1. INTRACRANIAL PRESSURE-VOLUME DYNAMICS2.CEREBRAL BLOOD VOLUME3.BBB4.CSF FORMATION & FLOW5.AETIOLOGY OF INTRACRANIAL PRESSURES AND TREATMENT6.CEREBRAL EDEMA7.HERNIATION SYNDROMES
Intracranial pressure- volume dynamicsPhysiologyThe 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 dynamicsAdult brain weighs about 1500 gms and contains 70% water.Water content of white matter - 68% & Cortex - 73%.Intracellular compartment - 1100-1300mlExtracellular space - 100-150mlIntracranial CSF volume - 75-100mlCerebral blood - 75-100ml
The volume of various compartments arecontrolled by local mechanisms such as : BBB CHOROID PLEXUS ENDOGENOUS BRAIN WATER PRODUCTION ARACHNOID VILLI
Systemic factors such as :VASOPRESSINATRIOPEPTIDESRENIN-ANGIOTENSINALDOSTERONE
Subcellular mechanisms of watertransport:Tight junction protiens in BBBPerivascularPeriependymal aquaporin family
These intracranial compartments are in dynamicequilibrium due to pulsations of heart and respiratoryregulated return of venous blood from the brain.MONROE-KELLY DOCTRINE If the volume of one of these compartmentsincreases, the volume of another must decrease tomaintain normal ICP (0-20mmhg).
CEREBRAL BLOOD VOLUMEIt is composed of arterial inflow,blood in thecapillaries and in the venous vessels.Cerebral blood flow is generally independent ofmean arterial pressure but it is closely regulated byarterial PaCO₂ systemically and locally by regionalfactors such as release of endothelin and NO.
The rate of venous out flow is controlled byintrathoracic pressure, patency of the majorvenous cranial sinuses and hydrostatic pressure.Under normal circumstances,cerebral bloodvolume totals about 150ml with average bloodvolumes in grey matter being 5.5ml blood per100ml of brain and 1.4ml blood per 100ml ofbrain 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 areassociated 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 beendocumented in healthy subjects and are probably caused by interaction between the cardiac and respiratory cycles.
Intracranial pressurewaveform recorded.. Following surgery foran intracranialtumour,there arebaseline oscillationsfrom 0-10mm hg withoccasional c waves of20-25mmhg. There is alsocharacteristic a waveor plateau wave thatlasts 5mts with apressure peak of 50-60mmhg.Pressure wavesof this magnitude canresult in brainherniations oralterations in conciousstate
Three pressure volume curves showing the changes in the intracranial pressure that can occur from a baselinepressure following a volumeinsult such as intracranialhaematoma.The curves representresponses of 3 individualssuch as a healthy Youngperson,middle aged person orelderly person with brainatrophy subject to the samevolume insult.For each givenunit of volume insult thepressure response is variablebecause of differences inbrain compliance.
RELATIONSHIP BETWEEN CEREBRAL PERFUSION PRESSURE AND INTRACRANIAL PRESSURE 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
Blood brain barrierLimits the egress of water and impedes efflux ofmost ions and other compounds from the vascularcompartment to brain extracellular space.Its role is to maintain a homeostatic environmentfor neurons to function effectively and to excludepotential toxic substances.
Blood-CSF barrier = Blood-brain barrier A physiological mechanism that alters thepermeability of brain capillaries, so that somesubstances, such as certain toxins and drugs, areprevented from entering brain tissue, while othersubstances are allowed to enter freely;Physically it consists of the capillary endothelialcells and their basement membranes and theprocesses of astrocytes associated with the capillarybeds 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 atransporter and receptor systems that controltransmembrane and transluminal physiology.Endothelial cells interconnected byintermembrane protiens comprise tight junctions
Tight junctions consists of 3 integral membrane protiens:ClaudinOccludinJunction adhesion moleculesAnd also a number of cytoplasmic accessoryprotiens such as zona occludens-1,2,3 and cingulin.
These cytoplasmic protiens link membraneprotiens to the cytoskeleton protien actin inorder to maintain the structural andfunctional integrity of the endothelium
A pericyte, also known as Rougetcell,adventitial cell or mural cell, isa connective tissue cell that occurs about small blood vessels
As a relatively undifferentiated cell(oligopotent), it serves to support thesevessels, but it can differentiate intoa fibroblast or a smooth muscle cell. In orderto migrate into the interstitium, the pericytehas to break the barrier, formed bythe basement membrane, which can beaccomplished by fusion with the membrane.Pericytes are important in blood-brainbarrier stability as well as angiogenesis.
Their expression of smooth muscle actin (SMA)and vimentin (or desmin in some cases wherethey are more likely to become smooth musclecells), and their adherence to the endovascularcells makes them very strong candidates forblood flow regulators in themicrovasculature, and indeed they have beenimplicated in blood flow regulation atthe capillary level. After ischemia, an irreversibleconstriction of pericytes may prevent brainblood flow being restored
Pericytes appear to play a key role inangiogenesis, structural integrity anddifferentiation of the vessel,and formation ofendothelial tight junctions.Astrocytic end feet release trophic factors arecritical for induction and maintenance of BBB.
The predominant aquaporin protien inCNS, aquaporin-4 is a major path way for osmoticallydriven water transport and is found within thepericapillary astrocytic foot processes,the externaland sub-ependymal glial limiting membrane,andwithin ependymal cells.Aquaporin-4 facilitates movement of water intoand out of the brain since disruption of the protiencan significantly alter patterns of brain oedema andwater clearance
Pathophysiological changes in the BBB, bloodosmolality, dysregulated blood flow, or increasedcapillary pressure will influence the permeabilityof BBB as well as passive diffusion of water, ions,protiens, and other compounds in the brain.
choroid plexus One of the delicate finger likeprocesses, consisting almost entirely of bloodvessels, which project into each of the fourventricles of the brain which are lined byspecialized ependymal cells which secretecerebrospinal fluid.
Choroid PlexusCSF FORMATION AND FLOW Formation of CSF at a pressure of 11 mmhg and at a rate of 0.3ml/mt 37
Cerebrospinal FluidFORMATION• 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 40
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
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 53
Etiologies of increased intracranial pressures1.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 syndrome2.INFECTIOUS:-Abcess or empyema with mass effect,Any meningitis or encephalitis(esp brucellosis,lyme disease,cryptococcosis)
6.TRAUMA:-Brain trauma with edema7.OTHERS:-Hydrocephalous,Pseudotumour cerebri,Reyes syndrome
Raised cerebral venous pressure have anaffect on intracranial pressurehaemodynamics and this has beenimplicated in pathogenesis of Idiopathicintracranial hypertension.
INDICATIONS FOR ICP MONITORING1. GCS <82. Severe head traumaICP WAVE FORMSA. PLATEAU A WAVESa. 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 toICP and risk for ischaemia.B. B WAVES:smaller surges in ICP to 20 mm hg for 1 to 2 mts
MANAGEMENT OF ↑ ICPMEASURE COMPARTMENT RECOMMENDEDGeneral Several Head of bed at 30 Normothermic Pain controlCSF drainage ↓ CSF External ventricular drain Lumbar drainHyperventilation ↓ blood Hyperventilation to PCO2 30 mm Hg (vasoconstriction)Osmotic diuresis ↓ brain volume Mannitol 0.25-1 g/kg bolus, then consider repeat q 8hr; titrate to serum osmolality < 310Barbiturates ↓ metabolic activity of Phenobarbital brain & thus blood flowHypothermai ↓ metabolic activity of Cooling blankets brain & thus blood flowSurgery ↓ brain If ICP not controlled by medical mx & surgical lesion present
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.
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 Reyes 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 asevere form of (sometimes fatal) altitudesickness. HACE is the result of swelling of braintissue from leakage of fluids from the capillariesdue to the effects of hypoxia onthe mitochondria-rich endothelial cells of theblood-brain barrier.Symptoms can includeheadache, loss of coordination(ataxia), weakness, and decreasing levels ofconsciousness including disorientation, loss ofmemory, hallucinations, psychotic behavior, andcoma. It generally occurs after a week or moreat high altitude.
Severe instances can lead to death if nottreated quickly. Immediate descent is anecessary life-saving measure (2,000 - 4,000feet). There are some medications(e.g. dexamethasone) that may be prescribedfor treatment in the field, but these requireproper medical training in their use. Anyonesuffering from HACE must be evacuated to amedical facility for proper follow-uptreatment. A gamow bag can sometimes beused to stabilize the sufferer before transportor descending.
Cingulate herniationIn 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 thebrainstem as the other types of herniation, but it mayinterfere with blood vessels in the frontal lobes thatare close to the site of injury (anterior cerebralartery), or it may progress to central herniation.Interference with the blood supply can causedangerous increases in ICP that can lead to moredangerous forms of herniation.
Symptoms for cingulate herniation are not welldefined.Usually occurring in addition to uncalherniation, cingulate herniation may present withabnormal posturing and coma.Cingulate herniation is frequently believed to be aprecursor to other types of herniation.
Central herniationIn central herniation, the diencephalon and parts ofthe temporal lobes of both of the cerebralhemispheres are squeezed through a notch in thetentorium cerebelli.Transtentorial herniation can occur when the brainmoves either up or down across the tentorium, calledascending and descending transtentorial herniationrespectively; however descending herniation is muchmore common.
Downward herniation can stretch branches of thebasilar artery (pontine arteries), causing them to tear andbleed, known as a Duret hemorrhage. The result is usuallyfatal.Radiographically, downward herniation is characterizedby obliteration of the suprasellar cistern from temporallobe herniation into the tentorial hiatus with associatedcompression on the cerebral peduncles.Upwards herniation, on the other hand, can beradiographically characterized by obliteration of thequadrigeminal cistern. Intracranial hypotension syndromehas been known to mimic downwards transtentorialherniation.
Uncal herniationIn uncal herniation, a common subtype oftranstentorial herniation, the innermost part of thetemporal lobe, the uncus, can be squeezed so muchthat it goes by the tentorium and puts pressure on thebrainstem, most notably the midbrain.The tentorium is a structure within the skull formedby the meningeal layer of the dura mater. Tissue maybe stripped from the cerebral cortex in a processcalled decortication
The uncus can squeeze the third cranial nerve, which may affectthe parasympathetic input to the eye on the side of the affectednerve, causing the pupil of the affected eye to dilate and fail toconstrict in response to light as it should.Pupillary dilation often precedes the somatic motor effects ofcranial nerve III compression, which present as deviation of the eyeto a "down and out" position due to loss of innervation to all ocularmotility muscles except for the lateral rectus (innervated by cranialnerve VI) and the superior oblique (innervated by cranial nerve IV).The symptoms occur in this order because the parasympatheticfibers surround the motor fibers of CNIII and are hence compressedfirst.
Compression of the ipsilateral posterior cerebral artery willresult in ischemia of the ipsilateral primary visual cortex andcontralateral visual field deficits in both eyes (contralateralhomonymous hemianopsia).Another important finding is a false localizing sign, the socalled Kernohans notch, which results from compression of thecontralateral cerebral crus containing descending corticospinaland some corticobulbar tract fibers. This leads to contralateral (opposite as herniation)hemiparesis. Since the corticospinal tract predominatelyinnervates flexor muscles, extension of the leg may also be seen
With increasing pressure and progression of the hernia there will bedistortion of the brainstem leading to Duret hemorrhages (tearing of smallvessels in the parenchyma) in the median and paramedian zones of themesencephalon and pons.The rupture of these vessels leads to linear or flamed shaped hemorrhages.The disrupted brainstem can lead to decorticate posture, respiratory centerdepression and death. Other possibilities resulting from brain stem distortioninclude 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 inthe midbrain and pons compression, possibly causing damage to the reticularformation. If untreated, death will ensue
Transcalvarial herniationIn transcalvarial herniation, the brain squeezesthrough a fracture or a surgical site in the skull. Also called "external herniation", this type ofherniation may occur during craniectomy, surgery inwhich a flap of skull is removed, preventing the pieceof skull from being replaced.
Upward herniationIncreased pressure in the posterior fossa can causethe cerebellum to move up through the tentorialopening in upward, or cerebellar herniation.The midbrain is pushed through the tentorial notch.
Tonsillar herniationIn tonsillar herniation, also called downwardcerebellar herniation, or "coning", the cerebellartonsils move downward through the foramenmagnum possibly causing compression of the lowerbrainstem and upper cervical spinal cord as they passthrough the foramen magnum. Increased pressure on the brainstem can result indysfunction of the centers in the brain responsible forcontrolling respiratory and cardiac function.
Tonsillar herniation of the cerebellum is also known as a ChiariMalformation (CM), or previously as Arnold Chiari Malformation(ACM).There are at least three types of Chiari malformation that arewidely recognized, and they represent very different diseaseprocesses with different symptoms and prognosis.These conditions can be found in asymptomatic patients as anincidental finding, or can be so severe as to be life-threatening.This condition is now being diagnosed more frequently byradiologists, as more and more patients undergo MRI scans oftheir heads
Cerebellar ectopia is a term used by radiologists to describecerebellar tonsils that are "low lying" but that do not meet theradiographic criteria for definition as a Chiari malformation.The currently accepted radiographic definition for a Chiarimalformation is that cerebellar tonsils lie at least 5mm belowthe level of the foramen magnum.Some clinicians have reported that some patients appear toexperience symptoms consistent with a Chiari malformationwithout radiographic evidence of tonsillar herniation.Sometimes these patients are described as having a Chiari[type] 0.
There are many suspected causes of tonsillarherniation including:Decreased or malformed posterior fossa (the lower,back part of the skull) not providing enough room forthe cerebellum, Hydrocephalus or abnormal CSF volume pushingthe tonsils out,Connective tissue disorders, such as Ehlers DanlosSyndrome.