Cerebrospinal fluid and intracranial pressure

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Cerebrospinal fluid and intracranial pressure

  1. 1. CEREBROSPINAL FLUID AND INTRACRANIAL PRESSURE
  2. 2. CEREBROSPINAL FLUID The cerebrospinal Fluid [CSF] is aclear, colorless transparent, tissue fluid present in the cerebral ventricles, spinal canal, and subarachnoid spaces.
  3. 3. FORMATIONCSF 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 theventricles and other brain capillaries (perivascular space).
  4. 4. 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.
  5. 5. The resulting characteristics of the CSF are: Osmotic pressure approximately equal to that of plasma sodium ion concentrationApproximately 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
  6. 6. Rate of formation: About 20-25 ml/hour550 ml/day in adults. Turns over 3.7 times a day Total quantity: 150 ml: 30-40 ml within the ventriclesAbout 110-120 ml in the subarachnoid space [ofwhich 75-80 ml in spinal part and 25-30 ml in the cranial part].
  7. 7. The brain tissue is separated fromthe plasma by three main interfaces(a) blood–brain barrier (BBB), (b) blood–cerebral spinal fluid barrier(BCSFB) (c) arachnoid cells underlying thedura mater.
  8. 8. WHAT IS THE BLOOD BRAIN BARRIERStructural and functional barrier which impedes and regulates the influx of most compounds from blood to brainFormed by• endothelial cells (BMEC) of capillary• Basement membrane• Foot process of astrocytes
  9. 9. WHAT IS BLOOD CSF BARRIERLumen of blood capillaries separated by ventricle Endothelial cell of capillaries Basement membrane Choroid epithelial cell with tight junction
  10. 10. REGIONS OF BRAIN NOT ENCLOSED BY BBB• Circumventricular organs – area postrema, – median eminence, – neurohypophysis, – pineal gland, – subfornical organ and – lamina terminalis
  11. 11. 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 havevesicular 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.
  12. 12. 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
  13. 13. COMPOSITION OF CSFProteins(Less than plasma)=20-40 mg/100mlGlucose( Less than plasma )=50-65 mg/100mlCholesterol= 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
  14. 14. CHARACTERISTICS OF CSFNature:Colour = Clear, transparentfluidSpecific gravity = 1.004-1.007Reaction = Alkaline and doesnot coagulateCells = 0-3/ cmmPressure = 60-150 mm of H2O
  15. 15. CIRCULATION OF CSF Lateral ventricle Foramen of Monro [Interventricular foramen] Thirdventricle Cerebral aqueduct Fourth ventricle: Foramen of megendie and formen of luschSubarachnoid space of Brain and Spinal cord
  16. 16. FUNCTIONS OF CSFA shock absorberA mechanical bufferAct as cushion between the brain andcraniumAct as a reservoir and regulates thecontents of the craniumServes as a medium for nutritionalexchangeTransport hormones and hormone releasing
  17. 17. 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
  18. 18. 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.
  19. 19.  communicating hydrocephalous : 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 .
  20. 20. 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
  21. 21. 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
  22. 22. • 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
  23. 23. Clinical signs and symptoms that suggest increased ICP include:2) Headache3) Nausea/vomiting4) Blurre vision5) Papilledema6) Somnolence alter level of consciousness7) Pupillary dilatation8) Cushing triad• Bradycardia• Hypertension• Irregular respiration
  24. 24. 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.
  25. 25. • 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
  26. 26. DISRUPT STRUCTURAL INTEGRATIY LOCAL EDEMAINCREASED COMPONENT IN CRANIUM
  27. 27. CHANGE IN VOLUME OF OTHERBRAIN HAS LIMITED SPACE TO EXPAND
  28. 28. COMPANSATION WILL OCCURE DISPLACEMENT INCREASED ABSORPTIONDECREASED CEREBRAL BLOOD VOLUME
  29. 29. ICP BEGAIN TO RISE CHANGE IN LEVEL OF CONSCIOUSNESSREDUCE CEREBRAL FURTHERBLOOD FLOW SWELLING
  30. 30. ISCHEMIA CUSHING REFLEX VASOMOTOR CENTER INCREASED ARTERIAL PRESSURE TO COMPANSATE ICF SYMPATHETIC RESPONSE
  31. 31. BRADYCARDIA IRREGULAR RESPIRATION HYPERTENSION
  32. 32. FURTHER SWELLINGAUTOREGULATIO PRODUCTION OF CSFDILATATION OF BVMAINTAIN CBF
  33. 33. INEFFECTIVE DECOMPANSATIONAUTOREGULATIONSHIFTING OF BRAIN TISSUE FROM HEIGHER PRESSURE TO LOW PRESSURE HERNIATION
  34. 34. ISCHEMIA DISTURBE VITAL CENTERCESSATION OF CBF COMAPERMENANT NEUROLOGICAL DEATH

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