Physiology of the Cerebrospinal Fluid and Intracranial Pressure Chapter 10 Presentation: S. Bahram Seif, Resident of Neurosurgery Isfahan University of Medical Sciences

Protective and Homeostatic Systems of the CNS Skull Bones (physical protection) CSF (hydraulic shock absorption) Continuous Turnover of Extracellular Fluid (substrate supply and cellular homeostasis) BBB

Protective Systems can Become Detrimental

Elevated ICP Congenital lesions Neoplasms Metabolic syndromes Infectious syndromes Infarction Hemorrhage Trauma

HISTORICAL CONSIDERATIONS Galen Hippocrates Early Egyptian physicians Removing Pieces Of Skull

Monro-Kellie Doctrine 19th Century Alexander Monro George Kellie Monro-Kellie Doctrine

Lumbar Puncture 1911 Quincke 1951 continuously ICP monitoring Lundberg

NORMAL INTRACRANIAL PRESSURE Upper limit of normal ICP: 15 mmHg Usual range is 5 to 10 mmHg Coughing or Sneezing: 30 to 50 mmHg

mmHg x 1.36 = cmH2O

ICP Evaluation Intraventricular Intraparenchymal Subdural Epidural

CSF Pulsatility Associated with Cardiac and Respiratory activity Changes in these pulsatile components can be one of the earliest signs

Cardiac Component Left ventricular contraction Peripheral arterial pulse Choroid plexus and pial arteries High-compliance venous blood vessels

Respiratory Component Generated by pressure changes in the thoracic and abdominal cavities

Percussion wave (WI), the most constant, Pulsations in large intracranial arteries. Tidal wave (W2), brain elastance. Dicrotic wave (W3), dicrotic notch in the arterial.

ICP is synonymous with CSF Pressure

Atmospheric pressure Hydrostatic pressure Filling pressure

As volume is added there are two principal routes for compensation

Distention of the spinal dura mater Displacement of CSF and blood

ICP depends on the total volume inside the skull

Intracranial Space: 1500-mL 87%: the Brain 9%: CSF (ventricles, cisterns, and subarachnoid space) 4%: blood

CSF Compartmental Extracellular space 164.5 mL

CSF Production Choroid plexuses Ventricular ependyma

Choroid Plexuses Invaginations of the pia mater into the ventricular cavities Roofs of the third and fourth ventricles Walls of the lateral ventricles

Energy-dependent secretion and reabsorption processes 0.35 to 0.37 mL/min

Higher sodium, chloride, and magnesium Lower potassium, calcium, urea, and glucose Similar osmolality

Peak Production Rates Late evening Early morning

CSF pressures of less than 5 mm Hg CSF Drainage Dural Venous System Even in CSF pressures of less than 5 mm Hg

NPH Ventricular enlargement Absence of elevated ICP

Gait disturbance Dementia Incontinence

Lumbar Pressures: 6 to 24 cm H2O.

Symptoms and Signs of Elevated Intracranial Pressure Depends greatly on the nature and anatomic location of the underlying pathologic condition Headache, vomiting and papilledema.

Cranial nerve palsies may arise as a result of pressure on brainstem nuclei (particularly abducens palsies)

Papilledema Reliable Objective Good specificity Sensitivity: observer dependent

Vital Sign Changes Cushing response: Arterial Hypertension and Bradycardia

CPP = MAP - ICP

Abnormal Respiration Cheyne-Stokes: diencephalic region Sustained hyperventilation: midbrain and upper pons Slow respiration: Midpontine Ataxic respirations: pontomedullary lesions Rapid shallow breathing: upper medullary lesions

Herniation Syndromes Most serious complication of raised lCP

Central Syndrome Progressive dysfunction of structures in a rostral to caudal direction 1st Diencephalic Structures: Change in behavior or even loss of consciousness, Cheyne-Stokes respiration Pupils :small, with a poor reactivity Contralateral hemiparesis Pupils fall into a midline fixed position

Uncal Syndrome Unilaterally dilated and poorly reactive pupil External oculomotor ophthalmoplegia Ipsilateral hemiparesis: pressure on the contralateral cerebral peduncle on the edge of the tentorium cerebelli

INTRACRANIAL PRESSURE MONITORING Benefitial for Outcome

A Waves (plateau waves) Increases of ICP for several minutes Return spontaneously to a new baseline which is usually slightly higher

Vasodilation: normal compensatory response to decreases in CPP, effective management involves the use of vasopressors

B Waves Vasodilation: secondary to respiratory fluctuations in PaC02 Ventilated patients

C Waves More rapid sinusoidal fluctuations occurring approximately every 10 seconds Fluctuations in arterial pressure.

Intracranial Hypertension 40% to 60% of severe head injuries Major factor in the deaths of 50% of all fatalities. ICP above 20 mm Hg is highly significant in predicting outcome

Indications GCS: 3 to 8 and an abnormal CT If CT is normal, 2 of these shoud be present: 1)Age older than 40 years 2)Unilateral or bilateral motor posturing 3)Systolic BP below 90 mm Hg GCS>8 and significant mass lesions

Reye's syndrom Fulminant Hepatic failure

METHODS Gold standard: Ventriculostomy Infection rises after 5 days (10%) Hemorrhagic Complications(2%) Parenchymal monitors: less than 1% infective complications. Parenchymal monitors: regional inaccuracy

Device is zeroed at the level of the foramen of monro, using the external acoustic meatus as an anatomic landmark.

There is no uniform agreement about the critical level of ICP beyond which treatment is mandatory. 15 mm Hg 20 mm Hg CPP

MANAGEMENT OF INTRACRANIAL PRESSURE

VCSF Temporary external drainage Ventriculosubgaleal shunt Ventriculoperitoneal shunt

Medications Acetazolamide, furosemide, and corticosteroids can transiently decrease CSF production. Acetazolamide also has a cerebral vasodilator effect & contraindicated in patients with closed head injury.

VBLOOD Hyperventilation: vasoconstriction of pial vessles Pa CO2 : 32-35 Head elevation

VBRAIN Prevention of cerebrovascular hypertension (Inderal) Colloid (Lund Protocol) Isotonic or hypertonic(Bollus) solutions

Steroids(Vasogenic & Intrestitial) Not effective in cytotoxic edema(TBI, Stroke, SAH, Meningitis, DKA)

Barbiturates Hypothermia Osmotic agents

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