question: Why does getting hit in the head hard enough make one go unconscious?
comment: In a nutshell trauma to the brain. Long story. There is a "pillow" of liquid in between the brain and skull. When someone is hit hard enough not even that cushion can stop the impact of brain against skull which causes damage much like punching a wall. This impact causes our brain to sort of reset which is why we get knocked out
passages: Little is known about what exactly causes one to be knocked unconscious, but many agree it is related to trauma to the brain stem. This usually happens when the head rotates sharply, often as a result of a strike. There are three general manifestations of such trauma:
  
  BULLET::::- a typical knockout, which results in a sustained (three seconds or more) loss of consciousness (comparable to general anesthesia, when the recipient emerges and has lost memory of the event),
   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).
   Section::::Causes.
  
  Brain injuries can result from a number of conditions including:
  
  BULLET::::- trauma; multiple traumatic injuries can lead to chronic traumatic encephalopathy. A coup-contrecoup injury occurs when the force impacting the head is not only strong enough to cause a contusion at the site of impact, but also able to move the brain and cause it to displace rapidly into the opposite side of the skull, causing an additional contusion.
  
  BULLET::::- open head injury
  
  BULLET::::- closed head injury
   In a survey of documented head injuries followed by unconsciousness, most of which involved sporting activities, two thirds of head impacts demonstrated a fencing response, indicating a high incidence of fencing in head injuries leading to unconsciousness, and those pertaining to athletic behavior. Likewise, animal models of diffuse brain injury have illustrated a fencing response upon injury at moderate but not mild levels of severity as well as a correlation between fencing, blood brain barrier disruption, and nuclear shrinkage within the LVN, all of which indicates diagnostic utility of the response. 
   Bullets can indirectly disrupt the CNS by damaging the cardiovascular system so that it can no longer provide enough oxygen to the brain to sustain consciousness. This can be the result of bleeding from a perforation of a large blood vessel or blood-bearing organ, or the result of damage to the lungs or airway. If blood flow is completely cut off from the brain, a human still has enough oxygenated blood in their brain for 10–15 seconds of wilful action, though with rapidly decreasing effectiveness as the victim begins to lose consciousness.
   A fighter who becomes unconscious from a strike with sufficient knockout power is referred to as having been "knocked out" or "KO'd" ("kay-ohd"). Losing balance without losing consciousness is referred to as being "knocked down" ("down but not out"). Repeated blows to the head, regardless whether they cause loss of consciousness, are known to gradually cause permanent brain damage. In severe cases this may cause strokes or paralysis. This loss of consciousness is commonly known as becoming "punch drunk" or "shot". Because of this, many physicians advise against sports involving knockouts.
  
  Section::::Knockdown.
   BULLET::::- a "flash" knockout, when a very transient (less than three seconds) loss of consciousness occurs (in the context of a knock-down), and the recipient often maintains awareness and memory of the combat
   Impact damage is the most common type of TBI, estimated at 75% of all TBI injuries, and results from the brain making physical contact with the skull. Impact-induced TBI is localized to the region of impact, although the depth varies by person and force of impact. While cerebrospinal fluid normally acts as a buffer between the brain and skull, during moments of extreme force (i.e. car collision or physical contact sports), this barrier can be overcome, resulting in an impact as the brain rams into the skull. During the moment of impact, some neurons die immediately from being crushed, while other neurons may be damaged to varying degrees and undergo apoptosis. Concussions are the most common and least damaging form of impact-induced TBI.
   The parts of the brain most affected by rotational forces are the midbrain and diencephalon. It is thought that the forces from the injury disrupt the normal cellular activities in the reticular activating system located in these areas and that this disruption produces the loss of consciousness often seen in concussion. Other areas of the brain that may be affected include the upper part of the brain stem, the fornix, the corpus callosum, the temporal lobe, and the frontal lobe. Angular accelerations of 4600, 5900, or 7900 rad/s are estimated to have 25, 50, or 80% risk of MTBI respectively.
   For a period of minutes to days after a concussion, the brain is especially vulnerable to changes in intracranial pressure, blood flow, and anoxia. According to studies performed on animals (which are not always applicable to humans), large numbers of neurons can die during this period in response to slight, normally innocuous changes in blood flow.
   The most common type of head injury in motorcycle accidents is closed head injury, meaning injury in which the skull is not broken as distinct from an open head injury like a bullet wound. Closed head injury results from violent acceleration of the head, which causes the brain to move around inside the skull. During an impact to the front of the head, the brain lurches forwards inside the skull, squeezing the tissue near the impact site and stretching the tissue on the opposite side of the head. Then the brain rebounds in the opposite direction, stretching the tissue near the impact site and squeezing the tissue on the other side of the head. Blood vessels linking the brain to the inside of the skull may also break during this process, causing dangerous bleeding.
   Contusions are identified with two forms of diagnosis: acceleration of the brain and direct trauma. A direct trauma injury is much more severe than an acceleration injury (in most cases) and requires much more intensive diagnosis and testing. The full extent of the injury may not be known until testing done in a hospital is complete.
   There are also theorized research that suggest early CTE might result from damaged blood vessels within the brain. That could trigger brain inflammation and, eventually, the development of proteins such as Tau believed to play a key role in CTE. This hypothesis was tested on adult mice; the researchers state that their brains possess similar attributes to that of human brains. Using a special device, the mice were given precise impacts that would lead to mild brain traumas similar to what an athlete would suffer in contact sports. The mice, whose brains were scanned using a specialized MRI, immediately showed changes to the electrical functions of their brains.
   The exact mechanism for the injuries, especially contrecoup injuries, is a subject of much debate. In general, they involve an abrupt deceleration of the head, causing the brain to collide with the inside of the skull. It is likely that inertia is involved in the injuries, e.g. when the brain keeps moving after the skull is stopped by a fixed object or when the brain remains still after the skull is accelerated by an impact with a moving object. Additionally, increased intracranial pressure and movement of cerebrospinal fluid following a trauma may play a role in the injury.
  
  Section::::Mechanisms.
   Section::::Mechanism.
  
  Section::::Mechanism.:Physical forces.
  
  The type, direction, intensity, and duration of forces all contribute to the characteristics and severity TBI. Forces that may contribute to TBI include angular, rotational, shear, and translational forces.
   Section::::Effects on unconsciousness.
  
  Generally, there are six abnormal states of consciousness that can result from a TBI: 
  
  BULLET::::- Stupor is a state of partial or near complete unconsciousness in which the patient is lethargic, immobile, and has a reduced response to stimuli.
  
  BULLET::::- Coma is a state in which the patient is totally unconscious and cannot be aroused even with strong stimuli.
   BULLET::::- Basilar skull fractures, those that occur at the base of the skull, are associated with Battle's sign, a subcutaneous bleed over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea and otorrhea.
  
  Because brain injuries can be life-threatening, even people with apparently slight injuries, with no noticeable signs or complaints, require close observation; They have a chance for severe symptoms later on. The caretakers of those patients with mild trauma who are released from the hospital are frequently advised to rouse the patient several times during the next 12 to 24 hours to assess for worsening symptoms.
   Damage may occur directly under the site of impact, or it may occur on the side opposite the impact (coup and contrecoup injury, respectively). When a moving object impacts the stationary head, coup injuries are typical, while contrecoup injuries are usually produced when the moving head strikes a stationary object.
  
  Section::::Mechanism.:Primary and secondary injury.
   There are five major features in conjunction with the definition:
  
  BULLET::::- Concussion may be caused either by a direct blow to the head, face, or neck or elsewhere on the body with an "implosive" force transmitted to the head.
  
  BULLET::::- Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously.
  
  BULLET::::- Concussion may result in neuro-pathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.
   Brain injury can occur at the site of impact, but can also be at the opposite side of the skull due to a "contrecoup" effect (the impact to the head can cause the brain to move within the skull, causing the brain to impact the interior of the skull opposite the head-impact). If the impact causes the head to move, the injury may be worsened, because the brain may ricochet inside the skull causing additional impacts, or the brain may stay relatively still (due to inertia) but be hit by the moving skull (both are contrecoup injuries).
   Studies on animals have shown that the brain may be more vulnerable to a second concussive injury administered shortly after a first. In one such study, a mild impact administered within 24 hours of another one with minimal neurological impairment caused massive breakdown of the blood brain barrier and subsequent brain swelling. Loss of this protective barrier could be responsible for the edema found in SIS.
  
  Animal studies have shown that the immature brain may be more vulnerable to brain trauma; these findings may provide clues as to why SIS primarily affects people under age 18.
  
  Section::::Diagnosis.
   Changes indicative of SIS may begin occurring in the injured brain within 15 seconds of the second concussion. Pathophysiological changes in SIS can include a loss of autoregulation of the brain's blood vessels, which causes them to become congested. The vessels dilate, greatly increasing their diameter and leading to a large increase in cerebral blood flow. Progressive cerebral edema may also occur. The increase of blood and brain volume within the skull causes a rapid and severe increase in intracranial pressure, which can in turn cause uncal and cerebellar brain herniation, a disastrous and potentially fatal condition in which the brain is squeezed past structures within the skull.
   BULLET::::1. Buoyancy: The actual mass of the human brain is about 1400–1500 grams; however, the net weight of the brain suspended in CSF is equivalent to a mass of 25-50 grams. The brain therefore exists in neutral buoyancy, which allows the brain to maintain its density without being impaired by its own weight, which would cut off blood supply and kill neurons in the lower sections without CSF.
  
  BULLET::::2. Protection: CSF protects the brain tissue from injury when jolted or hit, by providing a fluid buffer that acts as a shock absorber from some forms of mechanical injury.
   Even in the absence of an impact, significant acceleration or deceleration of the head can cause TBI; however in most cases a combination of impact and acceleration is probably to blame. Forces involving the head striking or being struck by something, termed "contact" or "impact loading", are the cause of most focal injuries, and movement of the brain within the skull, termed "noncontact" or "inertial loading", usually causes diffuse injuries. The violent shaking of an infant that causes shaken baby syndrome commonly manifests as diffuse injury. In impact loading, the force sends shock waves through the skull and brain, resulting in tissue damage. Shock waves caused by penetrating injuries can also destroy tissue along the path of a projectile, compounding the damage caused by the missile itself.
   "Tests": Skull x-rays check for a fracture. CT or MRI detect any bleeding in the skull. The Glasgow Coma Scale classifies the severity of brain injury, with a score of 15 as normal and progressively lower scores indicating greater neurologic injury to the brain.
  