BRAIN INJURY, VOL. 18, NO.

4 (APRIL 2004), 351–358

Review

Natural history of chronic subdural haematoma

K.-S. LEE
Department of Neurosurgery, Soonchunhyang University Chonan Hospital,
Chonan, Korea
(Received 3 January 2003; accepted 31 October 2003)
Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

This review will clarify the natural history of chronic subdural haematoma (SDH). Chronic SDH
has dual origins, one from subdural hygromas (SDG) and the other from acute SDHs. It occurs only
in patients with a suitable pre-morbid condition, i.e. sufficient potential subdural space (PSS). In
unresolved SDGs, proliferation of dural border cells produces the neomembrane. Unresolved SDGs
become chronic SDHs by repeated micro-haemorrhages from fragile new vessels, which were grown
into the neomembrane. When PSS is sufficient, acute SDHs may become chronic SDHs. Chronic
SDHs enlarge when rebleeding exceeds absorption and they become symptomatic. When the
neomembrane is matured, the neocapillary is no longer fragile. If absorption exceeds rebleeding,
the haematoma will disappear. Maturation of the neomembrane and stabilization of the neovasculature
eventually result in spontaneous resolution. The fate of chronic SDH depends on the pre-morbid
status, the dynamics of absorption-expansion and maturation of the neomembrane.
For personal use only.

Introduction
Weir [1] described that Wepfer was the first man who described the chronic
subdural haematoma (SDH) in 1656. In 1826, Bayle ascribed the pathophysiology
of chronic SDH to ‘chronic rebleeding’ [2]. Repeated micro-haemorrhage from the
neomembrane was observed in 1925 [3]. However, about 50 years were required
until this phenomenon was accepted as the mechanism of haematoma enlargement.
Nevertheless, the origin of this lesion is still obscure. Until 1985, asymptomatic
acute SDH was suggested as the origin [4]. Recently, the aetiology and natural
history of this lesion were dealt with as an unresolved question [5].
There are three kinds of traumatic subdural lesions; acute SDH, chronic SDH
and subdural hygroma (SDG). The author has reported several papers [6–13] on
these traumatic lesions. To clarify the origin, pathogenesis and natural history of
chronic SDH, the author summarizes these papers and reviews the literature.

Origin of chronic subdural haematoma

Traditionally, SDH has been classified as acute, sub-acute and chronic, according to
the temporal interval. Such a temporal classification may lead to a wrong concept
that chronic SDHs originated from the acute ones. Actually, the acute SDH rarely

Correspondence to: Kyeong-Seok Lee, MD, Department of Neurosurgery, Soonchunhyang

University Chonan Hospital, Bongmyong-dong 23-20, Chonan, 330-721, Korea. e-mail: kslshl@
schch.co.kr

Brain Injury ISSN 0269–9052 print/ISSN 1362–301X online # 2004 Taylor & Francis Ltd
http://www.tandf.co.uk/journals
DOI: 10.1080/02699050310001645801
 352 K.-S. Lee

becomes the chronic one [14, 15]. The clinical characteristics of chronic SDHs are
quite different from the acute one. The acute one can be a seed, but if the soil is
not suitable for the seed it cannot become a chronic SDH. The soil, in other words
the pre-morbid condition, is a more important pre-requisite. Chronic SDHs occur
most often in the elderly who have the suitable soil. They can be developed in
the adolescent when the condition is suitable, such as an arachnoid cyst, cerebral
atrophy or intracranial hypotension [16–21] with or without trauma.
There are three kinds of traumatic subdural lesions; acute SDH, chronic SDH
and SDG. They have the same aetiologies and the same locations; they result from
trauma and take place in the subdural space. However, they have clearly different
characteristics. The nature of the content, envelope and radiological features are
quite different [10]. Contrary to the acute SDH, chronic SDH is very similar to the
Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

SDG. These two lesions are frequently bilateral, commonly occur at the ends of the
life, may be developed later by trivial injuries without combined lesions and quite
often are asymptomatic. There are numerous papers [6, 7, 12, 22–37] reporting that
unresolved SDGs become chronic SDHs. Now, such a transformation is regarded
as a rule rather than an exceptional event.
SDG is a passive lesion, a lesion of ex vacuo [11]. It is developed at the site of the
least pressure in the cranial cavity. Therefore, the shape and posture of the skull may
determine the site of SDG [11]. Skulls are frequently asymmetrical. If a skull is
not symmetrical, the skull tends to lean on the flat side. Then, the brain tends to
sink down and the site of the least pressure will be the top, the opposite side of the
For personal use only.

flat side. If the angle between the mid-line and a tangential line is acute the skull
tends to lie on that side and the hygroma would be placed on the opposite side
(figure 1(A)). If a skull is symmetrical, the skull tends to stand upright and then the

Figure 1. If the angle between the midline and a tangential line is acute, the skull tends to lie on that side and the
hygroma would be placed on the opposite side (A). If the skull is symmetrical, the skull tends to stand upright
and then the hygroma will be bilateral (B). If the skull leans to the left side, then the hygroma will be on the
right side (C).
 Natural history of chronic subdural haematoma 353
Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

Figure 2. The site of chronic SDHs also depends on the shape and posture of the skull. It is really common that
the haematoma tends to place on the opposite side of the flat side (A, B). In a calcified chronic SDH, the
For personal use only.

lesion is on the opposite side of the flat side (C).

hygroma will be bilateral (figure 1(B)). If the skull leans to the left side, then the
hygroma will be on the right side (figure 1(C)).
It is really interesting that the site of chronic SDHs also depends on the shape
and posture of the skull [13]. It is really common that the haematoma tends to place
on the opposite side of the flat side (figure 2(A) and (B)), including a calcified
chronic SDH (figure 2(C)). Of course, there are no rules without exceptions. In
figure 3, the haematoma is on the same side of the flat side. The reason is that this
chronic SDH originated from the acute SDH, primarily developed on the same
side. The location of the chronic SDH depends not only on the cranial shape and
posture, but also on the origin of the haematoma, pressure difference of both sides
of the cranial cavity, the expansile force of the haematoma, and so on [13].
However, it is usual that if the haematoma is on the opposite side, it might originate
from the hygroma. If the haematoma is on the same side, it might originate from the
acute SDH. If the haematoma is bilateral, the origin will be SDG.

Fate of chronic subdural haematoma

Chronic SDH is not a static lesion, but an ever-changing lesion. The initial thin
neomembrane becomes matured, organized or even calcified with time. The amount
of rebleeding from the neomembrane depends on the fragility of the vessels,
the degree of haemolytic activities within the haematoma [38, 39] and the surface
area of the outer membrane. The wider the surface area of outer membrane, the
more extensive the neovascularity and the higher the fibrinolytic activity within
the haematoma, the more blood will be mixed [9]. Therefore, the density of the
haematoma changes from low density to high density in CT (figure 4) [9, 39].
 354 K.-S. Lee
Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

Figure 3. The haematoma is on the same side of the flat side. The reason is that this chronic SDH
originated from the acute SDH, primarily developed on the same side.
For personal use only.

H ounsfie ld N o.

90

Hyperdensity
Resolu
tion

46
age
at
ur

orrh
at
io

hem
n

Isodensity icro
M

22

Hypodensity

1-3 wk 3 months Time

Figure 4. Presumed sequential change of the density and its mechanisms of subdural haematomas
in computed tomography.

Not only the density, but also the size and components of the haematoma change
according to the fragility of the vessels, the degree of haemolytic activities and the
surface area of the neomembrane.
Chronic SDHs enlarge when rebleeding exceeds absorption and they become
symptomatic. Symptoms of the chronic SDH depend on the pressure and the
 Natural history of chronic subdural haematoma 355

reserving capacity of the cranial cavity. Brain atrophy or expandability of the skull
may increase the reserving capacity. When the reserving capacity is enough, it may
be asymptomatic for a longer period [40, 41], even more than a year [42]. Surgical
interventions, either one or two burr holes with or without irrigation, usually solve
the symptomatic chronic SDH. However, recurrence of the haematoma is common
after surgery. There are many factors related to the recurrence, such as old age,
pre-existing cerebral infarction, pre-operative CT density, pattern or extent of the
haematoma, signal intensity on the T1 MR imaging, intra-haematomal membrane,
persistence of subdural air after surgery, volume of the drainage and methods of
surgery [43–49]. A layered type of the haematoma density (figure 2(A)) may
result from prolonged recumbency, which separates the blood components and
fluid. Such types are common in the inactive aged patients with brain atrophy,
Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

who tend to lie down. According to the pathogenesis [10], any factors inhibiting
brain expansion or increasing the reserving capacity may precipitate the recurrence.
To reduce the recurrence rate, it is better to promote brain expansion or try to
reduce the repeated micro-haemorrhage from the neomembrane. Any therapy
causing shrinkage of the brain should be avoided.
A few chronic SDHs may resolve spontaneously [50–55]. As a possible mechan-
ism, some proposed vascular permeability change by steroids or mannitol [50, 55].
However, resolution may occur without steroids or mannitol [53]. Reduction of
the intra-cranial pressure by osmotic agents may reduce the symptoms of chronic
SDH, but often fails to resolve the haematoma [56]. Theoretically, mannitol may
For personal use only.

shrink the brain, increase the reserving capacity and eventually inhibit resolution.
Hydrocephalus may lead to an elevated counter pressure against SDHs and may have
some role in the resolution of chronic SDHs [52]. The main mechanism of resolu-
tion is maturation of the neomembrane [8]. When the neomembrane is matured,
the neocapillary is no longer fragile. If absorption or brain expansion exceeds
rebleeding, the haematoma will disappear. Maturation of the neomembrane and
stabilization of the neovasculature eventually bring about spontaneous resolution.
Figure 5 represents the natural history of three traumatic subdural lesions.
These subdural lesions are a family in a sense. Trauma may cause subdural bleeding
directly, resulting in acute SDH. Most of them require surgical removal. About one
third of them can be managed conservatively and are usually resolved [7, 10]. A few
of them, usually less than 5%, can be changed into chronic SDH [7, 14].
Separation of the dura-arachnoid junction is the first step for the development of
SDG [6]. When there is a sufficient subdural space, the hygroma will develop [6]. If
not, the hygroma never occur. When brain shrinkage exceeds brain expansion, the
hygroma would persist. Neomembrane formation, neovascularization and repeated
micro-haemorrhages from these fragile new vessels will change the hygroma to
chronic SDH [10]. When brain expansion exceeds brain shrinkage, the hygroma
would resolve [10]. Repeated micro-haemorrhage from the neomembrane is the
mechanism of haematoma enlargement [57]. The haemorrhage will continue until
the vessels are matured. Once the vessels are matured, the haematoma eventually
will be resolved [8].
In conclusion, the chronic SDH has dual origin; one from the acute SDH, the
other from the SDG. Sufficient potential subdural space is the pre-morbid condition
for the chronic SDHs. Any forces to shrink the brain can be the precipitating factors,
while the opposite forces to expand the brain will be the inhibiting factors. Such a
transformation or development of a new subdural lesion depends on the interaction
 356 K.-S. Lee

TRAUMA Separation of
Dura-Arachnoid Junction

Tear of Bridge Veins,

Tear of Cortical Vessels Sufficient space Insufficient space
Bleeding from Cortical Laceration

20-40% 3% SDG No Hygroma

ASDH Dissolution 12% 80-90%
Shrinkage>Expansion Shrinkage<Expansion
60-80%

Operative Removal Neomembrane

Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

Resolved
Neovascularization
Absorption
Rebleeding

Resolved Maturation CSDH

Figure 5. Schematic representation of the origin and pathogenesis of chronic subdural haematoma and relationship
among three traumatic subdural lesions.

of the pre-morbid status, the dynamics of absorption-expansion and maturation of

For personal use only.

the neomembrane.

References
1. WEIR, B.: The osmolarity of subdural hematoma fluid. Journal of Neurosurgery, 34: 528–533, 1971.
2. WILBERGER, J. E.: Pathophysiology of evolution and recurrence of chronic subdural hematoma.
Neurosurgery Clinics of North America, 11: 435–438, 2000.
3. PUTNAM, T. J. and CUSHING, H.: Chronic subdural hematoma: its pathology, its relation to
pachymeningitis hemorrhagica interna and its surgical treatment. Archives of Surgery, 11:
329–393, 1925.
4. COOPER, P. R.: Traumatic intracranial hematomas. In: W. H. Wilkins and S. S. Rengachary
(editors) Neurosurgery (New York: McGraw-Hill), pp. 1657–1666, 1985.
5. LIAU, L. M., BERGSNEIDER, M. and BECKER, D. P.: Pathology and pathophysiology of head injury.
In: J. R. Youmans (editor) Neurological Surgery, 4th edn, Vol. 3 (Philadelphia: W.B. Saunders
Company), pp. 1549–1594, 1996.
6. LEE, K. S., BAE, W. K., PARK, Y. T. et al.: The pathogenesis and fate of traumatic subdural
hygroma. British Journal of Neurosurgery, 8: 551–558, 1994.
7. LEE, K. S., DOH, J. W., BAE, H. G. et al.: Relations among traumatic subdural lesions. Journal of
Korean Medical Science, 11: 55–63, 1996.
8. LEE, K. S., BAE, W. K., DOH, J. W. et al.: The computed tomographic attenuation and the age of
subdural hematomas. Journal of Korean Medical Science, 12: 353–359, 1997.
9. LEE, K. S.: The pathogenesis and clinical significance of traumatic subdural hygroma. Brain Injury,
12: 595–603, 1998.
10. LEE, K. S., BAE, W. K., DOH, J. W. et al.: Origin of chronic subdural hematoma and relation to
traumatic subdural lesions. Brain Injury, 12: 901–910, 1998.
11. LEE, K. S., BAE, W. K., YOON, S. M. et al.: Location of the traumatic subdural hygroma; role of
gravity and cranial morphology. Brain Injury, 14: 355–361, 2000.
12. LEE, K. S., BAE, W. K., BAE, H. G. et al.: The fate of traumatic subdural hygroma in serial
computed tomographic scans. Journal of Korean Medical Science, 15: 560–568, 2000.
13. LEE, K. S., BAE, W. K., YOON, S. M. et al.: Location of the chronic subdural haematoma: role of
the gravity and cranial morphology. Brain Injury, 15: 47–52, 2001.
 Natural history of chronic subdural haematoma 357

14. CROCE, M. A., DENT, D. L., MENKE, P. G. et al.: Acute subdural hematoma: nonsurgical
management of selected patients. Journal of Trauma, 36: 820–827, 1994.
15. DOLINSKAS, C. S., ZIMMERMAN, R. A., BILANIUK, L. T. et al.: Computed tomography of post-
traumatic extracerebral hematomas. Journal of Trauma, 19: 163–169, 1979.
16. ULMER, S., ENGELLANDT, K., STILLER, U. et al.: Chronic subdural hemorrhage into a giant
arachnoidal cyst (Galassi classification type III). Journal of Computer Assisted Tomography, 26:
647–653, 2002.
17. PRABHU, V. C. and BAILES, J. E.: Chronic subdural hematoma complicating arachnoid cyst
secondary to soccer-related head injury: case report. Neurosurgery, 50: 195–197, 2002.
18. OKA, Y., KUMON, Y., OHTA, S. et al.: Chronic subdural hematoma associated with middle fossa
arachnoid cysts—three case reports. Neurologia Medico-Chirugica (Tokyo), 34: 95–99, 1994.
19. IMAIZUMI, S., ONUMA, T., KAMEYAMA, M. et al.: Organized chronic subdural hematoma requiring
craniotomy-five case reports. Neurologia Medico-Chirugica (Tokyo), 41: 19–24, 2001.
20. SCHIEVINK, W. I., MORREALE, V. M., ATKINSON, J. L. et al.: Surgical treatment of spontaneous
Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

spinal cerebrospinal fluid leaks. Journal of Neurosurgery, 88: 243–246, 1998.

21. MURAKAMI, M., MORIKAWA, K., MATSUNO, A. et al.: Spontaneous intracranial hypotension
associated with bilateral chronic subdural hematomas—case report. Neurologia Medico-Chirugica
(Tokyo), 40: 484–488, 2000.
22. HYODO, A., NOSE, T., ENOMOTO, T. et al.: Chronic subdural hematoma; changed its density from
low to high on follow-up CT. No Shinkei Geka, 8: 649–653, 1980.
23. YAMADA, H., WATANABE, T., MURATA, S. et al.: Developmental process of chronic subdural
collections of fluid based on CT scan findings. Surgical Neurology, 13: 441–448, 1980.
24. KOIZUMI, H., FUKAMACHI, A., WAKAO, T. et al.: Traumatic subdural hygromas in adults: on the
possibility of development of chronic subdural hematoma. Neurologia Medico-Chirugica (Tokyo),
21: 397–406, 1981.
25. TAKAHASHI, Y., SATO, H., INOUE, Y. et al.: CT findings and the evaluation of chronic subdural
For personal use only.

hematoma (part 1)—forecast of chronic subdural hematoma. Neurologia Medico-Chirugica (Tokyo),

21: 485–490, 1981.
26. OHNO, K., SUZUKI, R., MASAOKA, H. et al.: Chronic subdural hematoma preceded by persistent
traumatic subdural fluid collection. Journal of Neurology Neurosurgery and Psychiatry, 50: 1694–1697,
1987.
27. VON KOPP, W.: Zur dynamik und pathogenese traumatischer subduraler hygrome. Fortschritte auf
dem Gebiete der Rontgenstrahlen und der neuen bildgebenden Verfahren, 148: 530–536, 1988 (ROFO).
28. KOPP, W.: Zur pathogenese des chronischen subduralen haematoms. Fortschritte auf dem Gebiete der
Rontgenstrahlen und der neuen bildgebenden Verfahren, 152: 200–205, 1990 (ROFO).
29. PARK, H. B., LEE, C. R. and KIM, S. C.: Chronic subdural hematoma superimposed on post-
traumatic subdural hygroma. Journal of Korean Neurosurgical Society, 19: 126–130, 1990.
30. LUSINS, J. O. and LEVY, E. R.: MRI documentation of hemorrhage into post-traumatic subdural
hygroma. The Mount Sinai Journal of Medicine, 60: 161–162, 1993.
31. MURATA, K.: Chronic subdural hematoma may be preceded by persistent traumatic subdural
effusion. Neurologia Medico-Chirugica (Tokyo), 33: 691–696, 1993.
32. WHANG, K., HU, C., HONG, S. K. et al.: Clinical analysis of chronic subdural hematoma originated
from traumatic subdural hygroma. Journal of Korean Neurosurgical Society, 22: 898–904, 1993.
33. ISHIBASHI, A., YOKOKURA, Y. and MIYAGI, J.: Clinical analysis of nineteen patients with traumatic
subdural hygromas. Kurume Medical Journal, 41: 81–85, 1994.
34. LEE, H. W., HU, C., PYEN, J. S. et al.: Clinical analysis of traumatic subdural hygroma. Journal of
Korean Neurosurgical Society, 23: 515–521, 1994.
35. PARK, C. K., CHOI, K. H., KIM, M. C. et al.: Spontaneous evolution of posttraumatic subdural
hygroma into chronic subdural haematoma. Acta Neurochirugica (Wien), 127: 41–47, 1994.
36. NISHIMURA, K., MORI, K., SAKAMOTO, T. et al.: Management of subarachnoid fluid collection in
infants based on a long-term follow-up study. Acta Neurochirugica (Wien), 138: 179–184, 1996.
37. MURAKAMI, H., HIROSE, Y., SAGOH, M. et al.: Why do chronic subdural hematomas continue
to grow slowly and not coagulate? Role of thrombomodulin in the mechanism. Journal of
Neurosurgery, 96: 877–884, 2002.
38. NOMURA, S., KASHIWAGI, S., FUJISAWA, H. et al.: Characterization of local hyperfibrinolysis
in chronic subdural hematomas by SDS-PAGE and immunoblot. Journal of Neurosurgery, 81:
910–913, 1994.
 358 K.-S. Lee

39. NAKAGUCHI, H., TANISHIMA, T. and YOSHIMASU, N.: Factors in the natural history of chronic
subdural hematomas that influence their postoperative recurrence. Journal of Neurosurgery, 95:
256–262, 2001.
40. LILIANG, P. C., TSAI, Y. D., LIANG, C. L. et al.: Chronic subdural haematoma in young and
extremely aged adults: a comparative study of two age groups. Injury, 33: 345–348, 2002.
41. JEONG, J. E., KIM, G. K., PARK, J. T. et al.: A clinical analysis of chronic subdural hematoma
according to age factor. Journal of Korean Neurosurgical Society, 29: 748–753, 2000.
42. KOTWICA, Z. and BREZEZINSKI, J: A long course of chronic subdural haematomas. Acta
Neurochirugica (Wien), 85: 44–45, 1987.
43. OKADA, Y., AKAI, T., OKAMOTO, K. et al.: A comparative study of the treatment of chronic
subdural hematoma—burr hole drainage versus burr hole irrigation. Surgical Neurology, 57:
405–409, 2002.
44. OISHI, M., TOYAMA, M., TAMATANI, S. et al.: Clinical factors of recurrent chronic subdural
hematoma. Neurologia Medico-Chirugica (Tokyo), 41: 382–386, 2001.
Brain Inj Downloaded from informahealthcare.com by Central Michigan University on 12/31/14

45. MORI, K. and MAEDA, M.: Surgical treatment of chronic subdural hematoma in 500 consecutive
cases: clinical characteristics, surgical outcome, complications, and recurrence rate. Neurologia
Medico-Chirugica (Tokyo), 41: 371–381, 2001.
46. TANIKAWA, M., MASE, M., YAMADA, K. et al.: Surgical treatment of chronic subdural hematoma
based on intrahematomal membrane structure on MRI. Acta Neurochirugica (Wien), 143: 613–618,
2001.
47. KWON, T. H., PARK, Y. K., LIM, D. J. et al.: Chronic subdural hematoma: evaluation of the clinical
significance of postoperative drainage volume. Journal of Neurosurgery, 93: 796–799, 2000.
48. TSUTSUMI, K., MAEDA, K., IIJIMA, A. et al.: The relationship of preoperative magnetic resonance
imaging findings and closed system drainage in the recurrence of chronic subdural hematoma.
Journal of Neurosurgery, 87: 870–875, 1997.
49. SHIMOJI, T., SATO, K. and ISHII, S.: A pathogenesis of chronic subdural hematoma; it’s relationship
For personal use only.

to subdural membrane. No Shinkei Geka, 20: 131–137, 1992.

50. SUZUKI, J. and TAKAKU, A.: Nonsurgical treatment of chronic subdural hematomas. Journal of
Neurosurgery, 33: 548–553, 1970.
51. BENDER, M. B. and CHRISTOFF, N.: Nonsurgical treatment of subdural hematomas. Archives of
Neurology, 31: 73–79, 1974.
52. NAGANUMA, H., FUKAMACHI, A., KAWAKAMI, M. et al.: Spontaneous resolution of chronic subdural
hematomas. Neurosurgery, 19: 794–798, 1986.
53. PARLATO, C., GUARRACINO, A. and MORACI, A.: Spontaneous resolution of chronic subdural
hematoma. Surgical Neurology, 53: 312–315, 2000.
54. VOELKER, J.: Nonoperative treatment of chronic subdural hematoma. Neurosurgery Clinics of North
America, 11: 507–513, 2000.
55. GLOVER, D. and LABADIE, E. L.: Physiopathogenesis of subdural hematomas. Part 2: Inhibition of
growth of experimental hematomas with dexamethasone. Journal of Neurosurgery, 45: 393–397,
1976.
56. GJERRIS, F. and SCHMIDT, K.: Chronic subdural hematoma: surgery or mannitol treatment. Journal
of Neurosurgery, 40: 639–642, 1974.
57. MARKWALDER, T. M.: Chronic subdural hematomas: a review. Journal of Neurosurgery, 54:
637–645, 1981.