Week 1 - Head Injury & Stroke Flashcards
Explain the neuronal injury mechanism (how neurons get damaged).
• Neurons: require continuous O2 demand (functioning or not).
- Very specialised cells, die from lack of oxygen due to any reason e.g. ischaemia, infarction (commonest).
• Following injury - increased excitatory amino acids: glutamate and aspartate - inflammation.
- E.g. physical/chemical injury - lack of oxygen - the damaged neurons release excitatory amino acids (glutamate and aspartate), which causes stimulation, irritation and inflammation that spreads to the surrounding neurons as well.
• Increased cytokines → inflammation.
- Increased cytokine production - classic inflammation.
• Cell swelling, vacuolisation, loss of nissl granules (red neuron), nuclear pyknosis.
- Red neuron is the first microscopic appearance of dead neurons.
• Decreased glucose utilisation → increased catecholamines → further injury.
- Small damage in the CNS spreads to surrounding tissues - extension of injury.
- Microglia → macrophages → clearing, phagocytosis.
• Pathogenesis - damaged neuron dies then the microglia (small sedentary cells - not functioning - actually macrophages - from bone marrow) start activating → become large macrophages → clear area. First change - accumulation of macrophages (modified microglia), which begin clearing the area. - Astrocyte activation and proliferation → fibril Gliosis (healing) - no collagen scar*
• Activation of astrocytes → become bigger → start producing cytoplasmic processes just like axons-dendrites (fine fibres - not collagen). Glial cells become large and start producing glial fibres - replacement for the collagen in CNS. There are no fibroblasts in brain tissue - healing by astrocyte fibrosis known as Gliosis - healing of CNS. Collagen scars only form in brain when there is a chronic abscess (collagen tissue from blood vessel walls). All other CNS injuries heal without collagen scar*
- Excitatory amino acids – elevation of glutamate & aspartate after traumatic brain injury which cause swelling, vaculolization & neuronal death through influx of Cl, Na and Ca.
- Endogenous opioids cause behavioural suppression.
- Decreased glucose utilisation causes brain injury.
- Extracellular K causes oedema.
- Increased cytokines cause inflammation.
Identify the types of brain injury.
• Concussion (mild damage) - no visible injury, microscopic diffuse neuronal stress/damage. Spontaneous recovery.
- No visible injury or necrosis of cells. Only microscopic diffuse neuronal stress/damage that results in spontaneous recovery (no permanent damage).
• Contusion (moderate damage) - localised, visible injury with bleeding (bruise).
- Equivalent to bruise - in CNS known as contusion.
• Laceration (severe damage) - visible tear in brain tissue.
Intracranial haemorrhage
• Bleeding within the brain.
• 2 major types:
- Traumatic: 1. Epidural, 2. Subdural, 3. Subarachnoid, 4. Intracerebral (depend on levels).
- Non-traumatic: 1. HTN, 2. AV malformation, 3. Tumours (typically cause either intracerebral or subarachnoid haemorrhage).
Outline blunt head injury.
• Primary injury (at the site of injury):
- Concussion, contusion, laceration.
- Coup (at place of impact) and contra-coup (hits back due to force - mobile brain moving in skull cavity). Typically seen in post-mortem MVA.
- Diffuse axonal injury (extension of injury to surrounding tissues due to damaged neurons).
• Secondary injury:
- Inflammation (expansion).
- Haematoma.
- Oedema (formation) and infection (secondary).
• Post Traumatic Complications:
- Diffuse neuronal injury - leading to coma/death.
- Chronic - epilepsy, dementia (late phase loss of nervous tissue).
What are the 3 major types of intracranial haemorrhages?
Epidural:
• Young age.
• Arterial bleed.
• Usually due to severe trauma associated with a fracture.
• ‘Lens’ shape haemorrhage (outside dura mater - firmly attached to skull - fracture leads to small thick lens shape haematoma). Lemon.
Subdural: • Old age. • Venous bleed. • Delayed, ‘linear’. • Minor trauma (e.g. fall) results in rupture of the veins in the subdural space → spreads to larger areas over surface of brain as it is not firmly adhered - linear shaped haemorrhage. Banana.
Sub-arachnoid:
• Arterial
• No trauma, hypertension, atherosclerosis, AVM.
• Usually non-traumatic, in the arachnoid space (location of cerebral blood vessels) → cause bleeding secondary to hypertension, atherosclerosis or arterio-venous malformations (congenital abnormalities).
• Sudden, very severe headache, blood spreads all over the surface and into the sulci as well.
Describe epidural haematoma.
- Trauma - severe usually with fracture.
• Severe trauma due to fracture. - Loss of consciousness - concussion.
• Usually produce loss of consciousness due to concussion. - Regains after few minutes (lucid interval).
• Regain/recover consciousness after a few minutes. This period known as lucid interval. - Again unconscious - haemtoma compression.
• Arterial bleed expanding and compressing on brain → leads to LOC.
Typically patients present with trauma → LOC → regain consciousness for a short while → LOC. Poor prognosis.
Diagnostic tips: • Acute, severe trauma. • Skull fracture, arterial. • Small lens like haematoma. • Lucid interval - clinical.
- Accumulation of blood between skull and dura mater.
- Is associated with high trauma/temporal fracture/arterial bleed.
- Rapid progression (↑ intracranial pressure) with clearly defined margin.
- Mainly affects young fit people.
- Good prognosis with surgery as normal brain underneath.
• Young, arterial, trauma, fracture, ‘lens’.
Describe subdural haematoma.
• Typical clinical presentation - an 89-year-old woman presents to ED with a 2 week history of wobbly gait, frequent falls and new right sided weakness. Had bumped her head to a closed door 3 weeks ago. Note large crescent shaped haematoma. Over frontal and parietal lobe. Compressed ventricle.
Diagnostic tips:
• Elderly, delayed symptoms (usually weeks).
• Long interval between trauma and symptoms (not acute).
• Crescent shape of haematoma (unlike epidural - large haematoma, slowly developing - venous bleed, rupture of bridging veins from the dura to the subarachnoid. Subdural - below dura, above arachnoid).
• Extravasion of blood between dural & arachnoid membrane.
• Venous bleed (often due to rupture of bridging veins).
• Gradual onset (chronic) with wide distribution.
• Chronic presentation with personality change, memory loss, confusion.
• Mainly affects old people or very young with minor trauma.
• Bad prognosis as abnormal brain underneath.
• Morphology:
- Crescent shape of haematoma.
- Oedema, herniation, flattening.
• Old age, venous, delayed, ‘linear’.
Describe subarachnoid haemorrhage.
• Alone is not trauma condition.
Diagnostic tips:
• Elderly, no trauma* (may be trauma secondary to unconsciousness due to haemorrhage).
• Hypertension, AVM, aneurysms, diabetes mellitus etc.
- Due to hypertension, atherosclerosis, rupture of aneurysms etc - systemic cause
• Sudden severe headache (thunderclap).
- Patients present with sudden severe pain.
• Blood all over surface (including sulci and ventricles - subarachnoid space extends into ventricles).
- Extravasion of arterial blood into subarachnoid space
- Often due aneurysm rupture & usually spread throughout CSF pathways
- Presents as meningeal irritation with rapid ↑ in intracranial pressure
• Arterial, no trauma, hypertension, atherosclerosis, AVM.
Outline head injury - healing.
- Old contusions are present on the inferior frontal surface with a brownish yellow colour (haemosiderin - old haem.).
- Haemorrhage → Necrosis → Gliosis + Haemosiderin.
- No scarring, heals by liquefaction (necrosis).
Summary intracranial haemorrhages.
- Epidural
• Mechanism: skull fracture, arterial.
• Clinical: acute presentation with lucid interval followed by rapid increase in intracranial pressure. - Subdural
• Mechanism: shearing/torsion - bridging veins - slow.
• Clinical: slow presentation with personality change, memory loss and confusion elderly. - Subarachnoid
• Mechanism: arterial - atherosclerosis, hypertension, aneurysm.
• Clinical: meningeal irritation sudden severe headache with a rapid increase in intracranial pressure. - Intracerebral (cerebral hemisphere haemorrhage).
• Mechanism: trauma - contusion. Subdural haematoma.
• Clinical: increased intracranial pressure with focal deficits; profound coma, usually rapidly fatal.
Outline stroke.
• Stroke - acute neurological deficit (sensory, motor, visual) - clinical definition.
- Sudden loss of neurological function.
• CVA - cerebrovascular accident - pathology.
- Caused by obstruction, block, embolism or haemorrhage.
• Neurons aerobic - require continuous O2.
- Specialised cells that require continuous oxygen. Purely aerobic cells.
• ~10 min of ischaemia - irreversible injury.
- 10 mins of ischaemia is enough to cause cell death (irreversible injury).
• Brain ~2% of body weight, ~20% of cardiac output, ~20% body O2.
- Although only 2% of body weight, requires 20% CO and O2 - maintain vitality.
• CVA - ischaemic (thrombotic, embolic) and haemorrhagic.
- Ischaemic - obstruction to blood flow - may be thrombus or embolus.
- Haemorrhagic - break in blood vessel.
• Focal/global (hypotension/hypoxia/hypoglycaemia).
- Focal - one of branches involved.
- Global - whole brain involved - hypertension, hypoxia, hypoglycaemia. Global damage.
• Arterial/venous (infections).
- Can be also divided as arterial and venous. 99% clinically are arterial, venous infarctions occasionally can occur, usually secondary to infections.
• Transient (<24 hours without cell necrosis), evolving (progressive increase in symptoms), completed (stable symptoms or improvement).
• Sensitive areas (first to get damaged in global ischaemia) - border zone (watershed zone), basal ganglia etc.
- Some areas of brain more sensitive to lack or oxygen such as border zone (watershed zone), basal ganglia etc. (first to get damaged in global ischaemia).
Outline global ischaemia.
Aetiology
• Decreased oxygen, BP or glucose. Major artery block* (carotid artery).
Clinical features
• Ranges from mild confusion to total brain death. Acute/chronic.
- Can occur suddenly due to major block (e.g. embolic infarcts) or chronic (ischaemia or narrowing or decreased O2 in blood).
Morphology
• Watershed zone infarcts and lamellar necrosis - in chronic form.
- Most affected tissues are watershed zones (border area between areas supplied by major arteries).
- In between ACA, MCA, PCA zones - more susceptible to ischaemia.
- Chronic global ischaemia also characterised by lamellar necrosis - line of necrosis around the cortex. Usually seen in ventilator brains (chronic).
Identify the types of stroke (focal).
Clinical:
• Transient ischaemic attack - resolve <24h, no cell death.
- Neurological deficit resolves in <24h as there is no cell death.
- Typical in small blocks which clear off thrombus getting thrombolysed or just a spasm in the blood vessel.
• Evolving - increasing (thrombotic), atheroma → thrombosis.
- Typical in thrombotic. Increasing/forming atheroma leading to block (gradually developing thrombosis). Patient presents with symptoms and the symptoms become worse. Evolving stroke.
• Completed - embolic, no change.
- Typical of embolic in which the embolism suddenly blocks and remains stable (no change). Completed stroke.
Pathological:
• Arterial - ischaemic (embolic, thrombotic) and haemorrhagic.
• Venous (infections) - rare.
Differentiate between an ischaemic and haemorrhage stroke.
Ischaemic: 1. Thrombotic. 2. Embolic. • Atherosclerosis. • Commonest ~80%. • Mortality ~20%.
Haemorrhagic:
• Hypertension and atherosclerosis.
• Less common ~20%.
• Mortality ~80%.
- 99% of cases ischaemic or haemorhagic.
- Ischaemic more common clinically ~80% - can be thrombotic (thrombus formation over atheromatous plaque → evolving stroke) or embolic (atheromatous plaque somewhere else in major blood vessels e.g. aorta - separates and blocks vessel → completed stroke). Both due to block in blood vessel (embolic more common).
- Mortality is less in ischaemic compared to haemorrhagic.
- Haemorrhagic due to rupture of blood vessel and bleeding causing haematoma.
- Both types common in MCA - deep penetrating branches most common.
Pathogenesis:
Hypoxia, ischaemia and infarction
1. Is reduced blood supply to a portion of the brain (commonly due to atherosclerosis).
2. Decreased oxygenation to blood tissue results in ischaemic injury to the cells.
3. Prolonged ischemic cellular injury/occlusion → infarction → cell death.
4. As cerebral blood flow declines, different neuronal functions fail at different thresholds.
Haemorrhage resulting from rupture of CNS vessels
- Rupture of a blood vessel within the brain panenchyma (often into area of infarction).
- Explosive entry of blood into brain causes immediate cessation of function in that area as neurons are structurally disrupted & white matter fibre tracts are split apart.
- Haemorrhage may expand or be associated with oedema → progression neurological deficit.
What is the most common location of a stroke?
- Commonest stroke affects MCA deep branches - supplies the basal ganglia - thalamus, internal capsule, globus pallidus - area most commonly affected. When this area is affected → internal capsule damage → causes hemiplegia (internal capsule is where half of the body’s motor fibres cross over).
- Common presentation - hemiplegia - middle cerebral artery involving the internal capsule.
- Many other types, less common e.g. paraplegia, head and neck effected, vision effected (different features of infarcts of ACA, PCA or minor branches of MCA).
How come patients improve after a stroke?
• Area of cell death - central infarct area - umbra, surrounded by area of ischaemic damage/inflammation - penumbra that may recover following resolution (therapy).
- Area infarcted is always surrounded by area of inflammation in which there is no death (only temporary inflammation and stoppage of function). Therefore, when patients are recovering in hospital - improvements in nerve and muscle function are due to improvements in penumbra (not umbra). The umbra is permanent loss.
