Hydrocephalus: historical analysis and considerations for treatment

Springer Science and Business Media LLC - Tập 27 - Trang 1-17 - 2022
Alexandra Hochstetler1, Jeffrey Raskin2,3, Bonnie L. Blazer-Yost1
1Department of Biology, Indiana University Purdue University Indianapolis, Indianapolis, USA
2Division of Pediatric Neurosurgery, Ann and Robert H. Lurie Children’s Hospital, Chicago, USA
3Department of Neurosurgery, Northwestern University Feinberg School of Medicine, Chicago, USA

Tóm tắt

Hydrocephalus is a serious condition that affects patients of all ages, resulting from a multitude of causes. While the etiologies of hydrocephalus are numerous, many of the acute and chronic symptoms of the condition are shared. These symptoms include disorientation and pain (headaches), cognitive and developmental changes, vision and sleep disturbances, and gait abnormalities. This collective group of symptoms combined with the effectiveness of CSF diversion as a surgical intervention for many types of the condition suggest that the various etiologies may share common cellular and molecular dysfunctions. The incidence rate of pediatric hydrocephalus is approximately 0.1–0.6% of live births, making it as common as Down syndrome in infants. Diagnosis and treatment of various forms of adult hydrocephalus remain understudied and underreported. Surgical interventions to treat hydrocephalus, though lifesaving, have a high incidence of failure. Previously tested pharmacotherapies for the treatment of hydrocephalus have resulted in net zero or negative outcomes for patients potentially due to the lack of understanding of the cellular and molecular mechanisms that contribute to the development of hydrocephalus. Very few well-validated drug targets have been proposed for therapy; most of these have been within the last 5 years. Within the last 50 years, there have been only incremental improvements in surgical treatments for hydrocephalus, and there has been little progress made towards prevention or cure. This demonstrates the need to develop nonsurgical interventions for the treatment of hydrocephalus regardless of etiology. The development of new treatment paradigms relies heavily on investment in researching the common molecular mechanisms that contribute to all of the forms of hydrocephalus, and requires the concerted support of patient advocacy organizations, government- and private-funded research, biotechnology and pharmaceutical companies, the medical device industry, and the vast network of healthcare professionals.

Tài liệu tham khảo

Blitz AM, Ahmed AK, Rigamonti D. Founder of modern hydrocephalus diagnosis and therapy: Walter Dandy at the Johns Hopkins Hospital. J Neurosurg. 2018. https://doi.org/10.3171/2018.4.JNS172316.

Mokri B. The Monro–Kellie hypothesis: applications in CSF volume depletion. Neurology. 2001;56(12):1746–8.

Fact Sheet: Hydrocephalus Fact Sheet [Internet]. Bethesda (MD): National Library of Medicine (US); 2020 Apr cited]. [about 3 screens]. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Hydrocephalus-Fact-Sheet. Accessed 7 Jan 2022

Mazzini L, Campini R, Angelino E, Rognone F, Pastore I, Oliveri G. Posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. Arch Phys Med Rehabil. 2003;84(11):1637–41.

Fame RM, Cortés-Campos C, Sive HL. Brain ventricular system and cerebrospinal fluid development and function: light at the end of the tube: a primer with latest insights. BioEssays. 2020;42(3): e1900186.

Drake JM, Kestle J. Rational and methodology of the multicenter pediatric cerebrospinal fluid shunt design trial. Pediatric hydrocephalus treatment evaluation group. Childs Nerv Sys. 1996;12(8):434–47.

Marriott WM. The use of theobromin sodio salicylate (diuretin) in the treatment of hydrocephalus. Am J Dis Child. 1924;28:479–83.

Chan M, Amin-Hanjani S. Cerebrospinal fluid and its abnormalities. Hoboken: Wiley; 2010.

Liedtke W, Friedman JM. Abnormal osmotic regulation in trpv4-/- mice. Proc Natl Acad Sci USA. 2003;100(23):13698–703.

Lummis NC, Sanchez-Pavon P, Kennedy G, Frantz AJ, Kihara Y, Blaho VA, Chun J. LPA1/3 overactivation induces neonatal posthemorrhagic hydrocephalus through ependymal loss and ciliary dysfunction. Sci Adv. 2019;5(10):eaax2011.

Toft-Bertelsen TL, Barbuskaite D, Heerfordt EK, Lolansen SD, Andreassen SN, Rostgaard N, Olsen MH, Norager NH, Capion T, Rath MF, Juler M, MacAulay N. Lysopohosphatidic acid, a CSF marker in posthemorrhagic hydrocephalus that drives CSF acculumation via TRPV4-indced hyperactivation of NKCC1. BioRxiv. 2022. https://doi.org/10.1101/2022.01.24.477507.

Chu J, Jensen H, Holubkov R, Krieger MD, Kulkarni AV, Riva-Cambrin J, Rozzelle CJ, Limbrick DD, Wellons JC, Browd SR, Whitehead WE, Pollack IF, Simon TD, Tamber MS, Hauptman JS, Pindrik J, Naftel RP, McDonald PJ, Hankinson TC, Jackson EM, Rocque BG, Reeder R, Drake JM, Kestle JRW. Hydrocephalus Clinical Research Network; Hydrocephalus Clinical Research Network Members. The Hydrocephalus Clinical Research Network quality improvement initiative: the role of antibiotic-impregnated catheters and vancomycin wound irrigation. J Neurosurg Pediatr. 2022;18:1–8.