CEREBROSPINAL FLUID AND INTRACRANIAL PRESSURE DR IFRA ASHRAF

CEREBROSPINAL FLUID The 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 CSF CSF 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 SubstanceCSFPlasma Na K HCO PCO pH Osmolality Glucose

CHARACTERISTICS OF CSF Colour = Clear, transparent fluid Specific gravity = Reaction = Alkaline and does not coagulate Cells = 0-3/ cmm Pressure = mm of H2O

Rate of formation: About ml/hour 550 ml/day in adults. Turns over 3.7 times a day Total quantity: 150 ml: ml within the ventricles About ml in the subarachnoid space [of which ml in spinal part and ml in the cranial part]. DYNAMICS OF CSF

CIRCULATION OF CSF Lateral 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 CSF  A shock absorber  A mechanical buffer  Act as cushion between the brain and cranium  Act as a reservoir and regulates the contents of the cranium  Serves 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 BRAIN The 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 compartment  pressure 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)Headache 2)Nausea/vomiting 3)Blurre vision 4)Papilledema 5)Somnolence alter level of consciousness 6)Pupillary dilatation 7)Cushing triad Bradycardia Hypertension Irregular respiration

CAUSES mass effect such as brain tumor, hematoma, or abscesses brain tumorhematomaabscesses generalized brain swelling, acute liver failure, heart failureacute liver failure increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of veinsvenous sinus thrombosisheart failure obstruction to CSF flow and/or absorption can occur in hydrocephalus,, infection, carcinoma, granuloma, hemorrhage or obstruction in sinushydrocephalusinfectioncarcinomahemorrhage increased CSF production occurin meningitis, hemorrhage, or choroid plexus tumormeningitis

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 decompansation autoregulation shifting of brain tissue from heigher pressure to low pressure herniation

ISCHEMIA DISTURBE VITAL CENTER CESSATION OF CBF COMA PERMENANT NEUROLOGICAL DEATH