Serum Protein Exudation in Chronic Subdural Haematomas: a Mechanism for Haematoma Enlargement?

Fujisawa, Hironori; Nomura, Sadahiro; Tsuchida, Eiji; Ito, Hiroki

doi:10.1007/s007010050077

Cited by 35 publications

(20 citation statements)

References 8 publications

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“…There are several other markers and cell types not directly related to inflammation and angiogenesis and not discussed at length in the present review, but which may still have potentially important roles. These include aquaporin-1, a water channel, heavily expressed in the outer membranes which may contribute to fluid accumulation in CSDH growth [31]; high levels of linoleic acid residue, which have been found in association with recurrent CSDH [32] and a wide range of proteins, similar to those found in serum, suggesting exudation from the outer membrane vessels [33, 34]. CSF is also highlighted as a potential driver of CSDH formation, accumulating due to arachnoid tearing at the time of trauma and potentially continuing to leak into the subdural space.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy

Edlmann

Giorgi-Coll

Whitfield

et al. 2017

J Neuroinflammation

453

360

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Chronic subdural haematoma (CSDH) is an encapsulated collection of blood and fluid on the surface of the brain. Historically considered a result of head trauma, recent evidence suggests there are more complex processes involved. Trauma may be absent or very minor and does not explain the progressive, chronic course of the condition. This review focuses on several key processes involved in CSDH development: angiogenesis, fibrinolysis and inflammation. The characteristic membrane surrounding the CSDH has been identified as a source of fluid exudation and haemorrhage. Angiogenic stimuli lead to the creation of fragile blood vessels within membrane walls, whilst fibrinolytic processes prevent clot formation resulting in continued haemorrhage. An abundance of inflammatory cells and markers have been identified within the membranes and subdural fluid and are likely to contribute to propagating an inflammatory response which stimulates ongoing membrane growth and fluid accumulation. Currently, the mainstay of treatment for CSDH is surgical drainage, which has associated risks of recurrence requiring repeat surgery. Understanding of the underlying pathophysiological processes has been applied to developing potential drug treatments. Ongoing research is needed to identify if these therapies are successful in controlling the inflammatory and angiogenic disease processes leading to control and resolution of CSDH.

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Section: Introductionmentioning

confidence: 99%

Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy

Edlmann

Giorgi-Coll

Whitfield

et al. 2017

J Neuroinflammation

453

360

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“…Indeed, not all the protein in the haematoma is derived from serum protein exudation, but part is synthesised in situ and there is an inverse relation in subdural haematoma between the total protein concentration and albumin ratio. 16 The oncotic pressure of subdural fluid depends in a linear fashion on the total protein concentration. 17 We therefore suggest that the increased synthesis of extracellular components leads to an increased oncotic pressure in the fluid in the cavity, thereby contributing to haematoma or effusion enlargement.…”

Section: Discussionmentioning

confidence: 99%

High concentrations of procollagen propeptides in chronic subdural haematoma and effusion

Sajanti

Majamaa²

2003

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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Procollagen propeptides increase in the CSF after subarachnoid haemorrhage, reflecting increased collagen synthesis in the arachnoid. We studied the induction of dural collagen synthesis after cerebral trauma by measuring the carboxyterminal propeptide of type I procollagen (PICP) and the aminoterminal propeptide of type III procollagen (PIIINP) in 17 subdural haematoma or effusion fluid samples obtained at operation on days 10-85 after head trauma. The concentration of PICP was 78-fold higher and that of PIIINP 156-fold higher, relative to that in the serum. These results indicate that meningeal trauma is followed by a long lasting increase in dural collagen synthesis, and suggest that enhanced synthesis of the various extracellular matrix components may have a role in the development of chronic subdural haematoma or effusion.A fluid containing space has been postulated at the dura-arachnoid junction, but many studies offer compelling evidence that no such subdural space exists.

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“…The inflammatory and angiogenic process of the neomembrane, along with the cycle of re-bleeding, coagulation, and fibrinolysis are hypothesized to be at the center of the development and progression of CSDHs (4,6,8,12,19,30,31). In addition, traumatic subdural hygroma, defined as an accumulation of cerebrospinal fluid in the subdural space after trauma, is frequently associated with the development of CSDH (23).…”

Section: █ Discussionmentioning

confidence: 99%

“…Although the mechanism of CSF leakage (and its component βTP) in to the subdural space in CSDH remains unknown, two hypotheses were suggested: (1) CSF (and its component βTP) enters the subdural space of CSDH through the arachnoid tear that acts as a valve and (2) CSF (and its component βTP) crosses the inner membrane of the CSDH into the subdural space by diffusion/exudation (12). The former mechanism is supported by the high prevalence of preceding head trauma in patients with CSDH and subdural hygroma (SH), by the sporadic intraoperative identification of arachnoid tears, and by sporadic accumulation of tracer within the subdural space during cisternography in patients with SH, but the latter mechanism has not yet been observed or assessed (2,4,5,15,26,27). In our study, we hypothesized that higher intensity head traumas may be indicative of more CSF leakage into the subdural space.…”

Section: Laboratory Findingsmentioning

confidence: 98%

Chronic subdural hematoma preceded by high-impact trauma: does the intensity of trauma influence the pathogenesis of traumatic chronic subdural hematoma?

Park¹,

Lee²,

Park³

et al. 2015

Turkish Neurosurgery

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ABSTRACTof the meninges and the neo-membrane of hematoma have been recently clarified. Additionally, the roles of inflammatory, fibrinolytic, angiogenic, and coagulation-system factors in the CSDH have been investigated (3,7,8,12,22,32). Currently, CSDH is considered a chronic self-perpetuating inflammatory process involving the dura mater.Trauma is probably the most important risk factor for CSDH. Rupture of transversing veins by trauma is commonly known █ INTRODUCTION C hronic subdural hematoma (CSDH) is a commonly encountered neurosurgical disease that is more likely to occur under certain conditions, including advanced age, alcoholism, abnormal coagulation, dementia, seizure disorder, or after cerebrospinal fluid (CSF) diversion (13,17,18). Although the pathophysiology of CSDH has been controversial over the last several years, the ultrastructural anatomy AIm: The purpose of this study was to investigate whether the intensity of trauma influences the pathogenesis of traumatic chronic subdural hematoma (CSDH). mATERIAl and mEThODS: Thirty-one patients treated surgically for traumatic CSDH were divided into high-impact and lowimpact groups according to the intensity of trauma. They were respectively evaluated with respect to clinical and radiological findings at presentation, and the subdural concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), basic fibroblast growth factor, and beta-trace protein (βTP) [a highly specific protein in the cerebrospinal fluid (CSF)] related to the pathogenesis of CSDH. If βTP (subdural fluid/serum) was >2, an admixture of CSF to the subdural fluid was indicated. RESUlTS:The βTP (subdural fluid/serum) was >2 in all patients with a traumatic CSDH. The mean concentration of subdural βTP in the high-impact group was higher than in the low-impact group (6.1 mg/L versus 3.9 mg/L), and the difference was statistically significant (p=0.02). In addition, mean concentrations of IL-6, IL-8 and VEGF were higher in the high-impact group, as compared to the low-impact group, though the differences did not reach statistical significance.CONClUSION: Trauma may be related to CSF leakage into the subdural space in CSDH, and the intensity of trauma may influence the amount of CSF leakage. Although there is no direct correlation between the amount of CSF leakage and other subdural molecules, the intensity of trauma may be associated with larger concentrations of molecules in traumatic CSDH.

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Serum Protein Exudation in Chronic Subdural Haematomas: a Mechanism for Haematoma Enlargement?

Cited by 35 publications

References 8 publications

Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy

Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy

High concentrations of procollagen propeptides in chronic subdural haematoma and effusion

Chronic subdural hematoma preceded by high-impact trauma: does the intensity of trauma influence the pathogenesis of traumatic chronic subdural hematoma?

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