CEREBROSPINAL FLUID AND INTRACRANIAL

PRESSURE

DR IFRA ASHRAF

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%from the ependymal cells lining the ventricles and

other brain capillaries (perivascular space).

CHOROID PLEXUS• The choroid plexus consist of

highly vascularized, "cauliflower-like" masses of pia mater tissue that dip into pockets formed by ependymal cells.

• These ependymal cells have microvilli on the CSF side, form a continuous sheet around the choroid plexus.

MECHANISM OF FORMATION OF CSFCSF is formed primarily by

secretion (active

transportation) and by

filtration from the net works of

capillaries and ependymal cells

in the ventricles called choroid

plexus.

COMPOSITION OF THE CSF

• The composition of CSF is essentially the same as brain ECF

Substance CSF Plasma

Na+ 147 150

K+ 2.9 4.6

HCO3- 25 24.8

PCO2 50 39.5

pH 7.33 7.4

OsmolalityGlucose

28964

289100

CHARACTERISTICS OF CSF

Colour = Clear, transparent fluidSpecific gravity =1.004-1.007Reaction = Alkaline and does not coagulateCells = 0-3/ cmmPressure = 60-150 mm of H2O

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].

DYNAMICS OF CSF

CIRCULATION OF CSFLateral ventricle

Foramen of Monro [Interventricular foramen]

Third ventricle

Subarachnoid space

Fourth ventricle:

Cerebral aqueduct

Foramen of megendie , luschka

ABSORPTION OF CSF

The arachnoidal villi are fingerlike inward projections of the arachnoidal membrane through the walls into venous sinuses.

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

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

BARRIERS IN BRAINThe brain tissue is separated from the plasma by two main barrier

(a) blood–brain barrier (BBB),

(b) blood–cerebral spinal fluid barrier (BCSFB)

.

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 THE BLOOD BRAIN BARRIER

WHAT IS BLOOD CSF BARRIER

Lumen of blood capillaries separated by ventricle

Endothelial cell of capillaries Basement membrane Choroid epithelial cell with

tight junction

Blood CSF barrier

TIGHT JUNCTION

REGIONS OF BRAIN NOT ENCLOSED BY BBB

• Circumventricular organs –area postrema, –median eminence, –neurohypophysis, –pineal gland, –subfornical organ and –lamina terminalis

HYDROCEPHALLUS:• External hydrocephallus or communicating: Large amounts of CSF accumulates when the reabsorptive capacity of arachnoid villi decreases.

• Internal hydrocephallusr or non communicating : occurs when foramina of Luschka & Magendie are blocked or obstruction within ventricular system, resulting in distention of the ventricles.

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

Intracranial compartment is a rigid container and consists of three components•a. brain-80% of total volume •b. blood-10% of total volume •c. CSF-10% of total volume An increase in one of these components must be accompanied by an equivalent reduction in another to avoid a rise in ICP

MONRO-KELLIE HYPOTESIS

to maintain a normal ICP, a change in the volume of one compartment must be offset by a reciprocal change in the volume of another compartmentpressure is normally well-controlled through alterations in the volume of blood and CSF

• 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, hematoma,

or abscesses • generalized brain swelling , acute liver

failure, heart failure• increase in venous pressure can be due

to venous sinus thrombosis, heart failure, or obstruction of veins

• obstruction to CSF flow and/or absorption can occur in hydrocephalus , , infection, carcinoma, granuloma,  hemorrhage or obstruction in sinus

• increased CSF production  occurin meningitis, hemorrhage, or choroid plexus tumor

disrupt structural integrity

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 began to rise

change in level of consciousness

reduce cerebral further blood flow swelling

ischemia cushing reflex vasomotor center

increased arterial pressure to

compensate increased ICP

bradycardia irregular respiration hypertension

further swelling

autoregulatio 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