DIFFUSE AXONAL
INJURY
Dr Ajinkya Akre
Guided by – Dr Piyush Sir
Diffuse Axonal Injury
Primary brain injury characterized by the widespread
shearing, stretching,
and subsequent disconnection of axons.
Within the cerebral white matter, corpus callosum, and brainstem.
If patient has not gained consciousness
EPIDEMIOLOGY-
10% of all patients with TBI -
DAI was found in 56% of patients with moderate TBI
90% of patients with severe TBI.
Males -high male-to-female ratio (6.5:1).
Young Adults -20-40 years.
MECHANISM-
TYPES OF IMPULSIVE FORCES-
DAI is associated with rotational and angular acceleration.
CLASSIFICATION BASED ON
CLINICAL SEVERITY-
Traumatic coma of greater than 6 hours - DAI.
Based on clinical criteria
(1) Mild DAI—coma of 6- to 24-hours duration,
(2) Moderate DAI— coma of more than 24 hours without decerebrate
posturing
(3) Severe DAI—coma of more than 24 hours with decerebrate
posturing or flaccidity.
CLASSIFICATION
ADAMS CLASSIFICATION BASED ON RADIOLOGICAL FINDINGS-
Grade 1 -lesions to the subcortical lobar white matter or cerebellum
only),
Grade 2 -lesions in the corpus callosum, w/or w/o lesions in the lobar
white matter), and
Grade 3 -traumatic lesions in the brainstem in areas typical of DAI
(dorsolateral quadrant of the upper brainstem, superior cerebellar
peduncles) with or without lesions in the lobar white matter or corpus
callosum,
PHYSIOLOGICAL BASIS- [2]
The ascending reticular activating system (ARAS) – CONSCIOUSNESS
Travels through the pontomesencephalic tegmentum.
LESIONS AT THE REGION of the DORSOLATERAL OR rostral pons which
contains the raphe nuclei, locus coeruleus.
Remaining surviving axons are VULNERABLE to hypoxia, ischemia and
subsequent release of excitatory amino acids and free radicals. influx
of calcium ions.
Cytochrome C release and caspase activation in DAI – increased
proteolysis.
SECONDARY AXOTOMY-
AMYLOID PRECURSOR PROTEIN
ACCUMULATION
CAUSES INCREASED CALCIUM INFLUX
IN THE NODE OF RANVIER
LEADS TO DISORGANIZATION OF
MICROTUBULES AND
NEUROFILAMENTS.
HENCE BLOCK IN AXONAL TRANSPORT.
CLINICAL PRESENTATION
ALTERED SENSORIUM i.e. GCS < 9
DECEREBRATE RIGIDITY
HYPOTONIA
CHEYNE STOKES BREATHING
HYPER/HYPOTHERMIA
DOLLS EYE MOVEMENT +
ABSENT BAER.
GCS-P Score
Better predictor of prognosis
2: Neither pupil reacts to light.
1: One pupil doesn’t react to light.
0: Both pupils react to light.
Limitations of GCS – vision loss, hearing
loss, intubated patients, not speaking
the same language.
Assessment of sedated/comatose
patients-
Advantages of the FOUR score-
Monitoring Progression: Serial FOUR Scores are valuable for
monitoring
Prognostic Indicator for Severe TBI/DAI.
Used in Intubated Patients with DAI
Direct assessment of brainstem
MARSHALL CLASSIFICATION FOR
CT FINDINGS- (associated injuries)
DAI CAN ALSO BE ASSOCIATED WITH DIFFUSE INJURY TYPE I.
INVESTIGATIONS-
10% of cases of DAI – ASSOCIATED WITH VISIBLE HEMATOMA IN
DIFFUSE AXONAL INJURY DETECTED ON PLAIN CT SCAN.
MRI > CT
MRI modes – SWI > GRE imaging for diffuse axonal injury.
Reduced N-acetyl aspartate,
Elevation in choline related compounds,
Correlate clinically *
Chronic effects of head injury like demyelination, hemorrhage,
hemosiderin and old parenchymal injuries are better revealed with
MRI.
TREATMENT-
INITIAL STEPS –
AIRWAY
BREATHING
RESUSCITATION
MANAGING INTRACRANIAL PRESSURE –
Anticonvulsants: Short-term (around 7 days) use can prevent early post-
traumatic seizures, though long-term prevention is not established.
MANAGING INTRACRANIAL
PRESSURE -
Hyperventilation: hypocapnia » cerebral vasoconstriction » METABOLIC
AUTOREGULATION
PaCO2 maintained at 30-35 mmhg.
Head Elevation: 15-30 degree promotes venous outflow
Osmotherapy/Diuretics: Mannitol
Barbiturates: Effectively lower ICP through sedation, vasoconstriction,
and reduced cerebral metabolic rate, but can cause hypotension.
Loading dose (10 mg/kg) of thiopental given during 30 min.
Maintenance – 1mg/kg/hr
ICP MONITORING DEVICES.
Emerging Therapies: While progesterone treatment shows promise in
reducing morbidity and mortality, it's not yet routinely recommended.
[3]
PROGNOSIS-
OVERALL PROGNOSIS IS POOR
AVERAGE 2 months to regain consciousness - Grade 3 DAI
2 weeks - Grade 2
5-7 days - Grade 1.
SCALE OF PROGNOSIS-
VERY GOOD > GOOD > BAD >
WORSE
The presence of hemorrhagic lesions on initial CT imaging – Bad Prog
NO microhemorrhages on initial CT – Worse Prognosis
Traumatic hematomas occur as a spectrum in DAI –
Isolated dorsal brainstem hematoma. – Bad prognosis
Dorsal brainstem hematoma with cerebral cortical hematomas. – worse
prognosis
REFERENCES-
[1] Sandhu S, Soule E, Fiester P, Natter P, Tavanaiepour D, Rahmathulla G, et al.
Brainstem diffuse axonal injury and consciousness. J Clin Imaging Sci 2019;9:32.
[2] Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma. Brain.
2003;126:1524–36. doi: 10.1093/brain/awg166. [DOI] [PubMed] [Google Scholar]
[Ref list]
[3] Mesfin FB, Gupta N, Hays Shapshak A, et al. Diffuse Axonal Injury. [Updated
2023 Jun 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;
2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448102/
