What is the pathophysiology behind concussion/head
injury?

There are three mechanisms of damage that may occur in
traumatic brain  injury: primary, secondary, and
tertiary damage (Boss, 2006). •	Primary injury is caused
by the impact of the injury •	It involves neural injury,
glial injury (injury to the axon), and the vascular 
response (immediate).

•	Secondary injury includes cerebral edema, swelling,
hemorrhage,  infection, and increased ICP. •	Tissue
hypoxia occurs from inadequate perfusion. •	This type of
injury occurs from a compromise in the circulation or a
shift  in the brain matter.

•	Tertiary injury is caused by apnea, low blood
pressure, changes in  pulmonary resistance, or ECG
changes.

Focal brain injury includes specific, observable brain
lesions, including  contusions, hemorrhages, and
hematomas. •	Contusions usually occur from direct
contact, and the damage results  from the compression of
the skull at the point of impact along with the  rebound
effect.  The contusion and associated bleeding occur
from small  tears in the blood vessels, which occur from
the force of the blow.  The  severity of the contusion
is associated with the force of the blow (amount of 
energy transmitted); as well, the smaller the area of
impact, the greater the  severity of injury due to the
concentration of force. •	The hematomas can be
classified according to location: extradural,  subdural,
or intracerebral.    •	The source of bleeding in an
extradural hematoma is often an artery.   The temporal
fossa is the most common site.  Subdural hematomas can
occur  rapidly, within 48 hours of injury (acute), or
can be subacute, and develop  over the course of several
days to two weeks.  They are usually located at the  top
of the skull, often cause by tearing of the bridging
veins or torn cortical  veins and damaged venous
sinuses.  Increased ICP occurs as the mass  exands. 
Intracerebral hematomas are most common in the frontal
or  temporal lobe, and are cause by small blood vessel
injury by penetrating or  shearing forces.  The mass
expands, causing increased ICP and compression  of brain
tissues.

Diffuse brain injury involves injury to the axon.  It
can occur as a result of a  shaking effect, with
resultant high levels of acceleration or deceleration,
or  rotational effects, with rotational acceleration. 
These motions cause  shearing, tearing, or stretching of
nerve fibers, followed by axonal damage. The categories
of diffuse brain injury include: mild concussion,
classic  concussion, mild diffuse axonal injury (DAI),
moderate DAI, and severe DAI.   DAI prompts a prolonged
comatose period lasting greater than 6 hours due to 
axonal disruption.  •	Mild concussion involves temporary
disturbance of the axon.   Consciousness is not lost,
but there are effects to memory and attention  systems,
although brief.  There are three grades, with grade I
involving  momentary confusion and disorientation, up to
grade III, in which the  confusion and amnesic effects
may persist for several minutes. •	Classic cerebral
concussion is also termed class IV.  There is an 
immediate loss of consciousness that lasts for less than
6 hours.  There is a  presence of physiologic and
neurologic dysfunction, without substantial  anatomic
injury.  The dysfunction results from a diffuse
disconnect in the  brain stem reticular activating
system, which in conjunction with the cerebral  cortex
regulates vital reflexes including cardiovascular and
respiratory  function, and for maintaining wakefulness
•	In mild DAI, the coma lasts from 6-24 hours.  There
may be residual  deficit after recovery. •	In moderate
DAI, there is widespread physiologic damage throughout
the  cerebral cortex and diencephalon, with actual
tearing of some of the axons.   Coma often lasts greater
than 24 hours, and there is a lack of prominent brain 
stem signs. •	In severe DAI, there is severe axonal
mechanical disruption in many areas  of the brain,
including both hemispheres, and extending to the brain
stem  and diencephalon.  

This summary was adapted from: Boss, B. (2006).
Alterations of neurologic function. In McCance, K. L, & 
Huether, S. E. (Eds.). Pathophysiology: The Biologic
Basis for Disease in Adults  and Children (5th ed, pp.
547-555). St. Louis: Elsevier Mosby.