Editing Normal pressure hydrocephalus (section)

==Pathogenesis==
Every day, the body makes roughly 600–700 ml of CSF, and about the same amount is reabsorbed into the bloodstream. [[Hydrocephalus]] is caused by an imbalance between the amount of fluid produced and its absorption rate. Enlarged ventricles put increased pressure on the adjacent cortical tissue and cause myriad effects in the patient, including distortion of the fibers in the [[corona radiata]]. This leads to an increase in [[intracranial pressure]] (ICP). The ICP gradually falls but remains slightly elevated, and the CSF pressure reaches a high normal level of 15 to 20&nbsp;cm H<sub>2</sub>O. Measurements of ICP, therefore, are not usually elevated. Because of this, patients do not exhibit the classic signs that accompany increased intracranial pressure such as headache, nausea, vomiting, or altered consciousness, although some studies have shown pressure elevations to occur intermittently.<ref>{{Cite journal |last=Factora |first=Ronan |date=May 2006 |title=When do common symptoms indicate normal pressure hydrocephalus? |url=https://pubmed.ncbi.nlm.nih.gov/16708712 |journal=Cleveland Clinic Journal of Medicine |volume=73 |issue=5 |pages=447–450, 452, 455–456 passim |doi=10.3949/ccjm.73.5.447 |doi-broken-date=23 May 2025 |issn=0891-1150 |pmid=16708712|s2cid=38707248 }}</ref><ref>{{Citation |last1=Pinto |first1=Venessa L. |title=Increased Intracranial Pressure |date=2024 |work=StatPearls |url=http://www.ncbi.nlm.nih.gov/books/NBK482119/ |access-date=2024-01-25 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29489250 |last2=Tadi |first2=Prasanna |last3=Adeyinka |first3=Adebayo}}</ref>

The exact pathogenesis is unknown, but consensus on some mechanisms include:<ref name=":2">{{Citation |last1=M Das |first1=Joe |title=Normal Pressure Hydrocephalus |date=2023 |work=StatPearls |url=http://www.ncbi.nlm.nih.gov/books/NBK542247/ |access-date=2024-01-22 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=31194404 |last2=Biagioni |first2=Milton C.}}</ref>
* An imbalance exists between production and resorption of CSF.
* The resistance to CSF outflow is often elevated.
* The disease is not caused by overproduction of CSF or obstruction of CSF flow at the ventricles.<ref name=":2" />

The syndrome is often divided into two groups, '''primary''' (also called '''idiopathic''') and '''secondary''', based on cause. The underlying etiology of primary NPH has not yet been identified. Primary NPH affects adults age 40 years or older, most commonly in adults over 60.<ref name="ReferenceA">{{Cite journal |last1=Oliveira |first1=Louise Makarem |last2=Nitrini |first2=Ricardo |last3=Román |first3=Gustavo C. |date=2019 |title=Normal-pressure hydrocephalus: A critical review |journal=Dementia & Neuropsychologia |volume=13 |issue=2 |pages=133–143 |doi=10.1590/1980-57642018dn13-020001 |issn=1980-5764 |pmc=6601311 |pmid=31285787}}</ref> Secondary NPH can affect persons of any age and occurs due to conditions such as [[subarachnoid hemorrhage]], [[meningitis]], brain surgery, brain radiation, or [[traumatic brain injury]].<ref>{{Cite book |last=Greenberg |first=Mark |title=Handbook of Neurosurgery |publisher=Thiem e Medical Publishers, Inc. |year=2016 |isbn=978-1-62623-241-9 |edition=8th |location=New York |pages=404–405 |language=English}}</ref> These conditions are thought to lead to increased inflammation of the [[arachnoid granulation]]s, which further leads to decreased CSF reabsorption and therefore enlargement of ventricles.<ref>{{Cite journal |last1=Passos-Neto |first1=Carlos Eduardo Borges |last2=Lopes |first2=Cesar Castello Branco |last3=Teixeira |first3=Mauricio Silva |last4=Studart Neto |first4=Adalberto |last5=Spera |first5=Raphael Ribeiro |date=May 2022 |title=Normal pressure hydrocephalus: an update |journal=Arquivos de Neuro-Psiquiatria |volume=80 |issue=5 Suppl 1 |pages=42–52 |doi=10.1590/0004-282X-ANP-2022-S118 |issn=1678-4227 |pmc=9491444 |pmid=35976308}}</ref>

Symptoms of gait deviation, neurological impairment, and urinary incontinence seen in NPH are due to compression of the corresponding regions of the brain that control these functions. Gait abnormalities are thought to be due to compression of the [[corticospinal tract]] fibers in the [[corona radiata]] that coordinate motor movements of the legs.<ref name=":2" /> Compression of the [[brainstem]] as well as poor perfusion of the periventricular [[white matter]] in the [[prefrontal cortex]] are also thought to contribute to gait deviations in NPH.<ref name=":2" /> Dementia in NPH is most likely caused by ventricular enlargement compressing the [[Calvaria (skull)|calvarium]], which further leads to tearing of currently unidentified [[Nerve|nerve fibers]].<ref name=":2" /> Lastly, urinary incontinence is thought to be caused by stretching of the periventricular sacral fibers of the corticospinal tract fibers leading to loss of voluntary bladder contraction.<ref name=":2" /><ref>{{Cite journal |last1=Gleason |first1=P. L. |last2=Black |first2=P. M. |last3=Matsumae |first3=M. |date=October 1993 |title=The neurobiology of normal pressure hydrocephalus |url=https://pubmed.ncbi.nlm.nih.gov/8241789 |journal=Neurosurgery Clinics of North America |volume=4 |issue=4 |pages=667–675 |doi=10.1016/S1042-3680(18)30558-8 |issn=1042-3680 |pmid=8241789}}</ref>