Causes and Consequences of Increased Intracranial Pressure

Causes and Consequences of change magnitude intracranial insistencyCONSEQUENCES OF INCREASED INTRACRANIAL PRESSUREWhat is the intracranial Pressure?Intracranial Pressure (ICP) is the hydrostatic twinge of the cerebrospinal silver-tongued (CSF) in the subarachnoid quadrangle 4.Cerebrospinal bland is a watery changeful circulating in the subarachnoid space surrounding the principal and the spinal cord. This still is synthesized by the choroid plexus in noetic heart ventricles and it is absorbed by the arachnoid granulations into the venous sinus system. So the CSF is the surrounding nature of the champion.Increased intracranial wardrobeNormal values for intracranial instancy be varying with age. Normal values for adults and older children argon 10 to 15 mmHg, 3 to 7 mmHg for young children and 1.5 to 6 mmHg for term infants. ICP whitethorn be sub atmospheric in newborns 5.Commonly 5 to 15 mmHg (7.5 to 20 cm H2O) is concerned to be normal adult ICP value 5. 20 to 30 mmHg v alues be concerned as mild intracranial hypertensions b bely 20 to 25 mmHg values requires treatments and values more than than 40 mmHg are severe life threatening situations 5.Causes for adjoin intracranialPressureIncreased intracranial squelch give nonice be get arounded each by an increase in the pressure in CSF or by a space occupying lesion (such(prenominal) as wiz tumors, bleeding in the genius, fluid surrounding the headway or swelling of the flair waver. plainly in some situations those two types of reasons faecal matter be interrelated with each other. (e.g. When the brain is swelling, its vasculature becomes flavorless and this whitethorn lead to increase ICP. in that location is a theory called Monroe Kellie Doctrine. According to that hypothesis, skull is an enclosed rigid structure containing no compressive structures such as brain, business line and CSF. So an increase in one constituent or an expanding of one of them answers in an increase in the i ntracranial pressure 6 Pg.76.Intracranial = Brain + CSF + Blood + Mass lesionVolume garishnessvolume volume volume but in infants, in the case of their skulls are not completely ossified, their skulls are some kind of incompatible with this hypothesis.According to that hypothesis an expanding push-down list, an increase in brain water content , an increase in intellectual split volume (by vasodilatation or venous outflow obstruction) or increase in CSF are the factors for an increase in intracranial pressure 6 Pg.76.However thither are some compensatory mechanisms for regulating intracranial pressure increases 6 Pg.76.Immediate actions 1. reducing of CSF volume (CSF outflow to the lumbar theca.2. Decrease of noetic blood volume.Delayed actions Decrease of duplication cellular fluid. at that place are number of suit of clothess responsible for change magnitude intracranial pressure. They may be either runring individually or in combination with others.Primary causes for inc reased ICP7,8,9This is similarly called as Intracranial Causes. They proceed within the cranium.Brain tumor Tumors lead to increase in brain volume. So according to the Monroe Kellie doctrine ICP increased.Trauma There are dissimilar types of head injuries. They can be close or open (penetrating) injuries. It can be lead to concussion (shaking of the brain as a turn outant role of trauma), scalp injuries, skull fractures. Those traumas may cause to bleeding within the brain tissue or bleeding in the layers that surrounds the brain.There are three types of bleedings encounterring in the layers surround the brain.Subarachnoid hemorrhage bleeding into the subarachnoid space.Subdural hematoma bleeding into the subdural spaceExtradural hematoma Bleeding into the epidural space.All those types of bleedings cause in increasing ICP.Non traumatic intra rational hemorrhage These hemorrhages can occur by aneurysm of cerebral arteries in the brain. Aneurysms are localized excessive swellings of an arterial wall. So they have more potential to rupture and this leads to subarachnoid hemorrhage. ischemic stroke Stroke (or Brain Attack) is the death of brain cells due to an pitiable blood flow 4.So in strokes, as a response to the brain cell death, brain swelling occurs.Hydrocephalus Hydrocephalus is an increase in CSF volume. Cerebrospinal fluid is secreted by the choroid plexus of the lateral, third and poop ventricles and flows in a caudal direction and enters the sub arachnoid space by dint of the foramina of Lushka and Magendie. At the end of the circulation absorb into the arachnoid granulations. Rate of validation CSF usually is about 500ml/day.Hydrocephalus occurs commonly due to impaired assimilation and rarely by excessive secretion. There are two types of hydrocephalus, preventative hydrocephalus Obstruction of the CSF flow within the ventricular system.Communicating hydrocephalus Obstruction of the CSF flow outside the ventricular system.Incr eased intracranial pressure can be seen as a direct effect of hydrocephalus.idiopathic (benign) intracranial hypertension 6 Pg. 363 This term means an increase in intracranial pressure without any mass lesion or hydrocephalus. Some clearly determine causative links (e.g. venous outflow obstruction to CSF absorption) or obscured causal links (e.g. diet, endocrine, hematological, drugs) cause for that.Other causes Pseudotumorcerebri, pneumocephalus, abscess, cyst.2. Secondary causes for increased ICPThese are as well as called as extra cranial causes. So it is ca utilize by extra cranial factors. Examples overwhelm,Airway obstructionHypertension or hypotensionHypoxia or hypercarbia billetSeizuresHyperpyrexiaDrugsOther (High altitude, cerebral edema, hepatic failure )3. Post-operative causes for increased ICPThis type of intracranial hypertension may occur after a neurosurgical procedure.Mass lesion/hematoma/edemaAn increase of cerebral blood volume by vasodilation.Disturbances o f CSF flow.clinical symptoms appear with increased intracranial pressure 11, 12Headache 11Papilledema This is the swelling of the oculus nerve occur most of times as a result of increased intracranial pressure 10.Projectile be sick This is a vomiting without nausea.Increased blood pressureDouble visionPupils do not respond to changes in lowerVisual field abnormality qualifying of peripheral and wanting(p) nasal visions.Seizure or convulsionsNeurological problems include balance issues, numbness and tingling, memory loss, paralysis, slurred or garbled address or inability to talk.COMAStiff neck Neck becomes loosely stiff and painfulnessful. Some researchers says the reason for that is the stretching of the spinal nerve sheaths where they sacking the spinal cord by the pressure passing down from the brain 10.Pain in the armsLoss of consciousnessBack painShallow breathingIn addition to those symptoms, in infants can be seen following 12,Separated sutures on the skullBulgin g fontanellaeNot feeding or responding normallyConsequences of increased intracranial pressureIntracranial hypertension is winding with the pressure in the skull or in another words, the pressure well-nigh the brain and the spinal cord. Therefore increased intracranial pressure becomes a life threatening situation. There are some possibilities or consequences of increased intracranial pressure involved.These complications can be categorized into different topics such as Displacement effects, Hydrocephalus, complications in cerebral perfusion, seizures.Displacement effects 5,3,6 pg. 76-80The cranial cavity is divided into compartments, separated by dural folds called falx cerebri and tentorium cerebelli. These folds limit brain structures within those compartments, but due to a space occupying lesion, pressure gradients occur in in the midst of these compartments. As a result brain shifts and hernia occur. This hernia can be categorized into two subjects,Supratentorial hernia (un cal, central, cingulate, transclaviral)Infratentorial herniation (upward, tonsillar)Supratentorial herniationSubfalcine herniation In this case the cingulate gyrus is pushed laterally away(p) from the expanding mass (like hematoma) beneath the falx cerebri. This may interfere with blood vessels in the facade lobes which are placed at the site of injury. This may cause intracranial bleeding and severe rise in intracranial pressure and more dangerous types of herniation. Symptoms are not clear related to this herniation but usually present with abnormal posturing and coma. This type of herniation can be a precursor to other types of herniation.Uncal (transtentorial, uncinate, mesial temporal) herniation This is the herniation of the Uncas in medial temporal lobe from the middle cranial pressure into the rear cranial fossa into the posterior cranial fossa across the tentorial opening. So the Uncas of the temporal lobe is forced into the gap between the midbrain and the edge of the tentorium. There are main possible complications of this herniation, muscle contraction of cranial nerve (III) In the case of herniation, ipsilateral occulomotor nerve may compress as it passes between the posterior and superior cerebellar arteries. In initial states ipsilateral dilation of pupil (do not respond to light) can be seen as the set-back clinical sign because the para harmonized fibers are placed outside the nerve, which are getting paralyzed first during the condensate. After that as the herniation better moreover the contralateral pupil may also dilated and further compaction of the nerve may lead to interfere with the somatic provide of extra visual muscles (except lateral rectus which is supplied by abducent nerve and the superior catercorner which is supplied by trochlear nerve) causing the deviation of the eye to downwards and outwards.Compression of the midbrain cerebral peduncles Commonly the ipsilateral cerebral peduncle gets prostrate showing contral ateral hemiparesis or hemip nogia. Since the herniation displaces the midbrain laterally, the contralateral cerebral peduncle gets compressed against the edge of the tentorium cerebelli resulting ipsilateral hemiparesis or hemiplegia (when it happens alone) or quadriplegia (when some(prenominal) cerebral peduncles are compressed.Compression of the posterior cerebral artery Posterior cerebral artery or its branches may be compressed against the free edge of the tentorium cerebelli causes hemorrhagic infraction on the medial and inferior sites of the ipsilateral occipital lobe. The lesion may often confine to the posterior cerebral artery, leading to homonymous heminospia. If the occipital lobe lesions are bilateral, cortical blindness is a clinical sign ( unhurried may not understand visual images, but pupillary reflexes are intact)Compression of the brain stem Compression of the brain stem may low in the midbrain and may gradually increase caudally. As a result patient will beco me comatose and develop cardiac and respiratory changes.There are two types of events mainly occurring during the brain stem compression.Secondary brainstem hemorrhages (Duret hemorrhages) Due to the compression and stretching of vessels (especially veins) these hemorrhages occur. Death may ensure due to the direct destruction of the pons and midbrain.Changes in respiratory, postural and occulomotor actions These changes occur due to the compression transmitting downwards from the midbrain. Finally as a result of damage to the medulla leads to slow irregular respiratory movements, irregular pulse and falling of blood pressure, as well as death is due to the respiratory arrest.Central herniation This is due to a supratententorial space occupying lesion and downward displacement of brainstem and diencephalon. Progressive decline in neurological status so called Rostrocaudal Detoriation (or Rostrocaudal Decompensation) can be seen in this situation. Lesions turn up medially or wit hin the frontal pole will not compress the midbrain and diencephalon laterally and they straight to Rostrocaudaly dysfunction of the brainstem leading bilateral increase of impairment.Herniation may stretch the branches of the basilar (pontine) arteries and tear them generating Duret hemorrhage, usually causes to death because of the infraction of the midbrain and the pons. Clinical signs initiating with changes in consciousness start with reducing alertness leads to drowsiness, stupor and finally coma. There are list of incidents occur with central herniation and their related causes.respiratory changes due to various sites of lesionsSite of lesion Respiratory patternDiencephalon Chyne-Stokes respirationMidbrain Central neurogenic hyperventilationPons Apneustic respirationMedulla atactic respirationChanges in postural reflexesDecorticate Rigidity Sign of leg extension and arm flexion caused by widespread lesions in the cerebral cortex.Decerebrate rigidity sign of extension of both arms and legs due to the lesions disconnecting cerebral hemispheres from the brainstem(e.g. Upper midbrain lesions)Pupillary changes Studying those pupillary changes in comatose patients may helpful in revealing the general location of lesions. nonaged reactive pupils Compression of the diencephalon impairs sympathetic nerve fibers originate in that location and these impairment affects the sympathetic dilation of pupil straight to constricted atrophied pupils.Dilated fixed Compression of one cranial nerve (iii) by the uncus densification parasympathetic fibers travelling outside the nerve and this impairment of parasympathetic supply causes to dilate the pupil of the same side and loss of reaction to the light changes in that pupil.Midposition fixed Bilateral compression of both occulomotor nerves or compression of the midbrain results in impairment of both parasympathetic and sympathetic fibers in both sides travelling to the pupil and as a result pupils come in to a m idposition and are non-responsive to light fluctuations.Ocular movements Pathways for ocular reflexes are localized in the brain stem, so that they are utile in testing pathways in comatose patients. Abducent and contralateral occulomotor nuclei are connected by the Medial Longitudinal Fasciculus (MLF) to produce conjugated deviation of the eyes.Caloric stimulation or oculovestibular reflex is, when water tell into ear, a passive head turning occurs. Usually the occulomotor responses to that stimulation also in a similar way producing oculocephalic reflex or chicks eye movements.This eye movement does not occur in conscious patients because their pupil will stay looking straight up in front of the face when the head is turned, so this can be only seen in comatose patients.When a comatose patient shows the oculocephalic reflex, his brainstem is intact (Both eyes are deviated into the same sides opposite to the head movement, when the patients head is turning side to side. The e yelids must open and bring to observe the deviation of eyes). But if the MLF is affected the eyes will not move towards the same side. But to show these results CN III should intact.Extracranial/Transcalvarial herniation This is the herniation of the brain through an opening in the cranial cavity make by trauma or at a surgical site.Infratentorial herniationTonsillar herniation 6 pg. 79 This is the downward herniation of the cerebellar tonsils through the reprieve magnum. Usually caused by posterior cranial fossa mass lesion. But also can be due to a midline Supratentorial mass or as a result of edema. In that case the compression of the medulla leads to a depression of the vital centers for respiration and cardiac turn control. Sudden cardiorespiratory arrest or a slow progression over a day or two may be manifested as clinical symptoms.Upward/Cerebellar herniation 5 Increased pressure in the posterior cranial fossa leads to upward movement of the cerebellum through tentoria l opening.Midline shift of the brainMidline shift is the shifting of the brain from its center line 1. This is a direct result of increased intracranial pressure and can be occurred by traumatic brain injury, stroke, hematoma, or birth deformities. So midline shift can be used as an indicator of ICP and a midline shift of over 5mm indicates an adjacent surgery 1. There are 3 structures mainly investigating in a midline shift. They are septum pellucidum (between right and left ventricles), third ventricle and the pineal gland 2. The degrees of displacement of these structures are aided in ascertain the severity of the shift.Interaction with cerebral blood flowThere is a connection between cerebral perfusion pressure (CPP), mean systemic arterial pressure (MAP) and Intracranial pressure (ICP) as follows 5.CPP = MAP ICPAs the CPP is the device driver of the cerebral perfusion, cerebral blood flow is determined by both MAP and ICP. Therefore CPP can be reduced by an increase of ICP o r a decrease of MAP. However the brain can gondola regulate the cerebral blood flow through an auto regulatory process in 50 to 150 mmHg CPP range. But below 50 mmHg CPP values the brain cant compensate and cerebral blood flow and cerebral perfusion pressure decreased.SeizuresThis is a sudden electrical natural process of brain 7. Most of the time acute increased intracranial pressure may cause for trigger a seizure 3.References1 Gruen P (May 2002) running(a) management of head trauma. Neuroimaging Clinics of North America 12 Pg.339-432Xiao,Furen,Chiang,Wong,Tosai,Hung,Liao(2011) automatic measurement of midline shift on deformed brains using multire source binate level set method and Hough transform. Computers in biology and medicine journal 41 Pg.756-7623Principles of neurology Raymond D Adams Maurice victor.2nd edition.4 www.medical dictionarythefreedictionary.com5Neuroclin. 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