INTRACRANIAL PRESSURE

AND

CEREBRAL EDEMA

1. INTRACRANIAL PRESSURE-VOLUME DYNAMICS

2.CEREBRAL BLOOD VOLUME

3.BBB

4.CSF FORMATION & FLOW

5.AETIOLOGY OF INTRACRANIAL PRESSURES AND TREATMENT

6.CEREBRAL EDEMA

7.HERNIATION SYNDROMES

Intracranial pressure- volume dynamics

Physiology

The skull is a fixed structure not allowing expansion.

Intracranial volume (1900 cubic cm) consists of three compartments:

Brain (80%) Blood (10%) CSF (10%)

Intracranial pressure - volume dynamics

Adult brain weighs about 1500 gms and contains 70% water.Water content of white matter - 68% & Cortex - 73%.

Intracellular compartment - 1100-1300mlExtracellular space - 100-150ml

Intracranial CSF volume - 75-100ml

Cerebral blood - 75-100ml

The volume of various compartments are controlled by local mechanisms such as :

BBBCHOROID PLEXUSENDOGENOUS BRAIN WATER PRODUCTIONARACHNOID VILLI

Systemic factors such as :

VASOPRESSIN

ATRIOPEPTIDES

RENIN-ANGIOTENSIN

ALDOSTERONE

Subcellular mechanisms of water transport:

Tight junction protiens in BBB

Perivascular

Periependymal aquaporin family

These intracranial compartments are in dynamic equilibrium due to pulsations of heart and respiratory regulated return of venous blood from the brain.

MONROE-KELLY DOCTRINE

If the volume of one of these compartments increases, the volume of another must decrease to maintain normal ICP (0-20mmhg).

CEREBRAL BLOOD VOLUME

It is composed of arterial inflow,blood in the capillaries and in the venous vessels.

Cerebral blood flow is generally independent of mean arterial pressure but it is closely regulated by arterial PaCO₂ systemically and locally by regional factors such as release of endothelin and NO.

The rate of venous out flow is controlled by intrathoracic pressure, patency of the major venous cranial sinuses and hydrostatic pressure.

Under normal circumstances,cerebral blood volume totals about 150ml with average blood volumes in grey matter being 5.5ml blood per 100ml of brain and 1.4ml blood per 100ml of brain for white matter.

The ICP waveform can also be analysed in the time domain - i.e. ICP waveform trend over time. This

may reveal typical Lundberg waves of ICP . A paper chart record connected to an analogue output from the ICP transducer often provides better

resolution than digital recording for detection of Lundberg waves. Lundberg A waves “or plateau waves” are steep increases in ICP lasting for 5 to

10 minutes. They are always pathological and represent reduced intracranial hypertension

indicative of early brain herniation. Lundberg B waves are oscillations of ICP at a frequency of 0.5

to 2 waves/min and are associated with an unstable ICP. Lundberg B waves are possibly the

result of cerebral vasospasm, because during the occurrence of these waves, increased velocity in the middle cerebral artery can be demonstrated

on transcranial Doppler.

Lundberg C waves are oscillations with a frequency of 4-8 waves/min. They have been

documented in healthy subjects and are probably caused by interaction between the cardiac and

respiratory cycles.

Intracranial pressure waveform recorded

.. Following surgery for an intracranial tumour,there are baseline oscillations from 0-10mm hg with occasional c waves of 20-25mmhg. There is also characteristic a wave or plateau wave that lasts 5mts with a pressure peak of 50-60 mmhg.Pressure waves of this magnitude can result in brain herniations or alterations in concious state

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Three pressure volume curves showing the changes in the intracranial pressure that can occur from a baseline pressure following a volume insult such as intracranial haematoma.

The curves represent responses of 3 individuals such as a healthy Young person,middle aged person or elderly person with brain atrophy subject to the same volume insult.For each given unit of volume insult the pressure response is variable because of differences in brain compliance.

FORMULA NORMAL

ICP 0 – 20 mm Hg

CPP = MAP - ICP 70 – 100 mm Hg

CBF = CPP / CVR 20 – 70 ml/100 g/min

MAP = DBP + 1/3 PP 70 – 110 mm Hg

RELATIONSHIP BETWEEN CEREBRAL PERFUSION PRESSURE AND INTRACRANIAL PRESSURE

Blood brain barrier

Limits the egress of water and impedes efflux of most ions and other compounds from the vascular compartment to brain extracellular space.

Its role is to maintain a homeostatic environment for neurons to function effectively and to exclude potential toxic substances.

Blood-CSF barrier = Blood-brain barrier

A physiological mechanism that alters the permeability of brain capillaries, so that some substances, such as certain toxins and drugs, are prevented from entering brain tissue, while other substances are allowed to enter freely;

Physically it consists of the capillary endothelial cells and their basement membranes and the processes of astrocytes associated with the capillary beds that serve the brain and spinal cord tissue.

Cellular elements of BBB

ENDOTHELIAL CELLS

ASTROCYTIC END FEET OR FOOT PROCESSES

PERICYTE

Within the structural components of bbb lie a transporter and receptor systems that control transmembrane and transluminal physiology.

Endothelial cells interconnected by intermembrane protiens comprise tight junctions

Tight junctions consists of 3 integral membrane protiens:

Claudin

Occludin

Junction adhesion molecules

And also a number of cytoplasmic accessory protiens such as zona occludens-1,2,3 and cingulin.

These cytoplasmic protiens link membrane protiens to the cytoskeleton protien actin in order to maintain the structural and functional integrity of the endothelium

A pericyte, also known as Rouget cell,adventitial cell or mural cell, is a connective tissue cell that

occurs about small blood vessels

As a relatively undifferentiated cell (oligopotent), it serves to support these vessels, but it can differentiate into a fibroblast or a smooth muscle cell. In order to migrate into the interstitium, the pericyte has to break the barrier, formed by the basement membrane, which can be accomplished by fusion with the membrane. Pericytes are important in blood-brain barrier stability as well as angiogenesis.

Their expression of smooth muscle actin (SMA) and vimentin (or desmin in some cases where they are more likely to become smooth muscle cells), and their adherence to the endovascular cells makes them very strong candidates for blood flow regulators in the microvasculature, and indeed they have been implicated in blood flow regulation at the capillary level. After ischemia, an irreversible constriction of pericytes may prevent brain blood flow being restored

Pericytes appear to play a key role in angiogenesis, structural integrity and differentiation of the vessel,and formation of endothelial tight junctions.

Astrocytic end feet release trophic factors are critical for induction and maintenance of BBB.

The predominant aquaporin protien in CNS, aquaporin-4 is a major path way for osmotically driven water transport and is found within the pericapillary astrocytic foot processes,the external and sub-ependymal glial limiting membrane,and within ependymal cells.

Aquaporin-4 facilitates movement of water into and out of the brain since disruption of the protien can significantly alter patterns of brain oedema and water clearance

Pathophysiological changes in the BBB, bloodosmolality, dysregulated blood flow, or increased capillary pressure will influence the permeability of BBB as well as passive diffusion of water, ions, protiens, and other compounds in the brain.

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Cerebrospinal fluid &

its circulation

choroid plexus

One of the delicate finger like processes, consisting almost entirely of blood vessels, which project into each of the four ventricles of the brain which are lined by specialized ependymal cells which secrete cerebrospinal fluid.

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Choroid Plexus

Formation of CSF at a pressure of 11 mmhg and at a rate of 0.3ml/mt

CSF FORMATION AND FLOW

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Cerebrospinal Fluid

FORMATION

• Secreted by choroid plexuses into each ventricle

• Choroid plexus are areas where the lining wall of the ventricle is very thin and has a profusion of capillaries

• At a pressure of 11mmHg

• At a rate of .3ml/mt

FACTORS INFLUENCING CSF FORMATION:

CSF Pressure

Hypoxia

pH

Hypoglycaemia

Drugs like acetazolamide, frusemide, amiloride, omeprazole, steroids

DRAINAGE

• From the roof of the 4th ventricle CSF flows through foramina into the subarachnoid space and completely surrounds the brain and spinal cord

• When CSF pressure is higher than venous pressure CSF passes into the blood and when the venous pressure is higher the arachnoid villi collapse, preventing the passage of blood constituents into the CSF

• The CSF passes back into blood through tiny diverticula of arachnoid mater called arachnoid villi (arachnoid granulations), which project into the venous sinuses

• Some reabsorption of CSF by cells in the walls of the ventricles occurs

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Force of circulation

• Movement of the CSF is by pulsating blood vessels, respiration and changes of posture

• CSF is secreted continuously at a rate of about 0.5ml per minute i.e. 720 ml per day

• Total CSF in the brain 120 ml

• CSF pressure can be measured by attaching a vertical tube to the lumbar puncture needle – 10 cm water

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Etiologies of increased intracranial pressures

1.VASCULAR:-ICH with mass effect,Epidural haemorrhage with mass effect,SAH,Large hemispheric stroke with mass effect,Venous thrombosis,Jugular vein ligation (radical neck dissection),SVC syndrome

2.INFECTIOUS:-Abcess or empyema with mass effect,Any meningitis or encephalitis(esp brucellosis,lyme disease,cryptococcosis)

3.INFLAMMATORY:-Behcets syndrome,SLE,Sarcoidosis

4.NEOPLASTIC:_Mass lesion,Carcinomatous meningitis

5.TOXIC/METABOLIC:-Vit A intoxication,

Endocrine disturbances, like-Adrenal insufficiency,Hyper-or hypoparathyroidism,Hyperthyroidism,

Hep encephalopathy,

Certain medications, like-Anabolic steroids,T.C,Cyclosporine

6.TRAUMA:-Brain trauma with edema

7.OTHERS:-Hydrocephalous,Pseudotumour cerebri, Reyes syndrome

Raised cerebral venous pressure have an affect on intracranial pressure haemodynamics and this has been implicated in pathogenesis of Idiopathic intracranial hypertension.

INDICATIONS FOR ICP MONITORING

1. GCS <8

2. Severe head trauma

ICP WAVE FORMS

A. PLATEAU A WAVES

a. Sudden surges in ICP to 50 to 80 mm hg lasting 5 to 20 mtsb. Presence of A waves suggests failing compliance of the brain to ICP and risk for ischaemia.

B. B WAVES:

smaller surges in ICP to 20 mm hg for 1 to 2 mts

MEASURE COMPARTMENT RECOMMENDEDGeneral Several Head of bed at 30

NormothermicPain control

CSF drainage ↓ CSF External ventricular drainLumbar drain

Hyperventilation ↓ blood (vasoconstriction)

Hyperventilation to PCO2 30 mm Hg

Osmotic diuresis ↓ brain volume Mannitol 0.25-1 g/kg bolus, then consider repeat q 8hr; titrate to serum osmolality < 310

Barbiturates ↓ metabolic activity of brain & thus blood flow

Phenobarbital

Hypothermai ↓ metabolic activity of brain & thus blood flow

Cooling blankets

Surgery ↓ brain If ICP not controlled by medical mx & surgical lesion present

MANAGEMENT OF ↑ ICP

CEREBRAL EDEMA:

Definition: Excess accumulation of water in the intra- and/or extracellular spaces of the brain.

Previously engorgement of cerebral vasculature was considered to be a major factor in brain swelling associated with neurotruma, however it is now considered that cytotoxic brain edema is the predominant factor causing brain swelling after neuro trauma.

Classification:Vasogenic edema:

• The disruption of the cerebral capillary provides the underlying mechanism for vasogenic edema.

The amount of edema is greatest in the white matter (increased water and sodium in the extracellular spaces, decreased potassium); but the same changes may take place in grey

matter but less so.

The astrocytes become swollen.

• This type of edema is seen in response to trauma, tumors, focal inflammation, and late stages of cerebral ischemia.

Edema vasogénico

Edema vasogénico

Interstitial oedema:-

• CSF pushed into extracellular space in preiventricular white matter in hydrocehalous

Cytotoxic edema:

• This is due to the derangement in cellular metabolism resulting in inadequate functioning of the sodium and potassium pump in the glial cell membrane.

As a result there is cellular retention of sodium and water.

There are swollen astrocytes in grey and white matter.

• Cytoxotic edema is seen with various intoxications (dinitrophenol, triethyltin, hexachlorophene, isoniazid) and in Reye's syndrome, severe hypothermia, and early ischemia.

Osmotic edema:

• Normally CSF and ECF osmolality in the brain is slightly greater than that of plasma.

• There is passage of water down abnormal gradient creating cerebral edema.

• When plasma is diluted by (SIADH syndrome of inappropriate Anti diuretic hormones, water intoxication, hemodialysis)

Hydrostatic edema:

• This form of cerebral edema is seen in acute, malignant hypertension.

• It is thought to result from direct transmission of pressure to cerebral capillary with transudation of fluid into the ECF.

High Altitude Cerebral EdemaHigh altitude cerebral edema (or HACE) is a severe form of (sometimes fatal) altitude sickness. HACE is the result of swelling of brain tissue from leakage of fluids from the capillaries due to the effects of hypoxia on the mitochondria-rich endothelial cells of the blood-brain barrier.Symptoms can include headache, loss of coordination (ataxia), weakness, and decreasing levels of consciousness including disorientation, loss of memory, hallucinations, psychotic behavior, and coma. It generally occurs after a week or more at high altitude.

Severe instances can lead to death if not treated quickly. Immediate descent is a necessary life-saving measure (2,000 - 4,000 feet). There are some medications (e.g. dexamethasone) that may be prescribed for treatment in the field, but these require proper medical training in their use. Anyone suffering from HACE must be evacuated to a medical facility for proper follow-up treatment. A gamow bag can sometimes be used to stabilize the sufferer before transport or descending.

Clinical presentation

• Headache• Tinnitus • Vomiting• Visual obscuration ,visual loss• Papilledema • Diplopia• Hypertension and Bradycardia• Herniation syndromes

TYPE PATHOGENESIS COMPOSITITION

LOCATION CSF FORMATION RATE

BBB

1.VASOGENIC BBB BREAKDOWN

WATER,Na AND PLASMA PROTIENS

PRIMARY EXTRACELLULAR, SECONDARY INTRACELLULAR

NOT ↑ DISTURBED

2.CYTOTOXIC DISTURBANCE OF CELLULAR METABOLISM

WATER,Na INTRACELLULAR ____

UNDISTURBED

3.OSMOTIC OSMOTIC GRADIENT

WATER INTRACELLULAR & EXTRACELLULAR

↑ UNDISTURBED

4.HYDROSTATIC HYDROSTATIC GRADIENT

WATER,Na EXTRACELLULAR ____ UNDISTURBED

CLASSIFICATION OF CEREBRAL EDEMA BASED ON PATHOGENESIS

EDEMA VASOGENIC CYTOTOXIC INTERSTITIAL

1.PATHOLOGY ↑CAPILLARY PERMEABILITY

CELLULAR SWELLING

↑BRAIN WATER DUE TO ↓ABSORPTION OF CSF

2.LOCATION OF EDEMA

WHITE MATTER GRAY&WHITE MATTER

PERIVENTRICULAR WHITE MATTER

3.COMPOSITION PLASMA FILTRATE Ĉ PLASMA PROTEINS

↑IC WATER & Na CSF

4.ECF ↑↑ ↓ ↑↑

5.CAUSES TRAUMA, TUMOUR, ABSCESS,INFARCT(LATE STAGES)

INFARCTS(EARLY)WATER INTOXICATION

OBSTR/COMMUNICATING HYDROCEPHALOUS

6.STEROIDS ++ ___ _____

7.MANNITOL ++ ++ _____

HERNIATION SYNDROMES

Cerebral edemaPathological increase in the water content of the brain

Increased intracranial pressure

Neurological deterioration

Herniation

Death

HERNIATION SYNDROMES

SUPRATENTORIAL

A. SubfalcineB. Central (diencephalic)C. Tentorial (uncal)D.Transcalvarial(external herniation)INFRATENTORIAL

A. Upward cerebellarB. Tonsillar

Cingulate herniation

In cingulate or subfalcine herniation, the most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri, the dura mater at the top of the head between the two hemispheres of the brain.

Cingulate herniation can be caused when one hemisphere swells and pushes the cingulate gyrus by the falx cerebri.

This does not put as much pressure on the brainstem as the other types of herniation, but it may interfere with blood vessels in the frontal lobes that are close to the site of injury (anterior cerebral artery), or it may progress to central herniation.

Interference with the blood supply can cause dangerous increases in ICP that can lead to more dangerous forms of herniation.

Symptoms for cingulate herniation are not well defined.Usually occurring in addition to uncal herniation, cingulate herniation may present with abnormal posturing and coma.

Cingulate herniation is frequently believed to be a precursor to other types of herniation.

Central herniation

In central herniation, the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium cerebelli.

Transtentorial herniation can occur when the brain moves either up or down across the tentorium, called ascending and descending transtentorial herniation respectively; however descending herniation is much more common.

Downward herniation can stretch branches of the basilar artery (pontine arteries), causing them to tear and bleed, known as a Duret hemorrhage. The result is usually fatal.

Radiographically, downward herniation is characterized by obliteration of the suprasellar cistern from temporal lobe herniation into the tentorial hiatus with associated compression on the cerebral peduncles.

Upwards herniation, on the other hand, can be radiographically characterized by obliteration of the quadrigeminal cistern. Intracranial hypotension syndrome has been known to mimic downwards transtentorial herniation.

Uncal herniation

In uncal herniation, a common subtype of transtentorial herniation, the innermost part of the temporal lobe, the uncus, can be squeezed so much that it goes by the tentorium and puts pressure on the brainstem, most notably the midbrain.

The tentorium is a structure within the skull formed by the meningeal layer of the dura mater. Tissue may be stripped from the cerebral cortex in a process called decortication

The uncus can squeeze the third cranial nerve, which may affect the parasympathetic input to the eye on the side of the affected nerve, causing the pupil of the affected eye to dilate and fail to constrict in response to light as it should.

Pupillary dilation often precedes the somatic motor effects of cranial nerve III compression, which present as deviation of the eye to a "down and out" position due to loss of innervation to all ocular motility muscles except for the lateral rectus (innervated by cranial nerve VI) and the superior oblique (innervated by cranial nerve IV).

The symptoms occur in this order because the parasympathetic fibers surround the motor fibers of CNIII and are hence compressed first.

Compression of the ipsilateral posterior cerebral artery will result in ischemia of the ipsilateral primary visual cortex and contralateral visual field deficits in both eyes (contralateral homonymous hemianopsia).

Another important finding is a false localizing sign, the so called Kernohan's notch, which results from compression of the contralateral cerebral crus containing descending corticospinal and some corticobulbar tract fibers.

This leads to contralateral (opposite as herniation) hemiparesis. Since the corticospinal tract predominately innervates flexor muscles, extension of the leg may also be seen

With increasing pressure and progression of the hernia there will be distortion of the brainstem leading to Duret hemorrhages (tearing of small vessels in the parenchyma) in the median and paramedian zones of the mesencephalon and pons.

The rupture of these vessels leads to linear or flamed shaped hemorrhages.

The disrupted brainstem can lead to decorticate posture, respiratory center depression and death. Other possibilities resulting from brain stem distortion include lethargy, slow heart rate, and pupil dilation.

Uncal herniation may advance to central herniation.

A complication of an uncal herniation is a Duret hemorrhage. This results in the midbrain and pons compression, possibly causing damage to the reticular formation. If untreated, death will ensue

Transcalvarial herniation

In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull.

Also called "external herniation", this type of herniation may occur during craniectomy, surgery in which a flap of skull is removed, preventing the piece of skull from being replaced.

INFRATENTORIAL

Upward herniation

Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation.

The midbrain is pushed through the tentorial notch.

Upward herniation

Upward herniation

Tonsillar herniation

In tonsillar herniation, also called downward cerebellar herniation, or "coning", the cerebellar tonsils move downward through the foramen magnum possibly causing compression of the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum.

Increased pressure on the brainstem can result in dysfunction of the centers in the brain responsible for controlling respiratory and cardiac function.

Tonsillar herniation of the cerebellum is also known as a Chiari Malformation (CM), or previously as Arnold Chiari Malformation (ACM).

There are at least three types of Chiari malformation that are widely recognized, and they represent very different disease processes with different symptoms and prognosis.

These conditions can be found in asymptomatic patients as an incidental finding, or can be so severe as to be life-threatening.

This condition is now being diagnosed more frequently by radiologists, as more and more patients undergo MRI scans of their heads

Cerebellar ectopia is a term used by radiologists to describe cerebellar tonsils that are "low lying" but that do not meet the radiographic criteria for definition as a Chiari malformation.

The currently accepted radiographic definition for a Chiari malformation is that cerebellar tonsils lie at least 5mm below the level of the foramen magnum.

Some clinicians have reported that some patients appear to experience symptoms consistent with a Chiari malformation without radiographic evidence of tonsillar herniation. Sometimes these patients are described as having a 'Chiari [type] 0'.

There are many suspected causes of tonsillar herniation including:

Decreased or malformed posterior fossa (the lower, back part of the skull) not providing enough room for the cerebellum,

Hydrocephalus or abnormal CSF volume pushing the tonsils out,

Connective tissue disorders, such as Ehlers Danlos Syndrome.

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