- Trauma to brain and spinal cord is a significant cause of death and disability

- Very common nowadays, particularly as a consequence of RTAs

- Site of injury is crucially important (may be clinically silent [frontal lobe], severely disabling [spinal cord] or fatal [brain stem])

Types

Skull fracture

- Occurs in approximately 80% of fatal cases of head injuries

Types of Skull Fracture:

a) Linear (most common fracture – 69% patients)

b) Compound (break in skin/splintering of bone, increased risk of infection and meningitis due to laceration of scalp and tearing of dura)

c) Depressed (11% severe head injuries, comminuted fractures with broken bones displaced inwards, increased incidence of epilepsy)

Parenchymal damage

1. Concussion:

- Reversible, altered consciousness from head injury in absence of contusion

- Characteristic dysfunction includes LOC, temporary respiratory arrest and loss of reflexes

- Full recovery usually ensues (although amnesia for event often persists)

2. Contusion and Laceration:

- Injury occurs from collision of the brain with the skull

- Most common at frontal and temporal lobes (mainly affect the crests of gyri rather than sulci)

- Affects superficial layers of cortex most severely (opposite to ischaemic lesions)

- Contusion – rapid tissue displacement, disruption of vascular channels, and subsequent haemorrhage, tissue injury and oedema, pia-arachnoid stays intact

- Laceration – penetration of brain, with tissue tearing, vascular disruption, haemorrhage and injury along a linear path, pia-arachnoid is penetrated

Types of Contusion and Lacerations:

a) Fracture (occurs at site of fracture)

b) Coup (occurs at point of impact in absence of fracture)

c) Contrecoup (occurs diametrically opposite to site of impact)

d) Herniation (e.g. when cerebellar tonsils are impacted and bruised by foramen magnum)

e) Gliding (occurs at superior margins of cerebral hemispheres, usually by interference of dura with rotational movement of the brain)

Microscopic Features:

- In the earliest stages, there is oedema and haemorrhage

- During the next few hours, blood extravasates through the involved tissue, across the width of the cerebral cortex, and into the white matter and subarachnoid spaces

- Evidence of injury in neuronal cell body (i.e. nucleus pyknosis, eosinophilia, disintegration of cell) takes about 24h to develop

- Neutrophils precede the onset of macrophages

- Old traumatic lesions are depressed, retracted, yellow-brown patches

3. Diffuse axonal injury:

- Result of rotational movements of the brain within the skull (e.g. RTAs)

- Occurs in up to 50% of patients who develop coma shortly after trauma

- Lesions are most commonly found near angles of lateral ventricles and in brainstem

- Often occurs in absence of any skull fracture or contusion

- Two main features:

a) Small haemorrhagic lesions (in corpus callosum and dorsolateral quadrant of brainstem)

b) Widespread tearing of axons (usually at nodes of Ranvier)

Vascular injury

1. Extradural  (epidural) haemorrhage:

- 2% of all head injuries

- Occurs in potential space between skull and dura –> saucer-shaped haematoma

- Almost always result of skull fracture (usually of temporal bone) lacerating middle meningeal artery

- Associated with post-traumatic lucid interval of several hours, followed by rapid increase in ICP

2. Subdural haemorrhage:

- Occurs in potential space between dura and arachnoid resulting in extensive haematoma

- Usually caused by rupture of the small bridging veins or venous sinuses

- Can be acute or chronic [thickened dura and arachnoid], the latter is more common in:

a) Elderly (even with minimal trauma, due to cerebral atrophy and stretching of bridging veins)

b) Infants (due to thin-walled bridging veins)

- Appears as a collection of freshly clotted blood apposed along contour of brain surface without extension into depths of sulci

- Underlying brain is flattened

- Venous bleeding is self-limited, and organisation occurs:

i) Lysis of the clot (1 week)

ii) Growth of fibroblasts from dural surface into haematoma (2 weeks)

iii) Development of hyalinized connective tissue (1-3 months)

iv) Eventual retraction as granulation tissue matures, until only thin layer left ("subdural membranes")

- Organised haematomas are attached to the inner surface of the dura but not to the arachnoid!

3. Subarachnoid haemorrhage:

- Occurs in potential space between arachnoid and pia

- Usually secondary to superficial contusions or lacerations of the brain

- Larger haemorrhages –> arachnoid fibrosis –> meningeal irritation and raised ICP

4. Intracerebral haemorrhage:

- Caused by direct rupture of the intrinsic cerebral vessels at time of injury

- Classification:

a) Solitary (occur in association with cortical contusions, common in temporal and frontal lobes)

b) Multiple (associated with contrecoup lesions, often fatal!)

c) Burst lobe (intracerebral or intracerebellar haematoma in continuity with subdural haematoma)

Spinal cord injuries

1. Open:

- Rarer

- Usually result of direct trauma to spinal cord and nerve roots

- Can be:

a) Perforating (extensive disruption and haemorrhage)

b) Penetrating (incomplete cord transection, e.g. Brown-Sequard syndrome)

2.

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