Overview of Traumatic Brain Injury: Difference between revisions

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== Pathological Process  ==
== Pathological Process  ==


=== Mechanical Damage ===
=== Mechanical Damage === AKA '''Primary Damage '''and '''Primary Insult.''' Primary mechanical brain injury is the direct injury to the brain cells caused by the initial impact. This initial damage affects the cerebral circulation and results in cerebral ischaemia, which is thought to be a major factor leading to death following TBI.
 
AKA '''Primary Damage '''and'''Primary Insult.'''  
Primary mechanical brain injury is the direct injury to the brain cells caused by the initial impact.


=== Delayed non-mechanical Damage  ===
=== Delayed non-mechanical Damage  ===

Revision as of 17:30, 11 April 2016

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Definition[edit | edit source]

Traumatic Brain Injury [TBI}, also known as Head Injury and Acquired Brain Injury [ABI], is defined as injury to the brain which occurred as a result of trauma, and is non-progressive.

It occurs when an external force impacts the brain, & often is caused by a blow, bump, jolt or penetrating wound to the head. However, not all blows or jolts to the head cause TBI: some just cause bony damage to the skull but do not cause brain injury.

Causes of TBI[edit | edit source]

The 2 most common causes of TBI are:

  1. Falls  
  2. Road Traffic Accident [RTA] This includes vehicle collisions, pedestrians being hit by a vehicle, vehicle-cyclist and car-motorcyclist collisions as well as bicycle and motorbike crashes which do not involve another vehicle.

Until recently, RTA was the primary cause of brain injury, but an international study published in 2013 reported that "falls have now surpassed road traffic incidents as the leading cause of this injury"[1].

Incidence of TBI[edit | edit source]

One study found that TBI was "a major cause of death and disability on the United States, contributing to about 30% of all injury deaths[2]".

A 2010 study looked at data from several nations, and reported that: "each year 235 000 Americans are hospitalized for non-fatal TBI, 1.1 million are treated in emergency departments, and 50 000 die. The northern Finland birth cohort found that 3.8% of the population had experienced at least 1 hospitalization due to TBI by 35 years of age. The Christchurch New Zealand birth cohort found that by 25 years of age 31.6% of the population had experienced at least 1 TBI, requiring medical attention (hospitalization, emergency department, or physician office). An estimated 43.3% of Americans have residual disability 1 year after injury. The most recent estimate of the prevalence of US civilian residents living with disability following hospitalization with TBI is 3.2 million."[3]

Clinically Relevant Anatomy
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Mechanism of Injury
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Closed head injury[edit | edit source]

Often occurs as a result of RTA, or a blow to the head, or a fall where the head strikes the floor or another hard surface..

In closed head injury, the skull is not penetrated, but it is frequently fractured.

Generally there is both focal and diffuse axonal damage.

Open head injury[edit | edit source]

This is caused by a penetrating wound, eg. by a weapon or from a bullet.

In these cases the skull is penetrated.

The brain injury is usually largely focal axonal damage.

Deceleration injury[edit | edit source]

This frequently occurs in RTA, when rapid deceleration occurs as the skull meets a stationary object, causing the brain to move inside the skull.

Mechanical brain injury occurs due to axonal shearing, contusion and brain oedema.

Pathological Process[edit | edit source]

=== Mechanical Damage === AKA Primary Damage and Primary Insult. Primary mechanical brain injury is the direct injury to the brain cells caused by the initial impact. This initial damage affects the cerebral circulation and results in cerebral ischaemia, which is thought to be a major factor leading to death following TBI.

Delayed non-mechanical Damage[edit | edit source]

AKA Secondary Damage. Non-mechanical brain injury is caused by ischaemic, cytotoxic and inflammatory processes.

One of the most significant factors is the excessive release of glutamate and aspartate, which alter cell wall permeability which ultimately leads to destruction of axons[4].

Clinical Presentation[edit | edit source]

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Diagnostic Procedures[edit | edit source]

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Outcome Measures[edit | edit source]

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Management / Interventions
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Differential Diagnosis
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Key Evidence[edit | edit source]

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Resources
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Case Studies[edit | edit source]

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Recent Related Research (from Pubmed)[edit | edit source]

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References[edit | edit source]

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  1. Changing patterns in the epidemiology of traumatic brain injuryfckLRBob Roozenbeek, Andrew I. R. Maas & David K. Menon Nature Reviews Neurology 9, 231-236 (April 2013)
  2. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. Faul M, Xu L, Wald MM, Coronado VG. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010
  3. The Epidemiology of Traumatic Brain InjuryfckLRCorrigan, John D. PhD, ABPP; Selassie, Anbesaw W. DrPH; Orman, Jean A. (Langlois) ScD, MPH The Epidemiology of Traumatic Brain Injury March/April 2010 - Volume 25 - Issue 2
  4. Axonal Damage in Traumatic Brain Injury. Smith DH, Meaney DF. The Neuroscientist. 2000, 6: 483-495