Week 5- Lecture 1b - Alterations in Central Nervous System Function Flashcards
What is included in the forebrain
telencephalon - cerebral cortex, basal ganglia, hippocampus, amygdala
diencephalon - thalamus, hypothalamus, epithalamus
what is included in the midbrain
mesencephalon - tectum, tegmentum
What is included in the hindbrain
cerebellum, pons, medulla
4 brain protection
bone (skull)
membranes (meninges)
Watery cushion (CSF)
BBB - helps maintain stable environment or the brain - separates neurons from blood borne substances such as hormones and neuro transmitters
CSF composition
watery solution formed from blood plasma - less protein and different ion concentrations than plasma
Functions of CSF
gives buoyancy to CNS structures
protects CNS from blows and other trauma
nourishes brain and carries chemical signals
What is the choroid plexus
hang from the roof of each ventricle
- clusters of capillaries enclosed by Pia mater and layer of ependymal cells
- produce CSF at constant rate
- keep it in motion
ependymal cells
- use ion pumps to control composition of CSF
- help cleanse CSF by removing wastes
normal volume of CSF 150ml
- replaced every 8 hours
- 500ml formed daily
BBB function
helps maintain stable environment for brain and separates neurons from some blood borne substances
BBB composition
continuous endothelium of capillary walls
thick basal lamina around capillaries
feet of astrocytes
- provide signal to endothelium for formation of tight junctions
- tight junctions complete, forming blood brain barrier
BBB function outlined
The blood brain barrier is a selective barrier that allows nutrients to move by facilitated diffusion. As it’s role is to maintain a stable environment for the brain, it denies metabolic wastes, proteins, most drugs, small nonessential amino acids and K+. Alcohol, nicotine and anaesthetics are all substances that are allowed to pass due to their fat solubility
BBB is absent in some areas - why?
the blood brain barrier is absent in areas like the hypothalamus and the vomiting centre. This is so hypothalamus can monitor water balance, temperature and metabolic activity of the body. The vomiting centre monitors for poisonous centres
Neuronal injury response is dependant on
the specific cell type involved
Support cells injury responses
astrogliosis
microgial nodules
ependymal damage which leads to CSF alterations
Injury responses of neuron
neuropathy
axonal damage
demyelination
Astrogliosis
Astrogliosis is where an astrocyte responds to local injury by the process of proliferation (forms a glial scar)
Contusions, wounds, tumours, abscesses, hemorrhages are all common causes of tissue injury that elicit an astrogliosis response
Unchecked proliferation can lead to neoplastic transformation (glioma - brain cancer)
MOIs of CNS injury
Traumatic CNS injury
Ischemic CNS injury
Excitation injury
CNS pressure injury
Microglial
Has an immune response, reactive changes include nucleus extension ( rod cells)
Can join to astrocytes to form microglial nodule - brain contains very few lymphocytes - T-Lymphocites do not cross BBB
Ependymal cell damage response
CSF production transfer is altered with ependymal cell damage due to infection of ventricles and intraventricular haemorrhaging
Traumatic CNS injury
can have impaired neurologic functioning which can either be local or systemic (usually always systemic )
In terms of a local effect, this injury is to neuronal tissue transmitting signals to a specific area
A systemic effects involves injury to a site responsible for integrating transmission of impulses to multiple distant sites (usually CNS)
TBI aka concussion
MOIs include automobile accidents, falls, sports related injuries and “shaken baby syndrome”
TBIs can lead to changes in physical, intellectual, emotional and social abilities.
Can be categorised as closed head injury and open traumatic injury
Closed head injury
involves movement of the brain inside of the skull causing the injury
Open traumatic injury
involves exposure of brain structures such as the meninges and brain tissue
with this comes the risk of infection and also risk of further injury
Traumatic brain injuries
With traumatic brain injuries comes a lot of complications, these include increased seizure activity, concussion (which has temporary alterations in function -dizzy/unconscious), contusions (which has permanent damage - cortical contusions - may remain conscious
- brainstem contusions - always cause coma / injury to the reticular activiting system (RAAS)
Other complications include hepatomas, oedema, skull fractures, increased ICP, respiratory depression, Brain hernias
Diagnosis of TBIs
diagnosis tools for traumatic brain injury include
imaging modalities ( CT, MRI)
EEGs for brain activity
Lumbar puncture (spinal tap) : for analysis of CSF and check presence of blood (intracranial haemorrhaging)
Treatment for TBIs
Treatment for TBI’s is targeted towards the specific injury
surgery can be performed to evacuate haematomas
removal of foreign fragments
Reduce intracranial pressure (ICP)
Pain control
anticonvulsive medication (prevent seizures)
Respiratory support
Antibiotics to prevent infection
SCI
most SCI's are among males - may be result of fractures -contusions -compression of the vertebral column -trauma to the head or neck
neurologic damage is the result of
- pulling
- twisting
- severing
- compressing the neural tissue of the spinal cord
Different spinal cord injuries
lacerations - rip or tear from vertebral fracture, knife or bullet
transection : completely severed, penetrating trauma
incomplete transection
contusion: falls, acceleration/deceleration injury
compression : crushing
distraction : pulling spinal cord apart (top moved while bottom fixed)
Clinical manifestations of vertebrae fracture
localised pain
clinical manifestations of SCI
wide range
- from mild paresthesia (abnormal sensation) to quadriplegia (paralysis of all four extremities)
- level of SCI and severity contributes to neurologic deficit
Diagnosis for a traumatic SCI
X-ray for fractures
neuro examination
lumbar puncture
CT, MRI
Treatment for traumatic SCI
immediate immobilisation to prevent further injury
corticosteroids to lessen inflammation
further treatment : traction , casting, surgery
ischaemic central nervous system injury
inadequate perfusion to neurologic tissue
- impaired oxygenation
- tissue necrosis
cause of ischemia
- local ischemia (specific region of the brain
- occlusion of blood supply by thrombosis in a local vessel - global ischemia (larger areas of CNS affected
- inadequate blood supply to meet the needs of brain tissue
- global ischemia
spinal cord ischemia : occlusion of spinal blood vessels
6 steps of an ischemic CNS injury
- impaired blood flow lasting longer than a few minutes
- brain tissue infarction occurs
- cellular function ceases because of inability to use anaerobic processes or uptake glucose and glycogen
- infarction stimulates response to tissue injury that leads to inflammation
- inflammatory response leads to oedema development
- Oedema leads to increased intracellular pressure (ICP)
cell injury also cause local water, electrolyte imbalances and acidosis
- calcium, sodium, water build up
- free radical formation at injury site
- increased release of excitatory neurotransmitter (glutamate)
clinical manifestations of iscaemic CNS injury
sensory and motor functions are often affected
If injury in brain : manifestations reflect specific associated functions with motor deficits on contralateral side
loss of consciousness, weakness, difficulty speaking, impaired vision , paresthesia
diagnosis for Ischaemic CNS injury
CT, MRI, angiography to diagnose ischaemic blockage
PET scan: altered metabolism in surrounding tissue
treatment for ischaemic CNS injury
manage ICP
restore perfusion
thrombolytic therapy to dissolve clot
anticoagulation therapy to prevent future clot
excitation injury
pathologic consequences of increased impulse frequency, intensity, cascade of transmission
glutamate is the main excitatory neurotransmitter
- involved numerous higher order function
- glutamate binds to its receptor on postsynaptic membrane (many types of receptors)
- NMDA: N-Methyl-D-aspartate receptor is one subtype with affinity for glutamate
signal transduction initiated
IF : high levels of glutamate binds to NMDA, leads to prolonged action potentials
Prolonged action potentials leads to protein breakdown, formation of free radicals, DNA damage, breakdown of nucleus
excitation injury cont’
may result from cell inability to meet metabolic demand
- oxygen needs increase with increased neurologic activity
- risk of hypoxia increased
- if ischaemia is present, more glutamate Is released by the cells
- excitation is intensified by binding to NMDA receptor
tissue sensitive to hypoxia may suffer from permanent damage
- hippocampus
- cerebral cortex
manifestations of excitation injury
reduction in higher order function
cognitive and memory abilities
Excitation injury cont’ #2
cell death from glutamate may be prevented
- effects can be blocked
- excessive level can be removed from synapse
glutamate has wide range of involvement in normal cell functioning
pharmacological blocking is difficult
during periods of deteriorating brain functions excitatory responses may predominate
severe brain injury
difference is based on the injury site
impacted CNS involvement
A . flexor or decorticate posture
- damage to cerebral hemispheres above midbrain
B extensor or decerebrate posture
-damage to midbrain, brainstem
CNS pressure injury
skull and vertebral column : rigid structure
- restricted expansion
increase in pressure may result in injury : increased intracranial pressure cause : 1. excessive CSF volume 2. cerebral oedema 3. Space occupying lesion (tumour)
CNS pressure injury
excessive CSF volume
increased production
decreased absorption
- obstruction of the ventricular system
- obstruction may occur through inflammation, tumour, haemorrhaging or a congenital anomaly
CSF build up in the ventricles leads to dilation of ventricles
CNS pressure injury
oedema
- abnormal water accumulation
- vasogenic oedema : transfer of water and protein from the vascular to interstitial space (following permeability change, pressure change)
- Cytotoxic oedema : caused by hypoxia secondary to ischaemia - cellular swelling
manifestations
- altered consciousness
- intracranial hypertension
- neurologic deficit
CNS tumour can promote pressure injury
may obstruct CSF flow
promote brain displacement (brain herniation) to lower pressure area
- stimulation of vomiting centre of medulla : nausea
-personality challenges, memory loss, depression
increased ICP
common response to pathologic events is increased intracranial pressure
- leads to blood flow reduction
- ischemia
- death of brain cells
- damage to brain structure
- functional loss
manifestations of increased ICP
- headache
- vomiting
- papilledema (oedema of optical disk)
- mental deterioration
treatment of ICP
excessive CSF : surgical shunting from intraventricular spaces
- to peritoneum : ventriculoperitoneal shunt
- to right atrium : ventriculoatrial shunt
- catheter – left ventricle – internal jugular vein – right atrium
Cerebral oedema
- osmotic diuretics
- fluid removal and excretion
