Sandbox:khurram: Difference between revisions

Jump to navigation Jump to search
← Older edit
VisualWikitext
Khurram Afzal (talk | contribs)
Bureaucrats, bureaucrats, nocaptcha, Administrators, Widget editors
1,615 edits
No edit summary
Khurram Afzal (talk | contribs)
Bureaucrats, bureaucrats, nocaptcha, Administrators, Widget editors
1,615 edits
No edit summary
 
(104 intermediate revisions by 3 users not shown)
Line 1: Line 1:
__NOTOC__
{{CMG}}; {{AE}} {{MKA}}, {{S.G.}}


{{CMG}}; {{AE}}
===Differentiating [disease name] from other diseases on the basis of [symptom 1], [symptom 2], and [symptom 3]===


On the basis [symptom 1], [symptom 2], and [symptom 3], [disease name] must be differentiated from [disease 1], [disease 2], [disease 3], [disease 4], [disease 5], and [disease 6].
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Diseases
| colspan="6" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Clinical manifestations'''
! colspan="4" rowspan="2" |Para-clinical findings
| colspan="1" rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Gold standard'''
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Additional findings
|-
| colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
| colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Physical examination'''
|-
! colspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Lab Findings'''
! colspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Imaging'''
|-
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptoms of DVT
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptoms of Pulmonary Embolism
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptoms of Myocardial Infarction
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Tenderness in extremities
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Edema in extremities
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Warmth in extremities
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |PT
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |aPTT
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Doppler ultrasound
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Chest CT scan
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Antithrombin III deficiency]]<ref name="pmid19141163">{{cite journal |vauthors=Patnaik MM, Moll S |title=Inherited antithrombin deficiency: a review |journal=Haemophilia |volume=14 |issue=6 |pages=1229–39 |date=November 2008 |pmid=19141163 |doi=10.1111/j.1365-2516.2008.01830.x |url=}}</ref><ref name="Al HadidiWu2017">{{cite journal|last1=Al Hadidi|first1=Samer|last2=Wu|first2=Kristi|last3=Aburahma|first3=Ahmed|last4=Alamarat|first4=Zain|title=Family with clots: antithrombin deficiency|journal=BMJ Case Reports|year=2017|pages=bcr-2017-221556|issn=1757-790X|doi=10.1136/bcr-2017-221556}}</ref><ref name="pmid21772860">{{cite journal |vauthors=Konecny F |title=Inherited trombophilic states and pulmonary embolism |journal=J Res Med Sci |volume=14 |issue=1 |pages=43–56 |date=January 2009 |pmid=21772860 |pmc=3129068 |doi= |url=}}</ref>


Respiratory failure is defined as a failure in gas exchange due to an impaired respiratory system--either pump or lung failure, or both. The hallmark of respiratory failure is impairment in arterial blood gases. This review describes the mechanisms leading to respiratory failure, the indices that can be used to better describe gas exchange abnormalities and the physiologic and clinical consequences of these abnormalities. The possible causes of respiratory failure are then briefly mentioned and a quick reference to the clinical evaluation of such patients is made. Finally treatment options are briefly outlined for both acute and chronic respiratory failure.
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | Normal
| style="background: #F5F5F5; padding: 5px;" |
* Normal


* Reduces the Increase in [[PTT]] after administration of [[heparin]]
| style="background: #F5F5F5; padding: 5px;" |
* Evidence of [[deep vein thrombosis]] ([[DVT]])
* Should be used for diagnosis and follow up
| style="background: #F5F5F5; padding: 5px;" |
* [[Occlusion]] of  [[brachiocephalic]] [[vein]]
* Large [[thrombus]] in [[superior vena cava]]
| style="background: #F5F5F5; padding: 5px;" |
* Decreased [[plasma]] [[Antithrombin III|antithrombin]] ([[AT III]]) activity
| style="background: #F5F5F5; padding: 5px;" |
* [[Nephrotic syndrome]]
* Decreased inhibition of [[factor II]] and Xa
* [[Antithrombin]] is a natural [[anticoagulant]] that is lost in the [[urine]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Factor V Leiden mutation]]<ref name="pmid20626623">{{cite journal |vauthors=Mannucci PM, Asselta R, Duga S, Guella I, Spreafico M, Lotta L, Merlini PA, Peyvandi F, Kathiresan S, Ardissino D |title=The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease |journal=J. Thromb. Haemost. |volume=8 |issue=10 |pages=2116–21 |date=October 2010 |pmid=20626623 |doi=10.1111/j.1538-7836.2010.03982.x |url=}}</ref><ref name="pmid27797270">{{cite journal |vauthors=Campello E, Spiezia L, Simioni P |title=Diagnosis and management of factor V Leiden |journal=Expert Rev Hematol |volume=9 |issue=12 |pages=1139–1149 |date=December 2016 |pmid=27797270 |doi=10.1080/17474086.2016.1249364 |url=}}</ref><ref name="pmid15003896">{{cite journal |vauthors=Van Rooden CJ, Rosendaal FR, Meinders AE, Van Oostayen JA, Van Der Meer FJ, Huisman MV |title=The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis |journal=Haematologica |volume=89 |issue=2 |pages=201–6 |date=February 2004 |pmid=15003896 |doi= |url=}}</ref><ref name="pmid23615845">{{cite journal| author=Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L et al.| title=Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis. | journal=Thromb Haemost | year= 2013 | volume= 110 | issue= 1 | pages= 191-4 | pmid=23615845 | doi=10.1160/TH13-02-0163 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23615845  }}</ref><ref name="pmid12421138">{{cite journal |vauthors=Press RD, Bauer KA, Kujovich JL, Heit JA |title=Clinical utility of factor V leiden (R506Q) testing for the diagnosis and management of thromboembolic disorders |journal=Arch. Pathol. Lab. Med. |volume=126 |issue=11 |pages=1304–18 |date=November 2002 |pmid=12421138 |doi=10.1043/0003-9985(2002)126<1304:CUOFVL>2.0.CO;2 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |N/A
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |
* Recommended to do weekly
* [[Proximal]] [[DVT]] is more commonly observed as compared to [[distal]] [[DVT]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* N/A
| style="background: #F5F5F5; padding: 5px;" |
* Inactivates factor Va and factor VIIIa
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Protein C deficiency]]<ref>{{Cite journal
| author = [[Bernard Khor]] & [[Elizabeth M. Van Cott]]
| title = Laboratory tests for protein C deficiency
| journal = [[American journal of hematology]]
| volume = 85
| issue = 6
| pages = 440–442
| year = 2010
| month = June
| doi = 10.1002/ajh.21679
| pmid = 20309856
}}</ref><ref name="pmid11336597">{{cite journal |vauthors=Pescatore SL |title=Clinical management of protein C deficiency |journal=Expert Opin Pharmacother |volume=2 |issue=3 |pages=431–9 |date=March 2001 |pmid=11336597 |doi=10.1517/14656566.2.3.431 |url=}}</ref><ref name=":0">{{Cite journal
| author = [[Gustavo A. Rodriguez-Leal]], [[Segundo Moran]], [[Roberto Corona-Cedillo]] & [[Rocio Brom-Valladares]]
| title = Portal vein thrombosis with protein C-S deficiency in a non-cirrhotic patient
| journal = [[World journal of hepatology]]
| volume = 6
| issue = 7
| pages = 532–537
| year = 2014
| month = July
| doi = 10.4254/wjh.v6.i7.532
| pmid = 25068006
}}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | Normal
| style="background: #F5F5F5; padding: 5px;" |Normal / ↑
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypercoagulation]]
* Recurrent [[venous thromboembolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Venous thromboembolism]]
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Protein C]] functional [[assay]]
* [[ELISA]] [[assay]]: may produce [[false positive]] result in cross reaction with [[rheumatoid factor]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Factor VIII]] elevation in acute phase
* Functional [[assay]] should not be performed if patient is on [[warfarin]]
* [[Purpura fulminans]] ([[skin]] [[necrosis]]) could be a form of presentation
* Risk of [[thrombotic]] [[skin]] [[necrosis]] following [[warfarin]] administration
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Protein S deficiency]]<ref name=":0" /><ref>{{Cite journal
| author = [[Kristi J. Smock]], [[Elizabeth A. Plumhoff]], [[Piet Meijer]], [[Peihong Hsu]], [[Nicole D. Zantek]], [[Nahla M. Heikal]] & [[Elizabeth M. Van Cott]]
| title = Protein S testing in patients with protein S deficiency, factor V Leiden, and rivaroxaban by North American Specialized Coagulation Laboratories
| journal = [[Thrombosis and haemostasis]]
| volume = 116
| issue = 1
| pages = 50–57
| year = 2016
| month = July
| doi = 10.1160/TH15-12-0918
| pmid = 27075008
}}</ref><ref name="pmid21799399">{{cite journal |vauthors=Ji M, Yoon SN, Lee W, Jang S, Park SH, Kim DY, Chun S, Min WK |title=Protein S deficiency with a PROS1 gene mutation in a patient presenting with mesenteric venous thrombosis following total colectomy |journal=Blood Coagul. Fibrinolysis |volume=22 |issue=7 |pages=619–21 |date=October 2011 |pmid=21799399 |doi=10.1097/MBC.0b013e32834a0421 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |Normal
| style="background: #F5F5F5; padding: 5px;" |Normal / ↑
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypercoagulation]]
* Recurrent [[venous thromboembolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
* [[Thrombosis]] of [[superior mesenteric vein]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Protein S]] free [[antigen]] [[assay]]
| style="background: #F5F5F5; padding: 5px;" |
* When performing the gold standard test, beware of interference from samples positive for [[Factor V]] [[mutation]], [[protein C deficiency]] and oral [[anticoagulants]] ([[rivaroxaban]])
* Risk of [[thrombotic]] [[skin]] [[necrosis]] following [[warfarin]] administration
* Suspected in patients with a strong family history of [[VTE]]
* [[Post phlebitic syndrome]] 


Histologic and ultrastructural analysis of the injured lung has been integral to current concepts of pathogenesis of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). (a) A low-power light micrograph of a lung biopsy specimen collected two days after the onset of ALI/ARDS secondary to gram-negative sepsis demonstrates key features of diffuse alveolar damage, including hyaline membranes, inflammation, intra-alveolar red cells and neutrophils, and thickening of the alveolar-capillary membrane. (b) A higher-power view of a different field illustrates a dense hyaline membrane and diffuse alveolar inflammation. Polymorphonuclear leukocytes are imbedded in the proteinaceous hyaline membrane structure. The blue arrow points to the edge of an adjacent alveolus, which contains myeloid leukocytes. (c) An electron micrograph from a classic analysis of ALI/ARDS showing injury to the capillary endothelium and the alveolar epithelium. Abbreviations: A, alveolar space; BM, exposed basement membrane, where the epithelium has been denuded; C, capillary; EC, erythrocyte; EN, blebbing of the capillary endothelium; LC, leukocyte (neutrophil) within the capillary lumen. The histologic sections in panels a and b are used courtesy of Dr. K. Jones, University of California, San Francisco. Reprinted with permission from the American Thoracic Society.
* [[Fetal]] loss
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Prothrombin gene mutation G20210A|Prothrombin gene mutation]]<ref name="pmid17474891">{{cite journal| author=Cooper PC, Rezende SM| title=An overview of methods for detection of factor V Leiden and the prothrombin G20210A mutations. | journal=Int J Lab Hematol | year= 2007 | volume= 29 | issue= 3 | pages= 153-62 | pmid=17474891 | doi=10.1111/j.1751-553X.2007.00892.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17474891  }}</ref><ref name="pmid12421139">{{cite journal| author=McGlennen RC, Key NS| title=Clinical and laboratory management of the prothrombin G20210A mutation. | journal=Arch Pathol Lab Med | year= 2002 | volume= 126 | issue= 11 | pages= 1319-25 | pmid=12421139 | doi=10.1043/0003-9985(2002)126<1319:CALMOT>2.0.CO;2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12421139  }}</ref><ref name="pmid236158452">{{cite journal| author=Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L et al.| title=Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis. | journal=Thromb Haemost | year= 2013 | volume= 110 | issue= 1 | pages= 191-4 | pmid=23615845 | doi=10.1160/TH13-02-0163 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23615845  }}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |N/A
| style="background: #F5F5F5; padding: 5px;" |
* [[Proximal]] [[DVT]] is more commonly observed as compared to [[distal]] [[DVT]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* Detection of [[mutation]] using [[restriction enzyme]] and [[PCR]]
* [[DNA testing]] for [[prothrombin G20210A mutation]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Mutation]] causes increased production of [[prothrombin]]
* Increased [[blood]] levels of [[prothrombin]] lead to [[venous]] clots in the [[circulatory system]]
* [[Hormonal]] [[oral contraceptive pills]] can increase the risk of [[VTE]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Disseminated intravascular coagulation|Disseminated intravascular coagulation (DIC)]]<ref name="pmid25535423">{{cite journal |vauthors=Venugopal A |title=Disseminated intravascular coagulation |journal=Indian J Anaesth |volume=58 |issue=5 |pages=603–8 |date=September 2014 |pmid=25535423 |pmc=4260307 |doi=10.4103/0019-5049.144666 |url=}}</ref><ref name="pmid27276832">{{cite journal |vauthors=Makruasi N |title=Treatment of Disseminated Intravascular Coagulation |journal=J Med Assoc Thai |volume=98 Suppl 10 |issue= |pages=S45–51 |date=November 2015 |pmid=27276832 |doi= |url=}}</ref><ref name="pmid29178991">{{cite journal| author=Cui S, Fu Z, Feng Y, Xie X, Ma X, Liu T et al.| title=The disseminated intravascular coagulation score is a novel predictor for portal vein thrombosis in cirrhotic patients with hepatitis B. | journal=Thromb Res | year= 2018 | volume= 161 | issue=  | pages= 7-11 | pmid=29178991 | doi=10.1016/j.thromres.2017.11.010 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29178991  }}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |
* [[Portal vein thrombosis]] is observed in patients with coexistent [[hepatitis B]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* N/A
| style="background: #F5F5F5; padding: 5px;" |
* Elevated [[fibrin degradation products]] ([[D-dimers]])
* Decreased [[fibrinogen]]
* Decreased [[factor V]] and VIII
* Shistocytes (helmet [[cells]]) on [[peripheral blood smear]]
* [[Portal vein thrombosis]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Antiphospholipid  antibody syndrome]]<ref name="pmid24319251">{{cite journal |vauthors=Lim W |title=Antiphospholipid syndrome |journal=Hematology Am Soc Hematol Educ Program |volume=2013 |issue= |pages=675–80 |date=2013 |pmid=24319251 |doi=10.1182/asheducation-2013.1.675 |url=}}</ref><ref name="pmid19624461">{{cite journal |vauthors=Pengo V, Tripodi A, Reber G, Rand JH, Ortel TL, Galli M, De Groot PG |title=Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis |journal=J. Thromb. Haemost. |volume=7 |issue=10 |pages=1737–40 |date=October 2009 |pmid=19624461 |doi=10.1111/j.1538-7836.2009.03555.x |url=}}</ref><ref name="pmid243192512">{{cite journal| author=Lim W| title=Antiphospholipid syndrome. | journal=Hematology Am Soc Hematol Educ Program | year= 2013 | volume= 2013 | issue=  | pages= 675-80 | pmid=24319251 | doi=10.1182/asheducation-2013.1.675 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24319251  }}</ref><ref name="pmid29791828">{{cite journal| author=Garcia D, Erkan D| title=Diagnosis and Management of the Antiphospholipid Syndrome. | journal=N Engl J Med | year= 2018 | volume= 378 | issue= 21 | pages= 2010-2021 | pmid=29791828 | doi=10.1056/NEJMra1705454 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29791828  }}</ref><ref name="pmid23488294">{{cite journal| author=Kornacki J, Wirstlein P, Skrzypczak J| title=[Assessment of uterine arteries Doppler in the first half of pregnancy in women with thrombophilia]. | journal=Ginekol Pol | year= 2012 | volume= 83 | issue= 12 | pages= 916-21 | pmid=23488294 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23488294  }}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |N/A
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |
* Increased impedance of [[flow]] in [[uterine]] [[arteries]] at 12-20 weeks of [[gestation]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Antiphospholipid antibody]]
* [[Anticardiolipin antibody]]
* [[Lupus anticoagulant]]
* Anti-β2GPI [[antibody]]
| style="background: #F5F5F5; padding: 5px;" |
* Both, [[arterial]] and [[venous]] [[thrombosis]] can occur
* History of [[spontaneous abortions]]
* [[False positive]] [[VDRL]]
* [[Stroke]] and [[transient ischemic attack]] ([[TIA]]) are most common forms of presentation of [[arterial thrombosis]]
|}


==References==
{{Reflist|2}}


{{WH}}
{{WS}}
[[Category: (name of the system)]]


Respiratory failure occurs due mainly either to lung failure resulting in hypoxaemia or pump failure resulting in alveolar hypoventilation and hypercapnia. Hypercapnic respiratory failure may be the result of mechanical defects, central nervous system depression, imbalance of energy demands and supplies and/or adaptation of central controllers. Hypercapnic respiratory failure may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. In all these conditions, pathophysiologically, the common denominator is reduced alveolar ventilation for a given carbon dioxide production. Acute hypercapnic respiratory failure is usually caused by defects in the central nervous system, impairment of neuromuscular transmission, mechanical defect of the ribcage and fatigue of the respiratory muscles. The pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear. The most attractive hypothesis for this disorder is the theory of "natural wisdom". Patients facing a load have two options, either to push hard in order to maintain normal arterial carbon dioxide and oxygen tensions at the cost of eventually becoming fatigued and exhausted or to breathe at a lower minute ventilation, avoiding dyspnoea, fatigue and exhaustion but at the expense of reduced alveolar ventilation. Based on most recent work, the favoured hypothesis is that a threshold inspiratory load may exist, which, when exceeded, results in injury to the muscles and, consequently, an adaptive response is elicited to prevent and/or reduce this damage. This consists of cytokine production, which, in turn, modulates the respiratory controllers, either directly through the blood or probably the small afferents or via the hypothalamic-pituitary-adrenal axis. Modulation of the pattern of breathing, however, ultimately results in alveolar hypoventilation and carbon dioxide retention.


Respiratory failure occurs due mainly either to lung failure resulting in hypoxaemia or pump failure resulting in alveolar hypoventilation and hypercapnia. Hypercapnic respiratory failure may be the result of mechanical defects, central nervous system depression, imbalance of energy demands and supplies and/or adaptation of central controllers.
__NOTOC__
{{Astrocytoma}}
{{CMG}}; {{AE}} {{Fs}}
==Overview==
On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from [[oligodendroglioma]], [[meningioma]], [[hemangioblastoma]], [[pituitary adenoma]], [[schwannoma]], [[Primary central nervous system lymphoma|primary CNS lymphoma]], [[medulloblastoma]], [[ependymoma]], [[craniopharyngioma]], [[pinealoma]], [[Arteriovenous malformation|AV malformation]], [[brain aneurysm]], [[bacterial]] [[brain]] [[abscess]], [[tuberculosis]], [[toxoplasmosis]], [[hydatid cyst]], [[CNS]] [[cryptococcosis]], [[CNS]] [[aspergillosis]], and [[brain metastasis]].


Hypercapnic respiratory failure may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. In all these conditions, pathophysiologically, the common denominator is reduced alveolar ventilation for a given carbon dioxide production.
== Differentiating astrocytoma from other Diseases ==
=== Differentiating astrocytoma from other diseases on the basis of seizure, visual disturbance, and constitutional symptoms ===
On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from [[oligodendroglioma]], [[meningioma]], [[hemangioblastoma]], [[pituitary adenoma]], [[schwannoma]], [[Primary central nervous system lymphoma|primary CNS lymphoma]], [[medulloblastoma]], [[ependymoma]], [[craniopharyngioma]], [[pinealoma]], [[Arteriovenous malformation|AV malformation]], [[brain aneurysm]], [[bacterial]] [[brain]] [[abscess]], [[tuberculosis]], [[toxoplasmosis]], [[hydatid cyst]], [[CNS]] [[cryptococcosis]], [[CNS]] [[aspergillosis]], and [[brain metastasis]].
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! colspan="2" rowspan="4" |Diseases
| colspan="5" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Clinical manifestations'''
! colspan="3" rowspan="2" |Para-clinical findings
| colspan="1" rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Gold<br>standard'''
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Additional findings
|-
| colspan="4" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical examination
|-
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab Findings
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |MRI
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Immunohistopathology
|-
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Head-<br>ache
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Seizure
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Visual disturbance
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Constitutional
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Focal neurological deficit
|-
| rowspan="7" style="background: #DCDCDC; padding: 5px; text-align: center;" |Adult primary brain tumors
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Glioblastoma multiforme]]<br><ref name="pmid17964028">{{cite journal |vauthors=Sathornsumetee S, Rich JN, Reardon DA |title=Diagnosis and treatment of high-grade astrocytoma |journal=Neurol Clin |volume=25 |issue=4 |pages=1111–39, x |date=November 2007 |pmid=17964028 |doi=10.1016/j.ncl.2007.07.004 |url=}}</ref><ref name="pmid22819718">{{cite journal |vauthors=Pedersen CL, Romner B |title=Current treatment of low grade astrocytoma: a review |journal=Clin Neurol Neurosurg |volume=115 |issue=1 |pages=1–8 |date=January 2013 |pmid=22819718 |doi=10.1016/j.clineuro.2012.07.002 |url=}}</ref><ref name=":0">{{cite book | last = Mattle | first = Heinrich | title = Fundamentals of neurology : an illustrated guide | publisher = Thieme | location = Stuttgart New York | year = 2017 | isbn = 9783131364524 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" |−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" |−
| style="background: #F5F5F5; padding: 5px;" |
* [[Supratentorial]]
* Irregular ring-nodular enhancing lesions
* Central [[necrosis]]
* Surrounding [[vasogenic edema]]


Acute hypercapnic respiratory failure is usually caused by defects in the central nervous system, impairment of neuromuscular transmission, mechanical defect of the ribcage and fatigue of the respiratory muscles.
* Cross [[corpus callosum]] ([[butterfly glioma]])
| style="background: #F5F5F5; padding: 5px;" |
* [[Astrocyte]] origin


The pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear. The most attractive hypothesis for this disorder is the theory of “natural wisdom”. Patients facing a load have two options, either to push hard in order to maintain normal arterial carbon dioxide and oxygen tensions at the cost of eventually becoming fatigued and exhausted or to breathe at a lower minute ventilation, avoiding dyspnoea, fatigue and exhaustion but at the expense of reduced alveolar ventilation. Based on most recent work, the favoured hypothesis is that a threshold inspiratory load may exist, which, when exceeded, results in injury to the muscles and, consequently, an adaptive response is elicited to prevent and/or reduce this damage. This consists of cytokine production, which, in turn, modulates the respiratory controllers, either directly through the blood or probably the small afferents or via the hypothalamic-pituitary-adrenal axis. Modulation of the pattern of breathing, however, ultimately results in alveolar hypoventilation and carbon dioxide retention.
* [[Pleomorphism|Pleomorphic]] cell


β‐Endorphinscytokineshypercapniapump failurerespiratory muscles fatigue
* Pseudopalisading appearance
This study was supported by the Thorax Foundation, Athens, Greece.


Respiratory failure is a condition in which the respiratory system fails in one or both of its gas exchange functions, i.e. oxygenation of and/or elimination of carbon dioxide from mixed venous blood. It is conventionally defined by an arterial oxygen tension (Pa,O2) of <8.0 kPa (60 mmHg), an arterial carbon dioxide tension (Pa,CO2) of >6.0 kPa (45 mmHg) or both. Therefore, the diagnosis of respiratory failure is a laboratory one, but the important point to emphasise is that these cut-off values are not rigid; they simply serve as a general guide in combination with the history and clinical assessment of the patient.
* [[GFAP]] +


The respiratory system can be said to consist of two parts: the lung, i.e. the gas-exchanging organ, and the pump that ventilates the lungs 1. The pump consists of the chest wall, including the respiratory muscles, the respiratory controllers in the central nervous system (CNS) and the pathways that connect the central controllers with the respiratory muscles (spinal and peripheral nerves). Failure of each part of the system leads to a distinct entity (fig. 1⇓). In general, failure of the lung caused by a variety of lung diseases (e.g. pneumonia, emphysema and interstitial lung disease) leads to hypoxaemia with normocapnia or hypocapnia (hypoxaemic or type I respiratory failure). Failure of the pump (e.g. drug overdose) results in alveolar hypoventilation and hypercapnia (hypercapnic or type II respiratory failure). Although there is coexistent hypoxaemia, the hallmark of ventilatory failure is the increase in Pa,CO2. Undoubtedly, both types of respiratory failure may coexist in the same patient, as, for example, in patients with chronic obstructive pulmonary disease (COPD) and carbon dioxide retention, or in those with severe pulmonary oedema or asthmatic crisis, who first develop hypoxaemia and, as the disease persists or progresses, hypercapnia appears.
* [[Necrosis]] +


Fig. 1.—
* [[Hemorrhage]] +
Download figureOpen in new tabDownload powerpoint
Fig. 1.—
Types of respiratory failure. The respiratory system can be considered as consisting of two parts: 1) the lung; and 2) the pump.
The various types of respiratory failure are presented in a gas tension diagram (fig. 2⇓), which illustrates the various pathways. The solid line represents a respiratory exchange ratio of 0.8. The parallel dotted line shows the corresponding Pa,O2 and Pa,CO2 with an alveolar to arterial oxygen difference (DA‐aO2) of ∼0.67 kPa (5 mmHg), as occurs in normal lung. When a normal subject hyperventilates, alveolar oxygen (PA,O2) and carbon dioxide (PA,CO2) tension and Pa,O2 and Pa,CO2 move down the slope in the direction indicated by the letter H, with rises in PA,O2 and Pa,O2 and falls in PA,CO2 and Pa,CO2. When hypoventilation occurs, in the normal subject, due to drug overdose for example, PA,O2 and Pa,O2 and PA,CO2 and Pa,CO2 move up the slope in the direction shown by the letter D, with falls in PA,O2 and Pa,O2 and rises in PA,CO2 and Pa,CO2. It can be seen that, in the normal lung, when hypercapnia occurs (as in the case of alveolar hypoventilation due to CNS depression), Pa,O2 cannot fall to very low levels. For example, when PA,CO2 increases from 5.3 (40 mmHg) to ∼10.6 kPa (80 mmHg), PA,O2 decreases from ∼13.3 (100 mmHg) to ∼8.0 kPa (60 mmHg). Assuming a DA‐aO2 of 0.67–1.3 kPa (5–10 mmHg), the Pa,O2 is ∼5.3–6.7 kPa (40–50 mmHg). Thus, when the lung is normal, a severe degree of alveolar hypoventilation, resulting in marked carbon dioxide retention, is not associated with excessive hypoxaemia. In lung diseases, however, due to increased DA‐aO2, the same conditions lead to arterial hypoxaemia. Arrow Α, in figure 2⇓, shows a large DA‐aO2 (the horizontal distance between arrow Α and alveolar line D‐H), which is commonly observed in patients with pneumonia, atelectasis or acute respiratory distress syndrome (ARDS). Hyperventilation in these patients leads to very low Pa,CO2. Line Β depicts the pathway of patients with interstitial lung disease or pure emphysema. Line C depicts a mixed state in a patient with lung disease (hypoxaemia) and inadequate alveolar ventilation (V'A). In severe cases (tip of arrow), hypoxaemia is dominant despite hypercapnia and the situation is certainly more dangerous than in pure hypoventilation at an equal Pa,CO2. Patients usually reach line C starting from line Α or B. Patients with COPD or end-stage interstitial lung disease who have remained along the B arrow for a long time move to arrow C as a result of alveolar hypoventilation. Similarly, patients with a gas-exchange abnormality, as shown by arrow Α (acute asthma attack or pulmonary oedema), may move towards arrow B or C as the central controllers or respiratory muscles, or both, become unable to maintain adequate ventilation.


Hypoxaemic (type I) respiratory failure
* [[Vascular]] prolifration +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] in fifth and sixth decades of life
* Most of the time, focal [[neurological]] deficit is the presenting [[Sign (medical)|sign]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[oligodendroglioma]]<br><ref name="pmid26849038">{{cite journal |vauthors=Smits M |title=Imaging of oligodendroglioma |journal=Br J Radiol |volume=89 |issue=1060 |pages=20150857 |date=2016 |pmid=26849038 |pmc=4846213 |doi=10.1259/bjr.20150857 |url=}}</ref><ref name="pmid25943885">{{cite journal |vauthors=Wesseling P, van den Bent M, Perry A |title=Oligodendroglioma: pathology, molecular mechanisms and markers |journal=Acta Neuropathol. |volume=129 |issue=6 |pages=809–27 |date=June 2015 |pmid=25943885 |pmc=4436696 |doi=10.1007/s00401-015-1424-1 |url=}}</ref><ref name="pmid26478444">{{cite journal |vauthors=Kerkhof M, Benit C, Duran-Pena A, Vecht CJ |title=Seizures in oligodendroglial tumors |journal=CNS Oncol |volume=4 |issue=5 |pages=347–56 |date=2015 |pmid=26478444 |pmc=6082346 |doi=10.2217/cns.15.29 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Almost always in [[Cerebral hemisphere|cerebral hemisphers]] ([[Frontal lobe|frontal lobes]])


Four pathophysiological mechanisms account for the hypoxaemia seen in a wide variety of diseases: 1) ventilation/perfusion inequality, 2) increased shunt, 3) diffusion impairment, and 4) alveolar hypoventilation 2. Ventilation/perfusion mismatching is the most common mechanism and develops when there is decreased ventilation to normally perfused regions or when there are lung regions with a greater reduction in ventilation than in perfusion. With shunt, either intrapulmonary or intracardiac deoxygenated mixed venous blood bypasses ventilated alveoli, resulting in “venous admixture”. Diseases that increase the diffusion pathway for oxygen from the alveolar space to the pulmonary capillaries, decrease capillary surface area or shorten the transit time of the blood through the pulmonary capillaries prevent complete equilibration of alveolar oxygen with pulmonary capillary blood.
* Hypointense on T1
* Hyperintense on T2
* [[Calcification]]


In the absence of underlying pulmonary disease, hypoxaemia accompanying hypoventilation is characterised by normal DA‐aO2. In contrast, disorders in which any of the other three mechanisms are operative are characterised by broadening of the alveolar/arterial gradient resulting in severe hypoxemia.
* Chicken wire capillary pattern
| style="background: #F5F5F5; padding: 5px;" |
* [[Oligodendrocyte]] origin


Although changes in V'A can change Pa,CO2 considerably, this is not so for Pa,O2. Increases in V'A modestly increase Pa,O2. Owing to the sigmoidal shape of the oxyhaemoglobin dissociation curve, any effect of increasing ventilation on oxygen saturation is minimal above Pa,O2 of 7.3–8.0 kPa (55–60 mmHg). Hypoxaemia resulting from ventilation/perfusion inequality or diffusion abnormalities can easily be corrected by supplementing inspired oxygen, whereas even very high concentrations of inspired oxygen cannot correct hypoxaemia induced by increased pure shunt.
* [[Calcification]] +


Hypercapnic (type II) respiratory failure
* Fried egg cell appearance
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] is between 40 and 50 years of age.
* Most of the time, [[epileptic seizure]] is the presenting [[Sign (medicine)|sign]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Meningioma]]<br><ref name="pmid1642904">{{cite journal |vauthors=Zee CS, Chin T, Segall HD, Destian S, Ahmadi J |title=Magnetic resonance imaging of meningiomas |journal=Semin. Ultrasound CT MR |volume=13 |issue=3 |pages=154–69 |date=June 1992 |pmid=1642904 |doi= |url=}}</ref><ref name="pmid25744347">{{cite journal |vauthors=Shibuya M |title=Pathology and molecular genetics of meningioma: recent advances |journal=Neurol. Med. Chir. (Tokyo) |volume=55 |issue=1 |pages=14–27 |date=2015 |pmid=25744347 |doi=10.2176/nmc.ra.2014-0233 |url=}}</ref><ref name="pmid17509660">{{cite journal |vauthors=Begnami MD, Palau M, Rushing EJ, Santi M, Quezado M |title=Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization |journal=Hum. Pathol. |volume=38 |issue=9 |pages=1345–50 |date=September 2007 |pmid=17509660 |pmc=2094208 |doi=10.1016/j.humpath.2007.01.027 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Well circumscribed
* Extra-axial [[mass]]


The respiratory equation
* [[Meninges|Dural]] attachment
* [[CSF]] [[vascular]] cleft sign
* Sunburst appearance of the [[Vessel|vessels]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Arachnoid]] origin


The volume of carbon dioxide eliminated per minute (which in a steady state is equal to that produced by the body (V'CO2)) is dependent on the concentration of carbon dioxide in alveolar gas and οn V'A. This is obvious, since the conducting airways do not exchange gas. Thus V'CO2=V'A×alveolar CO2 concentrationor alveolar CO2 concentration=V'CO2/V'A. Alveolar CO2 concentration is the concentration of CO2 in the alveolar gas. Gas concentration is converted to gas pressure (Pgas) by the equation: Pgas (mmHg)=(%concentration×(barometric pressure-water vapour))/100. At sea level, barometric pressure is 670 and water vapour pressure at 37°C is 47 mmHg. It follows that Pgas (mmHg)=%concentration×713/100.
* [[Psammoma body|Psammoma bodies]]


By using factor k (0.863), the constant of proportionality, the “respiratory equation” is obtained, which relates V'A to Pa,CO2:
* Whorled spindle cell pattern
Embedded Image
| style="background: #F5F5F5; padding: 5px;" |
Since V'A=V'E−V'ds, where V'E is minute ventilation and V'ds dead space ventilation, this relation may be expressed as:
* [[Biopsy]]
Embedded Image
| style="background: #F5F5F5; padding: 5px;" |
where VT is tidal volume and fR respiratory frequency.
* Highest [[incidence]] is between 40 and 50 years of age.
* Most of the time, focal [[neurological]] deficit and [[epileptic seizure]] are the presenting [[signs]].


Equation 2 states that the Pa,CO2 rises if V'CO2 increases (e.g. hyperthermia) at constant V'A, or when, at a constant V'CO2, V'A decreases by virtue of: 1) a rise in V'ds/VT (by increasing V'ds, decreasing VT or both), 2) a decrease in V'E, and 3) both an increase in V'ds/VT and a decrease in V'E 3, 4.
* May be associated with [[Neurofibromatosis type II|NF-2]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Hemangioblastoma]]<br><ref name="pmid24579662">{{cite journal |vauthors=Lonser RR, Butman JA, Huntoon K, Asthagiri AR, Wu T, Bakhtian KD, Chew EY, Zhuang Z, Linehan WM, Oldfield EH |title=Prospective natural history study of central nervous system hemangioblastomas in von Hippel-Lindau disease |journal=J. Neurosurg. |volume=120 |issue=5 |pages=1055–62 |date=May 2014 |pmid=24579662 |pmc=4762041 |doi=10.3171/2014.1.JNS131431 |url=}}</ref><ref name="pmid17877533">{{cite journal |vauthors=Hussein MR |title=Central nervous system capillary haemangioblastoma: the pathologist's viewpoint |journal=Int J Exp Pathol |volume=88 |issue=5 |pages=311–24 |date=October 2007 |pmid=17877533 |pmc=2517334 |doi=10.1111/j.1365-2613.2007.00535.x |url=}}</ref><ref name="pmid2704812">{{cite journal |vauthors=Lee SR, Sanches J, Mark AS, Dillon WP, Norman D, Newton TH |title=Posterior fossa hemangioblastomas: MR imaging |journal=Radiology |volume=171 |issue=2 |pages=463–8 |date=May 1989 |pmid=2704812 |doi=10.1148/radiology.171.2.2704812 |url=}}</ref><ref name="pmid945331">{{cite journal |vauthors=Perks WH, Cross JN, Sivapragasam S, Johnson P |title=Supratentorial haemangioblastoma with polycythaemia |journal=J. Neurol. Neurosurg. Psychiatry |volume=39 |issue=3 |pages=218–20 |date=March 1976 |pmid=945331 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]


In daily clinical practice, as a patient becomes hypercapnic, more than one factor generally contributes to the rise in Pa,CO2.
* [[Cyst|Cystic]] lesion with a solid enhancing mural [[nodule]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Blood vessel]] origin


CARBON DIOXIDE PRODUCTION
* [[Capillary|Capillaries]] with thin walls
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Might secret [[erythropoietin]] and cause [[polycythemia]]
* May be associated with [[Von Hippel-Lindau Disease|von hippel-lindau syndrome]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pituitary adenoma]]<br><ref name="pmid3786729">{{cite journal |vauthors=Kucharczyk W, Davis DO, Kelly WM, Sze G, Norman D, Newton TH |title=Pituitary adenomas: high-resolution MR imaging at 1.5 T |journal=Radiology |volume=161 |issue=3 |pages=761–5 |date=December 1986 |pmid=3786729 |doi=10.1148/radiology.161.3.3786729 |url=}}</ref><ref name="pmid22584705">{{cite journal |vauthors=Syro LV, Scheithauer BW, Kovacs K, Toledo RA, Londoño FJ, Ortiz LD, Rotondo F, Horvath E, Uribe H |title=Pituitary tumors in patients with MEN1 syndrome |journal=Clinics (Sao Paulo) |volume=67 Suppl 1 |issue= |pages=43–8 |date=2012 |pmid=22584705 |pmc=3328811 |doi= |url=}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + [[Bitemporal hemianopia]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Endocrine]] abnormalities as a result of [[Pituitary adenoma|functional adenomas]] or pressure effect of non-functional [[Adenoma|adenomas]]
| style="background: #F5F5F5; padding: 5px;" |
* Isointense to normal [[pituitary gland]] in T1
| style="background: #F5F5F5; padding: 5px;" |
* [[Endocrine]] cell [[hyperplasia]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[MEN1]] disease.


For a young adult, V'CO2 is ∼200 mL·min−1 (or 110 mL·m2 in males and 96 mL·m2 in females). V'CO2 increases during hyperthermia by ∼14% for each degree Celsius rise in temperature, particularly during muscular activity. During inspiratory resistive breathing, the respiratory muscles, in this respect, may show a V'CO2 of 700–800 mL·min−1 5. In the same manner, shivering or an increase in muscle tone, as occurs in tetanus, leads to excessive V'CO2, with an up to three-fold increase, whereas muscular exercise may increase V'CO2>10‐fold. Under normal conditions, an increase in V'CO2 is detected early by the CNS and is then easily compensated for by increasing V'E to maintain a normal Pa,CO2. However, if a patient's ventilatory capacity is impaired, an increase in V'CO2 greatly stresses the ventilatory system and leads to an increase in Pa,CO2.
* Initialy presents with upper bitemporal quadrantanopsia followed by [[Bitemporal hemianopia|bitemporal hemianopsia]] (pressure on [[Optic chiasm|optic chiasma]] from below)


ALVEOLAR VENTILATION
*


Equations 1 and 2 imply that, at constant V'CO2 and a given V'ds, V'A changes when VT or fR are varied either at constant or reduced total ventilation. This means that there are four possibilities: 1) unchanged total ventilation with decreased fR, 2) unchanged total ventilation with increased fR, 3) decreased total ventilation with decreased fR, or 4) decreased VT.
*
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Schwannoma]]<br><ref name="DonnellyDaly2007">{{cite journal|last1=Donnelly|first1=Martin J.|last2=Daly|first2=Carmel A.|last3=Briggs|first3=Robert J. S.|title=MR imaging features of an intracochlear acoustic schwannoma|journal=The Journal of Laryngology & Otology|volume=108|issue=12|year=2007|issn=0022-2151|doi=10.1017/S0022215100129056}}</ref><ref name="pmid9639114">{{cite journal |vauthors=Feany MB, Anthony DC, Fletcher CD |title=Nerve sheath tumours with hybrid features of neurofibroma and schwannoma: a conceptual challenge |journal=Histopathology |volume=32 |issue=5 |pages=405–10 |date=May 1998 |pmid=9639114 |doi= |url=}}</ref><ref name="pmid28710469">{{cite journal |vauthors=Chen H, Xue L, Wang H, Wang Z, Wu H |title=Differential NF2 Gene Status in Sporadic Vestibular Schwannomas and its Prognostic Impact on Tumour Growth Patterns |journal=Sci Rep |volume=7 |issue=1 |pages=5470 |date=July 2017 |pmid=28710469 |doi=10.1038/s41598-017-05769-0 |url=}}</ref><ref name="HardellHansson Mild2003">{{cite journal|last1=Hardell|first1=Lennart|last2=Hansson Mild|first2=Kjell|last3=Sandström|first3=Monica|last4=Carlberg|first4=Michael|last5=Hallquist|first5=Arne|last6=Påhlson|first6=Anneli|title=Vestibular Schwannoma, Tinnitus and Cellular Telephones|journal=Neuroepidemiology|volume=22|issue=2|year=2003|pages=124–129|issn=0251-5350|doi=10.1159/000068745}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Split-fat sign
* Fascicular sign
* Often have areas of [[hemosiderin]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Schwann cell]] origin


Under conditions of unchanged total ventilation and decreased fR, for V'E to remain unchanged, VT must increase. This decreases V'ds/VT, thereby increasing V'A and decreasing Pa,CO2.
* S100+
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* It causes [[hearing loss]] and [[tinnitus]]


Under conditions of unchanged total ventilation and increased fR, for V'E to remain unchanged, VT must decrease. Such a change, however, increases the V'ds/VT ratio and, therefore, V'A decreases and Pa,CO2 increases. In the clinical setting, rapid, shallow breathing may well explain carbon dioxide retention in patients with COPD.
* May be associated with [[Neurofibromatosis type II|NF-2]] (bilateral [[Schwannoma|schwannomas]])
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Primary central nervous system lymphoma|Primary CNS lymphoma]]<br><ref name="pmid7480733">{{cite journal |vauthors=Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ |title=Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy |journal=Radiology |volume=197 |issue=3 |pages=649–54 |date=December 1995 |pmid=7480733 |doi=10.1148/radiology.197.3.7480733 |url=}}</ref><ref name="Paulus19992">{{cite journal|last1=Paulus|first1=Werner|journal=Journal of Neuro-Oncology|title=Classification, Pathogenesis and Molecular Pathology of Primary CNS Lymphomas|volume=43|issue=3|year=1999|pages=203–208|issn=0167594X|doi=10.1023/A:1006242116122}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Usually deep in the [[white matter]]


Under conditions of decreased total ventilation and decreased fR, the reduction in fR alone, without affecting V'ds/VT, leads to a certain decrease in V'A by virtue of a reduction in V'E.
* Single [[mass]] with ring enhancement
| style="background: #F5F5F5; padding: 5px;" |
* [[B cell]] origin


Under conditions of decreased total ventilation and decreased VT, there is a reduction in V'E caused by reducing the VT (without reducing fR), which results in an increase in V'ds/VT, and, consequently, in a rise in Pa,CO2. Thus, the drop in V'A is expected to be more pronounced than in the aforementioned cases.
* Similar to [[Non-Hodgkin lymphoma|non hodgkin lymphoma]] ([[Diffuse large B cell lymphoma|diffuse large B cell]])
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Usually in young [[immunocompromised]] patients ([[HIV]]) or old [[immunocompetent]] person.


Pathophysiology of ventilatory pump failure
*
|-
| rowspan="5" style="background: #DCDCDC; padding: 5px; text-align: center;" |Childhood primary brain tumors
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pilocytic astrocytoma]]<br><ref name="pmid179640282">{{cite journal |vauthors=Sathornsumetee S, Rich JN, Reardon DA |title=Diagnosis and treatment of high-grade astrocytoma |journal=Neurol Clin |volume=25 |issue=4 |pages=1111–39, x |date=November 2007 |pmid=17964028 |doi=10.1016/j.ncl.2007.07.004 |url=}}</ref><ref name="pmid228197182">{{cite journal |vauthors=Pedersen CL, Romner B |title=Current treatment of low grade astrocytoma: a review |journal=Clin Neurol Neurosurg |volume=115 |issue=1 |pages=1–8 |date=January 2013 |pmid=22819718 |doi=10.1016/j.clineuro.2012.07.002 |url=}}</ref><ref name=":02">{{cite book | last = Mattle | first = Heinrich | title = Fundamentals of neurology : an illustrated guide | publisher = Thieme | location = Stuttgart New York | year = 2017 | isbn = 9783131364524 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]


There are three major causes of pump failure leading to hypercapnia 6. 1) The output of the respiratory centres controlling the muscles may be inadequate (anaesthesia, drug overdose and diseases of the medulla), resulting in a central respiratory drive that is insufficient for the demand, or the respiratory centres may reflexively modify their output in order to prevent respiratory muscle injury and avoid or postpone fatigue. 2) There may be a mechanical defect in the chest wall, as is the case in flail chest, diseases of the nerves (Guillain-Barré syndrome) and anterior horn cells (poliomyelitis), or diseases of the respiratory muscles (myopathies). Severe hyperinflation, with flat diaphragm and reduced mechanical action of the inspiratory muscles, as in acute asthmatic attack, is one of the most common causes of impaired mechanical performance of the inspiratory muscles. 3) When working under excessive inspiratory load, the inspiratory muscles may become fatigued, i.e. they become unable to continue to generate an adequate pleural pressure despite an appropriate central respiratory drive and an intact chest wall.
* Solid and [[Cyst|cystic]] component
* Mostly in [[posterior fossa]]
* Usually in [[Cerebellar hemisphere|cerebellar hemisphers]] and [[Cerebellar vermis|vermis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Glial cell]] origin
*Solid and [[Cyst|cystic]] component


It is obvious that, when there is insufficient activation from the CNS, either temporally (e.g. anaesthesia and overdose) or permanently (e.g. diseases of the medulla), respiratory efforts are inadequate and hypoventilation ensues.
* [[GFAP]] +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Most of the time, [[Cerebellum|cerebellar]] dysfunction is the presenting [[signs]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Medulloblastoma]]<br><ref name="DorwartWara1981">{{cite journal|last1=Dorwart|first1=R H|last2=Wara|first2=W M|last3=Norman|first3=D|last4=Levin|first4=V A|title=Complete myelographic evaluation of spinal metastases from medulloblastoma.|journal=Radiology|volume=139|issue=2|year=1981|pages=403–408|issn=0033-8419|doi=10.1148/radiology.139.2.7220886}}</ref><ref name="Fruehwald-PallamarPuchner2011">{{cite journal|last1=Fruehwald-Pallamar|first1=Julia|last2=Puchner|first2=Stefan B.|last3=Rossi|first3=Andrea|last4=Garre|first4=Maria L.|last5=Cama|first5=Armando|last6=Koelblinger|first6=Claus|last7=Osborn|first7=Anne G.|last8=Thurnher|first8=Majda M.|title=Magnetic resonance imaging spectrum of medulloblastoma|journal=Neuroradiology|volume=53|issue=6|year=2011|pages=387–396|issn=0028-3940|doi=10.1007/s00234-010-0829-8}}</ref><ref name="BurgerGrahmann1987">{{cite journal|last1=Burger|first1=P. C.|last2=Grahmann|first2=F. C.|last3=Bliestle|first3=A.|last4=Kleihues|first4=P.|title=Differentiation in the medulloblastoma|journal=Acta Neuropathologica|volume=73|issue=2|year=1987|pages=115–123|issn=0001-6322|doi=10.1007/BF00693776}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]


Motor output emanating from the CNS needs to be transferred to the respiratory muscles, a process requiring anatomical and functional adequacy of the spinal cord, peripheral nerves and neuromuscular junction. Any disorder along this pathway results in insufficient inflation of the ribcage inadequate to generate subatmospheric pressure, which is essential for the air to flow into the lungs. Mechanical defects of the chest wall (flail chest, kyphoscoliosis and hyperinflation) are entities that predispose to alveolar hypoventilation since they impose additional work on the inspiratory muscles, which have to displace the noncompliant chest wall and lungs.
* Mostly in [[cerebellum]]


Since hyperinflation, commonly occurring in diseases characterised by airways obstruction and loss of elastic recoil of the lungs, has multiple adverse effects on inspiratory muscle function, it deserves to be discussed separately.
* Non communicating [[hydrocephalus]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Neuroectoderm]] origin


For humans to breathe spontaneously, the inspiratory muscles must generate sufficient force to overcome the elastic and resistive load of the respiratory system. Furthermore, the inspiratory muscles should be able to sustain the above mentioned load over time and adjust V'E in such a way that there is adequate gas exchange. Fatigue is the inability of the respiratory muscles to continue to generate sufficient pressure to maintain V'A 6. Fatigue should be distinguished from weakness, which is a fixed reduction in force generation not reversible by rest, although muscle weakness may predispose to muscle fatigue.
* Homer wright rosettes
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Drop metastasis]] ([[metastasis]] through [[CSF]])
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Ependymoma]]<br><ref name="YuhBarkovich2009">{{cite journal|last1=Yuh|first1=E. L.|last2=Barkovich|first2=A. J.|last3=Gupta|first3=N.|title=Imaging of ependymomas: MRI and CT|journal=Child's Nervous System|volume=25|issue=10|year=2009|pages=1203–1213|issn=0256-7040|doi=10.1007/s00381-009-0878-7}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]


Fatigue occurs when the energy supply to the respiratory muscles does not meet the demands. Factors predisposing to respiratory muscle fatigue are those that increase inspiratory muscle energy demands and/or decrease energy supplies 7. Energy demands are determined by the work of breathing and the strength and efficiency of the inspiratory muscles (fig. 3⇓)
* Usually found in [[Fourth ventricle|4th ventricle]]
* Mixed [[Cyst|cystic]]/solid [[lesion]]


Fig. 3.—
* Hydrocephalus
Download figureOpen in new tabDownload powerpoint
| style="background: #F5F5F5; padding: 5px;" |
Fig. 3.—
* [[Ependymal cell]] origin
Respiratory muscle endurance is determined by the balance between energy supplies (S) and demands (D). Normally, the supplies meet the demands and a large reserve exists. Whenever this balance weighs in favour of demands, the respiratory muscles ultimately become fatigued, leading to inability to sustain spontaneous breathing.
The work of breathing increases proportionally with the mean pressure developed by the inspiratory muscles per breath (mean tidal pressure (PI)), expressed as a fraction of maximum inspiratory pressure (PI,max), V'E, duty cycle (inspiratory time (tI)/total respiratory cycle (ttot)) and mean inspiratory flow rate (VT/tI) 6.


PI is increased if the elastic (stiff lungs, pulmonary oedema) or resistive (airways obstruction, asthma) load imposed on the inspiratory muscles is increased. Roussos et al. 8 directly related PI/PI,max with the time that the diaphragm can sustain the load imposed on it (endurance time). The critical value of PI/PI,max that could be generated indefinitely at functional residual capacity (FRC) was ∼0.60. Greater PI/PI,max were inversely related to the endurance time. The critical value of PI/PI,max increases when end-expiratory lung volume increases. Indeed, when lung volume was increased from FRC to FRC plus 50% inspiratory capacity, the critical value of PI/PI,max and the endurance time were diminished to very low values, 25–30% PI,max. Bellemare and Grassino 9 also found that the maximum pressure that can be sustained indefinitely decreases when tI/ttot increases and suggested that the product of PI/PI,max and tI/ttot defined a useful “tension time index” that is related to the endurance time. Whenever the tension time index is below a critical value (0.15 for the diaphragm), the load can be sustained indefinitely.
* Peri[[vascular]] pseudorosette
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Causes an unusually persistent, continuous [[headache]] in children.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Craniopharyngioma]]<br><ref name="pmid12407316">{{cite journal |vauthors=Brunel H, Raybaud C, Peretti-Viton P, Lena G, Girard N, Paz-Paredes A, Levrier O, Farnarier P, Manera L, Choux M |title=[Craniopharyngioma in children: MRI study of 43 cases] |language=French |journal=Neurochirurgie |volume=48 |issue=4 |pages=309–18 |date=September 2002 |pmid=12407316 |doi= |url=}}</ref><ref name="PrabhuBrown2005">{{cite journal|last1=Prabhu|first1=Vikram C.|last2=Brown|first2=Henry G.|title=The pathogenesis of craniopharyngiomas|journal=Child's Nervous System|volume=21|issue=8-9|year=2005|pages=622–627|issn=0256-7040|doi=10.1007/s00381-005-1190-9}}</ref><ref name="pmid766825">{{cite journal |vauthors=Kennedy HB, Smith RJ |title=Eye signs in craniopharyngioma |journal=Br J Ophthalmol |volume=59 |issue=12 |pages=689–95 |date=December 1975 |pmid=766825 |pmc=1017436 |doi= |url=}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + [[Bitemporal hemianopia]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypopituitarism]] as a result of pressure effect on [[pituitary gland]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Calcification]]
* Lobulated contour
* Motor-oil like fluid within [[tumor]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Ectoderm|Ectodermal]] origin ([[Rathke's pouch|Rathkes pouch]])


A weak muscle requires more energy in relation to its maximum energy consumption to perform a given amount of work. The force developed by a skeletal muscle that is sufficient to produce fatigue is a function of the maximum force that the muscle can develop. Any condition that decreases the maximum force decreases the muscle's strength and predisposes to fatigue. Such conditions include atrophy (a probable result of prolonged mechanical ventilation), immaturity, neuromuscular diseases and performance in an inefficient part of the muscle's length/tension characteristics 10, as in a state of acute hyperinflation, during which both the diaphragm and intercostal muscles work at a shorter length.
* [[Calcification]] +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Initialy presents with lower bitemporal quadrantanopsia followed by [[Bitemporal hemianopia|bitemporal hemianopsia]] (pressure on [[Optic chiasm|optic chiasma]] from above)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pinealoma]]<br><ref name="pmid6625640">{{cite journal |vauthors=Ahmed SR, Shalet SM, Price DA, Pearson D |title=Human chorionic gonadotrophin secreting pineal germinoma and precocious puberty |journal=Arch. Dis. Child. |volume=58 |issue=9 |pages=743–5 |date=September 1983 |pmid=6625640 |doi= |url=}}</ref><ref name="Sano1976">{{cite journal|last1=Sano|first1=Keiji|title=Pinealoma in Children|journal=Pediatric Neurosurgery|volume=2|issue=1|year=1976|pages=67–72|issn=1016-2291|doi=10.1159/000119602}}</ref><ref name="Baggenstoss1939">{{cite journal|last1=Baggenstoss|first1=Archie H.|title=PINEALOMAS|journal=Archives of Neurology And Psychiatry|volume=41|issue=6|year=1939|pages=1187|issn=0096-6754|doi=10.1001/archneurpsyc.1939.02270180115011}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + vertical gaze palsy
| style="background: #F5F5F5; padding: 5px;" |
* B-hCG rise leads to [[precocious puberty]] in [[Male|males]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hydrocephalus]] (compression of [[cerebral aqueduct]])
| style="background: #F5F5F5; padding: 5px;" |
* Similar to [[testicular seminoma]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* May cause prinaud syndrome ([[Vertical gaze center|vertical gaze]] palsy, pupillary light-near dissociation, lid retraction and convergence-retraction [[nystagmus]]
|-
| rowspan="2" style="background: #DCDCDC; padding: 5px; text-align: center;" |Vascular
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Arteriovenous malformation|AV malformation]]<br><ref name="KucharczykLemme-Pleghos1985">{{cite journal|last1=Kucharczyk|first1=W|last2=Lemme-Pleghos|first2=L|last3=Uske|first3=A|last4=Brant-Zawadzki|first4=M|last5=Dooms|first5=G|last6=Norman|first6=D|title=Intracranial vascular malformations: MR and CT imaging.|journal=Radiology|volume=156|issue=2|year=1985|pages=383–389|issn=0033-8419|doi=10.1148/radiology.156.2.4011900}}</ref><ref name="FleetwoodSteinberg2002">{{cite journal|last1=Fleetwood|first1=Ian G|last2=Steinberg|first2=Gary K|title=Arteriovenous malformations|journal=The Lancet|volume=359|issue=9309|year=2002|pages=863–873|issn=01406736|doi=10.1016/S0140-6736(02)07946-1}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Supratentorial]]: ~85%
* Flow voids on T2 weighted images
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[AVM]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Angiography]]
| style="background: #F5F5F5; padding: 5px;" |
* We may see bag of worms appearance in [[CT angiography]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Brain aneurysm]]<br><ref name="ChapmanRubinstein1992">{{cite journal|last1=Chapman|first1=Arlene B.|last2=Rubinstein|first2=David|last3=Hughes|first3=Richard|last4=Stears|first4=John C.|last5=Earnest|first5=Michael P.|last6=Johnson|first6=Ann M.|last7=Gabow|first7=Patricia A.|last8=Kaehny|first8=William D.|title=Intracranial Aneurysms in Autosomal Dominant Polycystic Kidney Disease|journal=New England Journal of Medicine|volume=327|issue=13|year=1992|pages=916–920|issn=0028-4793|doi=10.1056/NEJM199209243271303}}</ref><ref name="pmid25632331">{{cite journal |vauthors=Castori M, Voermans NC |title=Neurological manifestations of Ehlers-Danlos syndrome(s): A review |journal=Iran J Neurol |volume=13 |issue=4 |pages=190–208 |date=October 2014 |pmid=25632331 |pmc=4300794 |doi= |url=}}</ref><ref name="SchievinkRaissi2010">{{cite journal|last1=Schievink|first1=W. I.|last2=Raissi|first2=S. S.|last3=Maya|first3=M. M.|last4=Velebir|first4=A.|title=Screening for intracranial aneurysms in patients with bicuspid aortic valve|journal=Neurology|volume=74|issue=18|year=2010|pages=1430–1433|issn=0028-3878|doi=10.1212/WNL.0b013e3181dc1acf}}</ref><ref name="pmid28486967">{{cite journal |vauthors=Germain DP |title=Pseudoxanthoma elasticum |journal=Orphanet J Rare Dis |volume=12 |issue=1 |pages=85 |date=May 2017 |pmid=28486967 |pmc=5424392 |doi=10.1186/s13023-017-0639-8 |url=}}</ref><ref name="pmid27162847">{{cite journal |vauthors=Farahmand M, Farahangiz S, Yadollahi M |title=Diagnostic Accuracy of Magnetic Resonance Angiography for Detection of Intracranial Aneurysms in Patients with Acute Subarachnoid Hemorrhage; A Comparison to Digital Subtraction Angiography |journal=Bull Emerg Trauma |volume=1 |issue=4 |pages=147–51 |date=October 2013 |pmid=27162847 |pmc=4789449 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* In [[magnetic resonance angiography]], we may see [[aneurysm]] mostly in anterior circulation (~85%)
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain aneurysm]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Magnetic resonance angiography]]  and [[CT angiography]] ([[Angiography]] is reserved for patients who have negative [[Magnetic resonance angiography|MAR]] and [[CT angiography|CTA]])
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[autosomal dominant polycystic kidney disease]], [[Ehlers-Danlos syndrome]], [[pseudoxanthoma elasticum]] and [[Bicuspid aortic valve]]
|-
| rowspan="6" style="background: #DCDCDC; padding: 5px; text-align: center;" |Infectious
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Bacterial [[brain abscess]]<br><ref name="HaimesZimmerman1989">{{cite journal|last1=Haimes|first1=AB|last2=Zimmerman|first2=RD|last3=Morgello|first3=S|last4=Weingarten|first4=K|last5=Becker|first5=RD|last6=Jennis|first6=R|last7=Deck|first7=MD|title=MR imaging of brain abscesses|journal=American Journal of Roentgenology|volume=152|issue=5|year=1989|pages=1073–1085|issn=0361-803X|doi=10.2214/ajr.152.5.1073}}</ref><ref name="BrouwerTunkel2014">{{cite journal|last1=Brouwer|first1=Matthijs C.|last2=Tunkel|first2=Allan R.|last3=McKhann|first3=Guy M.|last4=van de Beek|first4=Diederik|title=Brain Abscess|journal=New England Journal of Medicine|volume=371|issue=5|year=2014|pages=447–456|issn=0028-4793|doi=10.1056/NEJMra1301635}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* [[Leukocytosis]]
* Elevated [[ESR]]
* [[Blood culture]] may be positive for underlying [[organism]]
| style="background: #F5F5F5; padding: 5px;" |
* Central hypodense signal and surrounding ring-enhancement in T1
* Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding [[edema]] in T2
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain abscess]]
| style="background: #F5F5F5; padding: 5px;" |
* Clinical presentation/ imaging
| style="background: #F5F5F5; padding: 5px;" |
* The most common causes of [[brain abscess]] are [[Streptococcus]] and [[Staphylococcus]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Tuberculosis]]<br><ref name="MorgadoRuivo2005">{{cite journal|last1=Morgado|first1=Carlos|last2=Ruivo|first2=Nuno|title=Imaging meningo-encephalic tuberculosis|journal=European Journal of Radiology|volume=55|issue=2|year=2005|pages=188–192|issn=0720048X|doi=10.1016/j.ejrad.2005.04.017}}</ref><ref name=":0" /><ref name="pmid19275620">{{cite journal |vauthors=Be NA, Kim KS, Bishai WR, Jain SK |title=Pathogenesis of central nervous system tuberculosis |journal=Curr. Mol. Med. |volume=9 |issue=2 |pages=94–9 |date=March 2009 |pmid=19275620 |pmc=4486069 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[acid-fast bacilli]] ([[AFB]]) smear in [[CSF]] specimen
* Positive [[CSF]] [[nucleic acid]] amplification testing
* [[Hyponatremia]] (inappropriate secretion of [[antidiuretic hormone]])
* Mild [[anemia]]
* [[Leukocytosis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hydrocephalus]] combined with marked basilar [[Meninges|meningeal]] enhancement
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain]] [[tuberculosis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[CSF]] analysis/ Imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]] [[infection]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Toxoplasmosis]]<br><ref name="pmid74807332">{{cite journal |vauthors=Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ |title=Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy |journal=Radiology |volume=197 |issue=3 |pages=649–54 |date=December 1995 |pmid=7480733 |doi=10.1148/radiology.197.3.7480733 |url=}}</ref><ref name="pmid27348541">{{cite journal |vauthors=Helton KJ, Maron G, Mamcarz E, Leventaki V, Patay Z, Sadighi Z |title=Unusual magnetic resonance imaging presentation of post-BMT cerebral toxoplasmosis masquerading as meningoencephalitis and ventriculitis |journal=Bone Marrow Transplant. |volume=51 |issue=11 |pages=1533–1536 |date=November 2016 |pmid=27348541 |doi=10.1038/bmt.2016.168 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Normal [[CSF]]
| style="background: #F5F5F5; padding: 5px;" |
* Multifocal [[Mass|masses]] with ring enhancement
* Mostly in [[basal ganglia]], [[thalami]], and corticomedullary junction.
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for brain [[toxoplasmosis]]
| style="background: #F5F5F5; padding: 5px;" |
* Clinical presentation/ imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]] [[infection]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Hydatid cyst]]<br><ref name="pmid27620198">{{cite journal |vauthors=Taslakian B, Darwish H |title=Intracranial hydatid cyst: imaging findings of a rare disease |journal=BMJ Case Rep |volume=2016 |issue= |pages= |date=September 2016 |pmid=27620198 |pmc=5030532 |doi=10.1136/bcr-2016-216570 |url=}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: left;" |
* Positive [[serology]] ([[Antibody]] detection for [[E. granulosus]]'')''
| style="background: #F5F5F5; padding: 5px;" |
* Honeycomb appearance
* [[Necrotic]] area
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[Hydatid cyst|hydatid cysts]]
| style="background: #F5F5F5; padding: 5px;" |
* Imaging
| style="background: #F5F5F5; padding: 5px;" |
* [[Brain]], [[eye]], and [[Spleen|splenic]] [[Cyst|cysts]] may not produce detectable amount of [[antibodies]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[CNS]] [[cryptococcosis]]<br><ref name="pmid25006721">{{cite journal |vauthors=McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ |title=Mold infections of the central nervous system |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=150–60 |date=July 2014 |pmid=25006721 |pmc=4840461 |doi=10.1056/NEJMra1216008 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[CSF]] [[antigen]] testing ([[coccidioidomycosis]])
* [[CSF]] [[Lymphocyte|lymphocytic]] [[pleocytosis]]
* Elevated [[CSF]] [[Protein|proteins]] and [[lactate]]
* Low [[CSF]] [[glucose]]
*
| style="background: #F5F5F5; padding: 5px;" |
* Dilated peri[[vascular]] spaces
* [[Basal ganglia]] [[Pseudocyst|pseudocysts]]


Finally, muscle efficiency, the ratio of external work performed to energy consumed, is an important factor in energy demands. Inspiratory muscle efficiency is known to fall in patients with hyperinflation. It has been shown that, for the same work of breathing, the oxygen cost is markedly higher in patients with emphysema than in normal subjects 11. This happens, in emphysematous patients, because either some inspiratory muscles may contract isometrically (they consume energy but do not perform work) or the inspiratory muscles are operating in an inefficient part of their force/length relationship: a more forceful contraction is required to produce a given pressure change, and an even greater degree of excitation is required to develop a given force. Thus both conditions lead to increased energy consumption for a given pressure development 12.
* Soap bubble brain lesions ([[cryptococcus neoformans]])
*
| style="background: #F5F5F5; padding: 5px;" |
* We may see numerous acutely branching septate [[Hypha|hyphae]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Laboratory|Lab]] data/ Imaging
* since [[brain]] [[Biopsy|biopsies]] are highly invasive and may may cause [[neurological]] deficits, we [[diagnose]] [[CNS]] [[fungal]] [[Infection|infections]] based on [[laboratory]] and imaging findings
| style="background: #F5F5F5; padding: 5px;" |
* It is the most common [[brain]] [[fungal infection]]


Factors determining the inspiratory muscle energy available are muscle blood flow, the Ca,O2 and the blood substrate concentration as well as the ability of the muscles to extract energy (fig. 3⇑).
* It is associated with [[HIV]], [[Immunosuppressive therapy|immunosuppressive therapies]], and [[Organ transplant|organ transplants]]
 
* In may happen in [[immunocompetent]] patients undergoing invasive procedures ( [[neurosurgery]]) or exposed to [[Contamination|contaminated]] devices or [[drugs]]
Diaphragmatic blood flow is essentially determined by the perfusion pressure, which is a function of cardiac output and peripheral vascular resistance, and the vascular resistance of the muscle, which is a function of the intensity and duration of contraction 13. As has been described in animal models, a reduction in cardiac output accompanying cardiogenic or septic shock is a cause of respiratory fatigue leading to severe alveolar hypoventilation, bradypnoea and respiratory arrest 14, 15. Energy supply to inspiratory muscles also depends on the ability of the muscle to increase blood flow in parallel with the increased work. The diaphragm has a greater capacity to increase blood flow than other skeletal muscles 16. However, the amount that the inspiratory muscle blood flow can be increased may be affected by the intensity and duration of muscle contraction. If the respiratory muscles remain contracted throughout the respiratory cycle, as occurs in asthma 17, the overall blood flow to the muscles may be less than that required. In addition, haemoglobin concentration and oxyhaemoglobin saturation influence the aerobic energy supply to the muscle and hence its endurance.
|-
 
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[CNS]] [[aspergillosis]]<br><ref name="pmid250067212">{{cite journal |vauthors=McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ |title=Mold infections of the central nervous system |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=150–60 |date=July 2014 |pmid=25006721 |pmc=4840461 |doi=10.1056/NEJMra1216008 |url=}}</ref>
Conditions characterised by inability of the muscles to extract and use energy, such as sepsis or cyanide poisoning, or diminished energy stores and glycogen depletion, as in extreme inanition, may potentially lead to respiratory muscle fatigue.
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
 
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
It is clear from the above discussion that fatigue may occur in a variety of clinical entities that alone or in combination result in an imbalance between respiratory muscle energy supplies and demands. No matter what the causes are, it is well known that fatigue is characterised by loss of force output 18, leading to inability of the respiratory muscles to develop adequate PI during tidal breathing, with consequent decreases in VT and V'E and hypercapnia.
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
 
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
When the respiratory muscles are extensively loaded, however, it is likely that feedback mechanisms modify the central drive, which, by exerting “central wisdom”, alters the ventilatory pattern and serves in reducing the load and alleviating fatigue, thus protecting the ventilatory pump from exhaustion, which, undoubtedly, is a terminal event.
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
 
| style="background: #F5F5F5; padding: 5px;" |
Although there are no data from patients to substantiate the existence of “central wisdom” in ventilatory failure, there is enough evidence to support this notion. The fact that the reduction in VT that followed resistive breathing in animals could be restored promptly to normal by administration of naloxone 19 or bilateral cervical vagotomy 20, as well as the fact that most hypercapnic patients with COPD can achieve normocapnia by voluntarily increasing their ventilation, implies that, although the subjects could increase their ventilation, they chose not to do so.
* Positive [[galactomannan]] [[antigen]] testing ([[aspergillosis]])
 
* [[CSF]] [[Lymphocyte|lymphocytic]] [[pleocytosis]]
Indeed, alterations in the pattern of breathing may occur as a result of loading in animals 19, normal subjects 21 and patients during weaning trials 22.
* Elevated [[CSF]] [[Protein|proteins]] and [[lactate]]
 
* Low [[CSF]] [[glucose]]
Patients with acute and chronic respiratory failure as well as normal subjects and animals subjected to fatiguing respiratory loads tend to adopt rapid shallow breathing, consisting of a decrease in VT and increased fR, whereas V'E remains constant or increases slightly. Although this pattern may not be efficient in terms of gas exchange, it may reduce the load on the muscle by decreasing the PI developed, thereby preventing fatigue from occurring 23–26. Moreover, in stable patients with COPD and carbon dioxide retention, this pattern of breathing may be sufficient to keep diaphragm contraction below the fatigue threshold 23, 27.
| style="background: #F5F5F5; padding: 5px;" |
 
* Multiple [[Abscess|abscesses]]
The neurophysiological mechanisms that cause an altered pattern of breathing are not well elucidated. Chemosensitivity-induced alterations in respiratory activity do not appear to be the explanation. Hypoxia- and hypercapnia-induced reductions in expiratory time (tE) are disproportionately greater than reductions in tI, so that tI/ttot increases. Moreover, VT/tI and VT increase rather than decrease 28.
* Ring enhancement
 
* Peripheral low signal intensity on T2
Rapid shallow breathing may be produced by activation of vagal irritant receptors in the airways 29, or may represent a behavioural response to minimise the sense of dyspnoea 30.
| style="background: #F5F5F5; padding: 5px;" |
 
* We may see numerous acutely branching septate [[Hypha|hyphae]]
Reflexes originating from mechanoreceptors in the contracting ribcage muscles and diaphragm (tendon organs, spindle organs, and type III and IV endings) probably play a role in shaping the rapid shallow pattern of breathing. In deeply anaesthetised animals, stretch of the intercostal muscles or increase in diaphragm tension may abruptly terminate inspiration 31. Activation of endogenous opioid pathways has also been postulated to alter the pattern of breathing, perhaps as a mechanism by which the sense of dyspnoea might be reduced 19, 32–35.
| style="background: #F5F5F5; padding: 5px;" |
 
* [[Laboratory|Lab]] data/ Imaging
Small-fibre afferents have been widely implicated in the response of central respiratory output to prolonged stresses such as shock, hypoxia, acidosis and vigorous exercise 15, 36, 37. It is possible that, during loaded breathing, afferents, through the small fibres, modulate endogenous opioids as an adaptive response to minimise breathlessness and avoid or delay the onset of respiratory muscle fatigue 38.
* since [[brain]] [[Biopsy|biopsies]] are highly invasive and may may cause [[neurological]] deficits, we [[diagnose]] [[CNS]] [[fungal]] [[Infection|infections]] based on [[laboratory]] and imaging findings
 
| style="background: #F5F5F5; padding: 5px;" |
Whatever the mechanisms, however, the limit of this strategy is that with rapid shallow breathing V'ds/VT is increased (see The respiratory equation section) with worsening of hypercapnia.
* It is associated with [[HIV]], [[Immunosuppressive therapy|immunosuppressive therapies]], and [[Organ transplant|organ transplants]]
* In may happen in [[immunocompetent]] patients undergoing invasive procedures ( [[neurosurgery]]) or exposed to [[Contamination|contaminated]] devices or [[drugs]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Other
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Brain metastasis]]<br><ref name="pmid29307364">{{cite journal |vauthors=Pope WB |title=Brain metastases: neuroimaging |journal=Handb Clin Neurol |volume=149 |issue= |pages=89–112 |date=2018 |pmid=29307364 |pmc=6118134 |doi=10.1016/B978-0-12-811161-1.00007-4 |url=}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Multiple [[Lesion|lesions]]
* [[Vasogenic edema]]
*
| style="background: #F5F5F5; padding: 5px;" |
* Based on the primary [[cancer]] type we may have different immunohistopathology findings.
| style="background: #F5F5F5; padding: 5px;" |
* History/ imaging
* If there is any uncertainty about [[etiology]], [[biopsy]] should be performed
| style="background: #F5F5F5; padding: 5px;" |
* Most common primary [[Tumor|tumors]] that [[metastasis]] to [[brain]]:
** [[Lung cancer]]
** [[Renal cell carcinoma]]
** [[Breast cancer]]
** [[Melanoma]]
** [[Gastrointestinal tract]]
|}
'''ABBREVIATIONS'''


CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli


==References==
==References==
Line 132: Line 746:
{{WH}}
{{WH}}
{{WS}}
{{WS}}
[[Category:Disease]]
[[Category:Neurology]]
[[Category:Neurosurgery]]
[[Category:Pathology]]
[[Category:Up-To-Date]]
[[Category:Oncology]]
[[Category:Medicine]]

Latest revision as of 18:31, 30 January 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M. Khurram Afzal, MD [2], Sogand Goudarzi, MD [3]

Differentiating [disease name] from other diseases on the basis of [symptom 1], [symptom 2], and [symptom 3]

On the basis [symptom 1], [symptom 2], and [symptom 3], [disease name] must be differentiated from [disease 1], [disease 2], [disease 3], [disease 4], [disease 5], and [disease 6].

Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings
Symptoms Physical examination
Lab Findings Imaging
Symptoms of DVT Symptoms of Pulmonary Embolism Symptoms of Myocardial Infarction Tenderness in extremities Edema in extremities Warmth in extremities PT aPTT Doppler ultrasound Chest CT scan
Antithrombin III deficiency[1][2][3] + + - + + + Normal
  • Normal
  • Reduces the Increase in PTT after administration of heparin
Factor V Leiden mutation[4][5][6][7][8] + + + + + + N/A ↑
  • N/A
  • Inactivates factor Va and factor VIIIa
Protein C deficiency[9][10][11] + + - + + + Normal Normal / ↑
Protein S deficiency[11][12][13] + + - + + + Normal Normal / ↑
Prothrombin gene mutation[14][15][16] + + - + + + ↑ N/A
Disseminated intravascular coagulation (DIC)[17][18][19] + + +/- + + + ↑ ↑
  • N/A
Antiphospholipid antibody syndrome[20][21][22][23][24] + + +/- + + + N/A ↑

References

  1. ↑ Patnaik MM, Moll S (November 2008). "Inherited antithrombin deficiency: a review". Haemophilia. 14 (6): 1229–39. doi:10.1111/j.1365-2516.2008.01830.x. PMID 19141163.
  2. ↑ Al Hadidi, Samer; Wu, Kristi; Aburahma, Ahmed; Alamarat, Zain (2017). "Family with clots: antithrombin deficiency". BMJ Case Reports: bcr-2017–221556. doi:10.1136/bcr-2017-221556. ISSN 1757-790X.
  3. ↑ Konecny F (January 2009). "Inherited trombophilic states and pulmonary embolism". J Res Med Sci. 14 (1): 43–56. PMC 3129068. PMID 21772860.
  4. ↑ Mannucci PM, Asselta R, Duga S, Guella I, Spreafico M, Lotta L, Merlini PA, Peyvandi F, Kathiresan S, Ardissino D (October 2010). "The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease". J. Thromb. Haemost. 8 (10): 2116–21. doi:10.1111/j.1538-7836.2010.03982.x. PMID 20626623.
  5. ↑ Campello E, Spiezia L, Simioni P (December 2016). "Diagnosis and management of factor V Leiden". Expert Rev Hematol. 9 (12): 1139–1149. doi:10.1080/17474086.2016.1249364. PMID 27797270.
  6. ↑ Van Rooden CJ, Rosendaal FR, Meinders AE, Van Oostayen JA, Van Der Meer FJ, Huisman MV (February 2004). "The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis". Haematologica. 89 (2): 201–6. PMID 15003896.
  7. ↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). "Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis". Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
  8. ↑ Press RD, Bauer KA, Kujovich JL, Heit JA (November 2002). "Clinical utility of factor V leiden (R506Q) testing for the diagnosis and management of thromboembolic disorders". Arch. Pathol. Lab. Med. 126 (11): 1304–18. doi:10.1043/0003-9985(2002)126<1304:CUOFVL>2.0.CO;2. PMID 12421138.
  9. ↑ Bernard Khor & Elizabeth M. Van Cott (2010). "Laboratory tests for protein C deficiency". American journal of hematology. 85 (6): 440–442. doi:10.1002/ajh.21679. PMID 20309856. Unknown parameter |month= ignored (help)
  10. ↑ Pescatore SL (March 2001). "Clinical management of protein C deficiency". Expert Opin Pharmacother. 2 (3): 431–9. doi:10.1517/14656566.2.3.431. PMID 11336597.
  11. ↑ 11.0 11.1 Gustavo A. Rodriguez-Leal, Segundo Moran, Roberto Corona-Cedillo & Rocio Brom-Valladares (2014). "Portal vein thrombosis with protein C-S deficiency in a non-cirrhotic patient". World journal of hepatology. 6 (7): 532–537. doi:10.4254/wjh.v6.i7.532. PMID 25068006. Unknown parameter |month= ignored (help)
  12. ↑ Kristi J. Smock, Elizabeth A. Plumhoff, Piet Meijer, Peihong Hsu, Nicole D. Zantek, Nahla M. Heikal & Elizabeth M. Van Cott (2016). "Protein S testing in patients with protein S deficiency, factor V Leiden, and rivaroxaban by North American Specialized Coagulation Laboratories". Thrombosis and haemostasis. 116 (1): 50–57. doi:10.1160/TH15-12-0918. PMID 27075008. Unknown parameter |month= ignored (help)
  13. ↑ Ji M, Yoon SN, Lee W, Jang S, Park SH, Kim DY, Chun S, Min WK (October 2011). "Protein S deficiency with a PROS1 gene mutation in a patient presenting with mesenteric venous thrombosis following total colectomy". Blood Coagul. Fibrinolysis. 22 (7): 619–21. doi:10.1097/MBC.0b013e32834a0421. PMID 21799399.
  14. ↑ Cooper PC, Rezende SM (2007). "An overview of methods for detection of factor V Leiden and the prothrombin G20210A mutations". Int J Lab Hematol. 29 (3): 153–62. doi:10.1111/j.1751-553X.2007.00892.x. PMID 17474891.
  15. ↑ McGlennen RC, Key NS (2002). "Clinical and laboratory management of the prothrombin G20210A mutation". Arch Pathol Lab Med. 126 (11): 1319–25. doi:10.1043/0003-9985(2002)126<1319:CALMOT>2.0.CO;2. PMID 12421139.
  16. ↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). "Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis". Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
  17. ↑ Venugopal A (September 2014). "Disseminated intravascular coagulation". Indian J Anaesth. 58 (5): 603–8. doi:10.4103/0019-5049.144666. PMC 4260307. PMID 25535423.
  18. ↑ Makruasi N (November 2015). "Treatment of Disseminated Intravascular Coagulation". J Med Assoc Thai. 98 Suppl 10: S45–51. PMID 27276832.
  19. ↑ Cui S, Fu Z, Feng Y, Xie X, Ma X, Liu T; et al. (2018). "The disseminated intravascular coagulation score is a novel predictor for portal vein thrombosis in cirrhotic patients with hepatitis B." Thromb Res. 161: 7–11. doi:10.1016/j.thromres.2017.11.010. PMID 29178991.
  20. ↑ Lim W (2013). "Antiphospholipid syndrome". Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
  21. ↑ Pengo V, Tripodi A, Reber G, Rand JH, Ortel TL, Galli M, De Groot PG (October 2009). "Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis". J. Thromb. Haemost. 7 (10): 1737–40. doi:10.1111/j.1538-7836.2009.03555.x. PMID 19624461.
  22. ↑ Lim W (2013). "Antiphospholipid syndrome". Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
  23. ↑ Garcia D, Erkan D (2018). "Diagnosis and Management of the Antiphospholipid Syndrome". N Engl J Med. 378 (21): 2010–2021. doi:10.1056/NEJMra1705454. PMID 29791828.
  24. ↑ Kornacki J, Wirstlein P, Skrzypczak J (2012). "[Assessment of uterine arteries Doppler in the first half of pregnancy in women with thrombophilia]". Ginekol Pol. 83 (12): 916–21. PMID 23488294.

Template:WH Template:WS


Astrocytoma Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Astrocytoma from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-Ray

Echocardiography and Ultrasound

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Study

Case #1

Sandbox:khurram On the Web

Most recent articles

cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Sandbox:khurram

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Sandbox:khurram

CDC on Sandbox:khurram

Sandbox:khurram in the news

Blogs on Sandbox:khurram

Directions to Hospitals Treating Astrocytoma

Risk calculators and risk factors for Sandbox:khurram

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Overview

On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from oligodendroglioma, meningioma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Differentiating astrocytoma from other Diseases

Differentiating astrocytoma from other diseases on the basis of seizure, visual disturbance, and constitutional symptoms

On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from oligodendroglioma, meningioma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Diseases Clinical manifestations Para-clinical findings Gold
standard 		Additional findings
Symptoms Physical examination
Lab Findings MRI Immunohistopathology
Head-
ache 		Seizure Visual disturbance Constitutional Focal neurological deficit
Adult primary brain tumors Glioblastoma multiforme
[1][2][3] 		+ +/− +/− − + −
  • Pseudopalisading appearance
oligodendroglioma
[4][5][6] 		+ + +/− − + −
  • Chicken wire capillary pattern
  • Fried egg cell appearance
Meningioma
[7][8][9] 		+ +/− +/− − + −
  • Well circumscribed
  • Extra-axial mass
  • Whorled spindle cell pattern
  • May be associated with NF-2
Hemangioblastoma
[10][11][12][13] 		+ +/− +/− − + −
Pituitary adenoma
[14][15][3] 		− − + Bitemporal hemianopia − −
  • It is associated with MEN1 disease.
Schwannoma
[16][17][18][19] 		− − − − + −
  • Split-fat sign
  • Fascicular sign
  • Often have areas of hemosiderin
  • S100+
Primary CNS lymphoma
[20][21] 		+ +/− +/− − + −
  • Single mass with ring enhancement
Childhood primary brain tumors Pilocytic astrocytoma
[22][23][24] 		+ +/− +/− − + −
Medulloblastoma
[25][26][27] 		+ +/− +/− − + −
  • Homer wright rosettes
Ependymoma
[28][3] 		+ +/− +/− − + −
  • Hydrocephalus
  • Causes an unusually persistent, continuous headache in children.
Craniopharyngioma
[29][30][31][3] 		+ +/− + Bitemporal hemianopia − +
Pinealoma
[32][33][34] 		+ +/− +/− − + vertical gaze palsy
  • May cause prinaud syndrome (vertical gaze palsy, pupillary light-near dissociation, lid retraction and convergence-retraction nystagmus
Vascular AV malformation
[35][36][3] 		+ + +/− − +/− −
Brain aneurysm
[37][38][39][40][41] 		+ +/− +/− − +/− −
Infectious Bacterial brain abscess
[42][43] 		+ +/− +/− + +
  • Central hypodense signal and surrounding ring-enhancement in T1
  • Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding edema in T2
  • Clinical presentation/ imaging
Tuberculosis
[44][3][45] 		+ +/− +/− + +
  • CSF analysis/ Imaging
Toxoplasmosis
[46][47] 		+ +/− +/− − +
  • Clinical presentation/ imaging
Hydatid cyst
[48][3] 		+ +/− +/− +/− +
  • Imaging
CNS cryptococcosis
[49] 		+ +/− +/− + +
  • We may see numerous acutely branching septate hyphae
CNS aspergillosis
[50] 		+ +/− +/− + +
  • Multiple abscesses
  • Ring enhancement
  • Peripheral low signal intensity on T2
  • We may see numerous acutely branching septate hyphae
Other Brain metastasis
[51][3] 		+ +/− +/− + + −
  • Based on the primary cancer type we may have different immunohistopathology findings.
  • History/ imaging
  • If there is any uncertainty about etiology, biopsy should be performed

ABBREVIATIONS

CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli

References

  1. ↑ Sathornsumetee S, Rich JN, Reardon DA (November 2007). "Diagnosis and treatment of high-grade astrocytoma". Neurol Clin. 25 (4): 1111–39, x. doi:10.1016/j.ncl.2007.07.004. PMID 17964028.
  2. ↑ Pedersen CL, Romner B (January 2013). "Current treatment of low grade astrocytoma: a review". Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
  4. ↑ Smits M (2016). "Imaging of oligodendroglioma". Br J Radiol. 89 (1060): 20150857. doi:10.1259/bjr.20150857. PMC 4846213. PMID 26849038.
  5. ↑ Wesseling P, van den Bent M, Perry A (June 2015). "Oligodendroglioma: pathology, molecular mechanisms and markers". Acta Neuropathol. 129 (6): 809–27. doi:10.1007/s00401-015-1424-1. PMC 4436696. PMID 25943885.
  6. ↑ Kerkhof M, Benit C, Duran-Pena A, Vecht CJ (2015). "Seizures in oligodendroglial tumors". CNS Oncol. 4 (5): 347–56. doi:10.2217/cns.15.29. PMC 6082346. PMID 26478444.
  7. ↑ Zee CS, Chin T, Segall HD, Destian S, Ahmadi J (June 1992). "Magnetic resonance imaging of meningiomas". Semin. Ultrasound CT MR. 13 (3): 154–69. PMID 1642904.
  8. ↑ Shibuya M (2015). "Pathology and molecular genetics of meningioma: recent advances". Neurol. Med. Chir. (Tokyo). 55 (1): 14–27. doi:10.2176/nmc.ra.2014-0233. PMID 25744347.
  9. ↑ Begnami MD, Palau M, Rushing EJ, Santi M, Quezado M (September 2007). "Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization". Hum. Pathol. 38 (9): 1345–50. doi:10.1016/j.humpath.2007.01.027. PMC 2094208. PMID 17509660.
  10. ↑ Lonser RR, Butman JA, Huntoon K, Asthagiri AR, Wu T, Bakhtian KD, Chew EY, Zhuang Z, Linehan WM, Oldfield EH (May 2014). "Prospective natural history study of central nervous system hemangioblastomas in von Hippel-Lindau disease". J. Neurosurg. 120 (5): 1055–62. doi:10.3171/2014.1.JNS131431. PMC 4762041. PMID 24579662.
  11. ↑ Hussein MR (October 2007). "Central nervous system capillary haemangioblastoma: the pathologist's viewpoint". Int J Exp Pathol. 88 (5): 311–24. doi:10.1111/j.1365-2613.2007.00535.x. PMC 2517334. PMID 17877533.
  12. ↑ Lee SR, Sanches J, Mark AS, Dillon WP, Norman D, Newton TH (May 1989). "Posterior fossa hemangioblastomas: MR imaging". Radiology. 171 (2): 463–8. doi:10.1148/radiology.171.2.2704812. PMID 2704812.
  13. ↑ Perks WH, Cross JN, Sivapragasam S, Johnson P (March 1976). "Supratentorial haemangioblastoma with polycythaemia". J. Neurol. Neurosurg. Psychiatry. 39 (3): 218–20. PMID 945331.
  14. ↑ Kucharczyk W, Davis DO, Kelly WM, Sze G, Norman D, Newton TH (December 1986). "Pituitary adenomas: high-resolution MR imaging at 1.5 T". Radiology. 161 (3): 761–5. doi:10.1148/radiology.161.3.3786729. PMID 3786729.
  15. ↑ Syro LV, Scheithauer BW, Kovacs K, Toledo RA, Londoño FJ, Ortiz LD, Rotondo F, Horvath E, Uribe H (2012). "Pituitary tumors in patients with MEN1 syndrome". Clinics (Sao Paulo). 67 Suppl 1: 43–8. PMC 3328811. PMID 22584705.
  16. ↑ Donnelly, Martin J.; Daly, Carmel A.; Briggs, Robert J. S. (2007). "MR imaging features of an intracochlear acoustic schwannoma". The Journal of Laryngology & Otology. 108 (12). doi:10.1017/S0022215100129056. ISSN 0022-2151.
  17. ↑ Feany MB, Anthony DC, Fletcher CD (May 1998). "Nerve sheath tumours with hybrid features of neurofibroma and schwannoma: a conceptual challenge". Histopathology. 32 (5): 405–10. PMID 9639114.
  18. ↑ Chen H, Xue L, Wang H, Wang Z, Wu H (July 2017). "Differential NF2 Gene Status in Sporadic Vestibular Schwannomas and its Prognostic Impact on Tumour Growth Patterns". Sci Rep. 7 (1): 5470. doi:10.1038/s41598-017-05769-0. PMID 28710469.
  19. ↑ Hardell, Lennart; Hansson Mild, Kjell; Sandström, Monica; Carlberg, Michael; Hallquist, Arne; Påhlson, Anneli (2003). "Vestibular Schwannoma, Tinnitus and Cellular Telephones". Neuroepidemiology. 22 (2): 124–129. doi:10.1159/000068745. ISSN 0251-5350.
  20. ↑ Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ (December 1995). "Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy". Radiology. 197 (3): 649–54. doi:10.1148/radiology.197.3.7480733. PMID 7480733.
  21. ↑ Paulus, Werner (1999). "Classification, Pathogenesis and Molecular Pathology of Primary CNS Lymphomas". Journal of Neuro-Oncology. 43 (3): 203–208. doi:10.1023/A:1006242116122. ISSN 0167-594X.
  22. ↑ Sathornsumetee S, Rich JN, Reardon DA (November 2007). "Diagnosis and treatment of high-grade astrocytoma". Neurol Clin. 25 (4): 1111–39, x. doi:10.1016/j.ncl.2007.07.004. PMID 17964028.
  23. ↑ Pedersen CL, Romner B (January 2013). "Current treatment of low grade astrocytoma: a review". Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
  24. ↑ Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
  25. ↑ Dorwart, R H; Wara, W M; Norman, D; Levin, V A (1981). "Complete myelographic evaluation of spinal metastases from medulloblastoma". Radiology. 139 (2): 403–408. doi:10.1148/radiology.139.2.7220886. ISSN 0033-8419.
  26. ↑ Fruehwald-Pallamar, Julia; Puchner, Stefan B.; Rossi, Andrea; Garre, Maria L.; Cama, Armando; Koelblinger, Claus; Osborn, Anne G.; Thurnher, Majda M. (2011). "Magnetic resonance imaging spectrum of medulloblastoma". Neuroradiology. 53 (6): 387–396. doi:10.1007/s00234-010-0829-8. ISSN 0028-3940.
  27. ↑ Burger, P. C.; Grahmann, F. C.; Bliestle, A.; Kleihues, P. (1987). "Differentiation in the medulloblastoma". Acta Neuropathologica. 73 (2): 115–123. doi:10.1007/BF00693776. ISSN 0001-6322.
  28. ↑ Yuh, E. L.; Barkovich, A. J.; Gupta, N. (2009). "Imaging of ependymomas: MRI and CT". Child's Nervous System. 25 (10): 1203–1213. doi:10.1007/s00381-009-0878-7. ISSN 0256-7040.
  29. ↑ Brunel H, Raybaud C, Peretti-Viton P, Lena G, Girard N, Paz-Paredes A, Levrier O, Farnarier P, Manera L, Choux M (September 2002). "[Craniopharyngioma in children: MRI study of 43 cases]". Neurochirurgie (in French). 48 (4): 309–18. PMID 12407316.
  30. ↑ Prabhu, Vikram C.; Brown, Henry G. (2005). "The pathogenesis of craniopharyngiomas". Child's Nervous System. 21 (8–9): 622–627. doi:10.1007/s00381-005-1190-9. ISSN 0256-7040.
  31. ↑ Kennedy HB, Smith RJ (December 1975). "Eye signs in craniopharyngioma". Br J Ophthalmol. 59 (12): 689–95. PMC 1017436. PMID 766825.
  32. ↑ Ahmed SR, Shalet SM, Price DA, Pearson D (September 1983). "Human chorionic gonadotrophin secreting pineal germinoma and precocious puberty". Arch. Dis. Child. 58 (9): 743–5. PMID 6625640.
  33. ↑ Sano, Keiji (1976). "Pinealoma in Children". Pediatric Neurosurgery. 2 (1): 67–72. doi:10.1159/000119602. ISSN 1016-2291.
  34. ↑ Baggenstoss, Archie H. (1939). "PINEALOMAS". Archives of Neurology And Psychiatry. 41 (6): 1187. doi:10.1001/archneurpsyc.1939.02270180115011. ISSN 0096-6754.
  35. ↑ Kucharczyk, W; Lemme-Pleghos, L; Uske, A; Brant-Zawadzki, M; Dooms, G; Norman, D (1985). "Intracranial vascular malformations: MR and CT imaging". Radiology. 156 (2): 383–389. doi:10.1148/radiology.156.2.4011900. ISSN 0033-8419.
  36. ↑ Fleetwood, Ian G; Steinberg, Gary K (2002). "Arteriovenous malformations". The Lancet. 359 (9309): 863–873. doi:10.1016/S0140-6736(02)07946-1. ISSN 0140-6736.
  37. ↑ Chapman, Arlene B.; Rubinstein, David; Hughes, Richard; Stears, John C.; Earnest, Michael P.; Johnson, Ann M.; Gabow, Patricia A.; Kaehny, William D. (1992). "Intracranial Aneurysms in Autosomal Dominant Polycystic Kidney Disease". New England Journal of Medicine. 327 (13): 916–920. doi:10.1056/NEJM199209243271303. ISSN 0028-4793.
  38. ↑ Castori M, Voermans NC (October 2014). "Neurological manifestations of Ehlers-Danlos syndrome(s): A review". Iran J Neurol. 13 (4): 190–208. PMC 4300794. PMID 25632331.
  39. ↑ Schievink, W. I.; Raissi, S. S.; Maya, M. M.; Velebir, A. (2010). "Screening for intracranial aneurysms in patients with bicuspid aortic valve". Neurology. 74 (18): 1430–1433. doi:10.1212/WNL.0b013e3181dc1acf. ISSN 0028-3878.
  40. ↑ Germain DP (May 2017). "Pseudoxanthoma elasticum". Orphanet J Rare Dis. 12 (1): 85. doi:10.1186/s13023-017-0639-8. PMC 5424392. PMID 28486967.
  41. ↑ Farahmand M, Farahangiz S, Yadollahi M (October 2013). "Diagnostic Accuracy of Magnetic Resonance Angiography for Detection of Intracranial Aneurysms in Patients with Acute Subarachnoid Hemorrhage; A Comparison to Digital Subtraction Angiography". Bull Emerg Trauma. 1 (4): 147–51. PMC 4789449. PMID 27162847.
  42. ↑ Haimes, AB; Zimmerman, RD; Morgello, S; Weingarten, K; Becker, RD; Jennis, R; Deck, MD (1989). "MR imaging of brain abscesses". American Journal of Roentgenology. 152 (5): 1073–1085. doi:10.2214/ajr.152.5.1073. ISSN 0361-803X.
  43. ↑ Brouwer, Matthijs C.; Tunkel, Allan R.; McKhann, Guy M.; van de Beek, Diederik (2014). "Brain Abscess". New England Journal of Medicine. 371 (5): 447–456. doi:10.1056/NEJMra1301635. ISSN 0028-4793.
  44. ↑ Morgado, Carlos; Ruivo, Nuno (2005). "Imaging meningo-encephalic tuberculosis". European Journal of Radiology. 55 (2): 188–192. doi:10.1016/j.ejrad.2005.04.017. ISSN 0720-048X.
  45. ↑ Be NA, Kim KS, Bishai WR, Jain SK (March 2009). "Pathogenesis of central nervous system tuberculosis". Curr. Mol. Med. 9 (2): 94–9. PMC 4486069. PMID 19275620.
  46. ↑ Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ (December 1995). "Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy". Radiology. 197 (3): 649–54. doi:10.1148/radiology.197.3.7480733. PMID 7480733.
  47. ↑ Helton KJ, Maron G, Mamcarz E, Leventaki V, Patay Z, Sadighi Z (November 2016). "Unusual magnetic resonance imaging presentation of post-BMT cerebral toxoplasmosis masquerading as meningoencephalitis and ventriculitis". Bone Marrow Transplant. 51 (11): 1533–1536. doi:10.1038/bmt.2016.168. PMID 27348541.
  48. ↑ Taslakian B, Darwish H (September 2016). "Intracranial hydatid cyst: imaging findings of a rare disease". BMJ Case Rep. 2016. doi:10.1136/bcr-2016-216570. PMC 5030532. PMID 27620198.
  49. ↑ McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ (July 2014). "Mold infections of the central nervous system". N. Engl. J. Med. 371 (2): 150–60. doi:10.1056/NEJMra1216008. PMC 4840461. PMID 25006721.
  50. ↑ McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ (July 2014). "Mold infections of the central nervous system". N. Engl. J. Med. 371 (2): 150–60. doi:10.1056/NEJMra1216008. PMC 4840461. PMID 25006721.
  51. ↑ Pope WB (2018). "Brain metastases: neuroimaging". Handb Clin Neurol. 149: 89–112. doi:10.1016/B978-0-12-811161-1.00007-4. PMC 6118134. PMID 29307364.

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Sandbox:khurram&oldid=1543625"