Neurosurgery notes/Trauma/Head Trauma general/Pathophysiology of Head Trauma

Pathophysiology of Head Trauma

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Head Trauma general

Pathophysiology of primary brain injury

  • Head trauma is classified into 2 pathophysiological stages that differ in mechanism and necessitate distinct clinical treatments.

      • Primary trauma

      • Due to a mechanical load that translates into deformation of cerebral tissue (e.g. neurons, glia, axons, and blood vessels), which then initiate cellular responses that lead to disturbances in autoregulation and metabolism.
      • The first signs of trauma range from
        • Concussion: rapid, indiscrete depolarization of cortical neurons to
        • Focal lesions:
          • Due to blunt impact,
          • To severe damage such as diffuse shearing of axonal integrity,
          • To acute vascular disruptions in the form of haematomas.

      Secondary injuries

      • Occur across a more protracted phase
      • Consist of (McHugh et al., 2007)
        • Cerebral hypoxia 20%
        • Hypotension 18%
        • Swelling
        • Raised ICP
      • Secondary insults + acute injury + hospitalization, correlate with poor outcome, and require imperative attention, stabilization, and surgical and/ or medical management.

Biomechanics of closed head injury

  • Closed head injuries: when the cranium and dura mater remain intact after impact
  • Mechanical loading to 5% gelatine in the human skull caused focal lesions to areas of indentation or fracture, and diffuse shearing throughout the subcortex occurred during rotation (Holbourn, 1944).
  • The primary phase of trauma from TBI is defined through the nature of the
    • Mechanical load,
    • Type of induced motion,
    • Duration and velocity of impact.
  • Forces along different axes produce unique modes of stress upon the head
    • Elongation
    • Compression,
    • Bending
    • Shear,
    • Torsion
  • External force generally translates into

      • Impact load

      • Occurs from collision typically with a short duration of 3– 7 ms measured in low velocity falls.
      • Can result in
        • Skull fracture
        • Extradural haematoma
        • Focal cerebral lesions
        • Contusions known as
          • Location
            • Higher incidence of coup and/ or contre- coup contusions in the frontotemporal and basal regions of brain, irrespective of the primary impact site.
            • The contre- coup lesion is associated with temporal and occipital impacts.
            • Cerebral rotation during impact is also thought to be a significant contributing factor to contre- coup lesions, although definitive evidence on convulsional gliding have yet to confirm this theory.
          • Coup (directly below impact)
            • High positive pressure is observed at the coup site
          • Contre- coup (diametrically opposite to impact)
            • Transmission of the force vector through the brain parenchyma generates a slapping effect to the contre- coup site.
            • At the cellular level, high negative pressure at the contre- coup site, the development and subsequent collapse of cavitation bubbles known as contre cavitations, along with the brain parenchyma bouncing against inner posterior skull are associated with the contre- coup lesions.
            • Elastic rebounding of the skull results in significant spikes in cerebrospinal fluid (CSF) pressure and worsen tissue damage.
          • Intracerebral haematomas
            • Frequently associated with contusions.
            • In the early stage after trauma, a contusion is haemorrhagic and more severe at the crest of gyrus than in the sulcus.
            • It is associated with swelling that subsides with time though discoloration remains.

      Impulsive load

      • Occurs due to inertial forces during translational or rotational motion.
      • Within normal physiological circumstances, CSF pressure provides a considerable dampening effect on brain displacement during motion, and the lack of CSF is shown to significantly increase convolutional gliding and shear strain
      • Brain displacement lags behind that of the skull and the affixed dura mater due to the inertial force of cerebral mass, and convolutional gliding occurs in varying degrees depending on the region of brain, inducing diffuse damage to white matter tracts.
      • Relative to the region of the skull base near the sella and suprasellar space, the brain parenchyma is more mobile.
      • White matter is stiffer than grey matter, thus more strain is distributed at the interface.
      • DAI
        • More susceptible
          • Vascular
          • Neural
          • Dural elements
            • Distal internal carotid arteries
            • Optic nerves,
            • Olfactory tracts,
            • Oculomotor nerves,
            • Pituitary stalk
          • Splenium of the corpus callosum
          • Dorsolateral brainstem

      Purely translational motion of the head and neck at linear acceleration of up to 1000 g. generally does not produce

      • ASDH
      • Diffuse petechial haemorrhages
      • Injuries to the cervical cord

      Linear acceleration + angular motion of the head and neck causes

      • ASDH
      • Diffuse petechial haemorrhages
      • Injuries to the cervical cord

      Angular acceleration

      • Deep-seated haematomas in the basal ganglia + DAI.

      Rotational

      • Often seen in vehicular accidents,
      • Shear strain
        • Axons and vessels are stretched or compressed beyond their physiologic limits → DAI
        • Subdural bridging veins → tearing → ASDH

      Single inertial load + minor terminal impact load

      • Eg severe extension/flexion whiplash trauma,
      • Causes
        • SDH
        • Gliding contusions
        • Spinal cord injuries

      Angular acceleration

      • The rotational axis is at either the occipital condyles or the base of the neck,
      • Amplifying the rotational load and shearing potential.
      • This correlates with sudden vehicular impacts, when translational motion is applied at the seat to induce inertial force onto the head and neck. Rear loading occurs when an applied force from behind causes the head to rotate back at the base of the neck, while front loading occurs when an applied force from the front causes the head to rotate forward.
  • Head motion
    • Can be
      • Translational
      • Rotational
    • Depending on the alignment of two axes:
      • The axis of force application,
      • The axis between the centre of gravity of the head and the atlanto- occipital joint.
  • Whether the head is fixed or free to extend/ flex by the neck is an important determinant for injury mechanism.
  • Static or quasistatic loading
    • A less common type of mechanical load
    • Gradual compression occurs with negligible velocity and acceleration
    • Eg: mechanistically similar to a closing elevator door.
    • A steady load results in skull fractures and cerebral injuries that are deeper than cortical contusions from an impact load.
    • In comparison to blunt impact trauma with relatively shorter duration and higher velocity,
    • Energy from crushing trauma tends to be transmitted to the foraminae and hiatus of the middle cranial fossa, causing in damage to the associated cranial nerves, sympathetic nerves, and intima of blood vessels

TBI classification by morphology

  • Focus on the extent of injury (focal vs. diffuse)
  • Anatomical location of injury with respect to the meninges
    • Extradural/ extra- axial vs.
    • Intracerebral/ intra- axial.
    • From with the extra- axial layer closest to the skull and proceeding inward to intracerebral tissue.

Neuroinflammation of brain injury

  • Burden of inflammation associated with admission GCS and eventually will predict Glasgow outcome score
  • Damage to brain and BBB allows systemic immune system to be exposed to brain antigens which the immune system has never been exposed before. This creates inflammation in brain
  • Drugs like IL1 blockers being investigated to modulate brain inflammation
  • Central chromatolysis
    • Is a histopathologic change seen in the cell body of a neuron, where the chromatin and cell nucleus are pushed to the cell periphery, in response to axonal injury
    • This response is associated with increased protein synthesis to accommodate for axonal sprouting.
    • Aetiology
      • Traumatic injuries
      • Vitamin deficiency
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