Pseudotumor cerebri pathophysiology: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 7: | Line 7: | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
The exact pathogenesis of pseudotumor cerebri is not completely understood. Idiopathic intracranial hypertension or pseudotumor cerebri is defined by the symptoms of increased intracranial pressure without any evidence of tumor.(1uptodate) | The exact pathogenesis of pseudotumor cerebri is not completely understood. Idiopathic intracranial hypertension or pseudotumor cerebri is defined by the symptoms of increased intracranial pressure which is the common final pathway of all IHH etiologies, without any evidence of tumor.(1uptodate) | ||
Any theory regarding the pathophysiology of this disease should explain the following statements: | Any theory regarding the pathophysiology of this disease should explain the following statements: | ||
| Line 15: | Line 15: | ||
* No evidence of cerebral edema(27 wall) | * No evidence of cerebral edema(27 wall) | ||
Some of the these theories are: | Some of the these theories are: | ||
* Increased production of CSF and reduced resorption: Normal CSF flow involves production at the [[choroid plexus]]es and absorption at the cranial and [[spinal nerve]] root arachnoid villi and granulations. Impaired CSF absorption at the [[superior sagittal sinus]] or along the spinal nerve roots could therefore explain IIH and has been documented in 75-100% of IIH patients.<ref name=Skau_et_al_2006/> Permeability along the blood-CSF barrier varies, producing an increasing [[oncotic pressure]] gradient between the CSF and venous system in a [[rostral]] to [[caudal]] progression.<ref name=Walker_2001>{{cite journal |author=Walker RW |title=Idiopathic intracranial hypertension: any light on the mechanism of the raised pressure? |journal=J. Neurol. Neurosurg. Psychiatr. |volume=71 |issue=1 |pages=1–5 |year=2001 |pmid=11413251 |url = http://jnnp.bmj.com/cgi/content/full/71/1/1}}</ref> It is speculated that variations in this oncotic pressure contribute to or impede CSF absorption | * Increased production of CSF and reduced resorption: Normal CSF flow involves production at the [[choroid plexus]]es and absorption at the cranial and [[spinal nerve]] root arachnoid villi and granulations. Impaired CSF absorption at the [[superior sagittal sinus]] or along the spinal nerve roots could therefore explain IIH and has been documented in 75-100% of IIH patients.<ref name="Skau_et_al_2006" /> Permeability along the blood-CSF barrier varies, producing an increasing [[oncotic pressure]] gradient between the CSF and venous system in a [[rostral]] to [[caudal]] progression.<ref name="Walker_2001">{{cite journal |author=Walker RW |title=Idiopathic intracranial hypertension: any light on the mechanism of the raised pressure? |journal=J. Neurol. Neurosurg. Psychiatr. |volume=71 |issue=1 |pages=1–5 |year=2001 |pmid=11413251 |url = http://jnnp.bmj.com/cgi/content/full/71/1/1}}</ref> It is speculated that variations in this oncotic pressure contribute to or impede CSF absorption.<ref name="Skau_et_al_2006" /> | ||
* obesity.(89 uptodate): Some evidences suggest that onesity can increase intra abdominal and intra cranial pressure and have a role in pathogenesis of IHH. (106 uptodate) In a study on 7 obese women with IHH it was seen that weith loss improved their symptoms.(107 uptodate) In the other hand higher level of leptin (a protein released from adipose tissue) was found in IHH patiets.(125) | * obesity.(89 uptodate): Some evidences suggest that onesity can increase intra abdominal and intra cranial pressure and have a role in pathogenesis of IHH. (106 uptodate) In a study on 7 obese women with IHH it was seen that weith loss improved their symptoms.(107 uptodate) In the other hand higher level of leptin (a protein released from adipose tissue) was found in IHH patiets.(125) | ||
* Vitamin A intoxication: There are some evidences of higher serum and CSF level of vitamin A, retinol and retinol binding protein can be related to IHH pathogenesis.(116-118) | * Vitamin A intoxication: There are some evidences of higher serum and CSF level of vitamin A, retinol and retinol binding protein can be related to IHH pathogenesis.(116-118) | ||
Revision as of 13:16, 27 July 2018
|
Pseudotumor cerebri Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Pseudotumor cerebri pathophysiology On the Web |
|
American Roentgen Ray Society Images of Pseudotumor cerebri pathophysiology |
|
Risk calculators and risk factors for Pseudotumor cerebri pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Pathophysiology
Pathogenesis
The exact pathogenesis of pseudotumor cerebri is not completely understood. Idiopathic intracranial hypertension or pseudotumor cerebri is defined by the symptoms of increased intracranial pressure which is the common final pathway of all IHH etiologies, without any evidence of tumor.(1uptodate)
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(25 wall)
- Normal ventricle size and lack of hydrocephalus(26 wall)
- No evidence of cerebral edema(27 wall)
Some of the these theories are:
- Increased production of CSF and reduced resorption: Normal CSF flow involves production at the choroid plexuses and absorption at the cranial and spinal nerve root arachnoid villi and granulations. Impaired CSF absorption at the superior sagittal sinus or along the spinal nerve roots could therefore explain IIH and has been documented in 75-100% of IIH patients.[1] Permeability along the blood-CSF barrier varies, producing an increasing oncotic pressure gradient between the CSF and venous system in a rostral to caudal progression.[2] It is speculated that variations in this oncotic pressure contribute to or impede CSF absorption.[1]
- obesity.(89 uptodate): Some evidences suggest that onesity can increase intra abdominal and intra cranial pressure and have a role in pathogenesis of IHH. (106 uptodate) In a study on 7 obese women with IHH it was seen that weith loss improved their symptoms.(107 uptodate) In the other hand higher level of leptin (a protein released from adipose tissue) was found in IHH patiets.(125)
- Vitamin A intoxication: There are some evidences of higher serum and CSF level of vitamin A, retinol and retinol binding protein can be related to IHH pathogenesis.(116-118)
- Sleep apnea: Sleep apnea can cause hypercarbia which can result in vasodilation and elevated intacranial pressure (74 uptodate)
- Sex hormones: In one study regarding IIH etiology which was done on 8 men with this disease, Four of them had abnormal FSH and LH level, 2 of them had estradiol abnormalities and seven of them had reduced testosterone level.(127 uptodate)
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
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].