1. Nervous system 1 Introduction, 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

12. 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)

13. 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)

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

15. Focal cerebral oedema in frontal lobe

16. Focal cerebral oedema in frontal lobe around metastatic carcinoma

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

18. Herniation of the brain

19. 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

20. Subfalcine hernia due to glioblastoma

21. 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 3 rd nerve –posterior cerebral artery –opposite cerebral peduncle

22. Tentorial herniation

23. Large tentorial hernia due to cerebral glioblastoma

24. Brain herniation

25. 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 Pontine haemorrhages after tentorial herniation

26. Central brainstem haemorrhage and necrosis following tentorial herniation

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

28. Tonsillar herniation

29. Cerebellar tonsillar necrosis following tonsillar herniation

30. 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?

31. 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

32. Brain – tearing missile injury

33. Cerebral contusions coup –immediately under site of injury contre coup –at opposite side of brain

34. Frontal, temporal and cerebellar contusions

35. Temporal lobe contusions

36. Coup and contre coup

37. 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

38. 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)

39. Skull fracture

40. Extradural v subdural haematoma

41. Extradural haematoma & multiple contusions

42. Extradural haemorrhage

43. Subdural haematoma

45. 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