This document outlines the essentials of intracranial pressure (ICP), including the physiology of cerebrospinal fluid (CSF) production and flow, normal ICP physiology and the pathophysiology of increased ICP. It discusses ICP waveform interpretation, monitoring technologies and treatment of elevated ICP. CSF is produced by the choroid plexus and absorbed through arachnoid villi. ICP is regulated by the Monroe-Kellie doctrine. Increased ICP can result from mass lesions, edema, venous outflow obstruction or CSF abnormalities. ICP monitoring is most accurate via external ventricular drain. Treatment focuses on reducing CSF volume and space-occupying lesions while maintaining cerebral perfusion pressure.

1. ESSENTIALS
OF
INTRACRANIAL PRESSURE
FACEBOOK: HAPPY FRIDAY KNIGHT
MARCH, 12TH, 2020

2. OUTLINES
• Production and flow of CSF
• Physiology of ICP and Pathophysiology of increased ICP
• ICP waveform and interpretation
• ICP monitoring and technology
• Treatment of elevated ICP

3. PRODUCTION AND FLOW OF
CEREBROSPINAL FLUID (CSF)

4. PRODUCTION AND FLOW OF CSF
• CSF: predominately produced by choroid plexuses
• Absorption at cranial and spinal arachnoid villi (granulations)
• Volume: 125 – 150 ml: 25 ml in ventricles, 125 ml in subarachnoid
spaces
• Active and delicately controlled secretion + normal absorption =
ICP stable

6. Sakka L, Coll G, Cazal J. Anatomy and physiology of cerebrospinal
fluid. European annals of otorhinolaryngology, head and neck
diseases. 2011;128:309-316.

7. • Variation
• Adult humans normally form CSF 0.35 ml/min  400 - 600 ml/day
• CSF dynamics affect brain metabolism
• CSF formation fluctuates in disease
• Hypersecretion: choroid plexus papillomas
• Hyposecretion: NPH, AD
PRODUCTION AND FLOW OF CSF

8. PHYSIOLOGY OF CSF: PRESSURE
• CSF Pressure: 10 – 15 mmHg in adult that varies with
• Systolic pulse wave
• Respiratoy cycle
• Abdominal pressure
• Jugular venous pressure
• State of arousal
• Physical activity
• posture

9. COMPOSITION OF CSF
• 99% water
• Na, Cl, Mg: higher concentration than those in plasma
• K, Ca: lower concentration than those in plasma
• CSF cell count: < 5cells/mL, no PMN, no RBC
• Loop diuretics and carbonic anhydrase: reduce CSF secretion and
turnover (3-5 times daily)

10. PHYSIOLOGY OF INTRACRANIAL PRESSURE (ICP)
AND PATHOPHYSIOLOGY OF INCREASED ICP

11. PHYSIOLOGY OF ICP
• ICP = CSF pressure
• dynamic
• Then ICP is reflective of
• CSF formation
• Volume storage or compliance
• CSF absorption

12. MONROE-KELLIE DOCTRINE
• Vother: volume of any abnormal component  hematoma, tumor
• Cranium is
• Nonexpandable
• incompressible

13. VOLUME
• Brain parenchyma: 1400 ml
• Cerebral blood volume: 150 ml
• CSF volume: 150 ml

14. Reilly P. Management of intracranial pressure and cerebral perfusion. Head injury. London, 1997.

15. CEREBRAL BLOOD FLOW
• CPP = MAP - ICP
• Pressure autoregulation: MAP 50-150 mmHg is autoregulated to
maintain constant CBF

17. PATHOPHYSIOLOGY
• A change in components at intracranial space

18. RESULTS OF RASING ICP
• CSF can be displaced from ventricles and subarachnoid spaces and
exit intracranial compartment via foramen magnum
• Intravenous blood: displaced via IJVs
• Arterial vasoconstriction: diffuse cerebral ischemia
• Cerebral herniation

20. RESULTS OF RASING ICP: CT BRAIN
• Midline shift
• Obliteration of CSF cisterns

21. PATHOPHYSIOLOGY: CSF
• Acute obstruction of CSF flow: acute hydrocephalus
• Hypersecretion of CSF: structurally or functionally alteration of
choroid plexus secretion
• Choroid plexus papillomas and hyperplasia
• Malabsorption of CSF: cribiform plate obstruction
• Obstruction of venous outflow

22. PATHOPHYSIOLOGY: BLOOD
• Arterial system
• Vasodilatation: hypercapnia, drug reaction
• Venous system
• Obstruction of venous outflow: thrombosis, inappropriate position
of head and neck, pneumothorax

23. PATHOPHYSIOLOGY: BRAIN EDEMA
• Vasogenic
• Cytotoxic
• Interstitial
• osmotic

24. PATHOPHYSIOLOGY: MASS OCCUPYING LESION
• Tumor
• Hemorrhage
• Infection: abscess

25. CLINICAL PRESENTATION OF RAISED ICP
• Quite unreliable
• pupil asymmetry
• Unilateral abnormal posture
• Signs of brain herniation: Cushing’s triad
• Hypertension
• Bradycardia
• Respiratory irregularity

26. ICP WAVEFORM AND INTERPRETATION

27. ICP WAVEFORM
• Gold standard: interventricular monitoring through
ventriculostomy
• Other technologies: devices inserted into
• Epidural space
• Subdural space
• Subarachnoid space
• Brain parenchyma

28. • 3 characteristic peak of decreasing height + correlate with arterial
waveform:
• P1: percussion wave  arterial pulse
• P2: tidal wave  cerebral compliance
• P3: dicrotic wave  aortic valve closure
ICP WAVEFORM: NORMAL

29. https://derangedphysiology.com/main/required-reading/neurology-and-neurosurgery/Chapter%201.0.5/interpretation-
intracranial-pressure-waveforms

30. https://derangedphysiology.com/main/required-reading/neurology-and-neurosurgery/Chapter%201.0.5/interpretation-
intracranial-pressure-waveforms
Cardiac cycle
• This reflects changes in intrathoracic pressure with respiration.
• This respiratory variation in ICP diminishes and eventually disappears altogether as
intracranial pressure increases.

31. ICP INTERPRETATION: RISING ICP
• Increasing all amplitudes
• Waveform morphology
doesn’t change

32. ICP INTERPRETATION: DECREASING CEREBRAL
PREFUSION
• Decrease amplitude of P1
• Due to P1=reflective of
arterial pulse in choroid
plexus
• Vasospasm if no raised ICP

33. ICP INTERPRETATION: DECREASING CEREBRAL
COMPLIANCE
• Prominent P2
• Increase in cerebral
bulk: edema
• Vasospasm if no
raised ICP

34. ICP INTERPRETATION: INCREASING ICP
• Flattening of ICP
breathing variation

35. ICP INTERPRETATION: LUNDBERG WAVES
• Pathological waveforms defined by Dr. Nils Lundberg
• Not frequently seen but if so, in patients with resistant to
therapeutic interventions, is the sign of worse outcome
• Designated as
• A: plateau wave
• B: pressure pulse
• C: Traube-Hering arterial waves

36. LUNDBERG “A” WAVES
• Plateau waves
• ICP elevation to 50 mmHg
for 2 – 20 minutes then
abrupt fall to baseline
• Intact cerebral blood flow
autoregulation
• But impending
uncontrollable ICP

37. LUNDBERG “A” WAVES
• 4 phases
1. Drift: decrease CPP  vasodilatation
2. Plateau: vasodilatation  increase ICP
3. Ischemic response phase: decrease CPP  cerebral ischemia 
brainstem vasomotor trigger  cushing response
4. Resolution: cushing response  restore CPP

38. LUNDBERRG “B” WAVES
• ICP elevation 10 – 20 mmHg
lasting 30 sec – 2 minutes
• Depends on periodic breathing
(PaCO2), increased ICP,
decrease cerebral compliance
• Unclear value in clinical
practice

39. LUNDBERG “C” WAVES
• Similar to B waves but
more rapid sinusoidal
fluctuation
• Seen in normal ICP
waveform
• Suggestive but not
pathognomonic of
increased ICP

40. ICP MONITORING: METHODS AND TECHNOLOGIES

41. ICP MONITORING: METHODS AND TECHNOLOGIES
• Anatomical locations of device insertion
• Standard ICP monitoring: external ventricular drain
• Indications
• Points of insertion
• Insertion technique
• Complications
• Other technologies

42. ANATOMICAL LOCATIONS OF DEVICE INSERTION
• Intraventricular – gold standard
• Intraparenchymal
• Subarachnoid
• Subdural
• epidural
https://www.openpr.com/news/476693/global-intracranial-
pressure-icp-monitoring-devices-market-raumedic-medtronic-
vittamed-spiegelberg-sophysa-ltd.html

43. EXTERNAL VENTRICULAR DRAIN
• A catheter placed into one of the ventricles through burr hole
• Gold standard
• Cost effective
• Most invasive
• Can also be used for CSF drainage and administration of medicine
intrathecally

44. Winn, H. Richard. Youmans and Winn’s Neurological Surgery. Phildelphia: Elsevier, 2017.

45. ICP MONITORING: INDICATIONS
• Traumatic brain injury with GCS ≤ 8
• Subarachnoid hemorrhage
• Intracranial tumor
• Intracranial hemorrhage
• Stroke
• Hydrocephalus
• CNS infection
• Fulminant hepatic failure

46. ICP MONITORING: POINTS OF INSERTION
• Anterior access
• Kocher: frontal (coronal) – 2
• Paine
• Tubbs - 6
• Kaufman - 5
• Posterior access
• Keen: posterior parietal - 1
• Frazier: occipital-parietal - 4
• Dandy: occipital - 3

47. KOCHER’S POINT
• 3 cm from midline
• 1 cm anterior to coronal
suture
• Point needle to nasion
and tragus
• Most common point
https://link.springer.com/referenceworkentry/10.1007%2F978-
3-642-00418-6_544

48. PAINE’S POINT
• 2.5 cm superior to supraorbital
margin
• Anterior edge of temporalis muscle
• Used in aneurysmal surgery via an
interhemispheric approach

49. TUBBS’ POINT
• Transorbital access to frontal
horn
• Just medial to midpapilary
point to roof of orbit

50. KAUFMAN’S POINT
• 4 cm superior to nasion
• 3 cm lateral to midline
• Cosmetic concern but rapidly
drained

51. KEEN’S POINT
• 3 FB superior and posterior to
unfold pinna
• Placement in trigone
• Point for VP shunt

52. FRAZIER’S POINT
• Occipital-parietal
• 6 cm above inion
• 3-4 cm from midline
• Point for VP shunt

53. DANDY’S POINT
• Occipital bur hole
• 3 cm above 2 cm lateral to inion
• Infants: correspond with lambdoid
suture in the midpupillary line
• Higher risk for visual impairment

54. INSERTION TECHNIQUE
• Right (non-dominant) side is preferred unless contraindication
• Kocher’s point: Incision is made in sagittal plane
• Elevate periosteum
• Apply self-retaining retractor
• Make a bur hole 1 – 2 cm anterior to coronal suture
• Control bleeding by bone wax and gelfoam
• Durotomy by blade No.11 and cauterize dural edge by bipolar

55. INSERTION TECHNIQUE
• Insert ventriculostomy needle perpendicular to brain surface (point to
nasion and tragus), not more than 7 cm depth
• Feel popping sensation and remove stylet
• Make a tunnel for the catheter
• Insert catheter
• Measure opened pressure, collect CSF, and measure closed pressure
• Fix catheter, hemostasis, and close the skin

56. COMPLICATIONS
• Intracranial and tract hemorrhage
• Infection: Ventriculitis
• Technical failure
• Over-drainage: transtentorial herniation
• Kinks and blockage by air, blood, and debris
• Inadvertent vascular injury.
• Pneumocephalus and pneumoventriculi.
• CSF leak.
• Accidental fracture
• Accidental pull
• Obstruction by choroid plexus, blood clot or proteinous plug

57. TECHNOLOGIES OF ICP MONITORING
• Fiberoptic intracranial pressure monitor
• Miniature strain gauge
• Spiegelberg parenchymal transducer
• Hummingbird synergy
• Telemetric ICP monitoring

58. TREATMENT OF INTRACRANIAL HYPERTENSION

59. PRINCIPLES
• ICP > 22 mmHg mandates aggressive clinical management (brain
trauma foundation 2016)
• Look for potential problems that exacerbate raised ICP
• Treat etiology:
• Space-occupying hematoma: craniotomy and evacuation
• Hydrocephalus: ventriculostomy and shunt
• Tumor: dexamethasone/excision
• Abscess: aspiration/excision

60. Czosnyka M, Pickard JD, Steiner LA. Principles of intracranial pressure
monitoring and treatment in Handbook of Clinical Neurology. Elsevier,
2017

61. FIRST LEVEL: PREVENTION
• Head elevation: up to 30o
• Maintain SBP:
• Age 50 – 69 keep SBP ≥ 100 mmHg, other keep SBP ≥ 110 mmHg
• Normocarbia (PaCO2 35 – 40 mmHg): no role of prophylactiv
hyperventilation
• Normothermia (36 – 37.5oC)
• Light sedation
• CT brain and check for surgical treatment options if ICP > 20 mmHg
• Avoid hyperglycemia

62. SECOND LEVEL: MORE INVASIVE
• CSF drainage in hydrocephalus
• Hyperosmolar treatment if evidence of herniation shown
• 20% mannitol 0.25 – 1 g/kg
• Hypertonic saline: keep Na < 155 meq/L
• Steroid in vasogenic edema
• Mild hyperventilation (PaCO2 30 – 34 mmHg): too long will cause
global ischemia

63. THIRD LEVEL: CONTROVERSY
• Decompressive craniectomy
• Consider deeper hypothermia: 33 – 34oC
• Consider barbiturate coma to maintain CPP

65. CONCLUSION

66. REFERENCES
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Sakka L, Coll G, Cazal J. Anatomy and physiology of cerebrospinal fluid. European annals of
otorhinolaryngology, head and neck diseases. 2011;128:309-316.
Tumani H, Huss A, and Buchhuber F. The cerebrospinal fluid and barriers – anatomic and physiologic
considerations in Handbook of clinical neurology. Vol3 (3rd series), 2018.
Kirkness CJ et al. Intracranial pressure waveform analysis: clinical and research implications. Journal of neuroscience
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67. REFERENCES
Kasprowicz M, Lalou DA, Czosnyka M, Garnett M, Czosnyka Z.
Intracranial pressure, its components and cerebrospinal fluid pressure–volume compensation. Acta Neurol
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Czosnyka M. Increased intracranial pressure: what to do and when?. www.ccmjournal.org. 2013:41(2):688-
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intracranial-pressure-waveforms

68. REFERENCES
https://www.researchgate.net/figure/Lundberg-waves-Lundberg-A-waves-are-ICP-increases-for-5-to-
10-minutes-They-reflect_fig2_311525129
Raboel PH et al. Intracranial pressure monitoring: invasive versus non-invasive methods – a review.
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69. REFERENCES
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