Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected. Unconsciousness tends to last longer for people with injuries on the left side of the brain than for those with injuries on the right. Symptoms are also dependent on the injury's severity. With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing, lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns. Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking. Mild TBI symptoms may also be present in moderate and severe injuries.

A person with a moderate or severe TBI may have a headache that does not go away, repeated vomiting or nausea, convulsions, an inability to awaken, dilation of one or both pupils, slurred speech, aphasia (word-finding difficulties), dysarthria (muscle weakness that causes disordered speech), weakness or numbness in the limbs, loss of coordination, confusion, restlessness, or agitation. Common long-term symptoms of moderate to severe TBI are changes in appropriate social behavior, deficits in social judgment, and cognitive changes, especially problems with sustained attention, processing speed, and executive functioning. Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in 60.9% of individuals with TBI. Cognitive and social deficits have long-term consequences for the daily lives of people with moderate to severe TBI, but can be improved with appropriate rehabilitation.

When the pressure within the skull (intracranial pressure, abbreviated ICP) rises too high, it can be deadly. Signs of increased ICP include decreasing level of consciousness, paralysis or weakness on one side of the body, and a blown pupil, one that fails to constrict in response to light or is slow to do so. Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP. Anisocoria, unequal pupil size, is another sign of serious TBI. Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.

Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them. Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat, and irritability.

Systems also exist to classify TBI by its pathological features. Lesions can be extra-axial, (occurring within the skull but outside of the brain) or intra-axial (occurring within the brain tissue). Damage from TBI can be focal or diffuse, confined to specific areas or distributed in a more general manner, respectively. However, it is common for both types of injury to exist in a given case.

Diffuse injury manifests with little apparent damage in neuroimaging studies, but lesions can be seen with microscopy techniques post-mortem, and in the early 2000s, researchers discovered that diffusion tensor imaging (DTI), a way of processing MRI images that shows white matter tracts, was an effective tool for displaying the extent of diffuse axonal injury. Types of injuries considered diffuse include edema (swelling) and diffuse axonal injury, which is widespread damage to axons including white matter tracts and projections to the cortex. Types of injuries considered diffuse include concussion and diffuse axonal injury, widespread damage to axons in areas including white matter and the cerebral hemispheres.

Focal injuries often produce symptoms related to the functions of the damaged area. Research shows that the most common areas to have focal lesions in non-penetrating traumatic brain injury are the orbitofrontal cortex (the lower surface of the frontal lobes) and the anterior temporal lobes, areas that are involved in social behavior, emotion regulation, olfaction, and decision-making, hence the common social/emotional and judgment deficits following moderate-severe TBI. Symptoms such as hemiparesis or aphasia can also occur when less commonly affected areas such as motor or language areas are, respectively, damaged.

One type of focal injury, cerebral laceration, occurs when the tissue is cut or torn. Such tearing is common in orbitofrontal cortex in particular, because of bony protrusions on the interior skull ridge above the eyes. In a similar injury, cerebral contusion (bruising of brain tissue), blood is mixed among tissue. In contrast, intracranial hemorrhage involves bleeding that is not mixed with tissue.

Hematomas, also focal lesions, are collections of blood in or around the brain that can result from hemorrhage. Intracerebral hemorrhage, with bleeding in the brain tissue itself, is an intra-axial lesion. Extra-axial lesions include epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intraventricular hemorrhage. Epidural hematoma involves bleeding into the area between the skull and the dura mater, the outermost of the three membranes surrounding the brain. In subdural hematoma, bleeding occurs between the dura and the arachnoid mater. Subarachnoid hemorrhage involves bleeding into the space between the arachnoid membrane and the pia mater. Intraventricular hemorrhage occurs when there is bleeding in the ventricles.

If symptoms of a head injury are seen after an accident, medical care is necessary to diagnose and treat the injury. Without medical attention, injuries can progress and cause further brain damage, disability, or death.

Because the brain swelling that produces these symptoms is often a slow process, these symptoms may not surface for days to weeks after the injury.

Common symptoms of a closed-head injury include:

- headache

- dizziness

- nausea

- slurred speech

- vomiting

Traumatic brain injury (TBI) is an exchangeable word used for the word concussion. This term refers to a mild brain injury. This injury is a result due to a blow to the head that could make the person’s physical, cognitive, and emotional behaviors irregular. Symptoms may include clumsiness, fatigue, confusion, nausea, blurry vision, headaches, and others. Mild concussions are associated with sequelae. Severity is measured using various concussion grading systems.

A slightly greater injury is associated with both anterograde and retrograde amnesia (inability to remember events before or after the injury). The amount of time that the amnesia is present correlates with the severity of the injury. In all cases the patients develop postconcussion syndrome, which includes memory problems, dizziness, tiredness, sickness and depression. Cerebral concussion is the most common head injury seen in children.

Diffuse axonal injury, or DAI, usually occurs as the result of an acceleration or deceleration motion, not necessarily an impact. Axons are stretched and damaged when parts of the brain of differing density slide over one another. Prognoses vary widely depending on the extent of damage.

Headache is the most common mTBI symptom. Others include dizziness, vomiting, nausea, lack of motor coordination, difficulty balancing, or other problems with movement or sensation. Visual symptoms include light sensitivity, seeing bright lights, blurred vision, and double vision. Tinnitus, or a ringing in the ears, is also commonly reported. In one in about seventy concussions, concussive convulsions occur, but seizures that take place during or immediately after concussion are not "post-traumatic seizures", and, unlike post-traumatic seizures, are not predictive of post-traumatic epilepsy, which requires some form of structural brain damage, not just a momentary disruption in normal brain functioning. Concussive convulsions are thought to result from temporary loss or inhibition of motor function, and are not associated either with epilepsy or with more serious structural damage. They are not associated with any particular sequelae, and have the same high rate of favorable outcomes as concussions without convulsions.

Cognitive symptoms include confusion, disorientation, and difficulty focusing attention. Loss of consciousness may occur, but is not necessarily correlated with the severity of the concussion if it is brief. Post-traumatic amnesia, in which events following the injury cannot be recalled, is a hallmark of concussion. Confusion, another concussion hallmark, may be present immediately or may develop over several minutes. A person may repeat the same questions, be slow to respond to questions or directions, have a vacant stare, or have slurred or incoherent speech. Other MTBI symptoms include changes in sleeping patterns and difficulty with reasoning, concentrating, and performing everyday activities.

Concussion can result in changes in mood including crankiness, loss of interest in favorite activities or items, tearfulness, and displays of emotion that are inappropriate to the situation. Common symptoms in concussed children include restlessness, lethargy, and irritability.

Geriatric trauma refers to a traumatic injury that occurs to an elderly person. The three prevailing causes of traumatic death in the elderly are falls (which account for 40% of traumatic death in this age group), traffic collisions and burns.

The symptoms of a cerebral contusion (bruising on the brain) depend on the severity of the injury, ranging from minor to severe. Individuals may experience a headache; confusion; sleepiness; dizziness; loss of consciousness; nausea and vomiting; seizures; and difficulty with coordination and movement. They may also have difficulty with memory, vision, speech, hearing, managing emotions, and thinking. Signs depend on the contusion's location in the brain.

Pain, especially headache, is a common complication following a TBI. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism. Other serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores, pneumonia or other infections, and progressive multiple organ failure.

The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. As many as 50% of people with penetrating head injuries will develop seizures. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma) though seizures can appear a decade or more after the initial injury and the common seizure type may also change over time. Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.

Neurostorms may occur after a severe TBI. The lower the Glasgow Coma Score (GCS), the higher the chance of Neurostorming. Neurostorms occur when the patient's Autonomic Nervous System (ANS), Central Nervous System (CNS), Sympathetic Nervous System (SNS), and ParaSympathetic Nervous System (PSNS) become severely compromised https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology . This in turn can create the following potential life-threatening symptoms: increased IntraCranial Pressure (ICP), tachycardia, tremors, seizures, fevers, increased blood pressure, increased Cerebral Spinal Fluid (CSF), and diaphoresis https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology. A variety of medication may be used to help decrease or control Neurostorm episodes https://www.brainline.org/story/neurostorm-century-part-3-3-new-way-life.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease, a chronic and progressive disorder, may develop years after TBI as a result of damage to the basal ganglia. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Skull fractures can tear the meninges, the membranes that cover the brain, leading to leaks of cerebrospinal fluid (CSF). 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 can also allow bacteria into the cavity, potentially causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space. 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.

Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

- Paralysis of facial muscles

- Damage to the nerves responsible for eye movements, which can cause double vision

- Damage to the nerves that provide sense of smell

- Loss of vision

- Loss of facial sensation

- Swallowing problems

Hydrocephalus, post-traumatic ventricular enlargement, occurs when CSF accumulates in the brain, resulting in dilation of the cerebral ventricles 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.

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 small blood vessels, but damage to larger ones 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 or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out.

Fluid and hormonal imbalances can also complicate treatment. 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 and hypothyroidism.

Another common problem is spasticity. In this situation, certain muscles of the body are tight or hypertonic because they cannot fully relax.

A progressive decline in central nervous system function leads to a loss of proprioception, balance and overall motor coordination, as well as a reduction in eye–hand coordination, reaction time and an unsteady gait. These degenerative changes are often accompanied by osteoarthritis (degenerative joint disease), which leads to a reduction in the range of motion of the head, neck and extremities. Furthermore, elderly people frequently take multiple medications for control of various diseases and conditions. The side effects of some of these medications may either predispose to injury, or may cause a minor trauma to result in a much more severe condition. For example, a person taking warfarin (Coumadin) and/or clopidogrel (Plavix) may experience a life-threatening intracranial hemorrhage after sustaining a relatively minor closed head injury, as a result of the defect in the hemostatic mechanism caused by such medications. The combined effects of these changes greatly predisposes elderly people to traumatic injury. Both the incidence of falls and the severity of associated complications increase with advancing age.

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury, and is a major cause of unconsciousness and persistent vegetative state after severe head trauma. It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.

DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.

In the mid 1970s, PTS was first classified by Bryan Jennett into early and late seizures, those occurring within the first week of injury and those occurring after a week, respectively. Though the seven-day cutoff for early seizures is used widely, it is arbitrary; seizures occurring after the first week but within the first month of injury may share characteristics with early seizures. Some studies use a 30‑day cutoff for early seizures instead. Later it became accepted to further divide seizures into immediate PTS, seizures occurring within 24 hours of injury; early PTS, with seizures between a day and a week after trauma; and late PTS, seizures more than one week after trauma. Some consider late PTS to be synonymous with post-traumatic epilepsy.

Early PTS occur at least once in about 4 or 5% of people hospitalized with TBI, and late PTS occur at some point in 5% of them. Of the seizures that occur within the first week of trauma, about half occur within the first 24 hours. In children, early seizures are more likely to occur within an hour and a day of injury than in adults. Of the seizures that occur within the first four weeks of head trauma, about 10% occur after the first week. Late seizures occur at the highest rate in the first few weeks after injury. About 40% of late seizures start within six months of injury, and 50% start within a year.

Especially in children and people with severe TBI, the life-threatening condition of persistent seizure called status epilepticus is a risk in early seizures; 10 to 20% of PTS develop into the condition. In one study, 22% of children under 5 years old developed status seizures, while 11% of the whole TBI population studied did. Status seizures early after a TBI may heighten the chances that a person will suffer unprovoked seizures later.

Post-traumatic seizures (PTS) are seizures that result from traumatic brain injury (TBI), brain damage caused by physical trauma. PTS may be a risk factor for post-traumatic epilepsy (PTE), but a person who has a seizure or seizures due to traumatic brain injury does not necessarily have PTE, which is a form of epilepsy, a chronic condition in which seizures occur repeatedly. However, "PTS" and "PTE" may be used interchangeably in medical literature.

Seizures are usually an indication of a more severe TBI. Seizures that occur shortly after a person suffers a brain injury may further damage the already vulnerable brain. They may reduce the amount of oxygen available to the brain, cause excitatory neurotransmitters to be released in excess, increase the brain's metabolic need, and raise the pressure within the intracranial space, further contributing to damage. Thus, people who suffer severe head trauma are given anticonvulsant medications as a precaution against seizures.

Around 5–7% of people hospitalized with TBI have at least one seizure. PTS are more likely to occur in more severe injuries, and certain types of injuries increase the risk further. The risk that a person will suffer PTS becomes progressively lower as time passes after the injury. However, TBI survivors may still be at risk over 15 years after the injury. Children and older adults are at a higher risk for PTS.

Traumatic brain injury (TBI, physical trauma to the brain) can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

Symptoms that may occur after a concussion – a minor form of traumatic brain injury – are referred to as post-concussion syndrome.

Cerebral contusion, Latin "contusio cerebri", a form of traumatic brain injury, is a bruise of the brain tissue. Like bruises in other tissues, cerebral contusion can be associated with multiple microhemorrhages, small blood vessel leaks into brain tissue. Contusion occurs in 20–30% of severe head injuries. A cerebral laceration is a similar injury except that, according to their respective definitions, the pia-arachnoid membranes are torn over the site of injury in laceration and are not torn in contusion. The injury can cause a decline in mental function in the long term and in the emergency setting may result in brain herniation, a life-threatening condition in which parts of the brain are squeezed past parts of the skull. Thus treatment aims to prevent dangerous rises in intracranial pressure, the pressure within the skull.

Contusions are likely to heal on their own without medical intervention.

DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse such as in shaken baby syndrome.

Immediate disconnection of axons could be observed in severe brain injury, but the major damage of DAI is delayed secondary axon disconnections slowly developed over an extended time course. Tracts of axons, which appear white due to myelination, are referred to as white matter. Lesions in both grey and white matters are found in postmortem brains in CT and MRI exams.

Besides mechanical breaking of the axonal cytoskeleton, DAI pathology also includes secondary physiological changes such as interrupted axonal transport, progressive swellings and degeneration. Recent studies have linked these changes to twisting and misalignment of broken axon microtubules, as well as tau and APP deposition.

A concussion, which is known as a subset traumatic brain injury (TBI), is when a force comes in contact with the head, neck or face, or fast movement of the head, causing a functional injury to the brain. Depending on where the location of impact, depends on the severity of the injury. It is short-lived impairment of neurological function, the brains ability to process information, which can be resolved in seven to ten days. Not all concussion involves the loss of consciousness, with it occurring in less than 10% of concussions. Second-impact syndrome is when a player has obtained a second concussion when you either return to field the same day, or return to play before a complete recovery from a previous concussion. This is a result from brain swelling, from vascular congestion and increased intracranial pressure, this can be fatal to a player as it is a very difficult medical injury to control. The brain is surrounded by cerebrospinal fluid, which protects it from light trauma. More severe impacts, or the forces associated with rapid acceleration, may not be absorbed by this cushion. Concussion may be caused by impact forces, in which the head strikes or is struck by something, or impulsive forces, in which the head moves without itself being subject to blunt trauma (for example, when the chest hits something and the head snaps forward). Chronic traumatic encephalopathy, or "CTE", is an example of the cumulative damage that can occur as the result of multiple concussions or less severe blows to the head. The condition was previously referred to as "dementia pugilistica", or "punch drunk" syndrome, as it was first noted in boxers. The disease can lead to cognitive and physical handicaps such as parkinsonism, speech and memory problems, slowed mental processing, tremor, depression, and inappropriate behavior. It shares features with Alzheimer's disease. Lamont sai od th PSCA after his incident::

Post-traumatic epilepsy (PTE) is a form of epilepsy that results from brain damage caused by physical trauma to the brain (traumatic brain injury, abbreviated TBI). A person with PTE suffers repeated post-traumatic seizures (PTS, seizures that result from TBI) more than a week after the initial injury. PTE is estimated to constitute 5% of all cases of epilepsy and over 20% of cases of symptomatic epilepsy (in which seizures are caused by an identifiable organic brain condition).

It is not known how to predict who will develop epilepsy after TBI and who will not. However, the likelihood that a person will develop PTE is influenced by the severity and type of injury; for example penetrating injuries and those that involve bleeding within the brain confer a higher risk. The onset of PTE can occur within a short time of the physical trauma that causes it, or months or years after. People with head trauma may remain at a higher risk for seizures than the general population even decades after the injury. PTE may be caused by several biochemical processes that occur in the brain after trauma, including overexcitation of brain cells and damage to brain tissues by free radicals.

Diagnostic measures include electroencephalography (EEG) and brain imaging techniques such as magnetic resonance imaging, but these are not totally reliable. Antiepileptic drugs do not prevent the development of PTE after head injury, but may be used to treat the condition if it does occur. When medication does not work to control the seizures, surgery may be needed. Modern surgical techniques for PTE have their roots in the 19th century, but trepanation (cutting a hole in the skull) may have been used for the condition in ancient cultures.

Seizures may occur after traumatic brain injury; these are known as post-traumatic seizures (PTS). However, not everyone who has post-traumatic seizures will continue to have post-traumatic epilepsy, because the latter is a chronic condition. However, the terms PTS and PTE are used interchangeably in medical literature. Seizures due to post-traumatic epilepsy are differentiated from non-epileptic post-traumatic seizures based on their cause and timing after the trauma.

A person with PTE suffers late seizures, those occurring more than a week after the initial trauma. Late seizures are considered to be unprovoked, while early seizures (those occurring within a week of trauma) are thought to result from direct effects of the injury. A provoked seizure is one that results from an exceptional, nonrecurring cause such as the immediate effects of trauma rather than a defect in the brain; it is not an indication of epilepsy. Thus for a diagnosis of PTE, seizures must be unprovoked.

Disagreement exists about whether to define PTE as the occurrence of one or more late, unprovoked seizures, or whether the condition should only be diagnosed in people with two or more. Medical sources usually consider PTE to be present if even one unprovoked seizure occurs, but more recently it has become accepted to restrict the definition of all types of epilepsy to include only conditions in which more than one occur. Requiring more than one seizure for a diagnosis of PTE is more in line with the modern definition of epilepsy, but it eliminates people for whom seizures are controlled by medication after the first seizure.

As with other forms of epilepsy, seizure types in PTE may be partial (affecting only part of one hemisphere of the brain) or generalized (affecting both hemispheres and associated with loss of consciousness). In about a third of cases, people with PTE have partial seizures; these may be simple or complex. In simple partial seizures, level of consciousness is not altered, while in complex partial seizures consciousness is impaired. When generalized seizures occur, they may start out as partial seizures and then spread to become generalized.

Concussions in England's professional rugby union are the most common injury gained. Concussion can occur where an individual experiences a minor injury to the head. Commonly occurring in high contact sporting activities; American football, boxing, and rugby. It can also occur in recreational activities like horse riding, jumping, cycling, and skiing. The reason being that it doesn't have to be something to strike you in the proximity of your brain, but can also be caused by rapid change of movement, giving the skull not enough time to move with your body, causing your brain to press against your skull. With rugby being such a contact and fast moving sport, it is no wonder why there is concussion and other head injuries occurring. With the development of equipment and training methods, these will help benefit the players on the field know what could happen and how they can help with preventing it.

Epidural hematoma is when bleeding occurs between the tough outer membrane covering the brain and the skull. Often there is loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again. Other symptoms may include headache, confusion, vomiting, and an inability to move parts of the body. Complications may include seizures.

The cause is typically head injury that results in a break of the temporal bone and bleeding from the middle meningeal artery. Occasionally it can occur as a result of a bleeding disorder or blood vessel malformation. Diagnosis is typically by a CT scan or MRI. When this condition occurs in the spine it is known as a spinal epidural hematoma.

Treatment in generally by urgent surgery in the form of a craniotomy or burr hole. Without treatment death typically results. The condition occurs in one to four percent of head injuries. Typically it occurs in young adults. Males are more often affected than females.

Epidural, subdural, and subarachnoid hemorrhages are extra-axial bleeds, occurring outside of the brain tissue, while intra-axial hemorrhages, including intraparenchymal and intraventricular hemorrhages, occur within it.

Epidural hematomas may present with a lucid period immediately following the trauma and a delay before symptoms become evident. After the epidural hematoma begins collecting, it starts to compress intracranial structures which may impinge on the CN III. This can be seen in the physical exam as a fixed and dilated pupil on the side of the injury. The eye will be positioned down and out, due to unopposed CN IV and CN VI innervation.

Other manifestations will include weakness of the extremities on the opposite side as the lesion (except in rare cases), due to compression of the crossed pyramid pathways, and a loss of visual field opposite to the side of the lesion, due to compression of the posterior cerebral artery on the side of the lesion.

The most feared event that takes place is tonsillar herniation which could result in respiratory arrest since the medullary structures are compromised. The trigeminal nerve (CN V) may be involved late in the process as the pons becomes compressed, but this is not a significant clinical presentation, since by that time the patient may already be dead. In the case of epidural hematoma in the posterior cranial fossa, the herniation is tonsillar and causes the Cushing's triad: hypertension, bradycardia, and irregular respiration.

Epidural bleeding is rapid because it is usually from arteries, which are high pressure. Epidural bleeds from arteries can grow until they reach their peak size at six to eight hours post injury, spilling from 25 to 75 cubic centimeters of blood into the intracranial space. As the hematoma expands, it strips the dura from the inside of the skull, causing an intense headache. Epidural bleeds can become large and raise intracranial pressure, causing the brain to shift, lose blood supply, or be crushed against the skull. Larger hematomas cause more damage. Epidural bleeds can quickly expand and compress the brain stem, causing unconsciousness, abnormal posturing, and abnormal pupil responses to light.

Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.

Other signs and symptoms of subdural hematoma can include any combination of the following:

- A history of recent head injury

- Loss of consciousness or fluctuating levels of consciousness

- Irritability

- Seizures

- Pain

- Numbness

- Headache (either constant or fluctuating)

- Dizziness

- Disorientation

- Amnesia

- Weakness or lethargy

- Nausea or vomiting

- Loss of appetite

- Personality changes

- Inability to speak or slurred speech

- Ataxia, or difficulty walking

- Loss of muscle control

- Altered breathing patterns

- Hearing loss or hearing ringing (tinnitus)

- Blurred Vision

- Deviated gaze, or abnormal movement of the eyes.