Relevant bibliographies by topics / Fluid; Volumes; Cerebral oedema

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Academic literature on the topic 'Fluid; Volumes; Cerebral oedema'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Fluid; Volumes; Cerebral oedema"

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Bersot, Carlos Darcy, Rafael Linhares, Carolina Araujo Barbosa, and Jose Eduardo Pereira. "Peri-operative fluid management during neurosurgical procedures." Nepal Journal of Neuroscience 18, no. 2 (June 1, 2021): 9–14. http://dx.doi.org/10.3126/njn.v18i2.33373.

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The management of fluids and electrolytes in neurosurgical patients aims to reduce the risk of cerebral oedema, reduce ICP and at the same time maintain haemodynamic stability and cerebral perfusion. Neurosurgical patients commonly receive diuretics (mannitol and furosemide), developing complications such as bleeding and diabetes insipidus. These patients may require large volumes of intravenous fluids and even blood transfusions for volume resuscitation, treatment of cerebral vasospasm, correction of preoperative dehydration or maintenance of haemodynamic stability. Goal-oriented therapy is recommended in neurological patients, with the aim of maintaining circulating volume and tolerating the changes induced by anaesthesia (vasodilation and myocardial depression).
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Fischer, R., C. Vollmar, M. Thiere, C. Born, M. Leitl, T. Pfluger, and RM Huber. "No Evidence of Cerebral Oedema in Severe Acute Mountain Sickness." Cephalalgia 24, no. 1 (January 2004): 66–71. http://dx.doi.org/10.1111/j.1468-2982.2004.00619.x.

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In a randomized, double-blind cross-over study 10 subjects were exposed to a simulated altitude of 4500 m for 10 h after administration of placebo, acetozolamide (250 mg bid) or theophylline (250 mg bid). T2-weighted magnetic resonances images (MRI) and diffusion weighted MRI were obtained directly after exposure to altitude under hypoxic conditions. Although eight of 10 subjects had moderate to severe acute mountain sickness (AMS), we found no evidence of cerebral oedema, irrespective of the medication taken. Almost all subjects showed a decrease in inner cerebrospinal fluid (iCSF) volumes (placebo −10.3%, P = 0.02; acetazolamide −13.2%, P = 0.008, theophylline −12.2%, n.s.). There was no correlation between AMS symptoms and fluid shift. However, we found a significantly positive correlation of large (>10 ml) iCSF volume and more severe AMS after administration of placebo ( r = 0.76, P = 0.01). Moderate to severe AMS after high altitude exposure for 10 h is associated with a decreased iCSF-volume independent of AMS severity or medication without signs of cerebral oedema.
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Lin, Hung-Jung, Chia-Ti Wang, Ko-Chi Niu, Chungjin Gao, Zhuo Li, Mao-Tsun Lin, and Ching-Ping Chang. "Hypobaric hypoxia preconditioning attenuates acute lung injury during high-altitude exposure in rats via up-regulating heat-shock protein 70." Clinical Science 121, no. 5 (May 20, 2011): 223–31. http://dx.doi.org/10.1042/cs20100596.

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HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the expression of HSP70 in lungs prior to the onset of HAE. At 2 weeks after the start of HHP, animals were exposed to a simulated HAE of 6000 m in a hypobaric chamber for 24 h. Immediately after being returned to ambient pressure, the non-HHP animals had higher scores of alveolar oedema, neutrophil infiltration and haemorrhage, acute pleurisy (e.g. increased exudate volume, increased numbers of polymorphonuclear cells and increased lung myeloperoxidase activity), increased pro-inflammatory cytokines [e.g. TNF-α (tumour necrosis factor-α), IL (interleukin)-1β and IL-6], and increased cellular ischaemia (i.e. glutamate and lactate/pyruvate ratio) and oxidative damage [glycerol, NOx (combined nitrate+nitrite) and 2,3-dihydroxybenzoic acid] markers in the BALF (bronchoalveolar fluid). HHP, in addition to inducing overexpression of HSP70 in the lungs, significantly attenuated HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage in the lungs. The beneficial effects of HHP in preventing the occurrence of HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage was reduced significantly by pretreatment with a neutralizing anti-HSP70 antibody. In conclusion, HHP may attenuate the occurrence of pulmonary oedema, inflammation, and ischaemic and oxidative damage caused by HAE in part via up-regulating HSP70 in the lungs.
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Ahmed, Shahad W. "Life threatening water intoxication." Iraqi Journal of Veterinary Medicine 44, no. 2 (December 28, 2020): 71–77. http://dx.doi.org/10.30539/ijvm.v44i2.978.

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Water intoxication is a fatal disorder associated with disturbance in brain function, known as hypo-osmolar syndrome which resulting from an excessive water intake, with dilutional hypernatremia leads to a potentially fatal outcome. A change in the electrolyte equilibrium such as this sudden drop in serum sodium level and then subsequent mortality. With hyponatremia, the plasma osmolality decreased leading to water movement into the brain according to the osmotic gradient, resulting in hyponatremic encephalopathy and cerebral oedema. Increased water intake such as in Psychogenic polydipsia is followed by urination of high amount of diluted urine (polyuria) which are the main initial symptoms of water intoxication with headache, blurred vision, nausea, tremor, and deterioration in psychosis. Other serious symptoms involve muscle spasms, Early detection of seizures and coma are more serious outcomes, Untreated cases may lead to death, Risk factor for water intoxication are Marathon runners, military population and athletes and due to this endurance events, these behaviors encouraging heavy sweating that result in heat exhaustion and consume large volumes of fluid, then hyponatremia developed as a result of excessive fluid substitution. Child abuse is other pediatric clinical cases reported with water intoxication. Psychogenic polydipsia which is psychiatric disorder with obsessive water drinking leading to a serious self-induced water intoxication (SIWI), water is normally metabolized and excreted by different means and it is mainly by kidneys in urine, evaporation through the skin, by respiratory system through the respired water vapor and little quantity of water was lost from the gastrointestinal tract (GI).The LD50 of water is > 90 ml/kg orally in rats. The current review illustrates the Life threatening effects of water when it is aggressively consumed.
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Foreman, J. H. "The effects of prolonged endurance exercise on the neurological system in horses." Comparative Exercise Physiology 8, no. 2 (January 1, 2012): 81–93. http://dx.doi.org/10.3920/cep11019.

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Horses compete routinely in endurance-type activities. Many of the various pathophysiological mechanisms which arise during endurance exercise have implications for the health and function of the neurological system. The development of centrally-mediated fatigue is a normal homeostatic physiological event with several possible mechanisms. Development of pathophysiological phenomena such as cerebral oedema may be near-terminal events during or after endurance exhaustion. Cellular damage resulting in cytotoxic cerebral oedema may result from decreases in circulating blood volume (dehydration), blood pressure, oxygen, and glucose, or increases in brain temperature. Vasogenic cerebral oedema arises from changes in cerebral vascular perfusion, tone, and permeability. Increased vascular permeability results from increased brain temperature, poor vascular integrity due to severe dehydration, disseminated intravascular coagulation due to hemoconcentration or endotoxemia, and iatrogenic overhydration during therapy. Clinical signs of intracranial disease after endurance exercise include staggering, shaking, ataxia, paresis, poor tongue tone, facial twitching, collapse, recumbency, seizures, and death. Treatment should include active and aggressive cooling, intravenous polyionic fluids, acid-base imbalance correction, intravenous glucose and calcium supplementation, non-steroidal anti-inflammatory agents once the patient is better hydrated, intra-nasal oxygen therapy if practicable, and achievement of a non-dependent head posture to prevent jugular venous hypertension and further increases in intracranial pressure. The prognosis for central fatigue is good with appropriate supportive care, but the prognosis for successful treatment of cerebral oedema must be considered guarded at best. Prevention is critical and must be through incorporation of mandatory rest stops with sufficient length and veterinary monitoring to allow prevention and detection of exhaustion, excessive dehydration, and neurological signs. Management flexibility in shortening or postponing rides in hot and humid conditions, mandated use of aggressive cooling techniques, and more restrictive entry criteria for upper level Fédération Equestre Internationale races should all be considered as viable options for optimising the safety of endurance horses.
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Bracher, Alexia, Beat Knechtle, Markus Gnädinger, Jolanda Bürge, Christoph Alexander Rüst, Patrizia Knechtle, and Thomas Rosemann. "Fluid intake and changes in limb volumes in male ultra-marathoners: does fluid overload lead to peripheral oedema?" European Journal of Applied Physiology 112, no. 3 (July 1, 2011): 991–1003. http://dx.doi.org/10.1007/s00421-011-2056-3.

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Brown, Mark A., Vivienne C. Zammit, and Sandra A. Lowe. "Capillary Permeability and Extracellular Fluid Volumes in Pregnancy-Induced Hypertension." Clinical Science 77, no. 6 (December 1, 1989): 599–604. http://dx.doi.org/10.1042/cs0770599.

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1. Capillary permeability was determined by the disappearance rate of Evans Blue dye from plasma in healthy non-pregnant women, normal third-trimester primigravidae and primigravidae with pregnancy-induced hypertension 2. Extracellular fluid volume was determined from the disappearance curves of injected mannitol in the same subjects and the plasma volume was measured by the Evans Blue dye dilution technique 3. In normal pregnancy capillary permeability was not altered from that of non-pregnant subjects. Although extracellular fluid volume and plasma volume were increased in normal pregnant compared with nonpregnant women, the distribution of fluid between plasma volume and interstitial fluid volume was unaltered 4. Women with established pregnancy-induced hypertension had a more rapid Evans Blue disappearance rate and a lower plasma volume than normal pregnant women, independent of the presence of proteinuria. Maternal plasma volume correlated positively and significantly with fetal birth weight in women with pregnancy-induced hypertension, emphasizing the important relationship between maternal plasma volume and fetal outcome 5. The increased capillary permeability in women with pregnancy-induced hypertension was associated with a reduction in the plasma volume/interstitial fluid volume ratio but a normal extracellular fluid volume, suggesting that the reduced plasma volume did not result from sodium loss but rather from a redistribution of the total extracellular fluid volume. These changes did not differ significantly in subgroups with and without oedema.
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Stoquart-ElSankari, Souraya, Olivier Balédent, Catherine Gondry-Jouet, Malek Makki, Olivier Godefroy, and Marc-Etienne Meyer. "Aging Effects on Cerebral Blood and Cerebrospinal Fluid Flows." Journal of Cerebral Blood Flow & Metabolism 27, no. 9 (February 21, 2007): 1563–72. http://dx.doi.org/10.1038/sj.jcbfm.9600462.

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Phase-contrast magnetic resonance imaging (PC-MRI) is a noninvasive reliable technique, which enables quantification of cerebrospinal fluid (CSF) and total cerebral blood flows (tCBF). Although it is used to study hydrodynamic cerebral disorders in the elderly group (hydrocephalus), there is no published evaluation of aging effects on both tCBF and CSF flows, and on their mechanical coupling. Nineteen young (mean age 27 ± 4 years) and 12 elderly (71 ± 9 years) healthy volunteers underwent cerebral MRI using 1.5 T scanner. Phase-contrast magnetic resonance imaging pulse sequence was performed at the aqueductal and cervical levels. Cerebrospinal fluid and blood flow curves were then calculated over the cardiac cycle, to extract the characteristic parameters: mean and peak flows, their latencies, and stroke volumes for CSF (cervical and aqueductal) and vascular flows. Total cerebral blood flow was ( P < 0.01) decreased significantly in the elderly group when compared with the young subjects with a linear correlation with age observed only in the elderly group ( R2 = 0.7; P = 0.05). Arteriovenous delay was preserved with aging. The CSF stroke volumes were significantly reduced in the elderly, at both aqueductal ( P < 0.01) and cervical ( P < 0.05) levels, whereas aqueduct/cervical proportion ( P = 0.9) was preserved. This is the first work to study aging effects on both CSF and vascular cerebral flows. Data showed (1) tCBF decrease, (2) proportional aqueductal and cervical CSF pulsations reduction as a result of arterial loss of pulsatility, and (3) preserved intracerebral compliance with aging. These results should be used as reference values, to help understand the pathophysiology of degenerative dementia and cerebral hydrodynamic disorders as hydrocephalus.
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Gove, C. D., R. D. Hughes, and Roger Williams. "Importance of Fluid Replacement in a Rat Model of Cerebral Oedema Formation in Acute Liver Failure." Clinical Science 74, s18 (January 1, 1988): 52P. http://dx.doi.org/10.1042/cs074052pb.

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Van Den Tooren, Harriet Kay, Viraj Bharambe, Nicholas Silver, and Benedict D. Michael. "Herpes simplex virus encephalitis in a patient receiving ustekinumab associated with extensive cerebral oedema and brainshift successfully treated by immunosuppression with dexamethasone." BMJ Case Reports 12, no. 8 (August 2019): e229468. http://dx.doi.org/10.1136/bcr-2019-229468.

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Herpes simplex virus (HSV) encephalitis affects 2–4 people per million/year. Immunocompomised patients can have atypical presentations of HSV encephalitis, including a lack of cerebrospinal fluid (CSF) pleocytosis. We present the case of a patient who was receiving ustekinumab therapy for psoriasis which inhibits interleukin (IL)-12 and IL-23 signalling pathways. The initial presentation was suggestive of encephalitis, but he was discharged prior to the reporting of HSV positivity due to the lack of CSF pleocytosis. On representation, he had worsening symptoms and imaging showed midline shift, indicating cerebral oedema despite the immunosupressant effects of ustekinumab. He required intensive care unit support and treatment with high dose aciclovir and dexamethasone; after a month of treatment he made a good recovery. This case is the first to report a link between ustekinumab and HSV encephalitis, and also emphasises that imunocompromised patients can lack CSF pleocytosis and develop significant cerebral oedema which responds to immune suppression.
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Dissertations / Theses on the topic "Fluid; Volumes; Cerebral oedema"

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Bothwell, John Henry Fordyce. "Swelling-activated organic osmolyte decrease in brain tissue preparations." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326110.

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Ásgeirsson, Bogi. "Post-traumatic brain oedema therapy a new approach based on aspects of brain volumen regulation and raised tissue pressure /." 1995. http://catalog.hathitrust.org/api/volumes/oclc/38078863.html.

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Thesis (Ph. D.)--Lund University, 1995.
Summary in Swedish. Contains reprints of 5 papers authored in part by the thesis author. eContent provider-neutral record in process. Description based on print version record.
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Books on the topic "Fluid; Volumes; Cerebral oedema"

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Whittle, Ian. Raised intracranial pressure, cerebral oedema, and hydrocephalus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0604.

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The brain is protected by the cranial skeleton. Within the intracranial compartment are also cerebrospinal fluid, CSF, and the blood contained within the brain vessels. These intracranial components are in dynamic equilibrium due to the pulsations of the heart and the respiratory regulated return of venous blood from the brain. Normally the mean arterial blood pressure, systemic venous pressure, and brain volume are regulated to maintain physiological values for intracranial pressure, ICP. There are a range of very common disorders such as stroke, and much less common, such as idiopathic intracranial hypertension, that are associated with major disturbances of intracranial pressure dynamics. In some of these the contribution to pathophysiology is relatively minor whereas in others it may be substantial and be a major contributory factor to morbidity or even death.Intracranial pressure can be disordered because of brain oedema, disturbances in CSF flow, mass lesions, and vascular engorgement of the brain. Each of these may have variable causes and there may be interactions between mechanisms. In this chapter the normal regulation of intracranial pressure is outlined and some common disease states in clinical neurological practice that are characterized by either primary or secondary problems in intracranial pressure dynamics described.
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Ostermann, Marlies, and Ruth Y. Y. Wan. Diuretics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0058.

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Fluid overload and chronic hypertension are the most common indications for diuretics. The diuretic response varies between different types and depends on underlying renal function. In patients with congestive heart failure, diuretics appear to reduce the risk of death and worsening heart failure compared with placebo, but their use in acute decompensated heart failure is questionable. Diuretics are also widely used in chronic kidney disease to prevent or control fluid overload, and treat hypertension. In acute kidney injury, there is no evidence that they improve renal function, speed up recovery, or change mortality. In patients with chronic liver disease and large volume ascites, paracentesis is more effective and associated with fewer adverse events than diuretic therapy, but maintenance treatment with diuretics is indicated to prevent recurrence of ascites. Mannitol has a role in liver patients with cerebral oedema and normal renal function. The use of diuretics in rhabdomyolysis is controversial and restricted to patients who are not fluid deplete. In conditions associated with resistant oedema (chronic kidney disease, congestive heart failure, chronic liver disease), combinations of diuretics with different modes of action may be necessary. Diuresis is easier to achieve with a continuous furosemide infusion compared with intermittent boluses, but there is no evidence of better outcomes. The role of combination therapy with albumin in patients with fluid overload and severe hypoalbuminaemia is uncertain with conflicting data.
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Waldmann, Carl, Neil Soni, and Andrew Rhodes. Obstetric emergencies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0031.

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Pre-eclampsia 518Eclampsia 520HELLP syndrome 522Postpartum haemorrhage 524Amniotic fluid embolism 526Pre-eclampsia is a common complication of pregnancy, UK incidence is 3–5%, with a complex hereditary, immunological and environmental aetiology.Abnormal placentation is characterized by impaired myometrial spiral artery relaxation, failure of trophoblastic invasion of these arterial walls and blockage of some vessels with fibrin, platelets and lipid-laden macrophages. There is a 30–40%, reduction in placental perfusion by the uterine arcuate arteries as seen by Doppler studies at 18–24 weeks gestation. Ultimately the shrunken, calcified, and microembolized placenta typical of the disease is seen. The placental lesion is responsible for fetal growth retardation and increased risks of premature labour, abruption and fetal demise. Maternal systemic features of this condition are characterized by widespread endothelial damage, affecting the peripheral, renal, hepatic, cerebral, and pulmonary vasculatures. These manifest clinically as hypertension, proteinuria and peripheral oedema, and in severe cases as eclamptic convulsions, cerebral haemorrhage (the most common cause of death due to pre-eclampsia in the UK), pulmonary oedema, hepatic infarcts and haemorrhage, coagulopathy and renal dysfunction....
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Modell, Jerome H., and Sean Kiley. Pathophysiology and management of drowning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0348.

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Drowning is a process beginning with airway submergence under a fluid medium, progressing to aspiration, and ultimately death in the absence of intervention. Aspiration of both fresh- and saltwater can cause pulmonary oedema, decreased compliance, intrapulmonary shunting, and severe hypoxia. Devastating neurological injury resulting from prolonged cerebral hypoxia is proportional to the duration of submersion and delay in effective resuscitation and oxygenation. Victims presenting to the emergency department awake and alert, or even stuporous, are likely to have a good neurological outcome with follow-up intensive care. Those presenting comatose are much more likely to have severe neurological deficits. Keys to survival are: timely rescue from the water, immediate initiation of aggressive supportive care regarding airway, cardiovascular and pulmonary function, and optimization of tissue oxygenation.
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Book chapters on the topic "Fluid; Volumes; Cerebral oedema"

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Kushi, H., M. Fujii, T. Shibuya, Y. Katayama, and T. Tsubokawa. "Oedema fluid clearance within cerebral contusion studied by MRI." In Proceedings of the XV Symposium Neuroradiologicum, 250–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79434-6_119.

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Kuroiwa, T., J. Yokofujita, H. Kaneko, and R. Okeda. "Accumulation of Oedema Fluid in Deep White Matter After Cerebral Cold Injury." In Brain Edema VIII, 84–86. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9115-6_29.

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McIntosh, T. K., H. Soares, M. Thomas, and K. Cloherty. "Development of Regional Cerebral Oedema After Lateral Fluid-Percussion Brain Injury in the Rat." In Brain Edema VIII, 263–64. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9115-6_89.

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Farne, Hugo, Edward Norris-Cervetto, and James Warbrick-Smith. "Headache." In Oxford Cases in Medicine and Surgery. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780198716228.003.0007.

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The sinister causes can be remembered using the mnemonic VIVID: . . . Vascular: subarachnoid haemorrhage (SAH), haematoma (subdural or extradural), cerebral venous sinus thrombosis, cerebellar infarct Infection: meningitis, encephalitis Vision-threatening: temporal arteritis, acute glaucoma, cavernous sinus thrombosis, pituitary apoplexy, posterior leucoencephalopathy Intracranial pressure (raised): space-occupying lesion (SOL; e.g. tumour, abscess, cyst), cerebral oedema (e.g. trauma, altitude), hydrocephalus, malignant hypertension, idiopathic intracranial hypertension Dissection: carotid dissection . . . The approach to headache is the same as that to pain anywhere in the body: you need to start by characterizing the pain. One useful way of doing this is by following another mnemonic, SOCRATES: . . . Site of pain, and has it moved since it began? Onset of pain—was it sudden or gradual, and did something trigger it? Character of pain—throbbing, dull ache, sharp stabbing? Radiation of pain—has the pain spread? . . . Attenuating factors—does anything make the pain better (e.g. position, medications)? Timing of pain—how long has it gone on for, has it been constant or coming and going? Is it worse at a particular time of the day? Exacerbating factors—does anything make the pain worse (e.g. lying down, standing up, coughing, fatigue)? Severity—on a scale of 0 to 10, where 10 is the worst pain ever (e.g. childbirth). In addition, you should enquire about the presence or absence of the following ‘red flags’: • Decreased level of consciousness. This is a worrying feature of any medical presentation. Combined with headache, SAH needs exclusion. If there is a history of head injury, it could suggest a subdural haematoma (fluctuating consciousness) or extradural haematoma (altered consciousness following a lucid interval). Meningitis and encephalitis can also affect consciousness. • Sudden onset, worst headache ever. Suggests SAH, with blood in the cerebrospinal fluid (CSF) irritating the meninges. It can be informative to ask the patient whether they remember the exact moment when the headache started—a very severe headache of almost instantaneous onset is characteristic of SAH. Patients describe it like, for example, ‘being hit on the back of the head with a bat’.
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Conference papers on the topic "Fluid; Volumes; Cerebral oedema"

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Tully, Brett, and Yiannis Ventikos. "Modelling Normal Pressure Hydrocephalus as a ‘Two-Hit’ Disease Using Multiple-Network Poroelastic Theory." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19135.

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The evolution of many cerebral diseases such as Alzheimer’s and Parkinson’s Disease, Hydrocephalus, Cerebral Oedema, Stroke, and Tumour are strongly correlated to a change in the transport properties of fluid in the brain. This research proposes a novel application of Multiple-Network Poroelastic Theory (MPET) to investigate cerebral hydrodynamics through a detailed investigation of multiscalar, spatio-temporal transport of fluid between the cerebral blood, cerebrospinal fluid (CSF) and brain parenchyma. Specifically, MPET is used to interrogate the clinical markers of Normal Pressure Hydrocephalus (NPH).
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