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Nervous system 1Introduction, raised intracranial
pressure and traumaProfessor John Simpson
This lecture will cover
• NS cell reactions to injury
• raised intracranial pressure, including herniation of the brain
• traumatic brain injury
What’s different about the nervous system to all other body systems?
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
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
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
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
How might diseases of the nervous present?
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
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
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)
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)
Raised intracranial pressureRaised intracranial pressure
Decompensation- causes “shifts” and herniation
Cushing reflex- haemodynamic changes (raised BP, slowed pulse)
Focal cerebral oedema infrontal lobe
Focal cerebral oedema in frontal lobe around metastaticcarcinoma
Sites of brain herniation
• subfalcine
• (trans)tentorial
• tonsillar
• (also through skull defect in trauma)
Herniation of the brain
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
Subfalcine herniadue to glioblastoma
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
Tentorial herniation
Large tentorial hernia due to cerebral glioblastoma
Brain 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
Pontine haemorrhages after tentorial herniation
Central brainstem haemorrhage and necrosis following tentorial herniation
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
Tonsillar herniation
Cerebellar tonsillar necrosisfollowing tonsillarherniation
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?
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
Brain – tearing missile injury
Cerebral contusions
• coup – immediately under site of injury
• contre coup– at opposite side of brain
Frontal, temporal and cerebellar contusions
Temporal lobe contusions
Coup and contre coup
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
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)
Skull fracture
Extradural v subdural haematoma
Extradural haematoma & multiple contusions
Extradural haemorrhage
Subdural haematoma
Subdural haematoma
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