CSF & intracranial pressure Flashcards
where is CSF located
between the ventricles and subarachnoid space
2 main types of meninges
- dura mater (pachymeninges)
- leptomeninges
- arachnoid
- pia
CSF production and the process involved
mostly produced by the choroid plexus
-mainly in lateral ventricles
involves 2 processes
- ultrafiltration across choroidal capillary wall
- active secretion by choroidal epithelium
choroid plexus structure
- fenestrated capillary network surrounded by a row of epithelial cells
- choroid plexus epithelial cells have tight junctions between them. They contain vesicles and lysosomes and have a microvilli brush border
CSF circulation
- CSF produced in lateral ventricles
- travels trough foramina munro
- goes into the midline of the 3rd ventricle
- passes through the sylvian aqueduct into 4th ventricle
- then leaves out through 3 foramen into subarachnoid space
CSF absorption
majority via the small arachnoid villi and larger arachnoid granulations
(herniations of arachnoid mater through dura into superior sagital sinus)
absorb CSF by unidirectional ‘bulk flow’
CSF total volume
150ml
mostly in subarachnoid space
(some in ventricles)
rate of CSF production
600ml/day
0.35ml/min
what does CSF absorption depend on
hydrostatic pressure in subarachnoid space
- not regulated by any transport process
CSF composition
clear and colourless
- WBC <5x10^6/L
- no neutrophils
- no RBC
- protein <0.45g/L
- glucose >2.5mmol/l
CSF changes in meningitis
increase WBC
increase protein
some cause low glucose (bacterial meningitis)
CSF in subarachnoid haemorrhage
increase in RBC
‘xanthochromia’ (yellow discolouration due to RBC breakdown - takes time)
CSF function
maintains environment for neurons and glia
mechanical cushion for brain
counters sudden increases in intracranial pressure
function of the BBB
- regulation of ionic balance in brain
- facilitates transport of essential substrates into brain e.g. oxygen
- barrier against the entry of potentially harmful molecules
metabolites need to be selectively transported across the endothelial cells
what does the BBB consist of?
- specialised endothelial cells
- thick basement membranes
- astrocytic processes on capillaries
describe the differences between systemic endothelial cells and brain endothelial cells
intracellular junctions
- systemic = fenestrated
- brain = tight
pinocytotic vesicles
- systemic = common - brain = uncommon
basement membrane
- systemic = thin - brain = thick
mitochondria
- systemic = + - brain = +++
transport across BBB
diffusion
-lipid soluble substances e.g.O2/CO2
active transport
- energy dependent
- glucose, some AA, vitamins
ion channels
factors affecting passage of molecule across BBB
- molecular weight (size)
- lipid solubility
- ionisation
- protein binding
- transport mechanism
disease processes involving the BBB
- disruption of tight junctions
- disruption of BM
- disruption of endothelial-astrocyte interaction
- altered function of specific transporter
- new BVs lacking features of BBB
how does meningitis affect the BBB
inflammatory response causes BBB breakdown
white cells and protein in the CSF
how do brain tumours affect the BBB
- abnormal BVs
- vessels can be ‘leaky’
- interstitial fluid accumulates (oedema)
how is intracranial pressure measured
- lumbar puncture
- intracranial pressure monitoring
normal CSF pressure
= 65-195mm of CSF (or water)
= 5-15mmHg
what are the 3 components of the intracranial contents and there values
brain 1300-1500mL
blood 75mL
CSF 75mL
intracranial volume fixed by skull
what is the Monro-Kellie doctrine concept
if you increase the volume of one intracranial component you must decrease another component.
If not ICP increases
compensatory mechanisms if ICP increases
- CSF displaced into SC
- cerebral veins collapse/compress
- increase in CSF absorption
- lumbrosacral dura distensible
causes of increased ICP
increase in volume of brain tissue
- e.g. tumour or oedema
increase in volume of CSF (hydrocephalus)
- obstruction or decreased absorption
increase in cerebral blood volume
- obstruction of venous outflow or loss of autoregulation
cushing’s signs and mechanism
cushings triad
- arterial hypertension
- slow HR
- slow RR
mechanism
- reduction in BF to medulla (due to direct distortion)
cerebral herniations
displacement of brain tissue:
- from one intracranial compartment to another - through foramen magnum into SC
midline shift
can cause compression of:
- brain
- cranial nerves
- BVs
transtentorial herniation
herniation of medial temporal lobe through tentorial notch
causes compression of midbrain, oculomotor nerve, posterior cerebral artery
tonsillar herniation
herniation of inferior cerebellum into SC (‘cerebellar tonsils’)
what does cerebral perfusion pressure depend on
mean arterial pressure and intracranial pressure
CPP = MAP - ICP
what does cerebrovascular autoregulation maintain
a constant cerebral BF over a wide range of cerebral perfusion pressures
what happens when there is a loss of cerebrovascular autoregulation (pressure outside of 60-150mmHg)
cerebral BF is proportional to arterial BP
what mediates the constriction and dilation of small cerebral arteries
vasoactive factors released by neurons
factors affecting ICP
- arterial BP
- increased venous pressure = increased ICP
- increased intrathoracic P increased venous P
- posture (lying, increases venous P)
- increased PaCO2 or decreased PaO2 = increased ICP
- decreased temp causes decreased ICP
why is the BBB important for neurons
provides a stable environment in which they can function
