TY - JOUR

T1 - CSF hypersecretion versus impaired CSF absorption in posthemorrhagic hydrocephalus

T2 - a systematic review

AU - Ben-Shoshan, Shai David

AU - Lolansen, Sara Diana

AU - Mathiesen, Tiit Illimar

AU - MacAulay, Nanna

N1 - Publisher Copyright: © 2023, The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.

PY - 2023

Y1 - 2023

N2 - Background: The molecular mechanisms underlying development of posthemorrhagic hydrocephalus (PHH) remain elusive. The aim of this systematic review was to evaluate existing literature on increased CSF secretion and impaired CSF absorption as pathogenic contributors to CSF accumulation in neonatal and adult PHH. Methods: The systematic review was conducted in accordance with the PRISMA guidelines. Relevant studies published before March 11th, 2023, were identified from PubMed and reference lists. Studies were screened for eligibility using predefined inclusion and exclusion criteria. Data from eligible studies were extracted and potential sources of bias were evaluated. Results: Nineteen studies quantified CSF production rates and/or CSF absorption capacity in human patients with PHH or animals with experimentally induced PHH. Increased CSF production was reported as early as 24 h and as late as 28 days post ictus in six out of eight studies quantifying CSF production rates in animals with experimentally induced PHH. Impaired CSF absorption was reported in all four studies quantifying CSF absorption capacity in human patients with PHH and in seven out of nine studies quantifying CSF absorption capacity in animals with experimentally induced PHH. Impaired CSF absorption was reported as early as 30 min and as late as 10 months post ictus. Conclusions: The pathological CSF accumulation in PHH likely arises from a combination of increased CSF secretion and impaired CSF absorption, which may manifest at different time scales following a hemorrhagic event. Emergent evidence on increased CSF secretion by the choroid plexus may herald a paradigm shift in our understanding of PHH.

AB - Background: The molecular mechanisms underlying development of posthemorrhagic hydrocephalus (PHH) remain elusive. The aim of this systematic review was to evaluate existing literature on increased CSF secretion and impaired CSF absorption as pathogenic contributors to CSF accumulation in neonatal and adult PHH. Methods: The systematic review was conducted in accordance with the PRISMA guidelines. Relevant studies published before March 11th, 2023, were identified from PubMed and reference lists. Studies were screened for eligibility using predefined inclusion and exclusion criteria. Data from eligible studies were extracted and potential sources of bias were evaluated. Results: Nineteen studies quantified CSF production rates and/or CSF absorption capacity in human patients with PHH or animals with experimentally induced PHH. Increased CSF production was reported as early as 24 h and as late as 28 days post ictus in six out of eight studies quantifying CSF production rates in animals with experimentally induced PHH. Impaired CSF absorption was reported in all four studies quantifying CSF absorption capacity in human patients with PHH and in seven out of nine studies quantifying CSF absorption capacity in animals with experimentally induced PHH. Impaired CSF absorption was reported as early as 30 min and as late as 10 months post ictus. Conclusions: The pathological CSF accumulation in PHH likely arises from a combination of increased CSF secretion and impaired CSF absorption, which may manifest at different time scales following a hemorrhagic event. Emergent evidence on increased CSF secretion by the choroid plexus may herald a paradigm shift in our understanding of PHH.

KW - Cerebrospinal fluid

KW - Cerebrospinal fluid absorption

KW - Cerebrospinal fluid production

KW - Choroid plexus

KW - Inflammation

KW - Posthemorrhagic hydrocephalus

U2 - 10.1007/s00701-023-05746-9

DO - 10.1007/s00701-023-05746-9

M3 - Review

C2 - 37642688

AN - SCOPUS:85169003444

VL - 165

SP - 3271

EP - 3287

JO - Acta Neurochirurgica

JF - Acta Neurochirurgica

SN - 0001-6268

ER -