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Raised Intracranial Tension

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RAISED INTRACRANIAL

TENSION(PART – 1)
D R . S I D D H A RT H
B
NORMAL VALUES
CSF PRODUCTION

• Cerebrospinal fluid (CSF) is a clear, colourless


ultrafiltrate of plasma with low protein content
(<40mg/dL - albumin)and few cells(3-5
lymphocytes).

• The CSF is mainly produced by the choroid


plexus, but also by the ependymal lining cells of
the brain’s ventricular system
RATE OF PRODUCTION AND
ABSORPTION
• Average rate of CSF formation is 21 to 22 mL/h (0.35
mL /min), or approximately 500 mL / day.

• Brain volume is normally approximately 1,400 mL.


• The entire reservoir of CSF is about 90 to 150 mL in the
normal adult, of which approximately 75 mL is intracranial,
75mL is vascular.
• Spinal CSF volume is about 50mL.

• Normal CSF pressure in recumbent position is 65 – 195


mm H2O
• Resorption requires a positive pressure of atleast 60
mmH2O in the subarachnoid space.
• CSF fills cerebral ventricles and subarachnoid
spaces around the brain and spinal cord.
• ISF(Interstitial fluid) circulates between the cells.

• Water moves into extracellular space along osmotic


gradient created at the Capillary – Abluminal
surface with the help of Na+/K+ ATPase pump.
• Glucose by Glut1 – Cerebral blood vessels
Glut3 – neurons
Glut5 - microglia
NEUROVASCULAR UNIT

• NEURONS, ASTROCYTES AND PERICYTES comprise


the Neurovascular (Gliovascular)Unit
• Total surface of capillary endothelial cells forms
the major interface between Blood and Brain.
(others – choroid plexus and arachnoid
granulations).
• At each of the above BBB interfaces, high
resistance junctions between cells exist – TIGHT
JUNCTIONS. (OCCLUDIN, CLAUDIN)
• These impede non lipid soluble substances,
charged substances, large molecules.
• On the abluminal surface of endothelial cells –
thin layer of basal lamina  Type 4 collagen 
binding sites for Laminin and fibronectin; act as
barriers to charged particles by heparan sulphate
• Entactin connects type 4 collagen and Laminin –
gives structure to capillary.
• Fibronectin from cells joins basal lamina to
endothelium

• Within the basal lamina – pericyte  smooth


muscle + macrophage
TIGHT JUNCTION
• Zona occludins tether tight junction proteins to
Actin in the endothelium.
• Occludin attaches to zona occludin
• Claudin attach to occludin and protrude into clefts
between cells – ZipLocked

• After injury, astrocytes release HYALURON 


impedes movement of fluids in extracellular
space and slows tissue repair.
LET’S DO THE MATH!

• Remember OHM’S LAW?


• E = IR

• Pcsf – Pv = I0 * R
• In the steady state, this flow rate is equal to the
rate of CSF production (0.3 mL/min).
• R0, the resistance to absorption, which under
normal circumstances is approximately 2 .5

• P csF = P v + I x R0.
• The product of I x R0 is only 0.8 mm Hg
• The main contribution to CSF
pressure-as measured by spinal
puncture-is the Venous Pressure
MONROE KELLIE DOCTRINE

• Total volume of fluid and tissue contained within the


skull is constant.

• The intact cranium and vertebral canal, together


with the relatively inelastic dura, form a rigid
container, such that an increase in the volume of
any of its contents-brain, blood, or CSF-will elevate
the ICP.
• Furthermore, an increase in any one of these
components must be at the expense of the other
two
CEREBRAL EDEMA

• CYTOTOXIC/Cellular Swelling
• VASOGENIC/Vascular leakage
• INTERSTITIAL
VASOGENIC EDEMA

• Damage to capillary (Proteases - MMPs, Free


radicals) disruption of BBB  expansion of
extracellular space.
• Protein and blood products enter brain tissue 
Increase oncotic pressure.

• Steroids suppress expression of MMPs and other


inflammatory mediators.
CYTOTOXIC EDEMA

• Pathological process that damages cell


membranes (activation of MMP2, MMP3,MMP
9,COX2) constricts extracellular space.

• Stroke causes failure of ATP pumps  Increase in


brain water.
• Seen within 24 – 72 hours after a stroke.

• IntraCerebral Hemorrhage causes both Cytotoxic


and Vasogenic edema( mass effect and release of
toxic blood products)
TREATMENT

• Reduction of volume in one of the 3


compartments-

1. Blood Volume – hyperventilation


2. CSF Volume – placing ventricular drains
3. Brain volume – mannitol(0.25-1g/kg)
• Steroids lower ICP in Vasogenic edema – reduce
blood vessel permeability.
• CONTRAINDICATED in treatment of edema
secondary to stroke/ hemorrhage
• Edema surrounding brain tumours respond
particularly well( Take contrast enchanced images
before giving steroid – closure of BBB –
enhancement of lesion can be missed)
BASIS FOR MRI

• Resonance signals detected by MRI are from


water molecule protons.
• Cytotoxic edema SHRINKS extracellular space –
restricts diffusion of water  APPARENT
DIFFUSION COEFFICIENT (ADC) shows a loss of
signal  appears BLACK on MRI, Whereas the
DIFFUSION WEIGHTED IMAGE (DWI) has a BRIGHT
signal (within minutes of cerebral ischaemia)

• Dark ADC + Bright DWI = INFARCT


CEREBRAL PERFUSION PRESSURE

• The numerical difference between ICP and mean


BP within the cerebral vessels

• normal value is 60 to 100 mm Hg


• When these compensatory
mechanisms have been
exhausted, ICP rises rapidly
with further increases in
volume until it reaches the
level comparable with the
pressure inside of cerebral
arterioles.

• At this point, the rise of ICP is


halted as cerebral arterioles
begin to collapse and the
blood flow completely ceases.
• The relationship between ICP and CBF and
functional effects was described thoroughly by
Symon and colleagues, as follows: [32]
• CBF of 50 mL/100 g/min: Normal
• CBF of 25 mL/100 g/min: Electroencephalogram
slowing
• CBF of 15 mL/100 g/min: Isoelectric
electroencephalogram
• CBF of 6 to 15 mL/100 g/min: Ischemic penumbra
• CBF of less than 6 mL/100 g/min: Neuronal death
CAUSES OF RAISED ICT

• Space-occupying lesions: Tumor, abscess, intracranial hemorrhage


(epidural hematoma, subdural hematoma, intraparenchymal
hematoma)
• CSF flow obstruction (hydrocephalus): Space-occupying lesion that
obstructs normal CSF flow, aqueductal stenosis, Chiari malformation
• Cerebral edema: Due to head injury, ischemic stroke with vasogenic
edema, hypoxic or ischemic encephalopathy, postoperative edema
• Increase in venous pressure: Due to cerebral venous sinus
thrombosis, heart failure, superior vena cava or jugular vein
thrombosis/obstruction
• Metabolic disorders: Hypo-osmolality, hyponatremia, uremic
encephalopathy, hepatic encephalopathy
• Increased CSF flow production: Choroid plexus tumors (papilloma or
carcinoma)
• Idiopathic intracranial hypertension
• Pseudo tumor cerebri
NEXT TIME……
THANK YOU

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