Elsevier

World Neurosurgery

Volume 108, December 2017, Pages 954-958
World Neurosurgery

Literature Review
Chronic Subdural Hematoma: A Perspective on Subdural Membranes and Dementia

https://doi.org/10.1016/j.wneu.2017.09.063Get rights and content

Objective

To review the complex pathogenesis of the subdural membrane and the link between head trauma, dementia, and dural lymphatics.

Methods

A thorough literature search of published English-language articles was performed using PubMed, Ovid, and Cochrane databases.

Results

Chronic subdural hematoma (cSDH) is a common intracranial pathology and a leading cause of reversible dementia. cSDH is projected to affect at least 60,000 new individuals in the United States annually by 2030. This condition can result from mild to moderate head trauma that leads to hemorrhaging in the dura-arachnoid interface. The short-term and long-term effects of cSDH and the subdural membrane on the pathogenesis of dementia and the newly discovered dural lymphatics is a topic of increasing importance.

Conclusions

Further research into the possible link between traumatic brain injury and cSDH in particular and dural lymphatics and intracranial fluid dynamics is warranted.

Introduction

Chronic subdural hematoma (cSDH) is a relatively common and debilitating pathologic entity that affects 1–5.3 per 100,000 individuals annually.1, 2 cSDH is particularly prevalent in elderly men, with >50% of cSDH cases occurring in patients >60 years old and the highest incidence (7.35 cases per 100,000) in adults 70–79 years old. It is projected to affect 60,000 Americans >65 years old annually by 2030.3, 4 Reasons for this lie in the increased risk factors, such as falls and use of anticoagulants, in elderly adults coupled with age-related cortical atrophy that distends small cerebral vessels and bridging veins.5, 6, 7, 8, 9

cSDH commonly develops over the course of ≥3 weeks following mild to moderate head trauma coupled with a chronic inflammatory reaction.10 After cSDH development, natural physiologic sequelae lead to a gradual enlargement of the cSDH, primarily through the formation of a subdural neomembrane.11 This subdural membrane is composed of inner and outer layers (Figure 1) that release antithrombotic and fibrinolytic molecules to liquefy the hematoma to prevent clot formation and facilitate cSDH reabsorption.12, 13 However, in cases where reabsorption is impaired or absent, the cSDH can expand and result in mass effects, blood flow impairment, and metabolic disturbances in the underlying cortex.14 The presence of blood alone in the subdural space is inadequate to induce cSDH; rather, chronic inflammation and other contributing factors, such as cerebral atrophy, may be the true etiologic factors underlying cSDH.15 We provide a brief overview of subdural membrane formation and discuss potential links between cSDH, dementia, and intracranial lymphatic systems.

Section snippets

Subdural Membrane Formation

The subdural membrane is an important contributor to the pathogenesis and clinical symptoms of cSDH. It consists of an inner and outer layer and forms within the dura-arachnoid meningeal interface.16 This interface creates a potential space, termed the subdural space, that consists of a tight group of cells known as the interface layer. This layer lines the inner dural border and forms the outermost arachnoid barrier. These 2 cellular components fuse within the interface layer and form a tight

Linking cSDH to Dementia and Dural Lymphatics

The clinical effects of treated and untreated cSDH have been broadly explored and overshadow the physiologic effects of cSDH on the underlying brain parenchyma. In addition to overt mass effect, the presence of a large cSDH can alter cerebral blood flow and result in ischemia and deleterious metabolic changes within the neuroparenchyma.37 cSDH evacuation has been shown to improve cerebral blood flow and cognitive function in patients.

Although the exact extent of the adverse physiologic effects

Conclusions

cSDH results from head injuries and is a type of TBI that affects approximately 1–5 in 100,000 individuals each year. cSDH is a leading cause of reversible dementia, in that surgical evacuation can lead to symptomatic improvement, yet multiple treatment options exist. Furthermore, an increasingly greater emphasis must be placed on the short-term and long-term effects of cSDH and the subdural membrane that accompanies it on the pathogenesis of dementia and the mechanistic role of newly

References (61)

  • L.B. Miranda et al.

    Chronic subdural hematoma in the elderly: not a benign disease: clinical article

    J Neurosurg

    (2011)
  • H. Baechli et al.

    Demographics and prevalent risk factors of chronic subdural haematoma: results of a large single-center cohort study

    Neurosurg Rev

    (2004)
  • M.A. Reymond et al.

    Aspirin as a risk factor for hemorrhage in patients with head injuries

    Neurosurg Rev

    (1992)
  • A.R. Wintzen et al.

    Subdural hematoma and oral anticoagulant therapy

    Arch Neurol

    (1982)
  • H. Mattle et al.

    Anticoagulation-related intracranial extracerebral haemorrhage

    J Neurol Neurosurg Psychiatry

    (1989)
  • E.M. Hylek et al.

    Risk factors for intracranial hemorrhage in outpatients taking warfarin

    Ann Intern Med

    (1994)
  • K. Torihashi et al.

    Independent predictors for recurrence of chronic subdural hematoma: a review of 343 consecutive surgical cases

    Neurosurgery

    (2008)
  • W. Schachenmayr et al.

    The origin of subdural neomembranes. I. Fine structure of the dura-arachnoid interface in man

    Am J Pathol

    (1978)
  • H. Ito et al.

    Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma

    J Neurosurg

    (1976)
  • H. Ito et al.

    Fibrinolytic enzyme in the lining walls of chronic subdural hematoma

    J Neurosurg

    (1978)
  • H. Yamamoto et al.

    Independent predictors of recurrence of chronic subdural hematoma: results of multivariate analysis performed using a logistic regression model

    J Neurosurg

    (2003)
  • E. Edlmann et al.

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

    J Neuroinflammation

    (2017)
  • T. Yamashima et al.

    The origin of inner membranes in chronic subdural hematomas

    Acta Neuropathol

    (1985)
  • R. Friede et al.

    The origin ofsubdural neomembranes. II. Fine structural of neomembranes

    Am J Pathol

    (1978)
  • A.G. Kolias et al.

    Chronic subdural haematoma: modern management and emerging therapies

    Nat Rev Neurol

    (2014)
  • T. Nagahori et al.

    Histological study of the outer membrane of chronic subdural hematoma: possible mechanism for expansion of hematoma cavity

    No Shinkei Geka

    (1993)
  • N. Kawano et al.

    Origin of the capsule of a chronic subdural hematoma—an electron microscopy study

    No Shinkei Geka

    (1988)
  • T. Yamashima et al.

    The role of endothelial gap junctions in the enlargement of chronic subdural hematomas

    J Neurosurg

    (1983)
  • S. Sato et al.

    Ultrastructural observations of the capsule of chronic subdural hematoma in various clinical stages

    J Neurosurg

    (1975)
  • J. Sajanti et al.

    High concentrations of procollagen propeptides in chronic subdural haematoma and effusion

    J Neurol Neurosurg Psychiatry

    (2003)
  • Cited by (0)

    Conflict of interest statement: R.S. is funded in part by a Medical Scientist Training Program grant from the National Institutes of Health (grant number T32-GM08620). All other authors have no conflicts to report.

    View full text