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

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

Non missile trauma

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

Blunt head trauma – focal damage

Focal damage Scalp lacerations

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)

Flat surfaces cause linear fractures

Angled / pointed objects → localized fractures

Focal lesions: Haemorrhage

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

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

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

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

Focal lesions: infection Predominantly due to skull fracture

Focal lesions: brain

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

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

Coup vs contrecoup

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

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

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

Diffuse traumatic axonal injury - macroscopic

Long term effects: diffuse traumatic axonal injury

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

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

Herniation Due to bleeding brain swelling

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

Missile injury

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

Chronic Traumatic Encephalopathy

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

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

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

CTE: TDP-43 pathology

Spinal injury

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

Spinal cord injury

Acute disc prolapse

Long term consequences Hydrocephalus secondary to SAH

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