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CEREBROSPINAL FLUID AND INTRACRANIAL
PRESSURE
CEREBROSPINAL FLUIDThe cerebrospinal Fluid [CSF] is a
clear, colorless transparent, tissue
fluid present in the cerebral
ventricles, spinal canal, and
subarachnoid spaces.
FORMATION CSF is largely formed by the choroid
plexus of the lateral ventricle and remainder in the third and fourth
ventricles.
About 30% of the CSF is also formed from the ependymal cells lining the
ventricles and other brain capillaries (perivascular space).
MECHANISM OF FORMATION OF CSF
CSF is formed primarily by secretion (active transportation) and also by
filtration from the net works of capillaries and ependymal cells in the
ventricles called choroid plexus.
The resulting characteristics of the CSF are:
Osmotic pressure approximately equal to that of plasma
sodium ion concentration Approximately equal to that of plasma
chloride ion About 15 per cent greater than in plasma
potassium ion approximately 40 per cent less
glucose 30 percent less
Rate of formation:
About 20-25 ml/hour
550 ml/day in adults. Turns over 3.7 times a day
Total quantity: 150 ml:
30-40 ml within the ventricles
About 110-120 ml in the subarachnoid space [of which 75-80 ml in spinal part and 25-30 ml in the
cranial part].
The brain tissue is separated from the plasma by three main interfaces
(a) blood–brain barrier (BBB),
(b) blood–cerebral spinal fluid barrier (BCSFB)
(c) arachnoid cells underlying the dura mater.
WHAT IS THE BLOOD BRAIN BARRIER
Structural and functional barrier which impedes and regulates the influx of most compounds from blood to brain
Formed by • endothelial cells (BMEC) of capillary• Basement membrane• Foot process of astrocytes
WHAT IS BLOOD CSF BARRIER
Lumen of blood capillaries separated by ventricle
Endothelial cell of capillaries Basement membrane Choroid epithelial cell with tight
junction
REGIONS OF BRAIN NOT ENCLOSED BY BBB
• Circumventricular organs –area postrema, –median eminence, –neurohypophysis, –pineal gland, –subfornical organ and – lamina terminalis
ABSORPTION OF CSF THROUGH ARACHNOID VILLI
The arachnoidal villi are fingerlike inward projections of the arachnoidal membrane
through the walls into venous sinuses.
The endothelial cells covering the villi have vesicular passages directly through the bodies
of the cells large enough to allow relatively free flow of (1) cerebrospinal fluid, (2)
dissolved protein molecules, and (3) even particles as large as red and white blood cells
into the venous blood.
REGULATION OF ABSORPTION
• Absorption of CSF occurs by bulk flow is proportionate to CSF pressure.:
• At pressure of 112 mm (normal average): filtration and absorption are equal.
• Below pressure of 68 mm CSF, absorption stops
COMPOSITION OF CSFProteins(Less than plasma)=20-40 mg/100 mlGlucose( Less than plasma )=50-65 mg/100 mlCholesterol= 0.2 mg/100 mlNa+(more)= 147 meq/Kg H2OCl+(more) =Ca+(less) = 2.3 meq/kg H2OUrea(less) = 12.0 mg/100 mlCreatinine = 1.5 mg/100 mlLactic acid = 18.0 mg/100 ml
CHARACTERISTICS OF CSFNature:Colour = Clear, transparent fluidSpecific gravity = 1.004-1.007Reaction = Alkaline and does not coagulateCells = 0-3/ cmmPressure = 60-150 mm of H2O
CIRCULATION OF CSFLateral ventricle
Foramen of Monro [Interventricular foramen]
Thirdventricle
Subarachnoid space of Brain and Spinal cord
Fourth ventricle:
Cerebral aqueduct
Foramen of megendie and formen of luschka
FUNCTIONS OF CSFA shock absorberA mechanical bufferAct as cushion between the brain and craniumAct as a reservoir and regulates the contents of the craniumServes as a medium for nutritional exchange Transport hormones and hormone releasing factors
Count. Function Remove metabolic wastes from CNS Serves as pathway for pineal secretion
to reach the pituitary gland. it protects against acute changes in
arterial and venous blood pressure; it is involved in intra-cerebral transport,
ex. hypothalamic releasing factors
HYDROCEPHALLUS:External hydrocephallus: Large amounts of
CSF accumulates when the reabsorptive capacity of arachnoid villi decreases.
Internal hydrocephallus: occurs when foramina of Luschka & Magendie are blocked or obstruction within ventricular system, resulting in distention of the ventricles.
Hydrocephalouscommunicating hydrocephalous :
fluid flows from the ventricular system into the subarachnoid space.
In communicating type blockage is in the subarchnoid space by blockage of arachnoidal villi themselves .
Non communicating : Fluid cant pass to the subarachnoid space In this type is blockage of the aqueduct of sylvius
. Obstruction of villi blockage ↑ CSF
pressure hydrocephalous may lead to edema .
INTRACRANIAL PRESSURE • ICP typically means the supratentorial CSF
pressure measured in the lateral ventricles or over the cerebral cortex.
• Normal ICP value is 10 mm Hg or130 mm of H2O
• Intracranial hypertension is defined as a sustained increase above 37 mm Hg or 300mm of H2O
MONORO-KELLIE HYPOTESIS
• The pressure-volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro-Kellie doctrine or the Monro-Kellie hypothesis.
• Since the cranium is a rigid structure with a fixed volume, comprising of CSF, brain, and blood. An increase in one of these components must be accompanied by an equivalent reduction in another to avoid a rise in ICP
• Initially, an increase in volume is met with little or no change in ICP. Ultimately, there is a point where minute increases in volume can result in a dramatic rise in ICP.
• Compensatory mechanisms that prevent the initial rise in ICP include:a) displacement of CSF from the cranial to spinal compartment,
b) decrease in production of CSF c) increase in absorption of CSF d) decrease in total cerebral blood volume
Clinical signs and symptoms that suggest increased ICP include:
1) Headache2) Nausea/vomiting3) Blurre vision4) Papilledema 5) Somnolence alter level of consciousness6) Pupillary dilatation7) Cushing triad• Bradycardia• Hypertension• Irregular respiration
CAUSES• mass effect such as brain tumor, infarction with
edema, contusions, subdural or epidural hematoma, or abscesses
• generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy, pseudotumor cerebri, . These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
• increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins.
• obstruction to CSF flow and/or absorption can occur in hydrocephalus , extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption
• increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
• Idiopathic or unknown cause (idiopathic intracranial hypertension)
• Cerebral venous sinus thrombosis
DISRUPT STRUCTURAL INTEGRATIY
LOCAL EDEMA
INCREASED COMPONENT IN CRANIUM
CHANGE IN VOLUME OF OTHER
BRAIN HAS LIMITED SPACE TO EXPAND
COMPANSATION WILL OCCURE
DISPLACEMENT INCREASED ABSORPTION
DECREASED CEREBRAL BLOOD VOLUME
ICP BEGAIN TO RISE
CHANGE IN LEVEL OF CONSCIOUSNESS
REDUCE CEREBRAL FURTHER BLOOD FLOW SWELLING
ISCHEMIA CUSHING REFLEX VASOMOTOR CENTER INCREASED ARTERIAL PRESSURE TO
COMPANSATE ICF
SYMPATHETIC RESPONSE
BRADYCARDIA IRREGULAR RESPIRATION HYPERTENSION
FURTHER SWELLING
AUTOREGULATIO PRODUCTION OF CSF DILATATION OF BV
MAINTAIN CBF
INEFFECTIVE DECOMPANSATIONAUTOREGULATION
SHIFTING OF BRAIN TISSUE FROM HEIGHER PRESSURE TO LOW PRESSURE
HERNIATION
ISCHEMIA DISTURBE VITAL CENTER
CESSATION OF CBF COMA
PERMENANT NEUROLOGICAL DEATH