Pseudotumor cerebri pathophysiology: Difference between revisions

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==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.


OR
==Pathophysiology==


It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
=== Physiology ===
* [[Cerebrospinal fluid]] lifecycle: 600 ml of [[CSF]] is produced daily. this amount will decrease with age. 2/3  of this fluid is produced by [[choroid plexus]] of [[Brain ventricle|brain ventricles]] and the other 1/3 by [[Ependymal cell|ependymal]] lining of [[Brain ventricle|ventricles]]. <ref name="pmid16344101">{{cite journal |vauthors=Redzic ZB, Preston JE, Duncan JA, Chodobski A, Szmydynger-Chodobska J |title=The choroid plexus-cerebrospinal fluid system: from development to aging |journal=Curr. Top. Dev. Biol. |volume=71 |issue= |pages=1–52 |date=2005 |pmid=16344101 |doi=10.1016/S0070-2153(05)71001-2 |url=}}</ref>
* [[CSF]] production is a energy consuming process and use [[Na/K ATPase]] to flow ions into lumen and attract water with it through [[aquaporins]].<ref name="pmid3132082">{{cite journal |vauthors=Maren TH |title=The kinetics of HCO3- synthesis related to fluid secretion, pH control, and CO2 elimination |journal=Annu. Rev. Physiol. |volume=50 |issue= |pages=695–717 |date=1988 |pmid=3132082 |doi=10.1146/annurev.ph.50.030188.003403 |url=}}</ref> [[CSF]] flows out to subarachnoid granulation where it can be absorbed.<ref name="pmid4369428">{{cite journal |vauthors=Tripathi BJ, Tripathi RC |title=Vacuolar transcellular channels as a drainage pathway for cerebrospinal fluid |journal=J. Physiol. (Lond.) |volume=239 |issue=1 |pages=195–206 |date=May 1974 |pmid=4369428 |pmc=1330945 |doi= |url=}}</ref> Some part of [[CSF]] flows into [[Lymphatic system|lymphatics]] of head and neck and some part absorbed through [[spine]].<ref name="pmid19002474">{{cite journal |vauthors=Weller RO, Djuanda E, Yow HY, Carare RO |title=Lymphatic drainage of the brain and the pathophysiology of neurological disease |journal=Acta Neuropathol. |volume=117 |issue=1 |pages=1–14 |date=January 2009 |pmid=19002474 |doi=10.1007/s00401-008-0457-0 |url=}}</ref><ref name="pmid15308484">{{cite journal |vauthors=Edsbagge M, Tisell M, Jacobsson L, Wikkelso C |title=Spinal CSF absorption in healthy individuals |journal=Am. J. Physiol. Regul. Integr. Comp. Physiol. |volume=287 |issue=6 |pages=R1450–5 |date=December 2004 |pmid=15308484 |doi=10.1152/ajpregu.00215.2004 |url=}}</ref>


OR
===Pathogenesis===
 
* The exact [[pathogenesis]] of pseudotumor cerebri is not completely understood. [[Idiopathic intracranial hypertension]] or pseudotumor cerebri is defined by the [[Symptom|symptoms]] of increased [[intracranial pressure]] which is the common final pathway of all [[Idiopathic intracranial hypertension|IIH]] etiologies, without any evidence of [[Intracranial mass]] lesions.<ref name="pmid12455560">{{cite journal |vauthors=Friedman DI, Jacobson DM |title=Diagnostic criteria for idiopathic intracranial hypertension |journal=Neurology |volume=59 |issue=10 |pages=1492–5 |date=November 2002 |pmid=12455560 |doi= |url=}}</ref>
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
Any theory regarding the [[pathophysiology]] of this disease should explain the following statements:
#  High [[incidence]] rate in women with childbearing age
# Reduced conductance to [[CSF]] outflow<ref name="pmid5468773">{{cite journal |vauthors=Bercaw BL, Greer M |title=Transport of intrathecal 131-I risa in benign intracranial hypertension |journal=Neurology |volume=20 |issue=8 |pages=787–90 |date=August 1970 |pmid=5468773 |doi= |url=}}</ref>
# Normal [[ventricle]] size and lack of [[hydrocephalus]]<ref name="pmid2392235">{{cite journal |vauthors=Jacobson DM, Karanjia PN, Olson KA, Warner JJ |title=Computed tomography ventricular size has no predictive value in diagnosing pseudotumor cerebri |journal=Neurology |volume=40 |issue=9 |pages=1454–5 |date=September 1990 |pmid=2392235 |doi= |url=}}</ref>
# No evidence of [[cerebral edema]]<ref name="pmid7848121">{{cite journal |vauthors=Wall M, Dollar JD, Sadun AA, Kardon R |title=Idiopathic intracranial hypertension. Lack of histologic evidence for cerebral edema |journal=Arch. Neurol. |volume=52 |issue=2 |pages=141–5 |date=February 1995 |pmid=7848121 |doi= |url=}}</ref>


OR
* The basic [[etiology]] behind every [[Idiopathic intracranial hypertension|IIH]] [[pathogenesis]] theory is Increased production of [[CSF]] and reduced resorption.


Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
* [[CSF]] Changes in Pseudotumor Cerebri: The production of [[CSF]] is constant so the main problem in [[Idiopathic intracranial hypertension|IIH]] [[pathogenesis]] is related to [[CSF]] absorbtaion. Many studies suggested that increased resistant to [[CSF]] absorbtion in the main cause of [[Idiopathic intracranial hypertension|IIH]] disease.<ref name="pmid7435599">{{cite journal |vauthors=Sklar FH, Reisch J, Elashvili I, Smith T, Long DM |title=Effects of pressure on cerebrospinal fluid formation: nonsteady-state measurements in dogs |journal=Am. J. Physiol. |volume=239 |issue=3 |pages=R277–84 |date=September 1980 |pmid=7435599 |doi=10.1152/ajpregu.1980.239.3.R277 |url=}}</ref><ref name="pmid4434179">{{cite journal |vauthors=Johnston I, Paterson A |title=Benign intracranial hypertension. II. CSF pressure and circulation |journal=Brain |volume=97 |issue=2 |pages=301–12 |date=June 1974 |pmid=4434179 |doi= |url=}}</ref><ref name="pmid3872097">{{cite journal |vauthors=Gjerris F, Soelberg Sørensen P, Vorstrup S, Paulson OB |title=Intracranial pressure, conductance to cerebrospinal fluid outflow, and cerebral blood flow in patients with benign intracranial hypertension (pseudotumor cerebri) |journal=Ann. Neurol. |volume=17 |issue=2 |pages=158–62 |date=February 1985 |pmid=3872097 |doi=10.1002/ana.410170209 |url=}}</ref><ref name="pmid7221863">{{cite journal |vauthors=Janny P, Chazal J, Colnet G, Irthum B, Georget AM |title=Benign intracranial hypertension and disorders of CSF absorption |journal=Surg Neurol |volume=15 |issue=3 |pages=168–74 |date=March 1981 |pmid=7221863 |doi= |url=}}</ref>


OR
* The venous sinuses: It has been suggested that primary or secondary venous outflow narrowing or can cause [[Idiopathic intracranial hypertension|IIH]].<ref name="pmid16350454">{{cite journal |vauthors=Owler BK, Parker G, Halmagyi GM, Johnston IH, Besser M, Pickard JD, Higgins JN |title=Cranial venous outflow obstruction and pseudotumor Cerebri syndrome |journal=Adv Tech Stand Neurosurg |volume=30 |issue= |pages=107–74 |date=2005 |pmid=16350454 |doi= |url=}}</ref><ref name="pmid15288385">{{cite journal |vauthors=Bateman GA |title=Idiopathic intracranial hypertension: priapism of the brain? |journal=Med. Hypotheses |volume=63 |issue=3 |pages=549–52 |date=2004 |pmid=15288385 |doi=10.1016/j.mehy.2004.03.014 |url=}}</ref> One of the causes of venous sinuses narrowing is [[Thrombotic events|thrombotic event]]. In one of the [[Idiopathic intracranial hypertension|IIH]] studies the amount of [[MTHFR]] was higher in [[Idiopathic intracranial hypertension|IIH]] patients (38%) in comparison to control group (14%). This result suggests that [[thrombophilia]]-hypofibrinolysis can cause [[Idiopathic intracranial hypertension|IIH]]. One other study demonstrated that [[fibrinogen]] level and [[RBC]] aggregation is higher in these patients.<ref name="pmid15746649">{{cite journal |vauthors=Glueck CJ, Aregawi D, Goldenberg N, Golnik KC, Sieve L, Wang P |title=Idiopathic intracranial hypertension, polycystic-ovary syndrome, and thrombophilia |journal=J. Lab. Clin. Med. |volume=145 |issue=2 |pages=72–82 |date=February 2005 |pmid=15746649 |doi=10.1016/j.lab.2004.09.011 |url=}}</ref><ref name="pmid17003926">{{cite journal |vauthors=Kesler A, Yatziv Y, Shapira I, Berliner S, Assayag EB |title=Increased red blood cell aggregation in patients with idiopathic intracranial hypertension. A hitherto unexplored pathophysiological pathway |journal=Thromb. Haemost. |volume=96 |issue=4 |pages=483–7 |date=October 2006 |pmid=17003926 |doi= |url=}}</ref>


* [[Sodium]] and Water Regulation: [[Aldosterone]] and [[Vasopressin]]: In addition to [[Kidney|kidneys]], [[aldosterone]] also works on [[epithelial cells]] of [[choroid plexus]] inhancing the [[Na-K ATPase]] and [[CSF]] production. Based on this, primary or secondary [[hyperaldosteronism]] can cause [[Idiopathic intracranial hypertension|IIH]].<ref name="pmid12960953">{{cite journal |vauthors=Weber KT |title=Aldosteronism revisited: perspectives on less well-recognized actions of aldosterone |journal=J. Lab. Clin. Med. |volume=142 |issue=2 |pages=71–82 |date=August 2003 |pmid=12960953 |doi=10.1016/S0022-2143(03)00062-3 |url=}}</ref><ref name="pmid12120824">{{cite journal |vauthors=Weber KT, Singh KD, Hey JC |title=Idiopathic intracranial hypertension with primary aldosteronism: report of 2 cases |journal=Am. J. Med. Sci. |volume=324 |issue=1 |pages=45–50 |date=July 2002 |pmid=12120824 |doi= |url=}}</ref> Like [[aldosterone]], [[AVP]] also works on [[Kidney|kidneys]] and [[CNS]] but it seems that the rise in [[AVP]] in [[Idiopathic intracranial hypertension|IIH]] is the result of increase [[intracranial pressure]] not the cause.<ref name="pmid3221220">{{cite journal |vauthors=Seckl J, Lightman S |title=Cerebrospinal fluid neurohypophysial peptides in benign intracranial hypertension |journal=J. Neurol. Neurosurg. Psychiatry |volume=51 |issue=12 |pages=1538–41 |date=December 1988 |pmid=3221220 |pmc=1032770 |doi= |url=}}</ref><ref name="pmid3676810">{{cite journal |vauthors=Seckl JR, Lightman SL |title=Intracerebroventricular arginine vasopressin causes intracranial pressure to rise in conscious goats |journal=Brain Res. |volume=423 |issue=1-2 |pages=279–85 |date=October 1987 |pmid=3676810 |doi= |url=}}</ref><ref name="pmid3535347">{{cite journal |vauthors=Sørensen PS |title=Studies of vasopressin in the human cerebrospinal fluid |journal=Acta Neurol. Scand. |volume=74 |issue=2 |pages=81–102 |date=August 1986 |pmid=3535347 |doi= |url=}}</ref>


[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
* [[Obesity]]: Some evidences suggest that [[obesity]] can increase intra abdominal and intracranial pressure and have a role in [[pathogenesis]] of [[Idiopathic intracranial hypertension|IIH]].<ref name="pmid9270586">{{cite journal |vauthors=Sugerman HJ, DeMaria EJ, Felton WL, Nakatsuka M, Sismanis A |title=Increased intra-abdominal pressure and cardiac filling pressures in obesity-associated pseudotumor cerebri |journal=Neurology |volume=49 |issue=2 |pages=507–11 |date=August 1997 |pmid=9270586 |doi= |url=}}</ref> In a study on 7 obese women with [[Idiopathic intracranial hypertension|IIH]] it was seen that weigh loss improved their [[Symptom|symptoms]].<ref name="pmid11319651">{{cite journal |vauthors=Sugerman HJ, Felton III WL, Sismanis A, Saggi BH, Doty JM, Blocher C, Marmarou A, Makhoul RG |title=Continuous negative abdominal pressure device to treat pseudotumor cerebri |journal=Int. J. Obes. Relat. Metab. Disord. |volume=25 |issue=4 |pages=486–90 |date=April 2001 |pmid=11319651 |doi= |url=}}</ref> In the other hand higher level of [[leptin]] (a protein released from [[adipose tissue]]) was found in [[Idiopathic intracranial hypertension|IIH]] patients.<ref name="pmid11971053">{{cite journal |vauthors=Lampl Y, Eshel Y, Kessler A, Fux A, Gilad R, Boaz M, Matas Z, Sadeh M |title=Serum leptin level in women with idiopathic intracranial hypertension |journal=J. Neurol. Neurosurg. Psychiatry |volume=72 |issue=5 |pages=642–3 |date=May 2002 |pmid=11971053 |pmc=1737898 |doi= |url=}}</ref> Obesity also cause increased [[plasminogen activator inhibitor]] activity which leads to hypofibrinolysis<ref name="pmid12960611">{{cite journal |vauthors=Bowles LK, Cooper JA, Howarth DJ, Miller GJ, MacCallum PK |title=Associations of haemostatic variables with body mass index: a community-based study |journal=Blood Coagul. Fibrinolysis |volume=14 |issue=6 |pages=569–73 |date=September 2003 |pmid=12960611 |doi=10.1097/01.mbc.0000061344.72909.44 |url=}}</ref> In the other hand the amount of [[ANP]] and [[Brain natriuretic peptide|BNP]] decreases as [[BMI]] increases.<ref name="pmid20553977">{{cite journal |vauthors=Skau M, Goetze JP, Rehfeld JF, Jensen R |title=Natriuretic pro-peptides in idiopathic intracranial hypertension |journal=Regul. Pept. |volume=164 |issue=2-3 |pages=71–7 |date=September 2010 |pmid=20553977 |doi=10.1016/j.regpep.2010.05.009 |url=}}</ref>


OR
* [[Vitamin A]]: both hypo and hypervitaminosis A are suggested to be related to [[Idiopathic intracranial hypertension|IIH]] [[pathogenesis]]. Hypovitaminosis A can interfere with absorbtion of [[CSF]] and hypervitaminosis A can activate the [[mineralocorticoid receptor]].<ref name="pmid6070689">{{cite journal |vauthors=Calhoun MC, Hurt HD, Eaton HD, Rousseau JE, Hall RC |title=Rates of formation and absorption of cerebrospinal fluid in bovine hypovitaminosis A |journal=J. Dairy Sci. |volume=50 |issue=9 |pages=1489–94 |date=September 1967 |pmid=6070689 |doi= |url=}}</ref><ref name="pmid5571041">{{cite journal |vauthors=Hayes KC, McCombs HL, Faherty TP |title=The fine structure of vitamin A deficiency. II. Arachnoid granulations and CSF pressure |journal=Brain |volume=94 |issue=2 |pages=213–24 |date=1971 |pmid=5571041 |doi= |url=}}</ref>


The progression to [disease name] usually involves the [molecular pathway].
* [[Corticosteroid|Corticosteroids]]: Corticosteroid withdrawal can decrease [[CSF]] absorbtion and increase [[intracranial pressure]].<ref name="pmid1141965">{{cite journal |vauthors=Johnston I, Gilday DL, Hendrick EB |title=Experimental effects of steroids and steroid withdrawal on cerebrospinal fluid absorption |journal=J. Neurosurg. |volume=42 |issue=6 |pages=690–5 |date=June 1975 |pmid=1141965 |doi=10.3171/jns.1975.42.6.0690 |url=}}</ref>


OR
* [[Sex hormones]]:Progesterone can increase [[CSF]] with its [[mineralocorticoid]] effect and [[estrogen]] can reduce cellular [[Tight junction|tight junctions]] and reduce [[CSF]] permeability.<ref name="pmid15746649">{{cite journal |vauthors=Glueck CJ, Aregawi D, Goldenberg N, Golnik KC, Sieve L, Wang P |title=Idiopathic intracranial hypertension, polycystic-ovary syndrome, and thrombophilia |journal=J. Lab. Clin. Med. |volume=145 |issue=2 |pages=72–82 |date=February 2005 |pmid=15746649 |doi=10.1016/j.lab.2004.09.011 |url=}}</ref><ref name="pmid17038551">{{cite journal |vauthors=Gorodeski GI |title=Estrogen decrease in tight junctional resistance involves matrix-metalloproteinase-7-mediated remodeling of occludin |journal=Endocrinology |volume=148 |issue=1 |pages=218–31 |date=January 2007 |pmid=17038551 |pmc=2398688 |doi=10.1210/en.2006-1120 |url=}}</ref>
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Pathophysiology==
===Physiology===
The normal physiology of [name of process] can be understood as follows:
 
===Pathogenesis===
*The exact pathogenesis of [disease name] is not completely understood.
OR
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Genetics==
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
*[Gene1]
*[Gene2]
*[Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]


==Associated Conditions==
== Associated Conditions ==
Conditions associated with [disease name] include:
* [Condition 1]
* [Condition 2]
* [Condition 3]


==Gross Pathology==
== Gross Pathology ==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].


==Microscopic Pathology==
== Microscopic Pathology ==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].


==References==
==References==

Latest revision as of 14:25, 29 November 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Pathophysiology

Physiology

Pathogenesis

Any theory regarding the pathophysiology of this disease should explain the following statements:

  1. High incidence rate in women with childbearing age
  2. Reduced conductance to CSF outflow[7]
  3. Normal ventricle size and lack of hydrocephalus[8]
  4. No evidence of cerebral edema[9]
  • CSF Changes in Pseudotumor Cerebri: The production of CSF is constant so the main problem in IIH pathogenesis is related to CSF absorbtaion. Many studies suggested that increased resistant to CSF absorbtion in the main cause of IIH disease.[10][11][12][13]
  • The venous sinuses: It has been suggested that primary or secondary venous outflow narrowing or can cause IIH.[14][15] One of the causes of venous sinuses narrowing is thrombotic event. In one of the IIH studies the amount of MTHFR was higher in IIH patients (38%) in comparison to control group (14%). This result suggests that thrombophilia-hypofibrinolysis can cause IIH. One other study demonstrated that fibrinogen level and RBC aggregation is higher in these patients.[16][17]

Genetics

Associated Conditions

Conditions associated with [disease name] include:

  • [Condition 1]
  • [Condition 2]
  • [Condition 3]

Gross Pathology

On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

References

  1. ↑ Redzic ZB, Preston JE, Duncan JA, Chodobski A, Szmydynger-Chodobska J (2005). "The choroid plexus-cerebrospinal fluid system: from development to aging". Curr. Top. Dev. Biol. 71: 1–52. doi:10.1016/S0070-2153(05)71001-2. PMID 16344101.
  2. ↑ Maren TH (1988). "The kinetics of HCO3- synthesis related to fluid secretion, pH control, and CO2 elimination". Annu. Rev. Physiol. 50: 695–717. doi:10.1146/annurev.ph.50.030188.003403. PMID 3132082.
  3. ↑ Tripathi BJ, Tripathi RC (May 1974). "Vacuolar transcellular channels as a drainage pathway for cerebrospinal fluid". J. Physiol. (Lond.). 239 (1): 195–206. PMC 1330945. PMID 4369428.
  4. ↑ Weller RO, Djuanda E, Yow HY, Carare RO (January 2009). "Lymphatic drainage of the brain and the pathophysiology of neurological disease". Acta Neuropathol. 117 (1): 1–14. doi:10.1007/s00401-008-0457-0. PMID 19002474.
  5. ↑ Edsbagge M, Tisell M, Jacobsson L, Wikkelso C (December 2004). "Spinal CSF absorption in healthy individuals". Am. J. Physiol. Regul. Integr. Comp. Physiol. 287 (6): R1450–5. doi:10.1152/ajpregu.00215.2004. PMID 15308484.
  6. ↑ Friedman DI, Jacobson DM (November 2002). "Diagnostic criteria for idiopathic intracranial hypertension". Neurology. 59 (10): 1492–5. PMID 12455560.
  7. ↑ Bercaw BL, Greer M (August 1970). "Transport of intrathecal 131-I risa in benign intracranial hypertension". Neurology. 20 (8): 787–90. PMID 5468773.
  8. ↑ Jacobson DM, Karanjia PN, Olson KA, Warner JJ (September 1990). "Computed tomography ventricular size has no predictive value in diagnosing pseudotumor cerebri". Neurology. 40 (9): 1454–5. PMID 2392235.
  9. ↑ Wall M, Dollar JD, Sadun AA, Kardon R (February 1995). "Idiopathic intracranial hypertension. Lack of histologic evidence for cerebral edema". Arch. Neurol. 52 (2): 141–5. PMID 7848121.
  10. ↑ Sklar FH, Reisch J, Elashvili I, Smith T, Long DM (September 1980). "Effects of pressure on cerebrospinal fluid formation: nonsteady-state measurements in dogs". Am. J. Physiol. 239 (3): R277–84. doi:10.1152/ajpregu.1980.239.3.R277. PMID 7435599.
  11. ↑ Johnston I, Paterson A (June 1974). "Benign intracranial hypertension. II. CSF pressure and circulation". Brain. 97 (2): 301–12. PMID 4434179.
  12. ↑ Gjerris F, Soelberg Sørensen P, Vorstrup S, Paulson OB (February 1985). "Intracranial pressure, conductance to cerebrospinal fluid outflow, and cerebral blood flow in patients with benign intracranial hypertension (pseudotumor cerebri)". Ann. Neurol. 17 (2): 158–62. doi:10.1002/ana.410170209. PMID 3872097.
  13. ↑ Janny P, Chazal J, Colnet G, Irthum B, Georget AM (March 1981). "Benign intracranial hypertension and disorders of CSF absorption". Surg Neurol. 15 (3): 168–74. PMID 7221863.
  14. ↑ Owler BK, Parker G, Halmagyi GM, Johnston IH, Besser M, Pickard JD, Higgins JN (2005). "Cranial venous outflow obstruction and pseudotumor Cerebri syndrome". Adv Tech Stand Neurosurg. 30: 107–74. PMID 16350454.
  15. ↑ Bateman GA (2004). "Idiopathic intracranial hypertension: priapism of the brain?". Med. Hypotheses. 63 (3): 549–52. doi:10.1016/j.mehy.2004.03.014. PMID 15288385.
  16. ↑ 16.0 16.1 Glueck CJ, Aregawi D, Goldenberg N, Golnik KC, Sieve L, Wang P (February 2005). "Idiopathic intracranial hypertension, polycystic-ovary syndrome, and thrombophilia". J. Lab. Clin. Med. 145 (2): 72–82. doi:10.1016/j.lab.2004.09.011. PMID 15746649.
  17. ↑ Kesler A, Yatziv Y, Shapira I, Berliner S, Assayag EB (October 2006). "Increased red blood cell aggregation in patients with idiopathic intracranial hypertension. A hitherto unexplored pathophysiological pathway". Thromb. Haemost. 96 (4): 483–7. PMID 17003926.
  18. ↑ Weber KT (August 2003). "Aldosteronism revisited: perspectives on less well-recognized actions of aldosterone". J. Lab. Clin. Med. 142 (2): 71–82. doi:10.1016/S0022-2143(03)00062-3. PMID 12960953.
  19. ↑ Weber KT, Singh KD, Hey JC (July 2002). "Idiopathic intracranial hypertension with primary aldosteronism: report of 2 cases". Am. J. Med. Sci. 324 (1): 45–50. PMID 12120824.
  20. ↑ Seckl J, Lightman S (December 1988). "Cerebrospinal fluid neurohypophysial peptides in benign intracranial hypertension". J. Neurol. Neurosurg. Psychiatry. 51 (12): 1538–41. PMC 1032770. PMID 3221220.
  21. ↑ Seckl JR, Lightman SL (October 1987). "Intracerebroventricular arginine vasopressin causes intracranial pressure to rise in conscious goats". Brain Res. 423 (1–2): 279–85. PMID 3676810.
  22. ↑ Sørensen PS (August 1986). "Studies of vasopressin in the human cerebrospinal fluid". Acta Neurol. Scand. 74 (2): 81–102. PMID 3535347.
  23. ↑ Sugerman HJ, DeMaria EJ, Felton WL, Nakatsuka M, Sismanis A (August 1997). "Increased intra-abdominal pressure and cardiac filling pressures in obesity-associated pseudotumor cerebri". Neurology. 49 (2): 507–11. PMID 9270586.
  24. ↑ Sugerman HJ, Felton III WL, Sismanis A, Saggi BH, Doty JM, Blocher C, Marmarou A, Makhoul RG (April 2001). "Continuous negative abdominal pressure device to treat pseudotumor cerebri". Int. J. Obes. Relat. Metab. Disord. 25 (4): 486–90. PMID 11319651.
  25. ↑ Lampl Y, Eshel Y, Kessler A, Fux A, Gilad R, Boaz M, Matas Z, Sadeh M (May 2002). "Serum leptin level in women with idiopathic intracranial hypertension". J. Neurol. Neurosurg. Psychiatry. 72 (5): 642–3. PMC 1737898. PMID 11971053.
  26. ↑ Bowles LK, Cooper JA, Howarth DJ, Miller GJ, MacCallum PK (September 2003). "Associations of haemostatic variables with body mass index: a community-based study". Blood Coagul. Fibrinolysis. 14 (6): 569–73. doi:10.1097/01.mbc.0000061344.72909.44. PMID 12960611.
  27. ↑ Skau M, Goetze JP, Rehfeld JF, Jensen R (September 2010). "Natriuretic pro-peptides in idiopathic intracranial hypertension". Regul. Pept. 164 (2–3): 71–7. doi:10.1016/j.regpep.2010.05.009. PMID 20553977.
  28. ↑ Calhoun MC, Hurt HD, Eaton HD, Rousseau JE, Hall RC (September 1967). "Rates of formation and absorption of cerebrospinal fluid in bovine hypovitaminosis A". J. Dairy Sci. 50 (9): 1489–94. PMID 6070689.
  29. ↑ Hayes KC, McCombs HL, Faherty TP (1971). "The fine structure of vitamin A deficiency. II. Arachnoid granulations and CSF pressure". Brain. 94 (2): 213–24. PMID 5571041.
  30. ↑ Johnston I, Gilday DL, Hendrick EB (June 1975). "Experimental effects of steroids and steroid withdrawal on cerebrospinal fluid absorption". J. Neurosurg. 42 (6): 690–5. doi:10.3171/jns.1975.42.6.0690. PMID 1141965.
  31. ↑ Gorodeski GI (January 2007). "Estrogen decrease in tight junctional resistance involves matrix-metalloproteinase-7-mediated remodeling of occludin". Endocrinology. 148 (1): 218–31. doi:10.1210/en.2006-1120. PMC 2398688. PMID 17038551.

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