1. J Robin Highley Senior Lecturer in Neuropathology UoS
Head injury
J Robin Highley
Senior Lecturer in Neuropathology UoS

4. Broad classification of head injury
Type of injury
Non-missile most common by far
Missile head injury where there is penetration of skull or brain
Distribution of the lesions
Focal
Diffuse brain lesions
Time course of damage following the traumatic event
Primary – due to immediate biophysical forces of trauma
Secondary – presenting some time after the traumatic event,
physiologial responses to trauma
effects of hypoxia/ischaema
infection

5. Non missile trauma

6. Damage after non missile trauma
Diffuse brain lesions
Focal
Diffuse axonal injury
Diffuse vasucular injury
Hypoxia-ischaemia
Swelling
Scalp
Contusions
Lacerations
Skull
Fracture
Meninges
Haemorrhage
Infection
Brain

7. Blunt head trauma
– focal damage

8. Focal damage
Scalp lacerations

9. Focal damage – skull fracture
Implies considerable force
↑ risk haematoma, infection & aerocele
Angled or pointed objects cause localized fractures that are often open or depressed
Flat surfaces cause linear fractures
Can extend to skull base (sometimes called contrecoup fractures)

10. Flat surfaces cause linear fractures

11. Angled / pointed objects → localized fractures

12. Focal lesions: Haemorrhage

13. Extradural haematoma ~ 10% severe head injuries, ~15% fatal ones
Usually associated with skull #
Occur slowly over hours
Usually a lucid interval
Causes death by
brain displacement
raised intracranial pressure
herniation

14. Subdural haematoma Usually due to tears in bridging veins
cross subdural space from superior surface of brain to midsagittal sinus
Can occur slowly (‘chronic’)
Usually surrounded by ‘membrane’ of granulation tissue

15. Traumatic subarachnoid haematoma
Causes:
Contusions/lacerations
Base of skull # (tear vessels)
Vertebral artery rupture/dissection
Intraventricular haemorrhage

16. Cerebral and cerebellar haemorrhage
Superficial: due to severe contusion
Deep: related to diffuse axonal injury

17. Focal lesions: infection
Predominantly due to skull fracture

18. Focal lesions: brain

19. Focal brain damage mechansisms
Contact Damage
At or just deep to the point of impact
Acceleration or deceleration damage
Force to head causes differential movement of skull & brain
Impact of inner surface of skull on underlying brain causes contusion
Traction on bridging veins causes subdural haemorrhage
Differential movement of brain tissue
causes shearing, traction and compressive stresses
damages blood vessels and axons

20. Focal brain lesions: contusion & laceration
Contusions
Superficial “bruises” of the brain
“Coup” at the site of impact
“Contre coup” – away from the site of impact
At first – haemorrhagic
Then become brown/orange and soft (days weeks)
Then indented or cavitated after months years
Lacerations
When contusion is sufficiently severe to tear the pia mater

22. Coup vs contrecoup

23. Diffuse lesions Diffuse axonal injury Diffuse vasucular injury
Swelling
Hypoxia-ischaemia

24. Traumatic axonal injury - some terms
Axonal injury – a non specific term
Traumatic axonal injury – can be focal or widespread
Diffuse axonal injury
A clinicopathological syndrome of widespread axonal damage (inc brainstem)
But can be caused by a variety of processes
Diffuse traumatic axonal injury

25. Traumatic axonal injury
Usually involves acceleration and deceleration of the head
Mild  recovery of consciousness ± long term, variable severity deficit
Severe  unconscious from impact & remain so or severe disability

26. Diffuse traumatic axonal injury - macroscopic

27. Long term effects: diffuse traumatic axonal injury

28. Diffuse vascular injury
Usually result in near immediate death
Multiple petechial haemorrhages throughout brain

29. Brain swelling occurs in ~75% patients
Leads to ↑ intra cranial pressure
Caused by:
congestive brain swelling
Vasodilation and ↑ cerebral blood volume
Vasogenic oedema
Extravasation of oedema fluid from damaged blood vessels
Cytotoxic oedema
Increased water content of neurons and glia

30. Herniation
Due to
bleeding
brain swelling

31. Hypoxia-ischaemia can be widespread or confined to vulnerable regions
HI often causes infarction and hypoxic ischaemic damage
Likely in patients who have had
Clinically evident hypoxia
Hypotension with systolic BP<80mmHg for ≥15 min
↑ intracranial pressure
can be widespread or confined to vulnerable regions
Susceptible neurones
Border zones between major cerebral territories

33. Missile injury

34. Missile head injury Depressed injuries do not penetrate skull
Penetrating injuries
Can cause focal damage
Often no loss of consciousness
Bullets usually low velocity
High risk of infection, E
pilepsy in 40% of survivors.
Perforating injuries
Missile enters and exits skull, passing though the brain
Bullets usually high velocity
Exit wound > entry wound
Shock waves and cavitation produce most of the damage
~10% gunshot wound cases survive 24h
~ 5% survive 7 or more days

35. Chronic Traumatic Encephalopathy

36. Chronic traumatic encephalopathy
Neurodegenerative condition usually seen 8-10 years after
repetitive mild traumatic brain injury
1/3 are progressive
Initially irritability, impulsivity, aggression, depression, memory loss
Then dementia, gait and speech problems, parkinsonism
Some have motor neurone disease like symptoms

37. Chronic traumatic encephalopathy
Atrophic: neocortex, hippocampus, diencephalon &mamillary bodies
Enlarged ventricles with fenustrated cavuum septum
Tau-positive neurofibrillary and astrocytic tangles
Frontal and temporal cortex and limbic regions
especially around depths of sulci and limbic regions

38. Perivascular astrocytic tangles
CTE:
Tau pathology AD
CTE
Cortex
Substantia nigra
Perivascular astrocytic tangles

39. CTE: TDP-43 pathology

40. Spinal injury

41. Types of spinal injury Types of injury
Indirect (usually closed)
Compression, flexion, extension, rotation → vertebral fracture/dislocation
Direct due to penetration by external object (e.g. knife)
Distribution: Cervical>thoracic>lumbar
Time course
Primary, immediate damage
Secondary, delayed damage

42. Spinal cord injury

43. Acute disc prolapse

44. Long term consequences
Hydrocephalus secondary to SAH

45. Time spent preparing this lecture
11/02/2015 6h to write it