Abstract
Hydrocephalus following intraventricular hemorrhage (IVH) is a complex neurological condition resulting from cerebrospinal fluid (CSF) circulation disruptions due to intraventricular blood entry. This review synthesizes current evidence on pathophysiology, mechanisms, and treatment strategies. Following IVH, erythrocyte lysis releases hemoglobin and iron, triggering oxidative stress and ferroptosis, while thrombin activation, TGF-β1-mediated fibrosis, inflammatory cascades, and ependymal damage collectively contribute to ventricular enlargement. Key animal models elucidate roles of oxidative stress, cytokines, and complement activation in IVH-induced injury. We highlight evolving insights into CSF absorption pathways and blood metabolite interactions, alongside persistent clinical challenges including delayed diagnosis and therapeutic limitations. Experimental approaches such as thrombolytics, iron chelators, and inflammatory inhibitors show preclinical potential but face significant translational barriers: thrombolytics reduced mortality in the CLEAR III trial yet failed to improve functional outcomes or shunt dependence; iron chelation lacks robust clinical validation; and TGF-β1 inhibition yields conflicting efficacy across models. Future research must address the interplay of blood components, inflammatory mediators, and structural damage, prioritizing biomarker discovery and rigorously validated therapeutic innovation.
Introduction
Hydrocephalus is characterized by the abnormal accumulation of cerebrospinal fluid (CSF) within the ventricular system, leading to ventricular enlargement. This condition arises from disruptions in CSF circulation, which may result from obstruction, secretion disorders, or absorption deficiencies (1, 2). The widely accepted theory of CSF circulation posits that approximately 80% of CSF is produced by the choroid plexus within the ventricular system, while the remaining 20% is generated through interstitial fluid transport from brain parenchyma. Following its production, CSF circulates through the ventricular system to the subarachnoid space, where it is reabsorbed into the venous system via arachnoid granulations, thus completing the CSF circulation pathway (3, 4).
Hydrocephalus is classified based on its etiology and mechanism. Mechanistically, it is divided into obstructive (non-communicating) and communicating hydrocephalus. Etiologically, hydrocephalus is categorized into congenital, idiopathic, and acquired forms (5). Clinically, acquired hydrocephalus, often referred to as secondary hydrocephalus, results from a range of neurological disorders such as intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), traumatic brain injury, brain tumors, and intracranial infections.
Among the various neurological conditions that can lead to hydrocephalus, intraventricular hemorrhage (IVH) is a prominent cause (6). IVH is commonly observed in both elderly individuals and neonates (7–10). In adults, IVH often follows spontaneous ICH, aneurysmal SAH, vascular malformations, or traumatic brain injury, which subsequently invade the ventricular system (11). Risk factors for IVH include advanced age, large hematoma volume, and hypertension (12, 13). The occurrence of IVH significantly impacts prognosis and notably increases the risk of developing hydrocephalus (14). Literature indicates that approximately 40% of adults with spontaneous ICH (non-traumatic) experience IVH, with 51–89% of these patients developing secondary hydrocephalus (15). In neonates, IVH frequently arises from germinal matrix hemorrhage (GMH) that affects the ventricular system (GMH-IVH). The germinal matrix is richly vascularized but contains numerous immature, irregular, and fragile capillaries and veins, making it prone to hemorrhage (16). GMH-IVH is most prevalent among extremely low birth weight infants (birth weight <1,500 grams), with approximately 20–30% of these infants developing GMH-IVH and around one-third progressing to hydrocephalus (17).
IVH inflicts direct damage to brain tissue, as well as contributes to both acute and chronic hydrocephalus. The mechanisms underlying secondary hydrocephalus following IVH remain incompletely understood (18). Elucidating these mechanisms is crucial for identifying therapeutic targets to mitigate both primary and secondary damage caused by IVH, thereby improving patient neurological outcomes. This review aims to explore the pathophysiological changes in brain tissue following IVH, key metabolic products, the mechanisms of hydrocephalus development, and current treatment strategies.
IVH and brain injury
IVH frequently induces a spectrum of primary and secondary brain injuries. Clinicians and researchers frequently employ grading systems to assess the extent of brain damage and prognosis associated with IVH (19). These grading systems consider factors including hematoma volume, location, and ventricular enlargement (20). Clinically, IVH often presents with increased intracranial pressure, varying degrees of consciousness disturbances, neurological deficits, and seizures. The underlying pathophysiological changes are primarily six-fold: periventricular white matter softening; ischemic infarction secondary to hemorrhage; release of harmful substances such as oxygen free radicals and inflammatory cytokines into the CSF circulation; hypotensive and increased intracranial pressure-induced reductions in cerebral perfusion pressure and ischemic damage to periventricular white matter; and the development of hydrocephalus post-ventricular enlargement, which exacerbates oxidative stress, inflammation, and intracranial pressure (19–21). In recent studies, more and more researchers have proved that hydrocephalus should be considered as an independent factor among the factors that cause brain injury. Wahjoeprumono et al. (22) conducted research that assessed the independent influence of hydrocephalus on brain injury. In this study, the researchers compared the mortality and functional outcome between ICH, IVH with hydrocephalus and ICH only (ICH + IVH + hydrocephalus group vs. ICH group). They found that the 30-day and 90-day mortality rate was higher in patients with ICH + IVH + hydrocephalus than in patients who were only diagnosed with ICH only. It’s noted that hydrocephalus leads to higher mortality and morbidity remains elusive, but the exact mechanism has not been explained clearly.
IVH and ferroptosis
In recent years, more and more studies have shown that neuronal death caused by hydrocephalus is closely related to the mechanism of ferroptosis. Zille, M et al. (23) investigated cell death mechanisms in cultured neurons exposed to hemoglobin or hemin and then compared it with all existing known cell death mechanisms. The researchers found that chemical inhibitors targeting ferroptosis and necroptosis provided protection from hemoglobin- and hemin-induced toxicity. Consistently, molecular markers indicative of both ferroptosis and necroptosis were elevated following ICH in both in vitro and in vivo settings. Z. Meng et al. (24) explored whether ferroptosis death markers can be used as auxiliary indicators for diagnosis of PHH. Consequently, the researchers revealed the induction of ferroptosis in the choroid plexus of PHH as demonstrated by the excess production of ROS and by lipid peroxidation. Thus, ferroptosis could be a biomarker in the diagnosis of PHH.
Blood and metabolic products
Erythrocytes, hemoglobin, and iron
Upon the entry of blood into the ventricular system, erythrocytes begin to lyse within 3 days, releasing substantial amounts of hemoglobin and iron. Numerous studies have demonstrated that both hemoglobin and iron play critical roles in the development and progression of hydrocephalus following hemorrhagic events. Strahle et al. (25) injected hemoglobin and iron into the lateral ventricles of neonatal mice, observing significant ventricular enlargement within 1 day. Similarly, Gao et al. (26) injected lysed erythrocytes and iron into the lateral ventricles of adult rats, resulting in marked ventricular enlargement within 1 day. Additionally, the administration of iron chelators has been shown to significantly reduce the severity of hydrocephalus in various IVH animal models (27). However, the clinical application of iron chelators remains limited, and their efficacy in preventing or mitigating post-IVH hydrocephalus is still debated, lacking robust clinical evidence. Future studies should focus on high-quality basic and clinical research to provide conclusive evidence. Moreover, the presence of macrophages in the ventricular system has been observed to engulf erythrocytes prior to their lysis, resulting in reduced levels of hemoglobin and iron in the CSF (28). Thus, activating phagocytic cells during the early stages of IVH may be a potential strategy to decrease the incidence of long-term hydrocephalus.
Platelets
Following IVH, platelets release transforming growth factor-beta 1 (TGF-β1), which promotes extracellular matrix protein synthesis and induces subarachnoid space fibrosis. This fibrosis leads to narrowing and obstruction of the subarachnoid space, disrupting CSF circulation and resulting in hydrocephalus (29, 30). In the 1990s, Tada et al. (31) successfully created a communicating hydrocephalus model in mice (10 days old) by injecting recombinant human TGF-β1 into the subarachnoid space, highlighting the significant role of TGF-β1 in hydrocephalus development. TGF-β1 has since been identified as a key biomarker in post-IVH hydrocephalus. Kitazawa et al. (32) reported elevated TGF-β1 levels in CSF following subarachnoid hemorrhage leading to communicating hydrocephalus. Similarly, increased TGF-β1 levels have been observed in the CSF of patients with post-IVH hydrocephalus. However, therapeutic targeting yields conflicting outcomes across models. Table 1 showed the summary of studies on therapeutic targeting TGF-β1 Aquilina et al. (33) found that TGF-β1 inhibition did not reduce ventricular enlargement in neonatal mice post-IVH, whereas Manaenko et al. (34) reported reduced ventricular enlargement and improved cognitive and motor functions with TGF-β1 inhibition in a GMH-IVH model. Conversely, Hoque et al. (35) observed no reduction in ventricular enlargement with TGF-β1 inhibition in a neonatal IVH model, and Yan et al. (36) demonstrated decreased lateral ventricle volume and reduced hydrocephalus incidence with TGF-β1 inhibition in a rat subarachnoid hemorrhage model. These discrepancies highlight TGF-β1’s context-dependent actions: Effective in fibrosis-dominant models (e.g., SAH) but ineffective in developing systems with compensatory inflammation or structural immaturity. Thus, while TGF-β1 is a valid biomarker, its therapeutic utility requires patient stratification.
Table 1
| Study | Model | Intervention | Key finding | Proposed mechanism |
|---|---|---|---|---|
| Aquilina (2013) | Neonatal IVH mice | TGF-β1 inhibition | No ventricle reduction | Immature arachnoid granulations |
| Manaengo (2016) | Rabbit GMH-IVH | Anti-TGF-β1 | Reduced ventricles & improved function | Fibrosis suppression |
| Hoque (2016) | Neonatal IVH rat | TGF-β1 blockade | No effect | Compensatory IL-1β upregulation |
| Yan (2015) | Rat SAH | TGF-β1 inhibition | Decreased hydrocephalus | Ependymal protection |
Summary of studies on therapeutic targeting TGF-β1.
Thrombin
Upon entering the ventricular system, the coagulation cascade is rapidly activated, resulting in substantial thrombin production. Thrombin has been shown to exacerbate brain injury following intracerebral hemorrhage (ICH) and may also contribute to the formation of hydrocephalus post-IVH (37). Gao et al. (37) demonstrated that thrombin exacerbated ventricular enlargement, disrupted the blood–brain barrier, and damaged the ependymal lining in a rat IVH model. The administration of thrombin inhibitors alleviated these pathological changes. The precise mechanism by which thrombin contributes to post-IVH hydrocephalus remains incomplete. Some studies suggest that thrombin may upregulate TGF-β1 expression, leading to subarachnoid space fibrosis and obstruction, thereby disrupting CSF circulation and causing hydrocephalus (38). Hao et al. (39) recently proposed that thrombin might induce hydrocephalus by downregulating endothelial cadherin in the choroid plexus, with PAR1/p-Src/p-PAK1 pathway inhibition potentially mitigating thrombin-induced hydrocephalus by upregulating endothelial cadherin expression. Future research may explore thrombin inhibition as a potential therapeutic target for post-IVH hydrocephalus.
Mechanisms of hydrocephalus following IVH
Blood clots
Early studies commonly attributed hydrocephalus following IVH to blood clots obstructing CSF pathways, particularly the aqueduct of Sylvius and the foramen of Magendie, leading to impaired CSF drainage and ventricular enlargement. Following IVH, blood rapidly disperses through the ventricles and subarachnoid space, forming clots that block CSF circulation and subsequently cause hydrocephalus. This has led to investigations into the use of thrombolytic agents, such as tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), in the early management of IVH to reduce the incidence of hydrocephalus. Several studies have shown that early administration of tPA and uPA can effectively reduce ventricular enlargement and decrease long-term hydrocephalus rates (40). Similarly, in subarachnoid hemorrhage models, Thomas et al. (41) observed that early thrombolytic therapy could significantly lower the incidence of hydrocephalus. However, the safety and efficacy of thrombolytics in IVH are still debated. Some reports suggest that thrombolytic therapy may worsen edema and induce severe inflammatory responses due to the release of metabolic products from lysed clots (42, 43). A recent multi-center, double-blind, randomized controlled trial (CLEAR III) found that although recombinant tPA reduced mortality at 6 months, it did not improve functional outcomes or reduce the likelihood of shunt placement (44). Thus, while early removal of clots is theoretically a promising approach for preventing hydrocephalus, its clinical adoption is limited by concerns about safety and efficacy, necessitating further high-quality evidence.
Arachnoid granulations dysfunction
CSF absorption is critical in the development of hydrocephalus following IVH. Traditionally, it is believed that arachnoid granulations, which protrude into the sagittal sinus, are primarily responsible for CSF absorption. Post-IVH, blood and its metabolites can cause fibrosis and inflammation of the arachnoid granulations, obstructing their function and leading to impaired CSF absorption and hydrocephalus (45, 46). However, this model may be incomplete, as arachnoid granulations vary across species, and some, such as rodents and preterm infants, lack these structures (47). Recent research suggests that other potential sites of CSF absorption, including the choroid plexus, pial membrane, lymphatic vessels, and even nasal lymphatics, could also play a role (48). The impact of IVH on these alternative absorption pathways remains under investigation and requires further validation.
Inflammatory response
Inflammatory responses are pivotal in the pathology of numerous neurological conditions, including trauma and stroke (49–51). IVH triggers significant inflammatory processes, which not only affect disease progression and prognosis but also contribute to the development of hydrocephalus (52–55). Post-IVH, inflammation leads to fibrosis of the arachnoid membrane and ependyma, causing obstruction of CSF pathways and hydrocephalus (50, 56, 57). Additionally, inflammation of the choroid plexus and ependyma has been linked to hydrocephalus. Simard et al. (58) demonstrated that NF-κB activation in these structures was associated with ventricular enlargement in a rat model of IVH. Recent findings suggest that targeting the TLR4-NF-κB pathway may reduce hydrocephalus severity (59). Complement activation, particularly of complement component 3, has also been implicated in post-IVH hydrocephalus. Studies have shown increased levels of complement C3 in the ventricles of rat models, and C3-deficient mice exhibited reduced brain injury and ventricular enlargement post-hemorrhage (60, 61). Comprehensive evaluation of complement inhibition as a therapeutic strategy is still needed.
Ependymal injury
Ependymal injury is a common consequence of IVH, impacting the functionality of the ependymal lining that lines the ventricles. Ependymal cells, with their cilia, facilitate CSF flow, and their damage can significantly affect CSF dynamics (62). Research indicates that IVH-related damage to ependymal cell junctions, such as N-cadherin, can lead to cell detachment and subsequent atrophy, narrowing, or occlusion of CSF pathways, resulting in hydrocephalus (63, 64). Additionally, ependymal cilia destruction impairs CSF flow and contributes to ventricular enlargement (65, 66).
Blood–brain barrier disruption
The blood–brain barrier (BBB) at the choroid plexus, composed of endothelial cells, basement membrane, pericytes, and astrocyte end-feet, is crucial for maintaining CSF homeostasis. IVH can disrupt this barrier, leading to increased protein levels in the CSF, including TNF-α, thrombopoietin, ferritin, TGF-β1, GFAP, and S-100 (67). This disruption can alter osmotic gradients, enhancing CSF secretion and promoting hydrocephalus. Krishnamurthy et al. (68) demonstrated that increased osmotic pressure in the choroid plexus could induce hydrocephalus without obstructing CSF pathways. This supports the theory that IVH-induced BBB damage elevates protein levels in the CSF, disrupting osmotic gradients and contributing to hydrocephalus development (Figure 1).
Figure 1
Summary of mechanisms of hydrocephalus following IVH.
Current treatment approaches
Pharmacological treatment
Pharmacological management typically involves diuretics such as acetazolamide and furosemide, which have been used in hopes of avoiding surgical intervention. However, their clinical efficacy has been suboptimal. Research from the 1990s, including a multicenter, randomized controlled trial, indicated that patients receiving acetazolamide and furosemide had higher rates of disability and a greater likelihood of undergoing shunt surgery compared to those receiving standard treatment (69). Subsequent trials also demonstrated no reduction in shunt implantation rates and an increased risk of disability in patients treated with these diuretics (70). A retrospective study by Kazan et al. (71) corroborated these findings, showing that acetazolamide and furosemide did not lower shunt implantation rates. Consequently, pharmacological treatments are rarely utilized in current clinical practice due to their limited effectiveness and potential to increase disability.
Surgical treatments
Choroid plexus cauterization
Choroid plexus cauterization (CPC) was an early surgical approach for treating hydrocephalus, particularly for communicating hydrocephalus. Although CPC achieved some success, it was associated with high mortality and morbidity rates, and long-term complications remain poorly understood (72, 73).
Endoscopic third ventriculostomy
Since the 1990s, ETV has been utilized primarily for obstructive hydrocephalus with patent basal cisterns, where it achieves success rates of 60–80% (74–76). ETV is generally considered successful when there is an obstruction between the third ventricle and the convexity of the brain’s subarachnoid space. However, its efficacy significantly declines in hemorrhage-related cases. Success rates drop to 37–45% in post-IVH hydrocephalus due to arachnoid fibrosis and subarachnoid space obstruction (77). Early failure occurs in >30% of cases within 6 months, often requiring salvage shunting (78), and extensive subarachnoid hemorrhage also reduces the success rate of ETV (75). Recently, ETV has been applied to certain cases of communicating hydrocephalus with favorable outcomes (79). The combination of ETV with CPC has been explored, with some studies suggesting that combined treatment is superior to ETV alone in pediatric hydrocephalus (80). However, other research indicates poor outcomes in preterm infants with IVH undergoing combined ETV and CPC, likely due to multiple obstructions in the CSF pathways (81). ETV remains a situational alternative to shunting, indicated only for obstructive hydrocephalus with radiologically confirmed basal cistern patency. Its limited efficacy in hemorrhage-related cases reflects permanent arachnoid damage that cannot be bypassed by ventriculostomy.
CSF shunt surgery
Currently, CSF shunt surgery remains the most common treatments (82). The frequently used shunt types include ventriculoperitoneal shunt (VPS), lumboperitoneal shunt (LPS), and ventriculoatrial shunt (VAS) (74–76, 78–81, 83–85). VPS is widely preferred for both adults and infants, while LPS is used for patients with communicating hydrocephalus following hemorrhage (86). After surgery, most patients experience rapid symptom relief and significant reduction in ventricular size.
Endoscopic hematoma evacuation
Endoscopic hematoma evacuation is a minimally invasive surgical evacuation of IVH using neuro-endoscopy, often combined with EVD (87). However, an adequately powered RCT comparing endoscopic hematoma evacuation plus EVD with EVD alone is still lacking and there is also still considerable uncertainty regarding patient selection, intraventricular hematoma volume, ICH volume, timing, and for the surgical procedure itself, including whether to perform septostomy and attempt to clear the contralateral ventricle, or whether to enter the third ventricle (87).
Stereotactic hematoma evacuation
Stereotactic techniques rapidly decompress ventricular systems by evacuating clots, restoring CSF dynamics which has a direct impact on hydrocephalus. In a guideline on stroke due to spontaneous ICH (87), there are four RCTs comparing minimal invasive surgical techniques with medical management. Minimal invasive surgery aimed at hematoma evacuation compared with standard medical treatment improved functional outcome (mRS score of 0–3) at 3–6 months (OR 1.84, 95% CI 1.29–2.61) and reduced the risk of death at 1–12 months (OR 0.49, 95% CI 0.30–0.81).
Lumber drainage
Lumbar drainage serves as a temporary CSF diversion tool for acute hydrocephalus, particularly in communicating types or as a perioperative adjunct. While it can rapidly alleviate symptoms, its use requires careful patient selection, infection prevention, and transition to permanent solutions to avoid complications. There are lack of trial investigating whether early insertion of a lumbar drainage leading to better functional outcome and reduced shunt dependency (87).
Choosing the optimal surgical approach
The optimal surgical approach remains a topic of debate among neurosurgeons. VPS is generally considered the first-line treatment (88). Comparatively, ETV is associated with lower infection rates but higher severe complication and failure rates, leading to limited use in treatment (89–91). LPS avoids direct brain tissue damage, but it has a slightly higher failure and over-drainage rate compared to VPS (92–95). A single-center, retrospective study advocate for LPS as a treatment for adults with post-hemorrhagic communicating hydrocephalus (96). However, there is a lack of randomized clinical trials comparing outcomes among different surgical approaches, highlighting the need for more high-quality, evidence-based research to inform clinical decision-making (97). Table 2 showed the summary of recent studies on clinical outcomes of hydrocephalus following intraventricular hemorrhage.
Table 2
| Study | Patients | Design | Group | Sample size | Conclusion |
|---|---|---|---|---|---|
| Kang et al., 2000 (98) | Adults | Retrospective | VPS vs. LPS | 32 vs. 22 | VPS better than LPS |
| Koksal et al., 2007 (99) | Infants | Retrospective | VSGS | 25 | VSGS was safe and effective |
| Chamiraju et al., 2014 (100) | Infants | Retrospective | ETV + CPC | 27 | Successful rate: 37% |
| Chrastina et al., 2018 (79) | Adults | Retrospective | ETV | 35 | Successful rate: 40% |
| Wang et al., 2019 (96) | Adults | Retrospective | VPS vs. LPS | 102 vs. 56 | Equal outcomes |
| Luther et al., 2020 (101) | Infants | Retrospective | VPS vs. ETV | 6,206 vs. 4,810 | VPS better than ETV |
Summary of recent studies on clinical outcomes of hydrocephalus following intraventricular hemorrhage.
ETV, endoscopic third ventriculostomy; CPC, choroid plexus cauterization; VPS, ventriculoperitoneal shunt; LPS, lumboperitoneal shunt; VSGS, ventriculosubgaleal shunt.
Potential treatment strategies for hydrocephalus in the future
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Activation of fibrinolysis and phagocytic Systems: Accelerating the dissolution of blood clots by enhancing fibrinolytic activity and the brain’s phagocytic response.
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Inhibition of complement-mediated Hemolysis: Suppressing complement activation to reduce red blood cell breakdown and associated inflammatory responses.
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Enhancement of iron chelation: Reducing brain iron deposition through chelation therapy to mitigate iron-induced neurotoxicity.
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Maintenance of ependymal cell Function: Targeting intercellular junction proteins in ependymal cells to reduce damage to cilia and maintain their normal function.
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Inhibition of TGF-β1: Reducing subarachnoid fibrosis by targeting Transforming Growth Factor-beta 1 (TGF-β1) to prevent excessive scarring and fibrosis.
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Early administration of thrombolytics: Administering thrombolytic agents early after hemorrhage to promote re-opening of blocked ventricles and subarachnoid spaces.
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Reduction of inflammatory responses: Mitigating inflammation in the choroid plexus and ependymal lining post-hemorrhage to prevent secondary damage and hydrocephalus.
Statements
Author contributions
HW: Writing – original draft, Formal analysis, Software, Data curation. XC: Software, Writing – original draft, Investigation. CY: Writing – review & editing, Supervision, Conceptualization. KW: Investigation, Writing – review & editing, Conceptualization. TS: Methodology, Writing – review & editing, Conceptualization, Software, Investigation.
Funding
The author(s) declare that no financial support was received for the research and/or publication of this article.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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References
1.
Skalicky P Mládek A Vlasák A De Lacy P Benes V Bradác O . Normal pressure hydrocephalus-an overview of pathophysiological mechanisms and diagnostic procedures. Neurosurg Rev. (2020) 43:1451–64. doi: 10.1007/s10143-019-01201-5
2.
Varagur K Sanka SA Strahle JM . Syndromic hydrocephalus. Neurosurg Clin N Am. (2022) 33:67–79. doi: 10.1016/j.nec.2021.09.006
3.
Rasmussen MK Mestre H Nedergaard M . Fluid transport in the BRAIN. Physiol Rev. (2022) 102:1025–151. doi: 10.1152/physrev.00031.2020
4.
Wichmann TO Damkier HH Pedersen M . A brief overview of the cerebrospinal fluid system and its implications for brain and spinal cord diseases. Front Hum Neurosci. (2022) 15:737217. doi: 10.3389/fnhum.2021.737217
5.
Wang ZY Zhang YY Hu F Ding J Wang X . Pathogenesis and pathophysiology of idiopathic normal pressure hydrocephalus. CNS Neurosci Ther. (2020) 26:1230–40. doi: 10.1111/cns.13526
6.
Koschnitzky JE Keep RF Limbrick DD McAllister JP Morris JA Strahle J et al . Opportunities in posthemorrhagic hydrocephalus research: outcomes of the hydrocephalus association Posthemorrhagic hydrocephalus workshop. Fluids Barriers CNS. (2018) 15:11. doi: 10.1186/s12987-018-0096-3
7.
Özek E Kersin SG . Intraventricular hemorrhage in preterm babies. Turk Pediatri Ars. (2020) 55:215–21. doi: 10.14744/TurkPediatriArs.2020.66742
8.
Wan YF Gao F Ye FH Yang W Hua Y Keep RF et al . Effects of aging on hydrocephalus after intraventricular hemorrhage. Fluids Barriers CNS. (2020) 17:8. doi: 10.1186/s12987-020-0169-y
9.
Yang M Kim S . Current status and associated factors of post-hemorrhagic hydrocephalus in infants of 22 to 28 weeks gestation with severe intraventricular hemorrhage in Korea: a Nationwide cohort study. J Korean Med Sci. (2024) 39:e139. doi: 10.3346/jkms.2024.39.e139
10.
Pindrik J Schulz L Drapeau A . Diagnosis and surgical Management of Neonatal Hydrocephalus. Semin Pediatr Neurol. (2022) 42:100969. doi: 10.1016/j.spen.2022.100969
11.
Pai A Hegde A Nair R Menon G . Adult primary intraventricular hemorrhage: clinical characteristics and outcomes. J Neurosci Rural Pract. (2020) 11:623–8. doi: 10.1055/s-0040-1716770
12.
Robles LA Volovici V . Hypertensive primary intraventricular hemorrhage: a systematic review. Neurosurg Rev. (2022) 45:2013–26. doi: 10.1007/s10143-022-01758-8
13.
Steiner T Diringer MN Schneider D Mayer SA Begtrup K Broderick J et al . Dynamics of intraventricular hemorrhage in patients with spontaneous intracerebral hemorrhage: risk factors, clinical impact, and effect of hemostatic therapy with recombinant activated factor VII. Neurosurgery. (2006) 59:767–74. doi: 10.1227/01.Neu.0000232837.34992.32
14.
Yang WS Shen YQ Zhang XD Zhao LB Wei X Xiong X et al . Hydrocephalus growth: definition, prevalence, association with poor outcome in acute intracerebral hemorrhage. Neurocrit Care. (2021) 35:62–71. doi: 10.1007/s12028-020-01140-w
15.
Chen QW Feng Z Tan Q Guo J Tang J Tan L et al . Post-hemorrhagic hydrocephalus: recent advances and new therapeutic insights. J Neurol Sci. (2017) 375:220–30. doi: 10.1016/j.jns.2017.01.072
16.
Ballabh P . Intraventricular hemorrhage in premature infants: mechanism of disease. Pediatr Res. (2010) 67:1–8. doi: 10.1203/PDR.0b013e3181c1b176
17.
Gilard V Tebani A Bekri S Marret S . Intraventricular hemorrhage in very preterm infants: a comprehensive review. J Clin Med. (2020) 9:2447. doi: 10.3390/jcm9082447
18.
Wu W Li Q . Mechanisms of hydrocephalus after intraventricular haemorrhage: a review. Childs Nerv Syst. (2024) 41:49. doi: 10.1007/s00381-024-06711-2
19.
Whitelaw A . Intraventricular haemorrhage and posthaemorrhagic hydrocephalus: pathogenesis, prevention and future interventions. Semin Neonatol. (2001) 6:135–46. doi: 10.1053/siny.2001.0047
20.
Papile LA Burstein J Burstein R Koffler H . Incidence and evolution of subependymal and intra-ventricular hemorrhage – study of infants with birth weights less than 1,500 gm. J Pediatr. (1978) 92:529–34. doi: 10.1016/s0022-3476(78)80282-0
21.
Del Bigio MR . Cell proliferation in human ganglionic eminence and suppression after prematurity-associated haemorrhage. Brain. (2011) 134:1344–61. doi: 10.1093/brain/awr052
22.
Wahjoepramono POP Sasongko AB Halim D Aviani JK Lukito PP Adam A et al . Hydrocephalus is an independent factor affecting morbidity and mortality of ICH patients: systematic review and meta-analysis. World Neurosurg X. (2023) 19:100194. doi: 10.1016/j.wnsx.2023.100194
23.
Zille M Karuppagounder SS Chen Y Gough PJ Bertin J Finger J et al . Neuronal death after hemorrhagic stroke in vitro and in vivo shares features of Ferroptosis and necroptosis. Stroke. (2017) 48:1033–43. doi: 10.1161/strokeaha.116.015609
24.
Meng Z Liu C Chen C di F Zhang S Liang X et al . The induction of ferroptosis in posthemorrhagic hydrocephalus. Brain Res. (2023) 1798:148133. doi: 10.1016/j.brainres.2022.148133
25.
Strahle JM Garton T Bazzi AA Kilaru H Garton HJL Maher CO et al . Role of hemoglobin and Iron in hydrocephalus after neonatal intraventricular hemorrhage. Neurosurgery. (2014) 75:696–706. doi: 10.1227/neu.0000000000000524
26.
Gao C Du HJ Hua Y Keep RF Strahle J Xi GH . Role of red blood cell lysis and iron in hydrocephalus after intraventricular hemorrhage. J Cereb Blood Flow Metab. (2014) 34:1070–5. doi: 10.1038/jcbfm.2014.56
27.
Meng H Li F Hu R Yuan Y Gong G Hu S et al . Deferoxamine alleviates chronic hydrocephalus after intraventricular hemorrhage through iron chelation and Wnt1/Wnt3a inhibition. Brain Res. (2015) 1602:44–52. doi: 10.1016/j.brainres.2014.08.039
28.
Zhao H Garton T Keep RF Hua Y Xi GH . Microglia/macrophage polarization after experimental intracerebral hemorrhage. Transl Stroke Res. (2015) 6:407–9. doi: 10.1007/s12975-015-0428-4
29.
Lipina R Reguli S Novácková L Podesvová H Brichtová E . Relation between TGF-β 1 levels in cerebrospinal fluid and ETV outcome in premature newborns with posthemorrhagic hydrocephalus. Childs Nerv Syst. (2010) 26:333–41. doi: 10.1007/s00381-009-1011-7
30.
Kuo LT Huang APH . The pathogenesis of hydrocephalus following aneurysmal subarachnoid hemorrhage. Int J Mol Sci. (2021) 22:5050. doi: 10.3390/ijms22095050
31.
Tada T Kanaji M Kobayashi S . Induction of communicating hydrocephalus in mice by intrathecal injection of human recombinant transforming growth-factor-beta-1. J Neuroimmunol. (1994) 50:153–8. doi: 10.1016/0165-5728(94)90041-8
32.
Kitazawa K Tada T . Elevation of transforming growth-factor-beta-1 level in cerebrospinal-fluid of patients with communicating hydrocephalus after subarachnoid hemorrhage. Stroke. (1994) 25:1400–4. doi: 10.1161/01.Str.25.7.1400
33.
Aquilina K Hobbs C Tucker A Whitelaw A Thoresen M . Do drugs that block transforming growth factor beta reduce posthaemorrhagic ventricular dilatation in a neonatal rat model?Acta Paediatr. (2008) 97:1181–6. doi: 10.1111/j.1651-2227.2008.00903.x
34.
Manaenko A Lekic T Barnhart M Hartman R Zhang JH . Inhibition of transforming growth factor-β attenuates brain injury and neurological deficits in a rat model of germinal matrix hemorrhage. Stroke. (2014) 45:828–34. doi: 10.1161/strokeaha.113.003754
35.
Hoque N Thoresen M Aquilina K Hogan S Whitelaw A . Decorin and colchicine as potential treatments for post-Haemorrhagic ventricular dilatation in a neonatal rat model. Neonatology. (2011) 100:271–6. doi: 10.1159/000327842
36.
Yan H Chen YJ Li LY Jiang J Wu G Zuo Y et al . Decorin alleviated chronic hydrocephalus via inhibiting TGF-β1/Smad/CTGF pathway after subarachnoid hemorrhage in rats. Brain Res. (2016) 1630:241–53. doi: 10.1016/j.brainres.2015.11.004
37.
Gao F Liu FY Chen Z Hua Y Keep RF Xi GH . Hydrocephalus after intraventricular hemorrhage: the role of thrombin. J Cereb Blood Flow Metab. (2014) 34:489–94. doi: 10.1038/jcbfm.2013.225
38.
Gao F Zheng M Hua Y Keep RF Xi GH . Acetazolamide attenuates thrombin-induced hydrocephalus. Acta Neurochir. (2016) 121:373–377. doi: 10.1007/978-3-319-18497-5_64
39.
Hao XD Le CS Zhang HM Shang DS Tong LS Gao F . Thrombin disrupts vascular endothelial-cadherin and leads to hydrocephalus via protease-activated receptors-1 pathway. CNS Neurosci Ther. (2019) 25:1142–50. doi: 10.1111/cns.13129
40.
Bosche B Mergenthaler P Doeppner TR Hescheler J Molcanyi M . Complex clearance mechanisms after intraventricular hemorrhage and rt-PA treatment-a review on clinical trials. Transl Stroke Res. (2020) 11:337–44. doi: 10.1007/s12975-019-00735-6
41.
Brinker T Seifert V Dietz H . Subacute hydrocephalus after experimental subarachnoid hemorrhage – its prevention by intrathecal fibrinolysis with recombinant tissue plasminogen-activator. Neurosurgery. (1992) 31:306–12. doi: 10.1227/00006123-199208000-00016
42.
Kramer AH Jenne CN Zygun DA Roberts DJ Hill MD Holodinsky JK et al . Intraventricular fibrinolysis with tissue plasminogen activator is associated with transient cerebrospinal fluid inflammation: a randomized controlled trial. J Cereb Blood Flow Metab. (2015) 35:1241–8. doi: 10.1038/jcbfm.2015.47
43.
Ducruet AF Hickman ZL Zacharia BE Grobelny BT Narula R Guo KH et al . Exacerbation of Perihematomal edema and sterile meningitis with intraventricular Administration of Tissue Plasminogen Activator in patients with intracerebral hemorrhage. Neurosurgery. (2010) 66:648–55. doi: 10.1227/01.Neu.0000360374.59435.60
44.
Hanley DF Lane K McBee N Ziai W Tuhrim S Lees KR et al . Thrombolytic removal of intraventricular haemorrhage in treatment of severe stroke: results of the randomised, multicentre, multiregion, placebo-controlled CLEAR III trial. Lancet. (2017) 389:603–11. doi: 10.1016/s0140-6736(16)32410-2
45.
Torvik A Bhatia R Murthy VS . Transitory block of arachnoid granulations following subarachnoid hemorrhage – postmortem study. Acta Neurochir. (1978) 41:137–46. doi: 10.1007/bf01809144
46.
Massicotte EM Del Bigio MR . Human arachnoid villi response to subarachnoid hemorrhage: possible relationship to chronic hydrocephalus. J Neurosurg. (1999) 91:80–4. doi: 10.3171/jns.1999.91.1.0080
47.
Oi S Di Rocco C . Proposal of “evolution theory in cerebrospinal fluid dynamics” and minor pathway hydrocephalus in developing immature brain. Childs Nerv Syst. (2006) 22:662–9. doi: 10.1007/s00381-005-0020-4
48.
Papaiconomou C Bozanovic-Sosic R Zakharov A Johnston M . Does neonatal cerebrospinal fluid absorption occur via arachnoid projections or extracranial lymphatics?Am J Phys Regul Integr Comp Phys. (2002) 283:R869–76. doi: 10.1152/ajpregu.00173.2002
49.
Schulz LN Varghese A Michenkova M Wedemeyer M Pindrik JA Leonard JR et al . Neuroinflammatory pathways and potential therapeutic targets in neonatal post-hemorrhagic hydrocephalus. Pediatr Res. (2024) 97:1345–57. doi: 10.1038/s41390-024-03733-z
50.
Sadegh C Xu H Sutin J Fatou B Gupta S Pragana A et al . Choroid plexus-targeted NKCC1 overexpression to treat post-hemorrhagic hydrocephalus. Neuron. (2023) 111:1591–1608.e4. doi: 10.1016/j.neuron.2023.02.020
51.
Johnsen L Friis KA Damkier HH . In vitro investigation of the effect of proinflammatory cytokines on mouse choroid plexus membrane transporters Ncbe and NKCC1. Fluids Barriers CNS. (2023) 20:71. doi: 10.1186/s12987-023-00474-9
52.
Shi KB Tian DC Li ZLG Ducruet AF Lawton MT Shi FD . Global brain inflammation in stroke. Lancet Neurol. (2019) 18:1058–66. doi: 10.1016/s1474-4422(19)30078-x
53.
Tschoe C Bushnell CD Duncan PW Alexander-Miller MA Wolfe SQ . Neuroinflammation after intracerebral hemorrhage and potential therapeutic targets. J Stroke. (2020) 22:29–46. doi: 10.5853/jos.2019.02236
54.
Bu YY Chen MY Gao T Wang X Li XT Gao F . Mechanisms of hydrocephalus after intraventricular haemorrhage in adults. Stroke Vasc Neurol. (2016) 1:e000003:23–7. doi: 10.1136/svn-2015-000003
55.
Wang Q Cheng J Liu F Zhu J Li Y Zhao Y et al . Modulation of cerebrospinal fluid dysregulation via a SPAK and OSR1 targeted framework nucleic acid in hydrocephalus. Adv Sci. (2024) 11:e2306622. doi: 10.1002/advs.202306622
56.
Kahle KT Klinge PM Koschnitzky JE Kulkarni AV MacAulay N Robinson S et al . Paediatric hydrocephalus. Nat Rev Dis Primers. (2024) 10:35. doi: 10.1038/s41572-024-00519-9
57.
Robert SM Reeves BC Kiziltug E Duy PQ Karimy JK Mansuri MS et al . The choroid plexus links innate immunity to CSF dysregulation in hydrocephalus. Cell. (2023) 186:764–785.e21. doi: 10.1016/j.cell.2023.01.017
58.
Simard PF Tosun C Melnichenko L Ivanova S Gerzanich V Simard JM . Inflammation of the choroid plexus and ependymal layer of the ventricle following intraventricular hemorrhage. Transl Stroke Res. (2011) 2:227–31. doi: 10.1007/s12975-011-0070-8
59.
Lin T Ding L Lin YC Liu C Wang C Wu D et al . Pharmacological inhibition of TLR4-NF-κB signaling by TAK-242 attenuates hydrocephalus after intraventricular hemorrhage. Int Immunopharmacol. (2022) 103:108486. doi: 10.1016/j.intimp.2021.108486
60.
Holste K Xia F Garton HJL Wan S Hua Y Keep RF et al . The role of complement in brain injury following intracerebral hemorrhage: a review. Exp Neurol. (2021) 340:113654. doi: 10.1016/j.expneurol.2021.113654
61.
Wang M Xia F Wan S Hua Y Keep RF Xi GH . Role of complement component 3 in early Erythrolysis in the hematoma after experimental intracerebral hemorrhage. Stroke. (2021) 52:2649–60. doi: 10.1161/strokeaha.121.034372
62.
Mirzadeh Z Han YG Soriano-Navarro M García-Verdugo JM Alvarez-Buylla A . Cilia organize ependymal planar polarity. J Neurosci. (2010) 30:2600–10. doi: 10.1523/jneurosci.3744-09.2010
63.
Del Bigio MR . Ependymal cells: biology and pathology. Acta Neuropathol. (2010) 119:55–73. doi: 10.1007/s00401-009-0624-y
64.
Guerra MM Henzi R Ortloff A Lichtin N Vío K Jiménez AJ et al . Cell junction pathology of neural stem cells is associated with ventricular zone disruption, hydrocephalus, and abnormal neurogenesis. J Neuropathol Exp Neurol. (2015) 74:653–71. doi: 10.1097/nen.0000000000000203
65.
Sawamoto K Wichterle H Gonzalez-Perez O Cholfin JA Yamada M Spassky N et al . New neurons follow the flow of cerebrospinal fluid in the adult brain. Science. (2006) 311:629–32. doi: 10.1126/science.1119133
66.
Klebe D McBride D Krafft PR Flores JJ Tang JP Zhang JH . Posthemorrhagic hydrocephalus development after germinal matrix hemorrhage: established mechanisms and proposed pathways. J Neurosci Res. (2020) 98:105–20. doi: 10.1002/jnr.24394
67.
Whitelaw A Rosengren L Blennow M . Brain specific proteins in posthaemorrhagic ventricular dilatation. Arch Dis Child Fetal Neonatal Ed. (2001) 84:90F–991F. doi: 10.1136/fn.84.2.F90
68.
Krishnamurthy S Li J Schultz L McAllister JP . Intraventricular infusion of hyperosmolar dextran induces hydrocephalus: a novel animal model of hydrocephalus. Cerebrospinal Fluid Res. (2009) 6:16. doi: 10.1186/1743-8454-6-16
69.
Kennedy C Campbell M Elbourne D Hope P Johnson A . International randomised controlled trial of acetazolamide and furosemide in posthaemorrhagic ventricular dilatation in infancy. Lancet. (1998) 352:433–40.
70.
Kennedy CR Ayers S Campbell MJ Elbourne D Hope P Johnson A et al . Randomized, controlled trial of acetazolamide and furosemide in posthemorrhagic ventricular dilation in infancy: follow-up at 1 year. Pediatrics. (2001) 108:597–607. doi: 10.1542/peds.108.3.597
71.
Kazan S Güra A Uçar T Korkmaz E Ongun H Akyuz M . Hydrocephalus after intraventricular hemorrhage in preterm and low-birth weight infants: analysis of associated risk factors for ventriculoperitoneal shunting. Surg Neurol. (2005) 64:77–81. doi: 10.1016/j.surneu.2005.07.035
72.
Scarff JE . Treatment of NONOBSTRUCTIVE (communicating) hydrocephalus by endoscopic cauterization of choroid plexuses. J Neurosurg. (1970) 33:1–18. doi: 10.3171/jns.1970.33.1.0001
73.
Pople IK Ettles D . The role of endoscopic choroid-plexus coagulation in the management of hydrocephalus. Neurosurgery. (1995) 36:698–702. doi: 10.1227/00006123-199504000-00009
74.
McElroy DB . Hydrocephalus in children. Nurs Clin North Am. (1980) 15:23–34. doi: 10.1016/S0029-6465(22)00520-5
75.
Warf BC . Comparison of endoscopic third ventriculostomy alone and combined with choroid plexus cauterization in infants younger than 1 year of age: a prospective study in 550 African children. J Neurosurg. (2005) 103:475–81. doi: 10.3171/ped.2005.103.6.0475
76.
Kulkarni AV Schiff SJ Mbabazi-Kabachelor E Mugamba J Ssenyonga P Donnelly R et al . Endoscopic treatment versus shunting for infant hydrocephalus in Uganda. N Engl J Med. (2017) 377:2456–64. doi: 10.1056/NEJMoa1707568
77.
Obaid S Weil AG Rahme R Bojanowski MW . Endoscopic third ventriculostomy for obstructive hydrocephalus due to intraventricular hemorrhage. J Neurol Surg A Cent Eur Neurosurg. (2015) 76:99–111. doi: 10.1055/s-0034-1382778
78.
Rekate HL . Selecting patients for endoscopic third ventriculostomy Review. Neurosurg Clin N Am. (2004) 15:39–49. doi: 10.1016/S1042-3680(03)00074-3
79.
Chrastina J Novák Z Zeman T Feitová V Hrabovsky D Ríha I . The results of Neuroendoscopic surgery in patients with posttraumatic and Posthemorrhagic hydrocephalus. World Neurosurg. (2018) 113:E113–21. doi: 10.1016/j.wneu.2018.01.186
80.
Ellenbogen Y Brar K Yang KY Lee Y Ajani O . Comparison of endoscopic third ventriculostomy with or without choroid plexus cauterization in pediatric hydrocephalus: a systematic review and meta-analysis. J Neurosurg Pediatr. (2020) 26:371–8. doi: 10.3171/2020.4.Peds19720
81.
Sacko O Boetto S Lauwers-Cances V Dupuy M Roux FE . Endoscopic third ventriculostomy: outcome analysis in 368 procedures clinical article. J Neurosurg Pediatr. (2010) 5:68–74. doi: 10.3171/2009.8.Peds08108
82.
Yang Y-C Liu S-H Hsu Y-H Wu Y-L Chu P-T Lin P-C . Cerebrospinal fluid predictors of shunt-dependent hydrocephalus after hemorrhagic stroke: a systematic review and meta-analysis. Neurosurg Rev. (2022) 45:1847–59. doi: 10.1007/s10143-022-01731-5
83.
Kulkarni AV Drake JM Mallucci CL Sgouros S Roth J Constantini S et al . Endoscopic third ventriculostomy in the treatment of childhood hydrocephalus. J Pediatr. (2009) 155:254–9. doi: 10.1016/j.jpeds.2009.02.048
84.
Bergsneider M Miller C Vespa PM Hu X . Surgical management of adult hydrocephalus. Neurosurgery. (2008) 62:643–59. doi: 10.1227/01.neu.0000316269.82467.f7
85.
Solou M Ydreos I Gavra M Papadopoulos EK Banos S Boviatsis EJ et al . Controversies in the surgical treatment of chronic subdural hematoma: a systematic scoping review. Diagnostics. (2022) 12:2060. doi: 10.3390/diagnostics12092060
86.
Pan IW Harris DA Luerssen TG Lam SK . Comparative effectiveness of surgical treatments for pediatric hydrocephalus. Neurosurgery. (2018) 83:480–7. doi: 10.1093/neuros/nyx440
87.
Steiner T Purrucker JC Aguiar de Sousa D Apostolaki-Hansson T Beck J Christensen H et al . European stroke organisation (ESO) and European Association of Neurosurgical Societies (EANS) guideline on stroke due to spontaneous intracerebral haemorrhage. Eur Stroke J. (2025):23969873251340815. doi: 10.1177/23969873251340815
88.
Anurag J Sandeep C Arunav S . Ventriculosubgaleal shunt: an institutional experience. Childs Nerv Syst. (2023) 39:2131–7. doi: 10.1007/s00381-023-05937-w
89.
Pinto FCG Saad F de Oliveira MF Pereira RM de Miranda FL Tornai JB et al . Role of endoscopic third ventriculostomy and ventriculoperitoneal shunt in idiopathic normal pressure hydrocephalus: preliminary results of a randomized clinical trial. Neurosurgery. (2013) 72:845–53. doi: 10.1227/NEU.0b013e318285b37c
90.
Welions JC Shannon CN Holubkov R Riva-Cambrin J Kulkarni AV Limbrick DD et al . Shunting outcomes in posthemorrhagic hydrocephalus: results of a hydrocephalus clinical research network prospective cohort study. J Neurosurg Pediatr. (2017) 20:19–29. doi: 10.3171/2017.1.Peds16496
91.
Kulkarni AV Drake JM Kestle JRW Kestle JR Mallucci CL Sgouros S et al . Endoscopic third ventriculostomy vs cerebrospinal fluid shunt in the treatment of hydrocephalus in children: a propensity score-adjusted analysis. Neurosurgery. (2010) 67:588–93. doi: 10.1227/01.Neu.0000373199.79462.21
92.
Sun T Li XP Zhang QM Zhou YC Guan JW . Efficacy and safety of Lumboperitoneal shunt in the treatment of all-cause communicating hydrocephalus: analysis of risk factors of shunt failure. World Neurosurg. (2019) 132:e956–62. doi: 10.1016/j.wneu.2019.06.070
93.
Karabatsou K Quigley G Buxton N Foy P Mallucci C . Lumboperitoneal shunts: are the complications acceptable?Acta Neurochir. (2004) 146:1193–7. doi: 10.1007/s00701-004-0392-3
94.
Kazui H Miyajima M Mori E Ishikawa M SINPHONI-2 Investigators . Lumboperitoneal shunt surgery for idiopathic normal pressure hydrocephalus (SINPHONI-2): an open-label randomised trial. Lancet Neurol. (2015) 14:585–94. doi: 10.1016/s1474-4422(15)00046-0
95.
Lehman RM . Complications of lumboperitoneal shunts. Neurosurgery. (2008) 63:376–6. doi: 10.1227/01.NEU.0000333957.02102.26
96.
Wang ZP Wang K Qian ZQ Zeng L Gao L . Lumboperitoneal and Ventriculoperitoneal shunt surgery for Posthemorrhagic communicating hydrocephalus: a comparison. World Neurosurg. (2019) 127:E638–43. doi: 10.1016/j.Wneu.2019.03.235
97.
Ho Y-J Chiang W-C Huang H-Y Lin S-Z Tsai S-T . Effectiveness and safety of ventriculoperitoneal shunt versus lumboperitoneal shunt for communicating hydrocephalus: a systematic review and meta-analysis with trial sequential analysis. CNS Neurosci Ther. (2023) 29:804–15. doi: 10.1111/cns.14086
98.
Kang SD . Efficacy of lumbo-peritoneal versus ventriculo-peritoneal shunting for management of chronic hydrocephalus following aneurysmal subarachnoid haemorrhage. Acta Neurochir. (2000) 142:45–9. doi: 10.1007/s007010050006
99.
Köksal V Öktem S . Ventriculosubgaleal shunt procedure and its long-term outcomes in premature infants with post-hemorrhagic hydrocephalus. Childs Nerv Syst. (2010) 26:1505–15. doi: 10.1007/s00381-010-1118-x
100.
Chamiraju P Bhatia S Sandberg DI Ragheb J . Endoscopic third ventriculostomy and choroid plexus cauterization in posthemorrhagic hydrocephalus of prematurity: clinical article. J Neurosurg Pediatr PED. (2014) 13:433–9. doi: 10.3171/2013.12.PEDS13219
101.
Luther E McCarthy D Sedighim S Niazi T . Endoscopic third ventriculostomy inpatient failure rates compared with shunting in post-hemorrhagic hydrocephalus of prematurity. Childs Nerv Syst. (2020) 36:559–68. doi: 10.1007/s00381-019-04465-w
Summary
Keywords
intraventricular hemorrhage, hydrocephalus, cerebrospinal fluid, erythrocyte lysis, thrombin, ependymal damage, inflammatory response
Citation
Wang H, Chen X, You C, Wu K and Sun T (2025) Navigating challenges in hydrocephalus following intraventricular hemorrhage: a comprehensive review of current evidence. Front. Neurol. 16:1630286. doi: 10.3389/fneur.2025.1630286
Received
17 May 2025
Accepted
04 August 2025
Published
18 August 2025
Volume
16 - 2025
Edited by
Sherief Ghozy, Mayo Clinic, United States
Reviewed by
Rawad Obeid, Beaumont Children’s Hospital, United States
Petra Octavian Perdana Wahjoepramono, Universitas Pelita Harapan, Indonesia
Updates
Copyright
© 2025 Wang, Chen, You, Wu and Sun.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Ke Wu, 3301862665@qq.com; Tong Sun, tongsun@stu.scu.edu.cn
†These authors have contributed equally to this work
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