Diffuse Brain Injury

TERRI SANDI SUSYANTO, dr

MENTOR :
RULLY HANAFI DAHLAN, dr, SpBS(K-Spine), Mkes
Definitions
Traumatic Brain Injury
“An insult to the brain, not of degenerative or
congenital nature caused by an external physical
force that may produce a diminished or altered
state of consciousness, which results in an
impairment of cognitive abilities or physical
functioning. It can also result in the disturbance of
behavioral or emotional functioning.”
Causes
An outside force impacts the
head causing the brain to
move

A direct blow to the head

A rapid acceleration and

deceleration of the head
Cause
Motor Vehicle Accident (50 %)
Fall (21 %)
Sport Injury (10 %)
Insidence of TBI
 In the United States, at least 1.4 million sustain a TBI each
year
51,000 die;
290,000 are hospitalized; and
1,224,000 million are treated an discharge from emergency
department
What Do We Mean by
Severity of Injury ?
Amount of brain tissue damage
Severity of TBI
GCS PTA LOC
<1 0–30
Mild 13–15
day minutes
>1 to <7 >30 min to
Moderate 9–12
days <24 hours
>24
Severe 3–8 >7 days
hours
Traumatic Brain Injury-
Classification
1. Fokal brain injury  confined to specific areas
◦ Contusion
◦ Intracranial hemorrharge
2. Diffuse brain injury 
distributed in a more general manner
◦ Mild  Concussion
◦ Severe  Diffuse Axonal Injury
Concussion
 It is at the mild end of the spectrum of
traumatic brain injury
 Reflecting transient brain dysfunction
 A sudden transient mechanical head
injury with disruption of neural activity
and a change in LOC
 No structural damage
 Reversible
Concussion
 Brief disruption in LOC
 Amnesia
 Headache
 Short duration : < 6 hours
Diffuse Axonal
Injury
Diffuse Axonal Injury
 Diffuse axonal injury (DAI) is a type of traumatic
brain injury (TBI) that results from a blunt injury to
the brain.
However, most traumatic brain injury patients with
diffuse axonal injury are identified to be in a severe
category
Clinical syndrome with LOC > 6hours after trauma,
without direct cause of LOC
Process takes approximately 12-24 hours
History
Stricth  Patologist (1965)
Brain Biopsy
 Diffuse degeneration of axon on post high
speed accident patient with head injury
Etiology
 high-speed motor vehicle accident
 most common mechanism involves an
accelerating and decelerating motion  Shearing
forces to the white matter tracts of the brain
 microscopic and gross damage to the axons in
the brain at the junction of the gray and white
matter.
 Diffuse axonal injury commonly affects white
matter tracts involved in the corpus callosum and
brainstem
 Epidemiology
epidemiology of diffuse axonal injury reflects the severity
of traumatic brain injury
Traumatic brain injury patients with lower GCS tend to
have a higher incident of diffuse axonal injury.
postmortem studies of severe traumatic brain
injury patients' brains have shown a significant number of
them to have a diffuse axonal injury
one can hypothesize that a significant number of severe
traumatic brain injury patients without mass lesions such as
subdural hematomas or epidural hematomas and low GCS
will have a diffuse axonal injury.
 Pathophysiology
The primary insults of diffuse axonal injury lead to
disconnection or malfunction of neurons
interconnection.
This affects numerous functional areas of the
brain.
Usually, patients with diffuse axonal
injury present with bilateral neurological
examination deficits frequently affecting the frontal
and temporal white matter, corpus callosum, and
brainstem
Rapid stretching of axons is thought to damage the axonal cytoskeleton and,
therefore, disrupt normal neuron function
Pathogenesis if Microscopic
Axonal Changes
Increased
cytoskeleton
damage + protein
accumulation =
axon disconnection
Axon Disconectiom
leads to irreversible
damage
Pathologic Feature :
Bulb Formation
Stages of DAI
The Adams Diffuse
Axonal Injury Classification:
Grade 1: Mild diffuse axonal injury with
microscopic white matter changes in cerebral
cortex, corpus callosum, and brainstem
Grade 2: Moderate diffuse axonal injury with
gross focal lesions in the corpus callosum
Grade 3: Severe diffuse axonal injury with
finding as grade 2 and additional focal lesions
in the brainstem.
 Clinical signs
DAI  after traumatic brain injury with GCS of
less than eight for more than six hours.
 LOC
 ICP
Decerebration or decortication
Global cerebral edema
Autonomic dysfunction
 Persistent vegetative state
 Evaluation
 Definitive diagnosis of diffuse axonal injury can
be made in postmortem pathologic examination
of brain tissue.
 in clinical practice, a diagnosis of diffuse axonal
injury is made by implementing clinical
information and radiographic findings
 It constitutes mostly microscopic damage, and it
is often not visible on imaging studies.
Axonal swellings revealed by the beta APP immunostain in DAI.
Microscopic evaluation of the brain tissue often shows
numerous swollen and disconnected axons
AXON RETRACTION BULB
 Radiology
 CT Scan  small punctate hemorrhages to white-
grey matter junction, corpus callosum, pons
 50-80% shows normal CT Scan
 A MRI, specifically Diffuse Tensor Imaging (DTI) is
imaging of choice for diagnosis of DAI
 recent report suggests that acute gradient-recalled
echo (GRD) MRI will enhance the detection of axonal
injury in grade 3 diffuse axonal injury patients,
suggesting that it is a better diagnostic tool.
 Grade 1 Axonal Injury
Typically located in the cortical-subcortical junction of cerebral hemispheres,
particularly in the frontal and parietal parasagittal white matter; Anterior temporal
white matter is another well known location of axonal injury

CT FLAIR SWI
SWI CT

Another case of axonal injury on SWI: Lesions

evident only in SWI sequence (arrows). Both CT and
Grade 1 axonal injury on SWI: Lesions typically FLAIR fail to demonstrate the axonal injuries
located along the parasagittal frontoparietal white
matter in the form of ‘rosary beads’ (arrow). Lesions
are difficult to identify in CT
 Grade 2 Axonal Injury
SWI
CT
Corpus callosal lesions often involve the posterior
body and splenium; lesions tend to be located to one
side of the midline. Associated lesions in septum
pellucidum and fornices may be seen.

Hemorrhagic axonal injury in the right side splenium. Also, note the smaller
lesion near right frontal horn (arrows). Lesions are not evident in CT.

SWI SWI – sagittal reformation

Gross specimen in coronal plane shows small hemorrhagic

lesions in the splenium of corpus callosum (arrows). Courtesy:
Greenfield’s Neuropathology, 8th Ed. p739.

Septum pellucidum and calloso-septal junction hemorrhagic

axonal injuries on SWI. Relationship is better appreciated in
sagittal reformation
 Grade III Diffuse Axonal Injury
(DAI)
Axonal injury typically affects the dorsolateral
portion of midbrain and rostral pons including the
superior cerebellar peduncles.

Gross specimen shows small hemorrhagic lesions in the

dorsolateral aspect of upper pons (arrow). Courtesy:
Greenfield’s Neuropathology, 8th Ed. p739.

Brainstem axonal injury may be associated with

abnormal pupillary light reflex. SWI can be
expected to demonstrate axonal lesions in these
patients. British Journal of Neurosurgery. 2011; 25: 596–605

Axonal injury in the brainstem: FLAIR image fails to demonstrate the

FLAIR SWI lesions. SWI mIP image demonstrates several foci of
microhemorrhages from DAI in the dorsolateral aspect of caudal
midbrain (arrow)
 LABORATORY TEST
Currently, there are no laboratory tests for
diagnosis diffuse axonal injury.
 Treatment / Management
 Preventions of secondary injuries and facilitating
rehabilitation.
 In the acute phase econdary injuries lead to
increased mortality
 Secondary injuries are related to low oxygen
delivery in the presence of hypotension, hypoxia,
edema, and intracranial hypertension
 Treatment / Management
 Initial treatment priority in traumatic brain
injury patients is focused on resuscitation
 ICP monitoring is indicated in patients with GCS
of less than 8
 Anesthesia, pain medicine
 Short-term, usually seven days, anticonvulsant
treatment  prevent early post-traumatic
seizures
 it is important to prevent hypertension that leads
to hypoperfusion
THANK YOU