contusions or localized bleeding, may develop and indicate damage to specific brain regions.^[11] Systemic effects from head injuries can involve autonomic responses as the body compensates for brain insult. Changes in vital signs, including the Cushing's triad of hypertension, bradycardia, and irregular respirations, signal rising intracranial pressure and potential brainstem compression.^[73] These alterations underscore the need for prompt monitoring in acute settings. Red flags in adult head injury presentations include worsening symptoms that suggest progression to life-threatening complications like herniation. Persistent or intensifying headache, repeated vomiting, or deteriorating level of consciousness warrant immediate intervention, as they may herald expanding hematomas or swelling.^[7] Additional indicators include unequal pupil sizes, severe focal weakness, or abnormal posturing, which correlate with elevated mortality risk if untreated.^[74]

In children and special populations

In children, head injuries often present with symptoms that differ from those in adults due to developmental limitations in communication and physiological responses. Young children may exhibit irritability, excessive crying, or crankiness rather than verbalizing headaches, making behavioral changes a key indicator. Vomiting, particularly persistent or projectile, can occur without a reported headache and signals potential intracranial pressure elevation. In infants, a bulging fontanelle is a critical sign of increased intracranial pressure from head trauma, often accompanied by lethargy or poor feeding. These manifestations pose diagnostic challenges, as children under 2 years may not localize pain or describe symptoms clearly, necessitating reliance on caregiver observations and physical exams.^[75]^[72]^[76]^[57] A subset of pediatric head injuries involves non-accidental trauma, such as abusive head trauma (AHT), formerly known as shaken baby syndrome, which is particularly prevalent in infants under 1 year. Indicators include retinal hemorrhages, subdural hematomas, and encephalopathy, often forming the classic triad suggestive of violent shaking or impact. Additional signs encompass seizures, apnea, macrocephaly, and tense anterior fontanelle, with 2025 studies emphasizing the specificity of high-grade retinal hemorrhages (grades 3A and 3B) for AHT diagnosis. Infants' anatomical vulnerabilities, including a large head-to-body ratio and weak neck muscles, heighten susceptibility, and early recognition is vital as abuse accounting for approximately 17% of brain injuries in children younger than 1 year, and up to 56% of serious cases.^[77] Diagnostic hurdles arise from overlapping accidental trauma presentations, but inconsistencies in injury history or multiple healing-stage fractures warrant child protection evaluation.^[78]^[57]^[79] In the elderly, head injury symptoms can be subtler and confounded by comorbidities, complicating timely diagnosis. Altered gait or unsteadiness may emerge as a primary manifestation, reflecting balance disruptions from even mild traumatic brain injury (TBI), alongside a history of recent falls as the leading mechanism. Cognitive changes like mild confusion or slowed responses might mimic age-related decline rather than acute injury. Elderly patients face a higher bleeding risk post-injury, particularly with subdural or intracerebral hemorrhages, exacerbated by anticoagulant use prevalent in this population—up to 80% of mild TBIs in older adults stem from falls, with anticoagulation doubling hemorrhage odds. These factors demand vigilant screening, as subtle signs can delay intervention and worsen outcomes.^[80]^[81]^[82] Among special populations, pregnant women with head injuries require consideration of fetal risks alongside maternal symptoms. Trauma can lead to placental abruption or direct fetal brain injury, elevating stillbirth risk by over 2.5-fold and preterm birth or low birth weight probabilities. Symptoms in the mother, such as headache or altered mental status, may parallel adult presentations but necessitate fetal monitoring, as even mild injuries threaten viability through hypoperfusion or direct impact. In intoxicated individuals, head injury symptoms are frequently masked by substance effects, with agitation, confusion, or lethargy attributable to alcohol or drugs rather than TBI. This overlap challenges assessment, as intoxication is a strong TBI predictor and affects up to 30% of trauma cases; routine head CT is often required to detect occult injuries despite normal vital signs. Serial evaluations post-sobriety are essential to unmask evolving neurological deficits.^[83]^[84]^[85]^[86]

Diagnosis

Clinical assessment

The clinical assessment of head injury begins with a systematic evaluation to determine the extent of injury and guide immediate care priorities. This involves obtaining a detailed history and performing a focused physical examination, often within the framework of advanced trauma life support protocols. The goal is to identify signs of neurological impairment, potential intracranial pathology, and associated injuries while stabilizing the patient.^[87] History taking is essential for contextualizing the injury and assessing severity. Clinicians inquire about the mechanism of injury, such as falls from height, motor vehicle collisions, or assaults, as high-energy mechanisms increase the risk of significant brain trauma. Duration of loss of consciousness (LOC) is documented precisely, with even brief LOC indicating potential concussion or more severe injury; amnesia, either retrograde (events before the injury) or anterograde (inability to form new memories post-injury), further suggests diffuse axonal injury or contusion. In cases where the patient cannot provide details, witnesses or emergency responders supply this information. Patients may present with symptoms like headache or vomiting, but the history prioritizes quantifiable elements like LOC to stratify risk.^[87]^[87]^[87] The physical examination focuses on neurological status and vital signs. The Glasgow Coma Scale (GCS) is the cornerstone for quantifying level of consciousness and classifying injury severity, originally developed to assess coma in brain-injured patients. It evaluates three components: eye opening (spontaneous: 4; to voice: 3; to pain: 2; none: 1), verbal response (oriented: 5; confused: 4; inappropriate words: 3; incomprehensible sounds: 2; none: 1), and motor response (obeys commands: 6; localizes pain: 5; withdraws from pain: 4; flexes to pain: 3; extends to pain: 2; none: 1), yielding a total score from 3 (deep coma) to 15 (fully alert). Scores are recorded as E-V-M (e.g., E3 V4 M5 = 12/15) and reassessed serially; mild injuries score 13-15, moderate 9-12, and severe ≤8. Adjustments are made for intubated patients (verbal score not applicable) or baseline deficits like aphasia. Pupil response is checked for size, equality, and reactivity to light, as fixed or dilated pupils may indicate herniation or third nerve compression. Motor and sensory checks involve testing limb strength, sensation, and reflexes to detect focal deficits suggestive of hematoma or contusion.^[88]^[88] Associated assessments integrate head injury evaluation with broader trauma care. The ABCs—airway maintenance with cervical spine protection, breathing adequacy, and circulation stability—are prioritized per Advanced Trauma Life Support (ATLS) guidelines to address life-threatening issues before detailed neurological exam. Cervical spine evaluation is mandatory in head-injured patients due to the high association with spinal injuries; immobilization is applied if GCS <15, focal neurology, or high-risk mechanisms are present, with further assessment for tenderness or deformity.^[89]^[87]^[87] For mild head injuries (GCS 13-15), triage tools like the Canadian CT Head Rule aid in identifying patients needing further evaluation. Developed for adults with minor trauma, it recommends head CT for high-risk factors (e.g., GCS <15 at 2 hours, suspected skull fracture, seizure) or medium-risk factors (e.g., amnesia >30 minutes, vomiting >2 episodes, age ≥65 years), reducing unnecessary imaging while detecting clinically important brain injuries with high sensitivity (nearly 100%). This rule applies only after initial stabilization and is not used in severe cases or children under 16.^[90]

Imaging and tests

Computed tomography (CT) scanning is the primary imaging modality for acute head injury evaluation, serving as the gold standard for detecting intracranial hemorrhages, fractures, and other immediate life-threatening abnormalities due to its speed, availability, and sensitivity to acute changes.^[91]^[92] Non-contrast CT is typically the initial study in emergency settings, allowing rapid identification of epidural or subdural hematomas, contusions, and skull fractures that require urgent intervention.^[93] Magnetic resonance imaging (MRI) complements CT in cases of suspected diffuse axonal injury (DAI), where it excels at visualizing shearing injuries to white matter tracts that may appear normal on CT.^[44] MRI sequences such as gradient-echo and diffusion tensor imaging are particularly useful for identifying microhemorrhages and axonal disruption in moderate to severe traumatic brain injury, aiding in prognosis when clinical findings suggest persistent neurological deficits.^[94]^[95] Advanced functional imaging techniques, including single-photon emission computed tomography (SPECT) and positron emission tomography (PET), assess cerebral perfusion and metabolism in traumatic brain injury, revealing hypoperfusion or hypometabolism in areas not evident on structural imaging.^[96] SPECT is valuable for detecting regional blood flow deficits in mild traumatic brain injury cases with normal CT and MRI, while PET provides quantitative data on glucose utilization, supporting differential diagnosis from conditions like post-traumatic stress disorder.^[97]^[98] Electroencephalography (EEG) is employed to evaluate for post-traumatic seizures, which occur in approximately 10-25% of severe head injury patients, often subclinical and detectable only through continuous monitoring.^[99] Continuous EEG is recommended in comatose patients with traumatic brain injury to identify non-convulsive seizures that exacerbate secondary injury, guiding anticonvulsant therapy.^[100] Laboratory tests play a supportive role in head injury diagnosis, with coagulation studies such as prothrombin time (PT), international normalized ratio (INR), and activated partial thromboplastin time (aPTT) essential for identifying trauma-induced coagulopathy, which affects approximately 35% of severe cases and increases hemorrhage risk.^[101] Toxicology screening, including blood alcohol levels and urine drug panels, is routinely performed to detect intoxicants that may mimic or complicate injury symptoms, influencing management decisions in acute settings.^[102] Blood-based biomarkers, such as glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase L1 (UCH-L1), are increasingly used in mild traumatic brain injury to predict the need for CT imaging, with FDA-approved tests showing high sensitivity (over 97%) for detecting intracranial lesions and helping reduce unnecessary scans as of 2025.^[103] As of 2025, artificial intelligence (AI) tools integrated with CT interpretation have emerged to accelerate bleed detection, with commercially available systems like qER.ai demonstrating a sensitivity of approximately 89% for post-traumatic intracranial hemorrhage in real-world emergency department use.^[104] These AI decision support systems prioritize abnormal scans for urgent review, improving workflow efficiency without replacing human oversight.

Management

Acute care

For mild head injuries (Glasgow Coma Scale [GCS] score 13-15, the majority of cases) and non-traumatic brain injury (TBI) head trauma, management focuses on observation, rest, over-the-counter pain relief (e.g., acetaminophen), and monitoring for deterioration such as worsening headache or vomiting; scalp lacerations require cleaning and suturing if needed, while isolated non-depressed skull fractures without neurological deficit are typically managed conservatively with follow-up imaging only if symptoms develop.^[8]^[4] Acute care for head injuries, particularly severe traumatic brain injuries (TBI) defined by a Glasgow Coma Scale (GCS) score of 3-8, begins with immediate stabilization to prevent secondary brain injury from hypoxia, hypotension, or elevated intracranial pressure (ICP). Initial management follows the ABCDE approach, prioritizing airway protection through early endotracheal intubation for patients with GCS <9, severe agitation, or loss of protective reflexes to ensure adequate oxygenation (PaO2 80-100 mm Hg) and ventilation (PaCO2 35-45 mm Hg).^[105] Circulation is maintained by targeting age-specific systolic blood pressure (SBP) thresholds—≥110 mm Hg for ages 15–49 or >70 years, or ≥100 mm Hg for ages 50–69 years—or mean arterial pressure (MAP) >80 mm Hg to support cerebral perfusion pressure (CPP) of at least 60 mm Hg, avoiding hypotension (SBP <90 mm Hg) which doubles mortality risk.^[106]^[105] ICP monitoring is recommended for comatose patients (GCS ≤8) with abnormal CT findings or risk factors such as age >40 years or abnormal posturing, using an external ventricular drain (EVD) as the gold standard to target ICP <22 mm Hg (20-25 mm Hg range acceptable).^[106]^[105] Continuous cerebrospinal fluid (CSF) drainage via EVD, zeroed at the midbrain level, is preferred over intermittent drainage to more effectively reduce ICP burden, particularly in the first 12 hours post-injury for GCS <6.^[106] Hyperventilation is reserved as a temporizing measure for cerebral herniation or refractory ICP, with mild hypocapnia (PaCO2 32-35 mm Hg) as a Tier II intervention and profound hyperventilation (PaCO2 <30 mm Hg) only briefly to avoid ischemia; prophylactic prolonged hyperventilation (PaCO2 ≤25 mm Hg) is not recommended due to risks of reduced cerebral blood flow.^[106]^[105] Surgical interventions are indicated based on diagnostic imaging such as CT scans revealing mass lesions or refractory ICP. Craniotomy for hematoma evacuation is performed for expanding lesions, such as epidural hematomas greater than 30 cm³ (regardless of GCS) or acute subdural hematomas with thickness greater than 10 mm or midline shift greater than 5 mm, ideally within 4 hours to prevent deterioration, using a large frontotemporoparietal approach.^[105]^[107] Decompressive craniectomy (DC) is a Tier III option for ICP >25 mm Hg unresponsive to medical therapies, with large frontotemporoparietal DC (>12x15 cm) recommended over smaller or bifrontal approaches for diffuse injury to reduce mortality, as supported by the RESCUEicp trial showing 21 additional survivors per 100 patients despite higher rates of vegetative states.^[106]^[105]^[108] Pharmacological management targets seizure prevention and ICP control. Anticonvulsants such as phenytoin or levetiracetam are administered prophylactically for 7 days post-injury in high-risk patients to reduce early posttraumatic seizures (<7 days), but not extended beyond to prevent late seizures, with no difference in efficacy between agents.^[106]^[105] For cerebral edema, osmotherapy with mannitol (0.25-1 g/kg bolus, osmolality ≤320 mOsm) is a first-line Tier I intervention when ICP is elevated and SBP >90 mm Hg, while hypertonic saline boluses (sodium ≤155 mEq/L) serve as an alternative, both more effective than placebo in lowering ICP.^[106]^[105] High-dose corticosteroids are contraindicated due to increased mortality.^[106] These interventions are guided by evidence-based protocols from the Brain Trauma Foundation (BTF) 4th Edition guidelines (2016, with 2020 DC update) and the American College of Surgeons (ACS) revised best practices (2024), which incorporate tiered ICP management via the SIBICC algorithm to tailor therapies by injury severity and emphasize multidisciplinary evaluation within 30 minutes for severe cases.^[106]^[105]^[109]

Rehabilitation and long-term support

Rehabilitation following a head injury, particularly traumatic brain injury (TBI), typically involves a multidisciplinary approach that integrates various therapeutic modalities to address physical, cognitive, and emotional impairments after the acute phase.^[110] This coordinated care, delivered by teams including physiatrists, neurologists, neuropsychologists, physical therapists, occupational therapists, speech-language pathologists, and social workers, aims to maximize functional recovery and community reintegration through interdisciplinary case conferences and shared health records.^[111] Physical therapy focuses on improving motor skills, balance, and mobility via targeted exercises such as gait training, which has been shown to enhance overall independence in daily activities.^[111] Occupational therapy supports adaptation to everyday tasks and work-related skills, contributing to higher rates of successful job retention post-injury.^[111] Speech therapy targets communication deficits, reducing social isolation by improving verbal and non-verbal expression.^[111] Cognitive and behavioral interventions form a core component of rehabilitation, employing both restorative techniques—like attention training programs—and compensatory strategies, such as external memory aids, to mitigate executive function and memory impairments.^[111] These interventions, often grounded in neuroplasticity principles, have demonstrated moderate effect sizes in improving cognitive outcomes, with gains in executive function measured at Hedges’ g = 0.48.^[111] Programs may include cognitive behavioral therapy adapted for TBI to address maladaptive thought patterns arising from injury-related changes.^[112] Long-term support extends beyond initial recovery to foster sustained independence, encompassing vocational retraining programs that facilitate return to work or education through skills assessment and job coaching.^[113] Early specialist vocational rehabilitation has been associated with improved employment outcomes, particularly for moderate to severe TBI cases.^[113] Psychological care is integral, targeting common comorbidities like post-traumatic stress disorder (PTSD) and depression, which affect up to 30-50% of survivors; interventions such as trauma-focused cognitive behavioral therapy help alleviate these symptoms and enhance quality of life.^[114] Community-based initiatives, including support groups and family education, further promote social participation and emotional resilience.^[110] Assistive devices play a key role in ongoing management, with mobile applications serving as memory aids to compensate for prospective memory deficits by providing reminders and task organization.^[115] These smartphone-based tools have shown feasibility in supporting cognitive independence, as evidenced in pilot studies where users reported reduced reliance on human cues for daily routines.^[116] By 2025, integration of tele-rehabilitation has expanded access to care, delivering remote therapy sessions that yield short-term improvements in functional independence and reduced anxiety, with effect sizes around 0.85.^[111] Neurofeedback technology, utilizing EEG-based training to enhance brain activity regulation, has emerged as a promising adjunct, leading to notable gains in attention and executive function over extended periods in severe TBI cases.^[111] These innovations, including brain-computer interfaces, support personalized, home-based recovery while bridging gaps in traditional service delivery.^[117]

Prognosis and Complications

Outcomes by severity

Head injuries are classified into mild, moderate, and severe categories primarily using the Glasgow Coma Scale (GCS), with mild corresponding to GCS 13-15, moderate to 9-12, and severe to 3-8.^[11] For mild head injuries, which account for 70-90% of traumatic brain injury (TBI) cases, the majority of individuals achieve full recovery within weeks to months. Specifically, over 70% of cases, particularly those related to sports or minor trauma, resolve symptoms like headache and dizziness within 2 weeks, with most achieving complete recovery by 4 weeks. However, 10-20% experience persistent post-concussive symptoms, such as cognitive or emotional difficulties, lasting beyond 3 months.^[11]^[118]^[119] In moderate head injuries, outcomes are more variable, with approximately 60-75% of patients attaining a good functional recovery at 12 months post-injury, defined as independence in daily activities. Despite this, there is a heightened risk of long-term disability, including cognitive impairments or motor deficits, affecting up to 40% of survivors and necessitating ongoing rehabilitation. Socioeconomic and racial disparities also influence outcomes, with underserved populations facing higher risks of long-term disability due to limited rehabilitation access, as of 2025.^[120]^[121]^[61] Severe head injuries carry the poorest prognosis, with mortality rates ranging from 30-50%, particularly among older adults and those with additional complications like hypotension. Among survivors, 50-70% experience significant impairments, such as persistent vegetative states or severe disabilities, limiting independence and quality of life.^[122]^[123]^[11] Several factors influence these outcomes across severities, including patient age—where older adults (typically over 65 years) face substantially worse recovery rates due to reduced neuroplasticity and comorbidities—and the timeliness of medical intervention. For instance, a GCS score below 8 at presentation is associated with a markedly elevated risk of poor outcomes, often doubling the likelihood compared to higher scores, underscoring the need for rapid airway management and intracranial pressure control.^[124]^[11]^[125]

Long-term effects

Head injuries, particularly traumatic brain injuries (TBI), can lead to persistent cognitive impairments that affect daily functioning long after the initial event. Memory loss is a common long-term consequence, often manifesting as difficulties in forming new memories or retrieving old ones, which can impair learning and independence.^[126] Executive dysfunction, including challenges with planning, decision-making, and impulse control, is also prevalent and tends to be more pronounced in moderate to severe cases, contributing to reduced problem-solving abilities.^[127] Among physical long-term effects, post-traumatic epilepsy represents a significant risk, with an estimated 10-20% of individuals experiencing seizures following severe TBI due to disrupted neural circuits.^[128] Chronic headaches, known as post-traumatic headaches, frequently persist for months or years, affecting 30–90% of survivors, particularly after mild TBI, and often resembling migraine patterns that exacerbate fatigue and sensitivity to stimuli.^[129] Psychosocial impacts extend beyond the physical, with depression occurring in nearly eight times more TBI survivors compared to the general population, driven by neurochemical changes and social isolation.^[130] This elevates suicide risk, as psychological disorders like depression post-TBI can increase the likelihood of suicidal ideation and attempts by several fold.^[131] In sports contexts, second-impact syndrome poses a rare but catastrophic psychosocial threat, where a subsequent head injury before full recovery from the first can lead to rapid brain swelling and high mortality, underscoring the need for extended recovery periods.^[75] Emerging research highlights chronic traumatic encephalopathy (CTE) as a delayed pathology from repetitive mild head injuries, characterized by tau protein accumulation and neurodegeneration, primarily in contact sports participants.^[51] As of 2025, biomarker studies have advanced detection, identifying early neuron loss and inflammation through blood and imaging markers in young athletes exposed to repeated impacts, enabling potential pre-symptomatic interventions.^[132]

Prevention

Strategies in daily life

Preventing head injuries in daily life involves adopting simple, evidence-based habits to mitigate common risks such as falls and traffic incidents. These strategies focus on personal actions that can significantly reduce the incidence of traumatic brain injuries without requiring specialized equipment or environments. Fall prevention is particularly crucial for older adults, who are at higher risk due to balance issues and environmental hazards. Home modifications, such as installing grab bars next to toilets and in bathtubs, can substantially lower fall risks by providing stable support during transfers. Non-slip mats in bathrooms and improved lighting throughout the home further enhance safety by reducing slips and improving visibility. Balance exercises, including tai chi or simple marches while holding onto stable surfaces, strengthen lower body muscles and improve postural stability, thereby decreasing the likelihood of falls in everyday activities. These interventions have been shown to reduce injurious falls and enhance mobility in older populations.^[133]^[134]^[135]^[136] Road safety measures are essential for protecting against head trauma from vehicle-related collisions. Always wearing seatbelts keeps occupants secured within the vehicle during crashes, preventing ejection and reducing the severity of head injuries by up to 45% in fatal incidents. For cyclists, using helmets that meet U.S. Department of Transportation standards can decrease the risk of head and brain injuries by 63% to 88%. Similarly, motorcyclists should wear DOT-approved helmets, which are 67% effective in preventing brain injuries and contribute to a 22% to 42% reduction in overall fatalities.^[137]^[138]^[139]^[140] Alcohol awareness plays a key role in averting head injuries linked to impaired judgment and coordination. Avoiding driving under the influence is critical, as alcohol intoxication is a leading predictor of traumatic brain injuries from motor vehicle crashes and falls. Sobriety checkpoints and personal commitment to alternatives like rideshares or designated drivers can prevent these incidents, with broader enforcement helping to reduce alcohol-related injuries.^[85]^[141] Basic education on recognizing risks during children's play helps safeguard young ones from head injuries. Parents and caregivers should supervise play closely, ensuring playground equipment is installed over shock-absorbing surfaces like mulch to cushion falls. For children ages 4-8, using booster seats in vehicles reduces serious head injuries by 45% compared to seat belts alone. Teaching children to avoid high-risk behaviors, such as climbing unstable structures or playing near traffic, fosters safer habits from an early age.^[142]^[143]

Sports and occupational measures

In sports, concussion protocols play a central role in preventing head injuries by standardizing the evaluation and gradual return-to-play process for affected athletes. The National Football League (NFL) implements a five-phase return-to-participation protocol, updated annually to incorporate the latest medical consensus, which begins with symptom-limited activity and progresses to full-contact practice only after clearance by team physicians and an independent neurological consultant.^[144]^[145] This stepwise approach, emphasizing rest and monitored exertion, has contributed to a historic low in concussions during the 2024 NFL season, with rates declining by up to 43% in certain plays due to rule changes like slower player speeds.^[146] Protective gear further mitigates risks in contact sports, though no equipment is entirely concussion-proof. Helmets certified to standards like those from the National Operating Committee on Standards for Athletic Equipment (NOCSAE) reduce the incidence of severe skull fractures and provide protection against traumatic brain injuries in activities such as football, cycling, and snowboarding, particularly when properly fitted.^[147]^[148] Mouthguards and devices like the FDA-cleared Q-Collar, which applies jugular vein compression to minimize brain slosh during impacts, provide additional layers of protection in sports like soccer and American football, though their efficacy against concussions varies and requires ongoing research.^[149] In soccer, the Fédération Internationale de Football Association (FIFA) permits non-dangerous protective headgear under Law 4 of the game's rules, allowing padded options for players at risk of head contact, though mandates are absent and adoption remains voluntary.^[150]^[151] Occupational measures emphasize regulated protective equipment and training to safeguard workers in high-risk environments. In construction, the Occupational Safety and Health Administration (OSHA) mandates hard hats under 29 CFR 1926.100 for areas with potential overhead hazards, requiring compliance with ANSI/ISEA Z89.1 standards for Type I (top-impact) or Type II (lateral-impact) helmets to prevent cranial injuries from falling objects or electrical shocks.^[152] These standards classify helmets by voltage resistance (e.g., Class G for general low-voltage use), ensuring broad applicability across sites and reducing head injury rates through routine inspections and replacements for damaged gear.^[153] For military personnel exposed to blast overpressure, training protocols focus on monitoring cumulative exposure and using specialized gear to limit traumatic brain injury (TBI). The Department of Defense's Blast Overpressure Reference and Information Guide outlines requirements for baseline cognitive assessments and exposure limits during breaching and weapons training, incorporating advanced helmets and standoff distances to attenuate shock waves.^[154] Recent 2024 initiatives include mandatory health evaluations post-training and enhanced protective protocols, addressing the "invisible" nature of primary blast TBIs that affect over 77% of helmeted soldiers in combat scenarios.^[155]^[156] In emerging fields like e-sports involving virtual reality (VR), risks of head-related injuries stem from prolonged headset use, including neck strain, headaches, and potential falls leading to impacts. A 2025 study on VR posture interventions reported that improper head positioning during immersive gaming exacerbates cervical fatigue and dizziness, prompting mitigations such as ergonomic headset designs, mandatory 15-20 minute breaks every hour, and visual cues in software to encourage neutral posture.^[157] Multidisciplinary guidelines from organizations like the International Esports Federation recommend adjustable VR setups and pre-session health screenings to minimize these repetitive strain risks, particularly for professional gamers logging 8-12 hours daily.^[158]

Epidemiology

Incidence and prevalence

Traumatic brain injury (TBI) affects millions worldwide annually, with an estimated 20.8 million incident cases in 2021 (95% uncertainty interval: 18.1–23.8 million) across all causes and severities.^[159] This global incidence equates to an age-standardized rate of approximately 259 cases per 100,000 population (95% UI: 226–296), with the majority—over 80%—burdening low- and middle-income countries due to higher rates of road traffic injuries, falls, and violence.^[159] Incidence rates vary by region, with higher rates in many high-income areas (e.g., 479–522 per 100,000 in parts of Europe and Australasia as of 2021) compared to some low-income regions (e.g., 162–183 per 100,000 in sub-Saharan Africa), though the majority of cases occur in low- and middle-income countries due to population size.^[159] In the United States, TBI results in nearly 2.8 million emergency department visits, hospitalizations, and deaths combined each year, based on data from 2013-2014, with emergency department visits alone accounting for about 2.5 million of these cases.^[160] More recent estimates suggest the annual figure for emergency department visits remains in the range of 2.7 to 3 million, underscoring the persistent public health challenge.^[161] The distribution of TBI severity shows that mild cases predominate, comprising 80-90% of incidents, while moderate TBIs account for about 10-11%, and severe TBIs represent less than 10%.^[162] Demographically, incidence peaks among males aged 15-24 years, who experience higher rates due to risk-taking behaviors and accidents, and among the elderly over 75 years, often from falls.^[160] Overall, males face a 40% higher risk than females across adulthood.^[163]

Trends and disparities

Over the past three decades, the global incidence rate of traumatic brain injury (TBI), which encompasses most head injuries, has declined, largely attributable to enhanced prevention and management strategies, including safety legislation that reduced traffic-related cases.^[159] In the United States, emergency department visits for bicycle-related TBIs decreased by 27.7% from 2009 to 2018, reflecting the impact of helmet laws and infrastructure improvements.^[164] Conversely, sports-related concussions have risen sharply since 2010, with reported cases in youth increasing by 71% in rough-contact sports according to insurance claims data, driven by greater awareness, diagnosis, and participation in high-risk activities like football.^[165] High school athletes experienced a more than fourfold increase in reported concussion rates over a 10-year period ending around 2019.^[166] Disparities in head injury incidence and outcomes persist across geographic and demographic lines. Rural residents face a 28% higher likelihood of severe TBI compared to urban dwellers, with fatality rates 23% higher overall, due to factors like longer transport times to trauma centers and higher rates of motor vehicle crashes on rural roads.^[167]^[168] Racial and ethnic minorities also experience elevated burdens; for instance, non-Hispanic Black individuals had TBI-related mortality rates approximately 25% higher than non-Hispanic Whites (22.3 vs. 17.8 deaths per 100,000) based on 2014 national data, with persistent gaps noted in recent analyses across urban-rural divides.^[169] American Indian/Alaska Native populations bear the highest rates, at 31.5 deaths per 100,000 as of 2021.^[170] These inequities are compounded by socioeconomic barriers to timely care and higher exposure to risk factors like occupational hazards.^[61] The COVID-19 pandemic (2020-2022) influenced head injury patterns, with overall trauma volumes declining due to lockdowns, but a notable shift toward home-based incidents. The proportion of emergency department visits for head injuries increased by 20% (adjusted odds ratio 1.2), largely from falls in residential settings, as restricted mobility and altered daily routines elevated domestic accident risks, particularly among children and older adults.^[171] Falls accounted for up to 40% of TBI cases during this period in some cohorts, reflecting reduced traffic and sports exposures offset by isolation-related vulnerabilities.^[172] Looking ahead, an aging global population is projected to substantially elevate severe head injury cases, as falls—the leading cause in those over 65—account for 70% of elderly TBIs. The U.S. elderly population (aged 65+) is expected to more than double to 80 million by 2050, potentially driving a proportional surge in severe cases unless prevention intensifies, with similar trends anticipated worldwide due to demographic shifts.^[173]^[174] This rise underscores the need for targeted interventions in geriatric care to mitigate long-term public health impacts.^[175]

History

Early understanding

The earliest documented understandings of head injuries date back to ancient civilizations, where interventions focused on relieving pressure from skull fractures. Around 400 BCE, the Greek physician Hippocrates described trephination—a surgical procedure involving drilling or scraping a hole in the skull—as a treatment for various types of cranial fractures, including fissured, contused, and depressed (hedra) fractures, to prevent complications such as pus accumulation or infection of the meninges.^[176] He emphasized performing the procedure promptly, ideally within three days of injury, using specialized instruments like the terephus (a rectangular saw) or terebra (a drill), while advising against operating on certain fracture patterns to avoid further brain damage.^[177] During the medieval period (roughly 500–1500 CE), treatment of head injuries remained largely conservative due to high risks of infection and limited anatomical knowledge, with surgery restricted to rare cases of evident skull depression or penetrating wounds. Physicians like the Persian scholar Avicenna (Ibn Sina, 980–1037 CE) advocated non-invasive approaches, recommending herbal remedies to manage symptoms such as pain and swelling; for instance, topical applications of opium poppy (Papaver somniferum) extracts for analgesia and enemas prepared from hot-temperament herbs like colocynth (Citrullus colocynthis) pulp to reduce intracranial swelling.^[178] European surgeons, influenced by Arabic texts, occasionally performed limited trephination to elevate depressed bone fragments but prioritized wound cleaning, bandaging, and purgatives over aggressive intervention, reflecting the era's emphasis on humoral balance and avoidance of fatal complications. In the 18th century, English surgeon Percivall Pott advanced recognition of specific head injury pathologies in his 1760 treatise A Surgical Observation Relative to the Head, where he first described extradural (epidural) hemorrhage as a collection of blood between the skull and dura mater, often resulting from arterial rupture after trauma, and recommended prompt surgical evacuation to alleviate symptoms like lucid intervals followed by deterioration.^[179] By the 19th century, French physicians such as Guillaume Dupuytren formalized the distinction between concussion (commotio cerebri)—characterized by transient loss of consciousness without visible brain damage—and contusion, which involved structural injury, based on clinical observations of symptoms like vomiting and sensory deficits.^[180] This period also saw the revival of craniotomy for head injuries, facilitated by Joseph Lister's 1867 introduction of antisepsis and the advent of general anesthesia in the 1840s, allowing safer removal of bone fragments and hematoma evacuation to reduce intracranial pressure.^[181]

Modern advancements

The development of the computed tomography (CT) scan in the 1970s revolutionized the diagnosis of head injuries by providing non-invasive, detailed cross-sectional images of the brain, allowing for rapid identification of hemorrhages, fractures, and other abnormalities that were previously difficult to detect without surgery.^[182] Invented by Godfrey Hounsfield, the first clinical CT scan of a human brain occurred on October 1, 1971, marking a pivotal shift toward evidence-based neuroimaging in traumatic brain injury (TBI) management.^[182] Complementing this, the Glasgow Coma Scale (GCS), introduced in 1974 by Graham Teasdale and Bryan Jennett, standardized the assessment of consciousness levels in TBI patients through a simple scoring system evaluating eye, verbal, and motor responses, facilitating consistent communication and prognosis across clinical settings.^[183] In the late 20th and early 21st centuries, the Brain Trauma Foundation published its first evidence-based guidelines for the management of severe TBI in 1995, synthesizing clinical data to recommend practices such as intracranial pressure monitoring and hyperosmolar therapy, which improved outcomes by standardizing care and reducing variability in treatment.^[184] Concurrently, the enactment of universal helmet laws in various jurisdictions, particularly for motorcyclists, led to significant reductions in head injury incidence; for instance, studies showed decreases in nonlethal head injuries by up to 29-69% following law implementation, alongside lower rates of traumatic brain injuries and fatalities.^[185] These public health measures, supported by epidemiological evidence, underscored the role of preventive legislation in mitigating TBI burden.^[186] From the 2010s to 2025, heightened public and medical awareness of concussions emerged, catalyzed by high-profile events such as the 2013 National Football League (NFL) settlement of $765 million with former players alleging concealment of long-term brain injury risks, which prompted widespread protocol changes in sports and accelerated research into chronic traumatic encephalopathy.^[187] Neuroprotective trials during this period, including phase 3 studies of progesterone in severe TBI, yielded mixed results but highlighted challenges in translating preclinical promise to clinical efficacy, with no overall mortality benefit observed in large cohorts.^[188] Advances in artificial intelligence (AI) for neuroimaging, meanwhile, enabled automated detection of TBI lesions on CT and MRI scans with accuracies exceeding 90%, improving diagnostic speed and prognostic predictions for outcomes like in-hospital mortality up to 95.6%.^[189] Post-2020 developments in blood-based biomarkers have further transformed TBI diagnosis, with FDA-cleared tests for glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1) allowing clinicians to rule out intracranial injuries in mild cases, potentially reducing unnecessary CT scans by up to 30% while maintaining high sensitivity.^[190] These biomarkers, measurable within hours of injury, provide objective evidence of neuronal damage and aid in stratifying patients for advanced care, addressing gaps in traditional imaging for concussion detection.^[103]

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[PDF] Traumatic Brain Injury: Imaging Patterns and Complications
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Traumatic Brain Injury and Artificial Intelligence: Shaping the Future ...
Advances in AI technology have shown promise in improving the detection and prioritization of findings in head CT scans for TBI treatment and care.
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Test selection and clinical integration of blood-based biomarkers for ...
Aug 25, 2025 · While no blood-based biomarkers can directly diagnose TBI, several FDA-cleared laboratory tests are now available to help reduce unnecessary CT ...
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The Diagnostic and Prognostic Role of Biomarkers in Mild Traumatic ...
May 28, 2025 · Beyond acute diagnosis, biomarkers such as NfL and tau protein can play a crucial role in predicting long-term outcomes. Patients who experience ...