Dural Graft-Induced Fibrotic Mass Twelve Years after Successful Treatment of Skull Base Non-Hodgkin Lymphoma Mimicking Recurrence: Case Report and Literature Review

doi:10.4236/ojmn.2014.41002

Paper Menu >>

Journal Menu >>

Open Journal of Modern Neurosurgery, 2014, 4, 7-12

Published Online January 2014 (http://www.scirp.org/journal/ojmn)

http://dx.doi.org/10.4236/ojmn.2014.41002

OPEN ACCESS OJMN

Dural Graft-Induced Fibrotic Mass Twelve Years after

Successful Treatment of Skull Base Non-Hodgkin

Lymphoma Mimicking Recurrence: Case Report and

Literature Review

Mario Teo1,2*, Sean Martin2, James Bowness1, Muftah Sam Eljamel1

1Department of Neurosurgery, Ninewells Hospital, Dundee, UK

2Department of Neurosurgery, Institute of Neurological Science, Glasgow, UK

Email: *marioteo@nhs.net

Received October 23, 2013; revised November 23, 2013; accepted December 1, 2013

permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In accordance of

ABSTRACT

Non-Hodgkin lymphoma involving the skull base is a very rare tumour. The role of surgery for these patients

remains controversial, as is the use of dural graft for CSF leak repair. With an increasing incidence of CNS

lymphoma, more atypical presentations are reported. It is, therefore, important to include lymphoma in the dif-

ferential diagnosis of skull base lesions as long-term remission is achievable for such patients, as shown in our

case. Dural graft used for CSF leak repair could present with delayed complication mimicking tumour recur-

rence. Relevant published literature is reviewed.

KEYWORDS

CNS Lymphoma; Skull Base; Dural Graft Repair; Delayed Complication

1. Introduction

Primary central nervous system (CNS) lymphoma is a

rare disease and accounts for 1% - 2% of intracranial tu-

mours [1,2]. Immunocompromised patients, including those

with organ transplantation, congenital immunodeficien-

cies, and acquired immunodeficiency syndrome (AIDS),

are at a particularly high risk of developing th is condition.

However, there has been an increasing incidence of pri-

mary CNS lymphoma among immunologically compe-

tent individuals [3].

Skull base primary CNS lymphoma is even rarer, but

has been reported [4-6]. In immunocompetent patients

with no predisposing history, the disease may not be sus-

pected, since clinically and radiolog ically, they can be in -

distinguishable from squamous cell carcinoma, metas-

tases, or intraosseous meningioma. The role of surgery

for CNS lymphoma, and more importantly, for skull base

lymphoma remains controversial as extensive skull base

surgery can lead to significant morbidity, and reconstruc-

tion is imperative.

We present a case of primary skull base lymphoma,

our surgical strategy, long-term outcome and the first re-

ported delayed complication of dural patch in such a pa-

tient.

2. Case Report

A 49-year-old man initially presen ted with a 3-week his-

tory of persistent right facial pain, which started in the

temporomandibular joint and spread to the right maxilla

and temple, and was associated with paraesthesia. Two

weeks later, he developed right eye ptosis, and visual dis-

turbance. Neurological examination revealed right II, III,

IV, V and VI cranial nerve palsies. MRI demonstrated a

large destructive lesion in the anterior cranial fossa with

breach of the cribriform plate, extension into the ethmoid

and sphenoid sinuses, right middle cranial fossa and right

Corresponding author.

M. TEO ET AL.

OPEN ACCESS OJMN

parapharyngeal space. He subsequently underw en t a joint

bifrontal craniotomy and transnasal approach for tumour

excision, and reconstruction of the anterior cranial fossa

floor. Postoperative recovery was initially hindered by

persistent CSF leak and pneumocephalus, where he un-

derwent a second procedure for the repair of the CSF fis-

tula using dural substitute (Neuro-Patch synthetic dural

substitute, Aesculap).

Subsequent tissue diagnosis confirmed high-grade ma-

lignant B-cell lymphoma. Further evaluation (including

CT chest, abdomen, pelvis, cerebrospinal fluid (CSF) ana-

lysis, serological investigations and bone marrow biopsy)

showed no evidence of immunosuppression, of systemic

disease, or of other tumours. He was then treated with

intravenous chemotherapy (cyclophosphamide, vincris-

tine, doxorubicin, prednisolone), prophylactic intrathecal

methotrexate and autologous peripheral blood stem cell

transplant. He made an excellent recovery with almost

complete resolution of his symptoms. He was followed

up regularly for 11 years with no evidence of recurrence.

At 12 years he reported nasal congestion. Surveillance

MRI showed a mass lesion with contrast enhancement in

the nasopharynx with suprasellar extension (Figure 1).

Transnasal biopsy revealed a fibrotic mass secondary to

previous dural graft, which was not infected, and did not

show any signs of integration with normal tissues. The

dural graft was removed with no subsequent CSF leak

and complete resolution of the mass and his symptoms.

16 years after his initial diagnosis of skull base lympho-

ma, he eventually died of causes unrelated to his malig-

nancy.

Figure 1. Surveillance MRI (T1 weighted, contrast, sagittal

brain) showed a mass lesion with contrast enhancement in

the nasopharynx with suprasellar extension, suspicious of

recurrent disease.

3. Discussion

Lymphoma is characterized by abnormal proliferation of

lymphoreticular tissue occurring nodally as Hodgkin’s

lymphoma or extranodally as non-Hodgkin lymphoma

(NHL). CNS lymphoma may occur as a primary disease

or as part of disseminated disease. Although lymphomas

of the skull base have been classified previously as non-

CNS, or extracerebral lymphomas, recent reports describ-

ed these lesions as atypical intracerebral or primary CNS

lymphomas [4,6-8].

CNS lymphomas are uncommon, but the incidence is

increasing in both immunocompetent and immunocom-

promised patients [3]. Historically, the median age of di-

agnosis of primary CNS lymphoma is 55 years for im-

munocompetent patients, and 31 years for AIDS patients,

though they can occur in all age groups. The male to fe-

male ratio is 3:2. They usually occur in the basal ganglia,

corpus callosum, thalamus, or periventricular region [9].

As the incidence of CNS lymphoma increases, more aty-

pical presentations of this disease will be encountered.

The differential diagnosis of a destructive l esion in the

anterior skull base, as described in this case, includes

squamous cell carcinoma arising from the paranasal si-

nuses, chordoma, metastasis, intraosseous meningioma

and esthesioneuroblastoma. Lymphoma, although uncom-

mon, should be included in the differential diagnosis of

such neoplasms of the skull base.

Nearly 30 cases of skull base lymphoma have been

reported in the literature, with less than 20 reported in

adults (Table 1) [4-8,10-13]. Including our patient, adults

with skull base lymphoma have a median age of 62 years,

and vary from 37 to 83 years. The majority of the pa-

tients were male [10], with male to female ratio 5 :3. The

interval from presentation to diagnosis varied from just

over a week to nearly a year. Those with cranial nerve

involvement often seek medical attention sooner, as com-

pared to other patients who present late due to raised in-

tracranial pressure symptoms from mass effect.

The initial role of surgery in the management of pri-

mary CNS lymphoma is usually tumour biopsy for tissue

diagnosis: the role of gross total resection is still contro-

versial, with reports of patients with long-term survival

after complete resection of a solitary brain lesion [14,15].

As seen in Table 1, nine patients with skull base lym-

phoma had tumour biopsy for diagnostic purposes only,

and six patients had partial resection of their lesions. We

present the only case of gross total resection (curative) of

skull base lymphoma with 14 years’ survival. Gross total

resection was carried out as a primary procedure instead

of biopsy, in view of this patient’s young age and our un-

derstanding of anterior skull base lesions at the time of

his initial presentation over a decade ago, extensive skull

base surgery was considered the best option for his sur-

vival.

M. TEO ET AL.

OPEN ACCESS OJMN

Table 1. Published liter ature on skull base primary lymphom a published in adult populati on. Abbreviations: N.A.: not avai-

lable, SB: sphe noid bone, ES: ethmoid si nus, CS: cavernous sinus, RP: retropharyngeal space, AF: anterior fossa, MF: mid-

dle fossa, PF: posterior fossa, Bx: biopsy, PR: partial resection, GTR: gross total resection, RT: radiotherapy, CT: chemo-

therapy, iv: intravenous, it: intrathecal.

Age Sex Symptom

Interval Pathology Involvement

Site Surgery Treatment Outcome Follow Up

Oyama et al. 1992 [10] 62 M 4 months B cell lymphoma SB, CS PR RT, CT Alive (R) 5 months

Shibata et al. 1992 [11] 74 F 10 days B cell lymphoma SB, ES, CS PR RT, CT Died 14 months

Tanaka et al. 1994 [12] 46 F 3 weeks B cell lymphoma SB, CS, PR RT, CT Died 10 months

Roman-Goldstein et al.

1998 [7] 37 M N.A. lymphoma ?type CS Bx RT, CT Alive 4 year s

62 M N.A. lymphoma ?type CS, SB, ES Bx CT, RT Died 18 months

51 F N.A. lymphoma ?type CS PR CT N.A. N.A.

69 M N.A. lymphoma ?type MF Bx CT N.A. N.A.

Jaiswal et al. 2000 [8] 40 M 6 months B cell lymphoma PF, CS PR CT, RT Alive 3 months

Dare et al. 2001 [5] 64 F 3 months B cell lymphoma SB, ES, CS, MF Bx RT, CT

(it, iv) Alive 1 year

71 M N.A. B cell lymphoma SB, ES, CS, AF Bx RT N.A. N.A.

73 M N.A. B cell lymphoma ES, AF Bx RT Died 20 months

83 M N.A. B cell lymphoma ES, AF Bx RT Alive 3 months

Tsai et al. 2002 [13] 60 F 2 months B cell lymphoma SB PR CT N.A. N.A.

Jung et al. 2004 [6] 56 F 2 months B cell lymphoma SB, CS Bx CT (iv, it) N.A. N.A.

Hans et al. 2005 [4] 64 M 9 months B cell lymphoma SB, ES Bx CT (iv), RT Alive 1 year

Teo et al. 2013 49 M 3 weeks B cell lymphoma SB, ES, MF, RP GTR CT (iv, it) Died 16 years

The options for treating primary CNS lymphoma have

evolved significantly during the last few decades. Radio-

therapy and chemotherapy, in isolation or in combination,

have significantly increased the survival of many immu-

nocompetent patients with primary CNS lymphoma. Ear-

ly reports indicated an increase in median survival from

3.3 months to 15.2 months for patients receiving radio-

therapy, but with a 5-year survival after treatment of only

7% [16,17]. Patients receiving concomitant chemothe-

rapy and radiotherapy live longer than those receiving ra-

diotherapy alone, with median survival ranges from 16 to

44.5 months; and 5-year survival rate of 20% - 30% [18-

20]. For those with skull base lymphomas, eight patients

had chemoradiotherapy, five patients had chemotherapy

alone, and three patients had radiotherapy in isolation.

Survival data for patients with skull base lymphoma

was available for eleven patients. Four died between 14

months and 20 months. Seven patients were still alive,

with our patient having the longest follow up at 14 years.

One patient represented at 5 months with recurrent dis-

ease, and had further chemoradiotherapy.

As shown in this case, long-term remission can be

achieved by aggressive treatment of skull base lympho-

ma. This patient had a combined transnasal and subfron-

tal operation for aggressive tumour resection due to both

intra- and extracranial tumour components. One of the

complicating factors with such aggressive surgical resec-

tion of the anterior cranial fo ssa floor is CSF leak, as was

encountered in our patient.

The repair of large dural defects is a problem faced by

many neurosurgeons dealing with anterior skull base

lesions. Various autografts, allograf ts, and artificial dural

substitutes have been used for some time. Many synthetic

plastics and fibres have been used; silastic membranes

are some of the more frequently used dural substitutes.

This is because they have many advantages for dural re-

pairs: the material is inexpensive, is easily fashioned to

size and shape, carries no risk of transmissible disease,

and minimally reacts with adjacent neural tissue s .

However, the use of silastic dural grafts is not risk free.

In 1974 the first case of haemorrhage associated with the

used of silastic dural substitute was reported [21], and se-

veral reports followed. Cervical myelopathy due to in-

folding of the dural graft [22], and spinal cord compres-

sion [23] due to formation of connective tissue around

the silastic grafts were also rep orted.

Delayed complications occurring after 10 years of si-

lastic dural graft used for cranial surgery were reported in

8 previous cases (Table 2) [24-30]. Among these cases,

silastic graft was used in four cases for supratentorial du-

ral repairs, all of which had previous excision of menin-

gioma and overlying dura. When patients presented with

neurological symptoms over a decade later, imaging

showed a mass lesion at the surgical site, with recurrent

M. TEO ET AL.

OPEN ACCESS OJMN

Table 2. Published literature of delayed complications encountered in patients with intracranial use of silastic dural graft.

Abbreviations: PF: posterior fossa, F: frontal, F/T: frontotemporal, P/O: parietooccipital, SAH: subarachnoid haemorrhage.

Age Sex Symptom

Interval (Years) Pathology Involvement Site Surgery

Simpson et al. 1984 [29] 15 M 10 Medulloblastoma PF Fibrotic mass & SAH

Simpson et al. 1984 [29] 22 M 10 Cerebellar astrocytoma PF Fibrotic mass & SAH

Gondo et al. 1991 [27] 14 F 11 Trauma PF Fibrotic haemorrhagic mass

Awwad et al. 1991 [25] 59 M 12 Meningioma F Fibrotic haemorrhagic mass

Berrington 1992 [26] 65 F 13 Meningioma F/T Fibrotic haemorrhagic mass

Ohbayashi et al. 1994 [30] 63 F 20 Meningioma P/O Fibrotic haemorrhagic mass

Siccardi et al. 1995 [28] 53 M 10 Meningioma F Fibrotic haemorrhagic mass

Robertson et al. 1997 [24] 31 F 14 Chiari PF Fibrotic haemorrhagic mass

Teo et al. 2013 61 M 12 Lymphoma Skull base Fibrotic mass

meningioma being the main differential diagnosis. Intra-

operatively, all four cases were found to have a fibrotic

haemorrhagic mass associated with the silastic dural graft,

and subsequent removal was performed with good post-

operative outcome.

The other four patients had silastic dural graft used for

posterior fossa repair. The patients presented with head-

ache and vomiting: two patients had cerebellar fibrotic

haemorrhagic mass, and the two others had SAH asso-

ciated with silastic dural graf t, to account for their symp-

toms. All patients subsequently had removal of the silas-

tic dural patch.

We, hereby, report the first case of delayed fibrotic

mass associated with synthetic dural graft mimicking tu-

mour recurrence when used in used in skull base recon-

struction.

Previous reports have demonstrated that local tissue

reaction can lead to the formation of a connective tissue

capsule or neomembrane around the silastic graft [31,32].

Due to the inert nature of the silastic g raft, adh esions are

lacking between the dural substitute and the neomem-

brane, creating a potential space. Excessive proliferation

of dural border cells and prominent sprouting of the de-

licate capillary network are two characteristics ascribed

to these neomembranes [33,34]. These sprouting capilla-

ries are fragile and can bleed easily. In addition, there is

little support from the surrounding fibrous tissue, making

these membranes susceptible to movement, so shearing

forces may be generated. Micro or macro haemorrhages

can therefore occur into the potential space between the

dural graft and the neomembrane.

The presence of neocapillaries around the silastic graft

would explain the enhancing nature of such a lesion in

our patient, and mimicking a recurrent tumour. Since our

patient was symptomatic, and with radiological suspicion

of tumour recurrence, he was brought back to theatre.

During surgical exploration, the dural graft was clearly

not incorporated into the anterior skull base and was eas-

ily removed. Despite the removal of the dural substitute,

no CSF leak was encoun tered. Therefore, the silastic graft

appears to have provided a platform for the reconstitution

of the anterior cranial fossa floor, despite its failure to

incorporate into the supporting structure. His symptoms

of nasal congestion resolved postoperatively with subse-

quent follow up imaging showing no evidence of mass

lesion.

Another consideration for this case was whether or not

we could have performed a tissue biopsy during initial

surgery, to make the diagnosis of skull base CNS lym-

phoma in order to commence the patient on chemoradio-

therapy, therefore avoiding CSF leak, anterior skull base

repair, and the subsequent delayed dural graft induced

complication. As mentioned earlier, in view of his young

age and our understanding of anterior skull base lesions

at the time of his initial presentation over a decade ago,

extensive skull base surgery was considered the best op-

tion for his survival. Although it is impossible to draw

definite conclusions from a single case, we believe that

gross total resection of the tumour has a significant role

for the long recurrence-free survival of this patient. With-

out long-term patient survival, we would not have en-

countered the subsequent delayed complications as seen

in this case.

4. Conclusions

With an increasing incidence of CNS lymphoma, more

atypical presentations are reported. It is therefore very

important to include lymphoma in the differential diag-

nosis of skull base lesions. The role of surgery in skull

base lymphoma is controversial, and we present a patient

who had curative gross total resection of the lesion and

chemotherapy.

We also report the first case of delayed complications

associated with neuro-patch graft used in skull base re-

construction. With the increasing types of synthetic dural

substitute available on the market nowadays, we have to

M. TEO ET AL.

OPEN ACCESS OJMN

be vigilant of the potential complications that could be

associated, even those occurring over a decade after in-

sertion. Though tumour recurrence remains the main con-

cern for patients with symptoms or radiological suspicion

on subsequent follow-up, this case highlights another pos-

sibility that we should keep in mind.

REFERENCES

[1] T. L. Helle, R. H. Britt and T. V. Colby, “Primary Lym-

phoma of the Central Nervous System: Clinopathological

Study of Experience at Stanford,” Journal of Neurosur-

gery, Vol. 60, No. 1, 1984, pp. 94-103.

http://dx.doi.org/10.3171/jns.1984.60.1.0094

[2] F. H. Hochberg and D. C. Miller, “Primary Central Ner-

vous System Lymphoma,” Journal of Neurosurgery, Vol.

68, No. 6, 1988, pp. 835-853.

http://dx.doi.org/10.3171/jns.1988.68.6.0835

[3] N. L. Eby, S. Guffer man, C . M. Fla nnel ly , S. C. Schol d, F.

S. Vogel and P. C. Burger, “Increasing Incidence of Pri-

mary Brain Lymphoma in the US,” Cancer, Vol. 62, No.

11, 1988, pp. 2461-2465.

http://dx.doi.org/10.1002/1097-0142(19881201)62:11<24

61::AID-CNCR2820621135>3.0.CO;2-M

[4] F. J. Hans, M. H. Reinges, K. Nolte, P. Reipke and T.

Krings, “Primary Lymphoma of the Skull Base,” Neuro-

radiology, Vol. 47, No. 7, 2005, pp. 539-542.

http://dx.doi.org/10.1007/s00234-005-1394-4

[5] O. Dare, R. V. Datta, T. R. Loree, W. L. Hicks and W.

Grand, “Sinonasal Non-Hodgkin’s Lymphom a with Skull

Base Involvement,” Skull Base, Vol. 11, No. 2, 2001, pp.

129-135. http://dx.doi.org/10.1055/s-2001-14433

[6] S. Jung, M. Zimmermann and V. Seifert, “Clivus Lym-

phoma,” Acta Neurochirurgica, Vol. 146, No. 5, 2004, pp.

533-534. http://dx.doi.org/10.1007/s00701-004-0244-1

[7] S. M. Roman-Goldst ein, A. Jones, J. B. Delashaw, S. Mc-

Menomey and E. A. Neuwelt, “Atypical Central Nervous

System Lymphoma at the Cranial Base: Report of Four

Cases,” Neurosurgery, Vol. 43, No. 3, 1998, pp. 613-615.

http://dx.doi.org/10.1097/00006123-199809000-00119

[8] K. Jaiswal, M. Tr ipathi, P. S. Cha ndra, M. C. Sharma a nd

A. K. Maha-patra, “An Unusual Case of Primary Lym-

phoma of the Skull Base Extending from Cerebellopon-

tine Angle to Cavernous Sinus and Orbit. A Case Report,”

Journal Neurosurg Science, Vol. 44, No. 3, 2000, pp.

145-148.

[9] J. M. Henry, R. R. Heff ner, S. H. Diiard, K. M. Earle and

R. L. Davis, “Primary Malignant Lymphomas of the Cen-

tral Nervous System,” Cancer, Vol. 34, No. 4, 1974, pp.

1293-1302.

http://dx.doi.org/10.1002/1097-0142(197410)34:4<1293::

AID-CNCR2820340441>3.0.CO;2-P

[10] H. Oyama, M. Nagane, S. Shibui, K. Nomura and K. Mu-

kai, “Skull Base Malignant Lymphoma: A Case Report

and Review of the Literature,” Japanese Journal of Cli-

nical Oncology, Vol. 22, No. 2, 1992, pp. 131-135.

[11] M. Shibata, M. Shimoda and O. Sato, “A Case of Bilate-

ral Panopthalmoplegia Caused by Paranasal Malignant

Lymphoma Extending into the Skull Base,” No Shinkei

Geka, Vol. 20, No. 6, 1992, pp. 717-721.

[12] S. Tanaka, H. Nihei, S. Manaka and T. Hori, “A Case of

Malignant Lymphoma in the Skull Base,” No Shinkei

Geka, Vol. 22, No. 1, 1994, pp. 73-78.

[13] V. W. Tsai, L. Ryba k, J. Espinosa, M. J. Kuhn, O. W. Ka-

mel, F. Mathews and F. R. Glatz, “Primary B-Cell Lym-

phoma of the Clivus: Case Report,” Surgical Neurology,

Vol. 58, No. 3-4, 2002, pp. 246-250.

http://dx.doi.org/10.1016/S0090-3019(02)00845-5

[14] K. G. Davies, G. C. Cole and R. D. Weeks, “Twenty Year

Survival Following Excision of Primary CNS Lymphoma

without Radiation Therapy: Case Report,” British Journal

of Neurosurgery, Vol. 8, N o. 4, 1994, pp. 487-491.

http://dx.doi.org/10.3109/02688699408995120

[15] W. Sonstein, K. Tabaddor and J. F. Ilena, “Solitary Pri-

mary CNS Lymphoma: Long Term Survival Following

Total Re-section,” Medical Oncology, Vol. 15, No. 1,

1998, pp. 61-65. http://dx.doi.org/10.1007/BF02787347

[16] S. A. Leibel and G. E. Sheline, “Radiation Therapy for

Neoplasms of the Brain,” Journal of Neurosurgery, Vol.

66, No. 1, 1987, pp. 1-22.

http://dx.doi.org/10.3171/jns.1987.66.1.0001

[17] D. F. Nelson, K. L. Martz, H. Bonner H, J. S. Nelson, J.

Newall, H. D. Kerman, J. W. Thomson and K. J. Murray,

“Non-Hodgkin’s Lymphoma of the Brain: Can High Dose,

Large Volume Radiation Therapy Improve Survival? Re-

port on a Prospective Trial by the Radiation Therapy On-

colgy Group (RTOG): RTOG 8315,” International Jour-

nal of Radiation Oncology, Biology, Physics, Vol. 23, No.

1, 1992, pp. 9-17.

http://dx.doi.org/10.1016/0360-3016(92)90538-S

[18] J. Y. Blay, T. Conroy, C. Chevreau, A. Thyss, N. Quesnel,

H. Eghbali, R. Bouabdallah, B. Coiffier, J. P. Wagner, A.

Le Mevel, D. Dramais-Marcel, “High-Dose Methotrexate

for the Treatment of Primary Cerebral Lymphomas: An

Analysis of Survival and Late Neurological Toxicity in a

Retrospective Series,” Journal of Clinical Oncology, Vol.

16, No. 3, 1998, pp. 864-871.

[19] M. Brada, D. Dearnaley, A. Horwich and H. J. G. Bloom,

“Management of Primary Cerebral Lymphoma with Ini-

tial Chemotherapy: Preliminary Results and Comparison

with Patients Treated with Radiotherapy Alone,” Interna-

tional Journal Radiation, Oncology, Biology, Physics,

Vol. 18, No. 4, 1990, pp. 787-792.

http://dx.doi.org/10.1016/0360-3016(90)90398-4

[20] L. M. DeAngelis, J. Yahalom, H. Thaler and U. Kher,

“Combined Modality Therapy for Primary CNS Lympho-

ma,” Journal of Clinical Oncology, Vol. 10, No. 4, 1992,

pp. 635-643.

[21] T. Banerjee, J. N. Merghe r and W. E. Hunt, “Unusual Com-

plications with use of Silastic Dural Substitute,” The Ame-

rican Surgeon, Vol. 40, No. 7, 1974, pp. 434-437.

[22] W. S. Fisher and E. G. Six, “Cervical Myelopathy from

Dural Substitute,” Neurosurgery, Vol. 13, No. 6, 1983, pp.

715-716.

http://dx.doi.org/10.1227/00006123-198312000-00020

[23] J. T. Keller, C. M. Ongkiko, M. C. Saunders, F. H. May-

field and S. B. Dunsker, “Repair of Spinal Defects: An

M. TEO ET AL.

OPEN ACCESS OJMN

Experimental Study,” Journal of Neurosurgery, Vol. 60,

No. 5, 1984, pp. 1022-1028.

http://dx.doi.org/10.3171/jns.1984.60.5.1022

[24] S. Robertson and A. Menezes, “Hemorrhagic Complica-

tions in Association with Silastic Dural Substitute: Pedi-

atric and Adult Case Reports with a Review of the Lit-

erature,” Neurosurgery, Vol. 40, No. 1, 1997, pp. 201-

206.

[25] E. E. Awwad, K. R. Smith Jr., D. S. Martin and A. Mane-

palli A, “Unusual Hemorrhage with Use of Synthetic Du-

ral Substitute: MR findings,” Journal of Computer Assis-

ted Tomography, Vol. 15, No. 4, 1991, pp. 618-620.

http://dx.doi.org/10.1097/00004728-199107000-00017

[26] N. R. Berrington, “Acute Extradural Hematoma Associat-

ed with Silastic Dural Substitute: Case Report,” Surgical

Neurology, Vol. 38, No. 6, 1992, pp. 469-470.

http://dx.doi.org/10.1016/0090-3019(92)90117-6

[27] G. Gondo, S. Nakayama, Y. Mochimatsu, F. Nakajima and

A. Hasegawa, “Posterior Fossa Hemorrhage 11 Years af-

ter the Use of Silastic Dural Substitute: Case Report,” No

Shinkei Geka, Vol. 19, No. 1, 1991, pp. 59-62.

[28] D. Siccardi and A. Ventimiglia, “Fibrotic-Haemorrhagic

Reaction to Synthetic Dural Substitute,” Acta Neurochi-

rurgica, Vol. 132, No. 1-3, 1995, pp. 148-149.

http://dx.doi.org/10.1007/BF01404864

[29] D. Simpson and A. Robson, “Recurrent Subarachnoid

Bleeding in Association with Dural Substitute: Report of

Three Cases,” Journal of Neurosurgery, Vol. 60, No. 2,

1984, pp. 408-409.

http://dx.doi.org/10.3171/jns.1984.60.2.0408

[30] N. Ohbayashi, T. Inagawa, Y. Katoh, K. Kumano, R. Na -

gasako and H. Hada, “Complication of Silastic Dural Sub-

stitute 20 Years after Dural Plasty,” Surgical Neurology,

Vol. 41, No. 4, 1994, pp. 338-341.

http://dx.doi.org/10.1016/0090-3019(94)90187-2

[31] R. Cohen, S. Aleksic and J. Ransohoff, “Inflamm atory Re-

action to Synthetic Dural Substitute: Case Report,” Jour-

nal of Neurosurgery, Vol. 70, No. 4, 1989, pp. 633-635.

http://dx.doi.org/10.3171/jns.1989.70.4.0633

[32] R. L. Friede and W. Schachenmayr, “The Origin of Sub-

dural Neomembranes: II—Fine Structures of Neomem-

branes,” pp. 69-84.

[33] W. Schachenmayr and R. L. Friede, “The Origin of Sub-

dural Neomembranes: I—Fine Structures of the Dura-ara-

chnoid Interface in Man,” American Journal of Pathology,

Vol. 92, No. 1, 1978, pp. 53-68.

[34] G. I. Schoefl, “Studies in Inflammation: III—Growing Ca-

pillaries: Their Structure and Permeability,” Virchows Ar-

chiv für pathologische Anatomie und Physiologie und für

klinische Medizin, Vol. 337, No. 2, 1963, pp. 97-141.

http://dx.doi.org/10.1007/BF00963592