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Diffuse Axonal Injury (DAI)

  1. Diffuse axonal injury represents the presence of wide spread axonal damage (white matter) in both hemispheres, secondary to severe head injury.
  2. DAI results from application of severe acceleration/deceleration or angular rotational to the brain which results in injuries to the axons by a shearing force shear injuries.

Pathobiological Features

  1. Focal (irreversible) disruption of axons (white matter) at multiple places in both hemispheres (occurs at the moment of injury) white matter tears.
  2. These white matter tears may be haemorrhagic or non hemorrhagic.
  3. When non haemorrhagic they are edematous (Non haemorrhagic lesions are not detected by CT scan but may be recognized on MRl as it picks up edema).
  4. The most frequent location of tears is in the white matter at the junction of GREY and white matter.

Frequent location of tears

  1. Lobar white matter at junction of Grey and white matter (commonest location) - Frontal/ Temporal lobe > Parietal lobe /Occipital lobes.
  2. Corpus Callosum (Second most commonly involved location).
  3. Brain stem (Third most commonly involved location).

Clinical presentation

  1. Clinical presentations may however range from symptoms of concussion to coma.
  2. Loss of consciousness is a common finding and DAI is the commonest cause of post traumatic vegetative state.
  3. Raised intracranial tension may or may not be associated.


  1. Many of these injuries are likely to go undetected by any imaging modality.
  2. DAI may be recognized on CT scan and MRI (MRI > CT scan).

CT scan

  1. CT scan often fails to recognize DAI lesions because most lesions are small and non haemorrhagic (CT scan is often normal).
  2. CT scan can usually detect only those lesions that are large and haemorrhagic.



MRI is more sensitive than CT scan for detecting DAI MRI can recognize smaller lesion than CT scan and also non haemorrhagic lesions from associated edema



Diffuse Axonal injury carries an extremely poor prognosis

Important Points:

Raised intracranial tension may be present in cases of Diffuse Axonal injury (DAI) but it is not seen in all cases of DAI. The presence of raised ICT is not needed for a diagnosis of DAI.

Acute Spinal Cord Injury


A. Spinal Shock

1. Refers to flaccidity and loss of reflexes seen after spinal cord injury.

2. The 'shock' here is to the 'injured cord' which makes it appear completely functionless although all areas are not necessary destroyed.

3. The duration of spinal shock is variable.

4. The clinical feature are

i. Flaccid Paralysis            

ii. Areflexia         

iii. Anesthesia

iv. Spinal shock is usually associated with Urinary Retention. The urinary bladder becomes areflexic during spinal shock and urinary retention develops in most cases.

v. Following the spinal shock phase reflex detrusor activity reappears

B. Neurogenic Shock

1. Produced as a result of loss of sympathetic tone.

2. Interruption of sympathetic vasomotor input after a high cervical spinal cord injury may result in neurogenic shock.

3. Classical picture of Neurogenic shock is Hypotension without tachycardia or cutaneous vasoconstriction i.e. Hypotension with Bradycardia with Skin hyperaemia and warmth

4. The mechanism of neurogenic shock after spinal cord injury is believed to be disruption of sympathetic flow with preserved and unopposed vagal (parasympathetic) tone

Cervical cord injury

  1. UMN Features below the site of lesion
    1. Lower limbs will show signs of UMN lesions and not LMN lesions
    2. Wasting and fasciculations are signs of LMN lesion and are not seen in the lower limbs in a patient with cervical injury
  2. LMN features at site of lesion
    1. Upper limbs may show signs of LMN lesion at the site of transaction
    2. Wasting and fasciculations are signs of LMN lesion and may be seen in the upper limbs in patient with cervical cord injury   
  3. Horner’s syndrome
    1. Homer's syndrome may be seen in cervical cord lesions

Cervical Cord Injury


Findings that indicate a cervical cord injury (in an unconscious patient)

  1. Flaccid Paralysis with Areflexia (Spinal shock)
  2. Flaccid Rectal sphincter or decreased tone of the rectal sphincter
  3. Hypotension with bradycardia (Neurogenic shock)
  4. Diaphragmatic Breathing
  5. Priapism (Autonomic transection) 
  6. Ability to flex but not extend the elbow
  7. Response on eliciting painful stimuli above the clavicle but not below the clavicle
  8. Decreased rectal sphincter tone
  9. Treatment: Injection methylprednisolone 30mg/kg within 3 hrs of injury

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