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Nervous system 1 Introduction, raised intracranial pressure and trauma

Nervous system 1 Introduction, raised intracranial pressure and trauma. Professor John Simpson. This lecture will cover. NS cell reactions to injury raised intracranial pressure, including herniation of the brain traumatic brain injury.

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Nervous system 1 Introduction, raised intracranial pressure and trauma

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  1. Nervous system 1Introduction, raised intracranial pressure and trauma Professor John Simpson

  2. This lecture will cover • NS cell reactions to injury • raised intracranial pressure, including herniation of the brain • traumatic brain injury

  3. What’s different about the nervous system to all other body systems?

  4. Why is the NS different? • brain and cord sit in closed spaces • autoregulation of blood flow • blood-brain barrier • high dependency on O2 and glucose • absence of lymphatics • limited immune surveillance • unique cell population with distinctive responses to injury and healing

  5. Microscopic structure of the nervous system • neurons (essentially end cells) • cell bodies - aggregated in grey matter • layers, ganglia, columns, nuclei • In specific domains • cell processes - include • axons in bundles in white matter • glial cells (capable of dividing) • astrocytes, oligodendrocytes and ependyma – neuroectodermal origin • microglia – mesodermal origin

  6. Glial cell roles • astrocytes • neuronal support, blood-brain barrier, healing and repair (by gliosis) • oligodendrocytes • myelin production (~ = Schwann cells in periphery) • ependyma • related to choroid plexus/CSF production • microglia • NS macrophages

  7. Cellular reaction to injury - neurons • cell death • in chronic disease, often seen as reduced cellularity • cell “degeneration” • variety of changes ~ disease, e.g. accumulations, inclusions • axonal reaction • regeneration possible if only axon damaged

  8. How might diseases of the nervous present?

  9. Symptoms and signs of NS disease • headache • neck stiffness • coma/impaired consciousness • loss or disturbance of movement • abnormal reflexes • muscle atrophy • sensory impairment/paraesthesia • visual disturbances • tinnitus/deafness

  10. Intracranial pressure (ICP) • major components of ICP • brain, CSF and blood • increased volume of any one will raise ICP, unless compensatory reduction in one/both of other components • presence of anything else “extra” inside skull will do the same • if ICP continues to increase, compensatory mechanisms will fail

  11. Common causes of raised ICP • intracranial expanding lesions (“space-occupying lesions”) – e.g. tumour, haematoma, abscess • hydrocephalus (excess CSF) • cerebral oedema – increase in brain water content, due to blood-brain barrier problem • localised (e.g. around tumours) • generalised (e.g. following severe head injury or hypoxic brain damage)

  12. Possible effects of raised ICP • compression of veins and ventricles • reduced CSF • flattening of gyri and narrowing of sulci • papilloedema • midline shift • herniation of parts of brain • eventual compression of vital brain stem centres • (before skull sutures fused, enlarged cranium)

  13. Raised intracranial pressure Decompensation - causes “shifts” and herniation Cushing reflex - haemodynamic changes (raised BP, slowed pulse)

  14. Focal cerebral oedema in frontal lobe

  15. Focal cerebral oedema in frontal lobe around metastatic carcinoma

  16. Sites of brain herniation • subfalcine • (trans)tentorial • tonsillar • (also through skull defect in trauma)

  17. Herniation of the brain

  18. Subfalcine herniation • (= supracallosal or cingulate hernia) • usually due to primary abnormality in one cerebral hemisphere • ipsilateral cingulate gyrus herniates under the free edge of falx • pericallosal arteries are compressed, so possible cerebral infarction • anterior cerebral artery may also be affected, causing larger infarct

  19. Subfalcine hernia due to glioblastoma

  20. Tentorial herniation • medial aspect of temporal lobe through tentorium • affects hippocampus • midbrain compressed and distorted • compressed aqueduct impairs CSF flow (obstructive hydrocephalus) • haemorrhage in pons and midbrain • risk to • ipsilateral 3rd nerve • posterior cerebral artery • opposite cerebral peduncle

  21. Tentorial herniation

  22. Large tentorial hernia due to cerebral glioblastoma

  23. Brain herniation

  24. Pontine haemorrhages after tentorial herniation Figure 28-3 Duret hemorrhage involving the brainstem at the junction of the pons and midbrain. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 2 February 2007 01:43 PM) © 2005 Elsevier

  25. Central brainstem haemorrhage and necrosis following tentorial herniation

  26. Tonsillar herniation • (= foramen magnum or foraminal herniation = coning) • cerebellar tonsils move down – with medulla form “cone” shape • exit from 4th ventricle blocked impairing CSF flow (obstructive hydrocephalus) • compression of breathing and cardiac centres in medulla

  27. Tonsillar herniation

  28. Cerebellar tonsillar necrosis following tonsillar herniation

  29. Lumbar puncture Lumbar puncture is dangerous and should be avoided if ICP raised. Why? Is there any way you might check for raised ICP before doing an LP?

  30. Traumatic brain injury • missile or non-missile - latter commoner • in non-missile, primary or secondary damage • primary – focal lesions (contusion/tear) or diffuse axonal injury • secondary – e.g. traumatic vascular injury with intracranial haematoma, oedema, herniation, infarction, hydrocephalus, infection • clinical effects • minor (?) - concussion • major – e.g. death, epilepsy, persistent vegetative state (PVS), post traumatic dementia

  31. Brain – tearing missile injury

  32. Cerebral contusions • coup • immediately under site of injury • contre coup • at opposite side of brain

  33. Frontal, temporal and cerebellar contusions

  34. Temporal lobe contusions

  35. Coup and contre coup

  36. Diffuse axonal injury • particularly in deep white matter • even with very minor trauma • axonal swelling and focal haemorrhage • contribute to cerebral oedema and raised ICP • long term effects variable

  37. Traumatic vascular injury • extradural • especially injury to middle meningeal artery • classical clinical presentation • subdural • dural veins, ? shearing stress • acute or chronic (? recurrent bleeding) • more common in the elderly and in any bleeding diathesis • injury often trivial /missed • (subarachnoid and intracerebral • usually secondary to contusions)

  38. Skull fracture

  39. Extradural v subdural haematoma

  40. Extradural haematoma & multiple contusions

  41. Extradural haemorrhage

  42. Subdural haematoma

  43. Subdural haematoma

  44. Spinal cord trauma • most often due to accidents and displacement of vertebral column +/- vascular problem • cord/nerve root compression, transection etc • effects depend on site and severity • paraplegia, quadriplegia, respiratory compromise

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