- Email: [email protected]
Endoscopic treatment of spinal epidural hematoma
460
Mackenzie et al/Steel et al
11. MarcelisJ, Silberstein SD. Spontaneouslow CSF pressure headache. Headache 1990; 30: 192-196. 12. RandoTA, Fishman RA. Spontaneousintracranial hypotension:report of two cases and review of the literature. Neurology 1992; 42: 481-487. 13. PannnlloSC, Reich JB, Krol G, Deck MDF, Posner YB.MRI changes in intracranial hypotension.Neurology 1993; 43: 919-926. 14. HortonJC, Fishman RA. Neurovisual findings in the syndrome of spontaneous intracranial hypotensionfrom dural cerebrospinalfluid leak. Ophthalmology 1994; 101: 244-251. 15. MokriB, Patisi JE, ScheithanerBW, Piepgras DG, Miller GM. Meningeal biopsy in intracranialhypotension: meningeal enhancementon MRI. Neurology 1995; 45: 1801-1807. 16. Renowden SA, Gregory R, Hyman N, Hilton-JonesD. Spontaneous intracradial hypotension.J Neurol Nenrosurg Psychiatry 1995; 59: 511-515. 17. Davenport RJ, Chataway HJS, Warlow CR Spontaneousintracranial hypotensionfrom a CSF leak in a patient with Marfan's syndrome.J Neurol Neurosurg Psychiatry 1995; 59: 516-519. 18. Schievink WI, Meyer FB, Atldnson JLD, Mokri B. Spontaneousspinal cerebrospinaifluid leaks and intracraniaihypotension.J Neurosurg 1996; 84: 598--605. 19. PaulsonGW, Klawans HL Jr. Benign orgasmic cephalgia. Headache 1994; 13: 181-187. 20. Schi.evinkWI, Reimer R, Folger WN. Surgical treatment of spontaneous intracranial hypotension associated with a spinal arachnoid diverticulum. J Neurosurg 1994; 80: 736-739. 21. Schreiber F, Haddad B. Lumbar & sacral cysts causing pain. J Neurosurg 1951; 8: 504-509. 22. TarlovIM. Spinal perineural and meningeal cysts. J Neurol Neurosurg Psychiatry 1970; 33: 833-843. 23. LakePA, Minclder J, Scanlan RL. Spinal epidural cyst: theories of pathogenesis. J Neurosurg 1974; 40: 774-778. 24. SableSG, Ramadan NM. Meningeal enhancement & low CSF pressure headache. An MRI study. Cephalgia 1991; 11: 275-26. 25. HochmanMS, Naidich TE Kobetz SA, Fernandez-MaitinA. Spontaneous intracranial hypotension with pachymeningealenhancementon MRI. Neurology 1992; 42: 1628-1630. 26. Fishman RA, Dillon WE Dural enhancementand cerebral displacement secondary to intracranialhypotension.Neurology 1993; 43: 609-611. 27. MokriB, Krueger BR, Miller GM, Piepgras DG. Meningeal gadolinium enhancementin low-pressureheadaches. J Neuroimaging 1993; 3: 11-15. 28. Good DC, Ghobrial M. Pathologic changes associated with intracranial hypotension & meningeal enhancementon MRI. Neurology 1993; 43: 2698-2700. 29. VandamLD, Dripps RD. Long-term follow-up of patients who received 10 098 spinal anaesthetics.JAMA 1965; 161: 586-591. 30. Abouleish E, de la Vega S, Blendinger t, Tic T-O. Long-term follow-up of epidural blood patch. Anesth Analg 1975; 54: 459-463.
This technique may be used for approaching intraspinal pathology in high risk patients where extensive exposure may be contraindicated. Journal of Clinical Neuroscience (1998)5(4), 460-463 © HarcourtBrace& Co. Ltd 1998
Keywords: ankylosing spondylitis, cervical spine, spinal epidural hematoma, spinal endoscopy Received 22 October 1996 Accepted 3 December 1997 Correspondence to: Edmund H. Frank, Tel: 1 503 494 8070, Fax: 1 503 494
7161
INTRODUCTION Spinal epidural hematomas (SEH) are rare, but well described, lesions. They may be spontaneous or occur following trauma. Twenty cases o f SEH occurring following trauma in patients with ankylosing spondylitis (AS) have been reported.l-12 The mortality and morbidity o f spinal trauma in patients with AS is high. In the 20 reported cases o f SEH associated with AS, nine died and only eight made a good recovery. ~ Cardiorespiratory complications accounted for 50% o f the deaths following spine trauma in such patients. Our patient suffered rapidly worsening cardiac failure immediately following his injury. Systemic anticoagulation was necessary for the investigation and m a n a g e m e n t o f his coronary disease. Systemic anticoagulation is contraindicated in the face o f a pre-existing SEH and/or an extensive laminectomy. Most surgeons advocate withholding anticoagulants for at least 2 4 4 8 h following spinal procedures. We report the use o f a malleable spinal endoscope via a limited cervical laminotomy to remove the h e m a t o m a in an effort to reduce the risk o f postoperative h e m a t o m a formation. Spinal endoscopy is being increasingly used in an effort to reduce the morbidity associated with extensive approaches to the spine. The majority o f uses reported to date involve anterior approaches for thoracic pathology.i315 This case is the first reported use o f the endoscope for a SEH. The etiology and m a n a g e m e n t o f SEH is reviewed and potential applications for this technique are discussed.
CASE R E P O R T
Endoscopic treatment of spinal epidural hematoma Timothy R. Steel FRACS,Jordi X. Kellogg MD, Todd A. Kuether MD, Jacques Favre MD, Edmund H. Frank MD Oregon Health Sciences University, Division of Neurosurgery,, L-472, 3181 SW Sam Jackson Park Road, Portland, OR 97201, USA
Summary We report the use of a spinal endoscope via a limited cervical laminotomy to evacuate a spinal epidural hematoma. The patient was a 75-year-old male with a 32-year history of ankylosing spondylitis. Following a low speed motor vehicle accident he developed a cervicothoracic epidural hematoma without an associated fracture. Despite a rapidly improving neurological state, his rapidly deteriorating cardiorespiratory state required systemic anticoagulaUon necessitating decompression of the hematoma. The hematoma was successfully removed via a limited C6 and C7 laminotomy using the endoscope and a malleable disposable aspirator. We conclude that epidural hematomas can be readily evacuated via endoscopic techniques without extensive laminectomy. Joumal of Clinical Neuroscience (1998) 5(4)
A 74-year-old male with a 32-year history o f AS was brought to our emergency room following a low speed roll-over motor vehicle accident. H e suffered no head injury or loss o f consciousness. On arrival he was unable to lie flat on the spine board due to his 40% kyphosis and he complained o f severe pain in his cervicothoracic region, but was neurologically intact. Within 15 rain o f admission he complained o f rapidly developing lower limb weakness and reduced sensation b e l o w his nipple line. On examination he had 2/5 strength in his lower limbs and reduced sensation to pin prick below his axillae. Joint position sense at his toes was absent. X-rays o f his cervical and thoracic spine revealed marked ankylosis but no fracture was seen. Computed tomography (CT) scans o f his C 4 - T 4 region with sagittal reconstruction showed the kyphosis but no fracture. Magnetic resonance image (MRI) scanning o f his cervicothoracic region was performed demonstrating a lesion lying dorsal to the spinal cord extending from C4 to T2 with significant compression o f the spinal cord (Figs. 1 & 2). The lesion was o f biconvex shape tapering superiorly and inferiorly. O n T l - w e i g h t e d images the lesion was isointense with the spinal cord and on T2-weighted images the lesion was heterogeneous and hypointense to the spinal cord; this was consistent with acute epidural hematoma. 4,t6 No evidence o f fracture was seen. At the time o f his neurological deterioration he was started on intravenous methylprednisolone as per the spinal cord injury
© Harcourt Brace & Co. Ltd 1998
Endoscopic treatment of SEHs 461
Fig. 3 Intraoperative view of the SEH (arrow) and thecal sac (star) via the endoscope.
Fig, 1 Sagittal T2-weighted MRI scan showing the lesion (hypointense to the spinal cord) posterior to and causing deviation of the spinal cord.
on the left side at the inferior border of C6 and the superior aspect of C7 exposing a bony opening of 20 mm diameter. After removal of the ligamentum, the SEH was encountered (Fig. 3). The clot itself was thick and tenacious. After removing the hematoma directly below the laminotomy the pulsatile irrigation of the endoscope combined with a malleable suction device was used to gently wash out the remainder of the clot, just as with an acute intracranial subdural hematoma. No acute bleeding site was encountered. The thecal sac was rapidly decompressed and returned to its normal position in the canal; using the endoscope adequate decompression in a rostral and caudal direction was ensured. Postoperatively the patient remained profoundly hypotensive and he was not extubated. An intra-aortic balloon pump was placed in the intensive care unit. This failed to significantly increase blood pressure. After discussion with the cardiology team and the patient's relatives, the patient was taken off pressor support and died shortly after.
DISCUSSION
Fig. 2 Axial T2-weighted MRI scan showing deviation of the spinal cord by the SEH.
protocol; (bolus dose 30 mg/kg followed by 5.4 mg/kg/h over 23 h). Within 2 h of initiation of the steroids his neurological examination had returned to normal apart from mild weakness of hip flexion (4/5); his sensation including joint position sense at the toes had returned to normal. He was admitted to the intensive care unit, while surgical decompression was planned. Whilst awaiting surgery the patient developed unstable angina associated with hypotensive episodes requiring pressor support. Urgent coronary angiography with possible angioplasty was planned followed by systemic heparinization; however, this could not be initiated until evacuation of the hematoma was carried out. At surgery we planned to expose C6 and C7 (the level of maximal depth of the hematoma) and perform a limited laminotomy only and evacuate the hematoma with the use of the spinal endoscope (Clams Murphy Scope, model 2125-161, Clarus Medical Minneapolis, MN, USA) and an angled disposable sucker. If we were not able to access the clot more extensive laminectomies were to be performed. Because of the patient's poor cardiorespiratory state we were unable to position the patient prone and elected a right lateral decubitus position. The hematoma was approached via a 6 cm incision over the spinous processes of C6 and C7. A bilateral muscle takedown was performed. Laminotomies were performed © Harcourt Brace & Co. Ltd 1998
More than 250 cases of SEH have been reported in the literature. 4,8,1~2° They may occur either spontaneously or following trauma and typically occur dorsal to the thecal sac in the cervicothoracic region. Thoracic and lumbar SEH have also been reported.IV'21 Spontaneous hematomas can be idiopathic, in which no etiology is found, and those arising secondary to some predisposing factor? 2 Anticoagulation, platelet dysfunction, neoplasms, vascular malformations, Paget's disease, lupus, hypertension and rheumatoid arthritis have all been reported as the underlying cause of SEH. 17'22,23 Spontaneous SEH may occur at rest or following trivial activities which may raise intraspinal venous pressure such as bending, straining or coughingJ 8,22The site of bleeding in such cases is assumed by many to be rupture of the valveless epidural veins (Batson's plexus) due to elevation of venous pressure. 18,19,24 Bleeding from epidural arteries has also been postulated as the source which may account for the more rapid neurological deterioration seen in some patients. 19,25 Traumatic SEH are uncommon in adults. 26 Almost half of reported cases have occurred in neonates and children. If a fracture occurs the hematoma may arise from exposed bone surfaces directly into the spinal canal, or from disruption of the vessels surrounding the thecal sac. Intraspinal epidural hematoma of definite traumatic origin occurs without spinal fracture in about 50% of cases particularly in the pediatric age group because of greater elasticity of the vertebral column. 4,26 The association of SEH and AS is well documented with 20 cases reported as of 1996Y 2 Eighteen of these have been in
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association with spinal fractures. 1,4,11,26 Two cases have been reported previously of hematoma formation without fracture. 2,6 In these cases such as ours, it has been assumed that movement of the spinal cord within the rigid spinal canal causes disruption to the epidural veins resulting in hemorrhage. Although no definitive bleeding site was encountered at operation we presume this to be the mechanism for the hematoma in our patient. The recommended management of SEH has been emergent decompressive laminectomy as soon as the diagnosis is reached. 4,6,11,18,19 In the pre-MRI era the diagnosis of SEH was rarely made in the absence of profound neurological deficits. Foo et aF 7 demonstrated in their review of 158 cases of spontaneous spinal hematoma that postoperative neurological recovery following surgery is proportionate to the severity of the sensorimotor impairment prior to intervention. Analysis of the literature reveals 15 cases of spontaneous SEH that have been successfully treated without surgery.16,19,2°,27 In recent reports 19,2°'27this has been due to rapid improvement or even early resolution of neurological deficits. Unfortunately only one of these reports indicates if methylprednisolone was administered; this may have accounted for the early and dramatic improvements made by our patient. No patient with an antemortem diagnosis of traumatic SEH has been successfully treated conservatively. There are no reports of SEH treated without decompression in patients with AS. In the case reported by Hissa, 6 myelography and subsequent surgery was delayed for 6 days; the patient's paraparesis improved following the administration of intravenous steroids on admission; however, deterioration subsequently occurred. Following decompression, the patient's deficits (spasticity and atonic bladder) gradually resolved over 6-8 months. This patient was not diagnosed with a thoracic hematoma initially as his severe kyphosis precluded his thoracic region entering the gantry of the MRI scanner. 6 AS patients have a far higher mortality and morbidity than the general population following spinal trauma." Reported mortality rates are commonly in the 30-35% range for AS patients with cervical spine injury and higher for those with spinal cord damage; l this is twice the mortality reported in patients without AS. The high incidence of early cardiorespiratory complications following spine injury due to systemic manifestations of the disease, such as rigid chest walls, pulmonary fibrosis and vascular degeneration, has been noted by many authors. 1,9'11'28'29Of the 20 reported cases of SEH occurring with AS, nine patients died, all within 1 month of injury. In six of these the diagnosis was made only at post-mortem. Neurological recovery is also greater in those patients with traumatic SEH without AS or spinal fracture. 26 Only eight of the 20 reported patients in the literature made a full recovery. In the remaining three patients delayed laminectomy was performed which revealed the hematoma. Major persisting neurological deficits resulted in all of these cases. 2'3'5 Despite our patient's improving neurological status, the size and location of the hematoma made evacuation imperative. However, the impending use of systemic anticoagulation made the standard treatment of extensive laminectomy and evacuation more hazardous due to the risk of postoperative hematoma formation. At our institution we have been using a malleable spinal endoscope (the Clams Murphy Scope, model 2125-161). We have predominantly been using this for the assessment of decompression and pedicle screw location in the lumbar spine. This has allowed us to substantially reduce the amount of bone removal required yet still confirm under direct vision that no further neural compression exists. By utilizing the endoscope with a curved aspirator we were able to limit the bony opening to a 2.0 cm defect. The pulsatile irrigation from the endoscope itself was able to loosen the clot which was then easily aspirated by the curved
Joumal of Clinical Neuroscience (1998) 5(4)
suction device. Because the endoscope itself was malleable we were able to pass the instrument a considerable distance rostrally and caudally (3 levels) to ensure adequate decompression. Using direct vision we could assess the extent of the clot removal in all directions. By limiting our bony exposure yet being able to evacuate the hematoma we were able to reduce our operative time (less than 1 h), and reduce the risk of postoperative hematoma formation following an extensive laminectomy in an anticoagulated patient. Unfortunately we were not able to assess the benefits of our technique postoperatively either clinically or with imaging studies due to the patient's rapid cardiorespiratory decline. The patient's family requested no autopsy be performed, which precluded post-mortem assessment of the hematoma removal. Neuroendoscopy and other minimally invasive techniques are being increasingly used in neurosurgery to minimize morbidity and complications related to large exposure. 13-15 Although the outcome was disappointing, in this case it represents the first description of the use of endoscopy to evacuate a SEH. We have demonstrated the technical feasibility of this procedure in the cervical spine. In high risk patients with intraspinal pathology such as in our case, increased availability and experience with spinal endoscopy may lead to reduced morbidity and mortality in the future.
REFERENCES
1. BohlmanHH. Acute fracturesand dislocationsof the cervicalspine.J Bone Joint Surg (Am) 1979;61A(8): 1119-1192. 2. DetwilerKN, Loftus CM, Godersky.Managementof cervical spineinjuries in patientswith ankylosingspondylitis.J Neurosurg 1990;72: 210-215. 3. FastA, Parikh S, Matin EL. Spinefracturesin ankylosingspondylitis.Arch Phys Med Rehabil 1986;67: 595-597. 4. Garza-MercadoR. Traumaticextraduralhematomaof the cervicalspine. Neurosurgery 1982;24: 410-414. 5. GnisoliaA, Bell RL, PeltierZF. Fracturesand dislocationsof the spine complicatingankylosingspondylitis: a report of six cases. J Bone Joint Surg (AM) 1967;49A: 339-344. 6. HissaE, BoumphreyF, Bay J. Spinalepiduralhematomaand ankylosing spondylitis. Clin Orthop 1986; 208: 225-227. 7. LowreyJ. Spinalepiduralhematomas.Experienceswith three patients. J Neurosurg 1959; 16: 508-513. 8. PeckerJ, Javelet A, LeMennG. Spondyloarthitieankyloanteet paraplegiepar hematorachisextra-duraltraumatique.Press Med 1960; 68:183-184. 9. RowedDW. Managementof cervicalspinalcord injury in altkylosing spondylitis:the intervertebraidisc as a cause of cord compression. J Neurosurg 1992; 77: 241-246. 10. SchneiderRC, Cherry G, PantekM. The syndromeof acute centralcervical spinal cord injury.J Neurosurg 1954; i 1: 546-577. 11. SweetWH. Cervicothoracicankylosingspondylitis.In: SchmidekHH, Sweet WH (eds). OperativeNeurosurgicalTechniques,3rd Edn. Philadelphia:WB Sannders, 1995. 12. Ver BrugghenA. Extradural spinalhemorrhage.Ann Surg 1946; 123: 154-159. 13. McAfeePC, Regan JR, Zdeblicket al. The incidenceof complicationsin endoscopic anteriorthoracolumbarspinal reconstructivesurgery. Spine 1995; 20(4): 1624-1632. 14. KarakhanVB, FilimonovBA, GrigorganYA, MitropolskyVB. Operative spinal endoscopy: Stereotopographyand surgicalpossibilities.Aeta Neuroehir 1994; 61 (suppl): 108-114. 15. RosetuhalO, DickmanC, LorenzR, SonntagVKM. Thoracicdisc herniation: Early resultsafter surgicaltreatmentusing microsurgicalendoscopy(abstract). ScientificProgram, AANS Meeting,Minneapolis1996: 152. 16. BoukobzaM, GuichardJP, BoissonetM, GeorgeB, ReizineD, GelbertF, MerlandJJ. Spinalepiduralhematoma:report of 11 cases and reviewof the literature. Neuroradiology 1994; 36: 456459. 17. Foo D, RossierAB. Preoperativeneurologicalstatusin predictingsurgical outcome of spinal epiduralhematomas.Surg Neurol 1981; 15: 389401. 18. PearBL. Spinalepiduralhematoma.Am J Radiol 1972; 115(1): 155-164. 19. ClarkeDB, BertrandG, TampieriO. Spontaneousspinalepiduralhematoma causingparaplegia: Resolutionand recoverywithoutsurgicaldecompression. Neurosurgery 1992;30(1): 108-111. 20. WagnerS, ForstingM, HackeW. Spontaneousresolutionof a large spinal epidural hematoma:case report. Neurosurgery 1996;38(4): 816 818.
© Harcourt Brace & Co. Ltd 1998
Endoscopic treatment of SEHs/Pseudoaneurysm
21. GundryLR, HeithoffKB. Epiduralhematomaof the lumbarspine: 18 surgicallyconfirmedcases. Radiology 1993; 187:427~43i. 22. LobitzB, GrateI. Acute epiduralhematomaof the cervicalspine: an unusual cause of neck pain. SouthMed J 1995; 88(5): 580-582. 23. MannaJW, Bail MR, Lee KS, McWhorterJM. Spontaneousspinal epidural hematomacomplicatingPaget's disease of the spine. Spine 1995; 14(8): 900-902. 24. CooperDW. Spontaneousspinal epiduralhematoma. J Neurosurg 1967; 26: 343 346. 25. BeattyRM, WinstonKR. Spontaneouscervicalepiduralhematoma.A considerationof etiology.J Neurosurg 1984;61: 143-148. 26. Foo D, RossierAB. Post-traumaticspinal epiduralhematoma.Neurosurgery 1982; 1i: 25-32. 27. KatoS, Seki H, Koshu K. Acute cervicalspinalepiduralhematomawith spontaneousresolution:case report. Neurol Med Clair(Tokyo) 1994;34: 23 26. 28. Fox MW, OnfrioBM, KilgoreJE. Neurologicalcomplicationsof ankylosing spondylitis. J Neurosurg 1993;78: 871-878. 29. Hunter3",Dubo HIC. Spinal fracturescomplicatingankylosingspondylitis. A long term follow-up study. ArthritisRheum 1983; 26: 751-759.
Pseudoaneurysm of anterior communicating artery following transsphenoidal surgery for craniopharyngioma A. Malik 1 MD, M. Goyal I MD, N. K. Mishra 1 MD, A. Verma 2 ach~ S. G a i k w a d 1 MD, V. S. Mehta 2 ach Departments of 1Neuroradiologyand 2Neurosurgery,Neuroseiences Centre, All India Institute of Medical Sciences, New Delhi, India 110 029
Summary Fusiform dilatation and pseudoaneurysm formation in arteries of the circle of Willis has been reported as a complication following surgery for craniopharyngiomas through craniotomies. We present a case of anterior communicating artery pseudoaneurysm following transsphenoidal surgery for craniopharygioma in an adult.
463
CASE REPORT A 26-year-old male patient was admitted with complaints of painless, progressive visual deterioration of 2 months' duration. There were no symptoms to suggest raised intracranial tension or hormonal dysfunction. The visual acuity was 6/9 on the right side and 6/36 on the left side. Examination of the left eye revealed primary optic atrophy and left temporal field cut off. Fundus examination and field charting of the right eye were normal. The sella was enlarged on skull roentgenogram. Preoperative magnetic resonance imaging (MRI) scan of the brain (Fig. 1) showed a large sellar mass with suprasellar extension. The mass was isointense to water on Tl-weighted imaging (T1WI) (TR 450 ms, TE 20 ms, NEX 3) and hyperintense on T2WI (TR 2705 ms, TE 90 ms, NEX 1). There was no evidence of encasement of the arteries of circle of Willis. The optic chiasm was elevated and compressed. The rest of the brain parenchyma was normal. Sublabial transsphenoidal surgery was performed. The patient had profuse bleeding from the operative site soon after the cystic mass was punctured. The contents of the cystic mass simulated 'machine oil' with few cholesterol crystals, consistent with the usual contents of a craniopharyngioma cyst. The bleeding was controlled by packing the sellar floor; complete excision of the tumour was not possible. On the third postoperative day the patient developed profuse cerebrospinal fluid rhinorrhoea necessitating reexploration. At surgery, through the transsphenoidal route, a small hole was seen in the diaphragma which was sealed with autologous fascia and biological glue; the postoperative course was uneventful. Postoperative non-enhanced computed tomography (CT) scan (Fig. 2) showed hyperdensity, suggestive of blood, in the tumour bed with left anterior cerebral artery (ACA) territory infarct involving the left basifrontal lobe and left caudate head. Intraarterial DSA performed 2 days after surgery (Fig. 3) showed spasm in the A1 segment of left ACA with a small AComA pseudoaneurysm. No other arterial abnormality was noted. Repeat DSA study performed after 3 months revealed the pseudoaneurysm to have enlarged in size (Fig. 4). The patient underwent left pterional craniotomy. At surgery the A I segment of left ACA was seen dipping into the sella along with a large pseudoaneurysm of the A C o m A which was successfully clipped.
Journal of Clinical Neuroscience (1998)5(4), 463-464 © HarcourtBrace& Co. Ltd 1998
Keywords : craniopharyngioma, magnetic resonance imaging, pseudoaneurysm, angiography, transsphenoidal surgery Received 22 October 1996 Accepted 10 December 1996 Correspondence to: Dr M. Goyal, Tel: 91 11 6594418, Fax: 91 11 6862663, E-mail: [email protected]
DISCUSSION Craniopharyngiomas are slow growing benign tumours arising from remnants of Rathke's pouch; 70% are both suprasellar and intrasellar in location, while 20% are located solely in the suprasellar region. The most common obstacle to the total removal of craniopharyngioma is dense adhesion to major arteries, usually of the circle of Willis, and lack of a clear plane of cleavage.
INTRODUCTION We report a case of anterior communicating artery (AcomA) pseudoaneurysm in an adult following transsphenoidal decompression of a craniopharyngioma. Histologically benign craniopharyngiomas usually produce symptoms by their growth within the sella and suprasellar cistern. Complete excision, although desired, is not always accomplished due to adhesion of the tumour to the adventitia of vessels in the circle of Willis. 1Fusiform dilatation and pseudoaneurysm formation in the supraclinoid internal carotid artery has been reported as a complication of surgical resection of craniopharyngioma through craniotomies. 2-~ However, AComA pseudoaneurysm formation following transsphenoidal surgery for craniopharyngioma has not been previously reported.
© Harcourt Brace & Co. Ltd 1998
Fig. 1 Preoperative T2-weighted coronal (A) and sagittal (B) MR image (TR 2705 ms, TE 90 ms) showing a large sellar and suprasellar mass with parasellar extension. No arterial abnormality is seen in the circle of Willis.
Joumal of Clinical Neuroscience (1998) 5(4)
Mackenzie et al/Steel et al
11. MarcelisJ, Silberstein SD. Spontaneouslow CSF pressure headache. Headache 1990; 30: 192-196. 12. RandoTA, Fishman RA. Spontaneousintracranial hypotension:report of two cases and review of the literature. Neurology 1992; 42: 481-487. 13. PannnlloSC, Reich JB, Krol G, Deck MDF, Posner YB.MRI changes in intracranial hypotension.Neurology 1993; 43: 919-926. 14. HortonJC, Fishman RA. Neurovisual findings in the syndrome of spontaneous intracranial hypotensionfrom dural cerebrospinalfluid leak. Ophthalmology 1994; 101: 244-251. 15. MokriB, Patisi JE, ScheithanerBW, Piepgras DG, Miller GM. Meningeal biopsy in intracranialhypotension: meningeal enhancementon MRI. Neurology 1995; 45: 1801-1807. 16. Renowden SA, Gregory R, Hyman N, Hilton-JonesD. Spontaneous intracradial hypotension.J Neurol Nenrosurg Psychiatry 1995; 59: 511-515. 17. Davenport RJ, Chataway HJS, Warlow CR Spontaneousintracranial hypotensionfrom a CSF leak in a patient with Marfan's syndrome.J Neurol Neurosurg Psychiatry 1995; 59: 516-519. 18. Schievink WI, Meyer FB, Atldnson JLD, Mokri B. Spontaneousspinal cerebrospinaifluid leaks and intracraniaihypotension.J Neurosurg 1996; 84: 598--605. 19. PaulsonGW, Klawans HL Jr. Benign orgasmic cephalgia. Headache 1994; 13: 181-187. 20. Schi.evinkWI, Reimer R, Folger WN. Surgical treatment of spontaneous intracranial hypotension associated with a spinal arachnoid diverticulum. J Neurosurg 1994; 80: 736-739. 21. Schreiber F, Haddad B. Lumbar & sacral cysts causing pain. J Neurosurg 1951; 8: 504-509. 22. TarlovIM. Spinal perineural and meningeal cysts. J Neurol Neurosurg Psychiatry 1970; 33: 833-843. 23. LakePA, Minclder J, Scanlan RL. Spinal epidural cyst: theories of pathogenesis. J Neurosurg 1974; 40: 774-778. 24. SableSG, Ramadan NM. Meningeal enhancement & low CSF pressure headache. An MRI study. Cephalgia 1991; 11: 275-26. 25. HochmanMS, Naidich TE Kobetz SA, Fernandez-MaitinA. Spontaneous intracranial hypotension with pachymeningealenhancementon MRI. Neurology 1992; 42: 1628-1630. 26. Fishman RA, Dillon WE Dural enhancementand cerebral displacement secondary to intracranialhypotension.Neurology 1993; 43: 609-611. 27. MokriB, Krueger BR, Miller GM, Piepgras DG. Meningeal gadolinium enhancementin low-pressureheadaches. J Neuroimaging 1993; 3: 11-15. 28. Good DC, Ghobrial M. Pathologic changes associated with intracranial hypotension & meningeal enhancementon MRI. Neurology 1993; 43: 2698-2700. 29. VandamLD, Dripps RD. Long-term follow-up of patients who received 10 098 spinal anaesthetics.JAMA 1965; 161: 586-591. 30. Abouleish E, de la Vega S, Blendinger t, Tic T-O. Long-term follow-up of epidural blood patch. Anesth Analg 1975; 54: 459-463.
This technique may be used for approaching intraspinal pathology in high risk patients where extensive exposure may be contraindicated. Journal of Clinical Neuroscience (1998)5(4), 460-463 © HarcourtBrace& Co. Ltd 1998
Keywords: ankylosing spondylitis, cervical spine, spinal epidural hematoma, spinal endoscopy Received 22 October 1996 Accepted 3 December 1997 Correspondence to: Edmund H. Frank, Tel: 1 503 494 8070, Fax: 1 503 494
7161
INTRODUCTION Spinal epidural hematomas (SEH) are rare, but well described, lesions. They may be spontaneous or occur following trauma. Twenty cases o f SEH occurring following trauma in patients with ankylosing spondylitis (AS) have been reported.l-12 The mortality and morbidity o f spinal trauma in patients with AS is high. In the 20 reported cases o f SEH associated with AS, nine died and only eight made a good recovery. ~ Cardiorespiratory complications accounted for 50% o f the deaths following spine trauma in such patients. Our patient suffered rapidly worsening cardiac failure immediately following his injury. Systemic anticoagulation was necessary for the investigation and m a n a g e m e n t o f his coronary disease. Systemic anticoagulation is contraindicated in the face o f a pre-existing SEH and/or an extensive laminectomy. Most surgeons advocate withholding anticoagulants for at least 2 4 4 8 h following spinal procedures. We report the use o f a malleable spinal endoscope via a limited cervical laminotomy to remove the h e m a t o m a in an effort to reduce the risk o f postoperative h e m a t o m a formation. Spinal endoscopy is being increasingly used in an effort to reduce the morbidity associated with extensive approaches to the spine. The majority o f uses reported to date involve anterior approaches for thoracic pathology.i315 This case is the first reported use o f the endoscope for a SEH. The etiology and m a n a g e m e n t o f SEH is reviewed and potential applications for this technique are discussed.
CASE R E P O R T
Endoscopic treatment of spinal epidural hematoma Timothy R. Steel FRACS,Jordi X. Kellogg MD, Todd A. Kuether MD, Jacques Favre MD, Edmund H. Frank MD Oregon Health Sciences University, Division of Neurosurgery,, L-472, 3181 SW Sam Jackson Park Road, Portland, OR 97201, USA
Summary We report the use of a spinal endoscope via a limited cervical laminotomy to evacuate a spinal epidural hematoma. The patient was a 75-year-old male with a 32-year history of ankylosing spondylitis. Following a low speed motor vehicle accident he developed a cervicothoracic epidural hematoma without an associated fracture. Despite a rapidly improving neurological state, his rapidly deteriorating cardiorespiratory state required systemic anticoagulaUon necessitating decompression of the hematoma. The hematoma was successfully removed via a limited C6 and C7 laminotomy using the endoscope and a malleable disposable aspirator. We conclude that epidural hematomas can be readily evacuated via endoscopic techniques without extensive laminectomy. Joumal of Clinical Neuroscience (1998) 5(4)
A 74-year-old male with a 32-year history o f AS was brought to our emergency room following a low speed roll-over motor vehicle accident. H e suffered no head injury or loss o f consciousness. On arrival he was unable to lie flat on the spine board due to his 40% kyphosis and he complained o f severe pain in his cervicothoracic region, but was neurologically intact. Within 15 rain o f admission he complained o f rapidly developing lower limb weakness and reduced sensation b e l o w his nipple line. On examination he had 2/5 strength in his lower limbs and reduced sensation to pin prick below his axillae. Joint position sense at his toes was absent. X-rays o f his cervical and thoracic spine revealed marked ankylosis but no fracture was seen. Computed tomography (CT) scans o f his C 4 - T 4 region with sagittal reconstruction showed the kyphosis but no fracture. Magnetic resonance image (MRI) scanning o f his cervicothoracic region was performed demonstrating a lesion lying dorsal to the spinal cord extending from C4 to T2 with significant compression o f the spinal cord (Figs. 1 & 2). The lesion was o f biconvex shape tapering superiorly and inferiorly. O n T l - w e i g h t e d images the lesion was isointense with the spinal cord and on T2-weighted images the lesion was heterogeneous and hypointense to the spinal cord; this was consistent with acute epidural hematoma. 4,t6 No evidence o f fracture was seen. At the time o f his neurological deterioration he was started on intravenous methylprednisolone as per the spinal cord injury
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Fig. 3 Intraoperative view of the SEH (arrow) and thecal sac (star) via the endoscope.
Fig, 1 Sagittal T2-weighted MRI scan showing the lesion (hypointense to the spinal cord) posterior to and causing deviation of the spinal cord.
on the left side at the inferior border of C6 and the superior aspect of C7 exposing a bony opening of 20 mm diameter. After removal of the ligamentum, the SEH was encountered (Fig. 3). The clot itself was thick and tenacious. After removing the hematoma directly below the laminotomy the pulsatile irrigation of the endoscope combined with a malleable suction device was used to gently wash out the remainder of the clot, just as with an acute intracranial subdural hematoma. No acute bleeding site was encountered. The thecal sac was rapidly decompressed and returned to its normal position in the canal; using the endoscope adequate decompression in a rostral and caudal direction was ensured. Postoperatively the patient remained profoundly hypotensive and he was not extubated. An intra-aortic balloon pump was placed in the intensive care unit. This failed to significantly increase blood pressure. After discussion with the cardiology team and the patient's relatives, the patient was taken off pressor support and died shortly after.
DISCUSSION
Fig. 2 Axial T2-weighted MRI scan showing deviation of the spinal cord by the SEH.
protocol; (bolus dose 30 mg/kg followed by 5.4 mg/kg/h over 23 h). Within 2 h of initiation of the steroids his neurological examination had returned to normal apart from mild weakness of hip flexion (4/5); his sensation including joint position sense at the toes had returned to normal. He was admitted to the intensive care unit, while surgical decompression was planned. Whilst awaiting surgery the patient developed unstable angina associated with hypotensive episodes requiring pressor support. Urgent coronary angiography with possible angioplasty was planned followed by systemic heparinization; however, this could not be initiated until evacuation of the hematoma was carried out. At surgery we planned to expose C6 and C7 (the level of maximal depth of the hematoma) and perform a limited laminotomy only and evacuate the hematoma with the use of the spinal endoscope (Clams Murphy Scope, model 2125-161, Clarus Medical Minneapolis, MN, USA) and an angled disposable sucker. If we were not able to access the clot more extensive laminectomies were to be performed. Because of the patient's poor cardiorespiratory state we were unable to position the patient prone and elected a right lateral decubitus position. The hematoma was approached via a 6 cm incision over the spinous processes of C6 and C7. A bilateral muscle takedown was performed. Laminotomies were performed © Harcourt Brace & Co. Ltd 1998
More than 250 cases of SEH have been reported in the literature. 4,8,1~2° They may occur either spontaneously or following trauma and typically occur dorsal to the thecal sac in the cervicothoracic region. Thoracic and lumbar SEH have also been reported.IV'21 Spontaneous hematomas can be idiopathic, in which no etiology is found, and those arising secondary to some predisposing factor? 2 Anticoagulation, platelet dysfunction, neoplasms, vascular malformations, Paget's disease, lupus, hypertension and rheumatoid arthritis have all been reported as the underlying cause of SEH. 17'22,23 Spontaneous SEH may occur at rest or following trivial activities which may raise intraspinal venous pressure such as bending, straining or coughingJ 8,22The site of bleeding in such cases is assumed by many to be rupture of the valveless epidural veins (Batson's plexus) due to elevation of venous pressure. 18,19,24 Bleeding from epidural arteries has also been postulated as the source which may account for the more rapid neurological deterioration seen in some patients. 19,25 Traumatic SEH are uncommon in adults. 26 Almost half of reported cases have occurred in neonates and children. If a fracture occurs the hematoma may arise from exposed bone surfaces directly into the spinal canal, or from disruption of the vessels surrounding the thecal sac. Intraspinal epidural hematoma of definite traumatic origin occurs without spinal fracture in about 50% of cases particularly in the pediatric age group because of greater elasticity of the vertebral column. 4,26 The association of SEH and AS is well documented with 20 cases reported as of 1996Y 2 Eighteen of these have been in
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association with spinal fractures. 1,4,11,26 Two cases have been reported previously of hematoma formation without fracture. 2,6 In these cases such as ours, it has been assumed that movement of the spinal cord within the rigid spinal canal causes disruption to the epidural veins resulting in hemorrhage. Although no definitive bleeding site was encountered at operation we presume this to be the mechanism for the hematoma in our patient. The recommended management of SEH has been emergent decompressive laminectomy as soon as the diagnosis is reached. 4,6,11,18,19 In the pre-MRI era the diagnosis of SEH was rarely made in the absence of profound neurological deficits. Foo et aF 7 demonstrated in their review of 158 cases of spontaneous spinal hematoma that postoperative neurological recovery following surgery is proportionate to the severity of the sensorimotor impairment prior to intervention. Analysis of the literature reveals 15 cases of spontaneous SEH that have been successfully treated without surgery.16,19,2°,27 In recent reports 19,2°'27this has been due to rapid improvement or even early resolution of neurological deficits. Unfortunately only one of these reports indicates if methylprednisolone was administered; this may have accounted for the early and dramatic improvements made by our patient. No patient with an antemortem diagnosis of traumatic SEH has been successfully treated conservatively. There are no reports of SEH treated without decompression in patients with AS. In the case reported by Hissa, 6 myelography and subsequent surgery was delayed for 6 days; the patient's paraparesis improved following the administration of intravenous steroids on admission; however, deterioration subsequently occurred. Following decompression, the patient's deficits (spasticity and atonic bladder) gradually resolved over 6-8 months. This patient was not diagnosed with a thoracic hematoma initially as his severe kyphosis precluded his thoracic region entering the gantry of the MRI scanner. 6 AS patients have a far higher mortality and morbidity than the general population following spinal trauma." Reported mortality rates are commonly in the 30-35% range for AS patients with cervical spine injury and higher for those with spinal cord damage; l this is twice the mortality reported in patients without AS. The high incidence of early cardiorespiratory complications following spine injury due to systemic manifestations of the disease, such as rigid chest walls, pulmonary fibrosis and vascular degeneration, has been noted by many authors. 1,9'11'28'29Of the 20 reported cases of SEH occurring with AS, nine patients died, all within 1 month of injury. In six of these the diagnosis was made only at post-mortem. Neurological recovery is also greater in those patients with traumatic SEH without AS or spinal fracture. 26 Only eight of the 20 reported patients in the literature made a full recovery. In the remaining three patients delayed laminectomy was performed which revealed the hematoma. Major persisting neurological deficits resulted in all of these cases. 2'3'5 Despite our patient's improving neurological status, the size and location of the hematoma made evacuation imperative. However, the impending use of systemic anticoagulation made the standard treatment of extensive laminectomy and evacuation more hazardous due to the risk of postoperative hematoma formation. At our institution we have been using a malleable spinal endoscope (the Clams Murphy Scope, model 2125-161). We have predominantly been using this for the assessment of decompression and pedicle screw location in the lumbar spine. This has allowed us to substantially reduce the amount of bone removal required yet still confirm under direct vision that no further neural compression exists. By utilizing the endoscope with a curved aspirator we were able to limit the bony opening to a 2.0 cm defect. The pulsatile irrigation from the endoscope itself was able to loosen the clot which was then easily aspirated by the curved
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suction device. Because the endoscope itself was malleable we were able to pass the instrument a considerable distance rostrally and caudally (3 levels) to ensure adequate decompression. Using direct vision we could assess the extent of the clot removal in all directions. By limiting our bony exposure yet being able to evacuate the hematoma we were able to reduce our operative time (less than 1 h), and reduce the risk of postoperative hematoma formation following an extensive laminectomy in an anticoagulated patient. Unfortunately we were not able to assess the benefits of our technique postoperatively either clinically or with imaging studies due to the patient's rapid cardiorespiratory decline. The patient's family requested no autopsy be performed, which precluded post-mortem assessment of the hematoma removal. Neuroendoscopy and other minimally invasive techniques are being increasingly used in neurosurgery to minimize morbidity and complications related to large exposure. 13-15 Although the outcome was disappointing, in this case it represents the first description of the use of endoscopy to evacuate a SEH. We have demonstrated the technical feasibility of this procedure in the cervical spine. In high risk patients with intraspinal pathology such as in our case, increased availability and experience with spinal endoscopy may lead to reduced morbidity and mortality in the future.
REFERENCES
1. BohlmanHH. Acute fracturesand dislocationsof the cervicalspine.J Bone Joint Surg (Am) 1979;61A(8): 1119-1192. 2. DetwilerKN, Loftus CM, Godersky.Managementof cervical spineinjuries in patientswith ankylosingspondylitis.J Neurosurg 1990;72: 210-215. 3. FastA, Parikh S, Matin EL. Spinefracturesin ankylosingspondylitis.Arch Phys Med Rehabil 1986;67: 595-597. 4. Garza-MercadoR. Traumaticextraduralhematomaof the cervicalspine. Neurosurgery 1982;24: 410-414. 5. GnisoliaA, Bell RL, PeltierZF. Fracturesand dislocationsof the spine complicatingankylosingspondylitis: a report of six cases. J Bone Joint Surg (AM) 1967;49A: 339-344. 6. HissaE, BoumphreyF, Bay J. Spinalepiduralhematomaand ankylosing spondylitis. Clin Orthop 1986; 208: 225-227. 7. LowreyJ. Spinalepiduralhematomas.Experienceswith three patients. J Neurosurg 1959; 16: 508-513. 8. PeckerJ, Javelet A, LeMennG. Spondyloarthitieankyloanteet paraplegiepar hematorachisextra-duraltraumatique.Press Med 1960; 68:183-184. 9. RowedDW. Managementof cervicalspinalcord injury in altkylosing spondylitis:the intervertebraidisc as a cause of cord compression. J Neurosurg 1992; 77: 241-246. 10. SchneiderRC, Cherry G, PantekM. The syndromeof acute centralcervical spinal cord injury.J Neurosurg 1954; i 1: 546-577. 11. SweetWH. Cervicothoracicankylosingspondylitis.In: SchmidekHH, Sweet WH (eds). OperativeNeurosurgicalTechniques,3rd Edn. Philadelphia:WB Sannders, 1995. 12. Ver BrugghenA. Extradural spinalhemorrhage.Ann Surg 1946; 123: 154-159. 13. McAfeePC, Regan JR, Zdeblicket al. The incidenceof complicationsin endoscopic anteriorthoracolumbarspinal reconstructivesurgery. Spine 1995; 20(4): 1624-1632. 14. KarakhanVB, FilimonovBA, GrigorganYA, MitropolskyVB. Operative spinal endoscopy: Stereotopographyand surgicalpossibilities.Aeta Neuroehir 1994; 61 (suppl): 108-114. 15. RosetuhalO, DickmanC, LorenzR, SonntagVKM. Thoracicdisc herniation: Early resultsafter surgicaltreatmentusing microsurgicalendoscopy(abstract). ScientificProgram, AANS Meeting,Minneapolis1996: 152. 16. BoukobzaM, GuichardJP, BoissonetM, GeorgeB, ReizineD, GelbertF, MerlandJJ. Spinalepiduralhematoma:report of 11 cases and reviewof the literature. Neuroradiology 1994; 36: 456459. 17. Foo D, RossierAB. Preoperativeneurologicalstatusin predictingsurgical outcome of spinal epiduralhematomas.Surg Neurol 1981; 15: 389401. 18. PearBL. Spinalepiduralhematoma.Am J Radiol 1972; 115(1): 155-164. 19. ClarkeDB, BertrandG, TampieriO. Spontaneousspinalepiduralhematoma causingparaplegia: Resolutionand recoverywithoutsurgicaldecompression. Neurosurgery 1992;30(1): 108-111. 20. WagnerS, ForstingM, HackeW. Spontaneousresolutionof a large spinal epidural hematoma:case report. Neurosurgery 1996;38(4): 816 818.
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21. GundryLR, HeithoffKB. Epiduralhematomaof the lumbarspine: 18 surgicallyconfirmedcases. Radiology 1993; 187:427~43i. 22. LobitzB, GrateI. Acute epiduralhematomaof the cervicalspine: an unusual cause of neck pain. SouthMed J 1995; 88(5): 580-582. 23. MannaJW, Bail MR, Lee KS, McWhorterJM. Spontaneousspinal epidural hematomacomplicatingPaget's disease of the spine. Spine 1995; 14(8): 900-902. 24. CooperDW. Spontaneousspinal epiduralhematoma. J Neurosurg 1967; 26: 343 346. 25. BeattyRM, WinstonKR. Spontaneouscervicalepiduralhematoma.A considerationof etiology.J Neurosurg 1984;61: 143-148. 26. Foo D, RossierAB. Post-traumaticspinal epiduralhematoma.Neurosurgery 1982; 1i: 25-32. 27. KatoS, Seki H, Koshu K. Acute cervicalspinalepiduralhematomawith spontaneousresolution:case report. Neurol Med Clair(Tokyo) 1994;34: 23 26. 28. Fox MW, OnfrioBM, KilgoreJE. Neurologicalcomplicationsof ankylosing spondylitis. J Neurosurg 1993;78: 871-878. 29. Hunter3",Dubo HIC. Spinal fracturescomplicatingankylosingspondylitis. A long term follow-up study. ArthritisRheum 1983; 26: 751-759.
Pseudoaneurysm of anterior communicating artery following transsphenoidal surgery for craniopharyngioma A. Malik 1 MD, M. Goyal I MD, N. K. Mishra 1 MD, A. Verma 2 ach~ S. G a i k w a d 1 MD, V. S. Mehta 2 ach Departments of 1Neuroradiologyand 2Neurosurgery,Neuroseiences Centre, All India Institute of Medical Sciences, New Delhi, India 110 029
Summary Fusiform dilatation and pseudoaneurysm formation in arteries of the circle of Willis has been reported as a complication following surgery for craniopharyngiomas through craniotomies. We present a case of anterior communicating artery pseudoaneurysm following transsphenoidal surgery for craniopharygioma in an adult.
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CASE REPORT A 26-year-old male patient was admitted with complaints of painless, progressive visual deterioration of 2 months' duration. There were no symptoms to suggest raised intracranial tension or hormonal dysfunction. The visual acuity was 6/9 on the right side and 6/36 on the left side. Examination of the left eye revealed primary optic atrophy and left temporal field cut off. Fundus examination and field charting of the right eye were normal. The sella was enlarged on skull roentgenogram. Preoperative magnetic resonance imaging (MRI) scan of the brain (Fig. 1) showed a large sellar mass with suprasellar extension. The mass was isointense to water on Tl-weighted imaging (T1WI) (TR 450 ms, TE 20 ms, NEX 3) and hyperintense on T2WI (TR 2705 ms, TE 90 ms, NEX 1). There was no evidence of encasement of the arteries of circle of Willis. The optic chiasm was elevated and compressed. The rest of the brain parenchyma was normal. Sublabial transsphenoidal surgery was performed. The patient had profuse bleeding from the operative site soon after the cystic mass was punctured. The contents of the cystic mass simulated 'machine oil' with few cholesterol crystals, consistent with the usual contents of a craniopharyngioma cyst. The bleeding was controlled by packing the sellar floor; complete excision of the tumour was not possible. On the third postoperative day the patient developed profuse cerebrospinal fluid rhinorrhoea necessitating reexploration. At surgery, through the transsphenoidal route, a small hole was seen in the diaphragma which was sealed with autologous fascia and biological glue; the postoperative course was uneventful. Postoperative non-enhanced computed tomography (CT) scan (Fig. 2) showed hyperdensity, suggestive of blood, in the tumour bed with left anterior cerebral artery (ACA) territory infarct involving the left basifrontal lobe and left caudate head. Intraarterial DSA performed 2 days after surgery (Fig. 3) showed spasm in the A1 segment of left ACA with a small AComA pseudoaneurysm. No other arterial abnormality was noted. Repeat DSA study performed after 3 months revealed the pseudoaneurysm to have enlarged in size (Fig. 4). The patient underwent left pterional craniotomy. At surgery the A I segment of left ACA was seen dipping into the sella along with a large pseudoaneurysm of the A C o m A which was successfully clipped.
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Keywords : craniopharyngioma, magnetic resonance imaging, pseudoaneurysm, angiography, transsphenoidal surgery Received 22 October 1996 Accepted 10 December 1996 Correspondence to: Dr M. Goyal, Tel: 91 11 6594418, Fax: 91 11 6862663, E-mail: [email protected]
DISCUSSION Craniopharyngiomas are slow growing benign tumours arising from remnants of Rathke's pouch; 70% are both suprasellar and intrasellar in location, while 20% are located solely in the suprasellar region. The most common obstacle to the total removal of craniopharyngioma is dense adhesion to major arteries, usually of the circle of Willis, and lack of a clear plane of cleavage.
INTRODUCTION We report a case of anterior communicating artery (AcomA) pseudoaneurysm in an adult following transsphenoidal decompression of a craniopharyngioma. Histologically benign craniopharyngiomas usually produce symptoms by their growth within the sella and suprasellar cistern. Complete excision, although desired, is not always accomplished due to adhesion of the tumour to the adventitia of vessels in the circle of Willis. 1Fusiform dilatation and pseudoaneurysm formation in the supraclinoid internal carotid artery has been reported as a complication of surgical resection of craniopharyngioma through craniotomies. 2-~ However, AComA pseudoaneurysm formation following transsphenoidal surgery for craniopharyngioma has not been previously reported.
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Fig. 1 Preoperative T2-weighted coronal (A) and sagittal (B) MR image (TR 2705 ms, TE 90 ms) showing a large sellar and suprasellar mass with parasellar extension. No arterial abnormality is seen in the circle of Willis.
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