Spinal Cord Injuries
❖ Primary spinal cord injury: initial mechanical trauma and
immediate tissue destruction
➢ If not immediately mobilized
➢ Longitudinal stretch of cord
Injury Description
Cord concussion Results in temporary disruption of cord-mediated functions
Cord contusion Bruising of neural tissue causes swelling and temporary loss of cord-
mediated function
Cord compression Pressure on cord causes ischemia to tissues; must be decompressed to
prevent permanent damage to spinal cord
laceration Tearing of neural tissue of spinal cord; may be reversible if only slight
damage sustained by neural tissues; may result in permanent loss of
cord-mediated functions of spinal tracts are disrupted
Transection Severing of spinal cord causes permanent loss of function
Complete All tracts in spinal cord are completely disrupted; all cord-mediated
functions below transection are completely and permanently lost
incomplete Some tracts in spinal cord remain intact, together with functions
mediated by these tracts; has potential for recovery although function is
temporarily lost
Hemorrhage Bleeding into neural tissue as a result of blood vessel damage;
usually no major loss of function
Damage or Causes local ischemia
obstruction of
spinal blood
supply
❖ Secondary spinal cord injury
➢ Cascade of vascular, cellular, and biochemical events
beginning minutes after injury and continuing for weeks
■ Hemorrhages- central gray matter
■ Inflammation
■ Edema-white matter impairs microcirculation of the cord
■ Ischemia
➢ C1-C4
■ Swelling may be life-threatening because CV and respiratory
control functions can be lost
➢ Vertebral Injuries
,■ Acceleration, deceleration, deformation forces occurring at impact
, Clinical findings : temporary loss of spinal cord functions below the lesion
★ Develop immediately after injury
❖ Spinal shock: temporary loss of spinal cord functions below the lesion
➢ Develops immediately after injury
➢ Caused by cord hemorrhage, edema, or anatomic transection
➢ Activity of cells AT and BELOW the level of injury cease
➢ Complete loss of reflex function, flaccid paralysis, absence of
sensation, loss of bladder and rectal control, drop in BP, bradycardia,
poor circulation
➢ Damage to SNS results in loss of thermal control
■ Hypothalamus cannot regulate body heat through vasoconstriction
■ Assumes temp of air known as poikilothermia
■ Generally lasts 2-3 days
❖ Neurogenic shock/vasogenic shock
➢ Cervical or upper thoracic cord injury above T6
➢ Absence of sympathetic activity
➢ Symptoms
■ Vasodilation
■ Hypotension
■ Bradycardia
■ Failure of body temp regulation
➢ Paraplegia: paralysis of lower half of body
➢ Quadriplegia: paralysis of all extremities
■ Complete
● Level of injury is above C6
■ Incomplete
● Function at or above C6 preserved
◆ Shoulder, upper arm, some forearm muscle control intact
❖ Autonomic hyperreflexia: syndrome of sudden massive reflex
sympathetic discharge r/t spinal cord injury at level T6 or above
➢ Manifestations
■ Flexor spasms
■ Severe HTN
■ Pounding headache
■ Blurred vision
■ Profuse sweating
■ Nasal congestion
■ Nausea
■ Piloerection
■ Bradycardia
➢ Emergency medical management
Type of Injury Mechanism
, PRIMARY BRAIN INJURY
FOCAL BRAIN INJURY Localized injury from impact
CLOSED BRAIN INJURY Blunt trauma
Coup Injury is directly below site of forceful impact
Contrecoup Injury is on opposite side of brain from site of forceful
impact
Epidural hematoma Vehicular accidents, minor falls, sporting accidents
Subdural hematoma Forceful impact: vehicular accidents or falls, especially
in elderly persons or persons with chronic alcohol
abuse
Subarachnoid hemorrhage Bleeding caused by forceful impact, usually vehicular
*worst headache of my life accidents or long distance falls
OPEN INJURY Penetrating trauma: missiles, bullets, sharp objects i.e.
knives, ice picks
Compound fracture Objects strike head with great force or head strikes
object forcefully; temporal blows, occipital blows,
upward impact of cervical vertebrae
DIFFUSE AXONAL INJURY Traumatic shearing forces, tearing of axons from
twisting and rotational forces with injury over
widespread brain areas; moving head strikes hard,
unyielding surface or moving object strikes stationary
head; torsional head motion without impact
SECONDARY BRAIN INJURY
SYSTEMIC PROCESSES Hypotension, hypoxia, anemia, hypercapnia,
hypocapnia
INTRACEREBRAL Inflammation, cerebral edema, ICP, brain herniation,
PROCESSES decreased cerebral perfusion pressure; ischemia
Cellular processes Release of excitatory neurotransmitters (glutamate);
failure of cell ion pumps, mitochondrial failure,
disruption of blood brain barrier
➔ · Types of traumatic brain injury: alteration in brain function or other
evidence of brain pathology caused by an external force such as MVA or falls
◆ Primary: direct impact
● Focal Brain Injury 2/3rds head injury deaths
○ Observable bain lesion
○ Force of impact typically produces
◆ Contusions
◆ Subdural hematomas
❖ Primary spinal cord injury: initial mechanical trauma and
immediate tissue destruction
➢ If not immediately mobilized
➢ Longitudinal stretch of cord
Injury Description
Cord concussion Results in temporary disruption of cord-mediated functions
Cord contusion Bruising of neural tissue causes swelling and temporary loss of cord-
mediated function
Cord compression Pressure on cord causes ischemia to tissues; must be decompressed to
prevent permanent damage to spinal cord
laceration Tearing of neural tissue of spinal cord; may be reversible if only slight
damage sustained by neural tissues; may result in permanent loss of
cord-mediated functions of spinal tracts are disrupted
Transection Severing of spinal cord causes permanent loss of function
Complete All tracts in spinal cord are completely disrupted; all cord-mediated
functions below transection are completely and permanently lost
incomplete Some tracts in spinal cord remain intact, together with functions
mediated by these tracts; has potential for recovery although function is
temporarily lost
Hemorrhage Bleeding into neural tissue as a result of blood vessel damage;
usually no major loss of function
Damage or Causes local ischemia
obstruction of
spinal blood
supply
❖ Secondary spinal cord injury
➢ Cascade of vascular, cellular, and biochemical events
beginning minutes after injury and continuing for weeks
■ Hemorrhages- central gray matter
■ Inflammation
■ Edema-white matter impairs microcirculation of the cord
■ Ischemia
➢ C1-C4
■ Swelling may be life-threatening because CV and respiratory
control functions can be lost
➢ Vertebral Injuries
,■ Acceleration, deceleration, deformation forces occurring at impact
, Clinical findings : temporary loss of spinal cord functions below the lesion
★ Develop immediately after injury
❖ Spinal shock: temporary loss of spinal cord functions below the lesion
➢ Develops immediately after injury
➢ Caused by cord hemorrhage, edema, or anatomic transection
➢ Activity of cells AT and BELOW the level of injury cease
➢ Complete loss of reflex function, flaccid paralysis, absence of
sensation, loss of bladder and rectal control, drop in BP, bradycardia,
poor circulation
➢ Damage to SNS results in loss of thermal control
■ Hypothalamus cannot regulate body heat through vasoconstriction
■ Assumes temp of air known as poikilothermia
■ Generally lasts 2-3 days
❖ Neurogenic shock/vasogenic shock
➢ Cervical or upper thoracic cord injury above T6
➢ Absence of sympathetic activity
➢ Symptoms
■ Vasodilation
■ Hypotension
■ Bradycardia
■ Failure of body temp regulation
➢ Paraplegia: paralysis of lower half of body
➢ Quadriplegia: paralysis of all extremities
■ Complete
● Level of injury is above C6
■ Incomplete
● Function at or above C6 preserved
◆ Shoulder, upper arm, some forearm muscle control intact
❖ Autonomic hyperreflexia: syndrome of sudden massive reflex
sympathetic discharge r/t spinal cord injury at level T6 or above
➢ Manifestations
■ Flexor spasms
■ Severe HTN
■ Pounding headache
■ Blurred vision
■ Profuse sweating
■ Nasal congestion
■ Nausea
■ Piloerection
■ Bradycardia
➢ Emergency medical management
Type of Injury Mechanism
, PRIMARY BRAIN INJURY
FOCAL BRAIN INJURY Localized injury from impact
CLOSED BRAIN INJURY Blunt trauma
Coup Injury is directly below site of forceful impact
Contrecoup Injury is on opposite side of brain from site of forceful
impact
Epidural hematoma Vehicular accidents, minor falls, sporting accidents
Subdural hematoma Forceful impact: vehicular accidents or falls, especially
in elderly persons or persons with chronic alcohol
abuse
Subarachnoid hemorrhage Bleeding caused by forceful impact, usually vehicular
*worst headache of my life accidents or long distance falls
OPEN INJURY Penetrating trauma: missiles, bullets, sharp objects i.e.
knives, ice picks
Compound fracture Objects strike head with great force or head strikes
object forcefully; temporal blows, occipital blows,
upward impact of cervical vertebrae
DIFFUSE AXONAL INJURY Traumatic shearing forces, tearing of axons from
twisting and rotational forces with injury over
widespread brain areas; moving head strikes hard,
unyielding surface or moving object strikes stationary
head; torsional head motion without impact
SECONDARY BRAIN INJURY
SYSTEMIC PROCESSES Hypotension, hypoxia, anemia, hypercapnia,
hypocapnia
INTRACEREBRAL Inflammation, cerebral edema, ICP, brain herniation,
PROCESSES decreased cerebral perfusion pressure; ischemia
Cellular processes Release of excitatory neurotransmitters (glutamate);
failure of cell ion pumps, mitochondrial failure,
disruption of blood brain barrier
➔ · Types of traumatic brain injury: alteration in brain function or other
evidence of brain pathology caused by an external force such as MVA or falls
◆ Primary: direct impact
● Focal Brain Injury 2/3rds head injury deaths
○ Observable bain lesion
○ Force of impact typically produces
◆ Contusions
◆ Subdural hematomas
