Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Cavernous Sinus Syndromes

  • Author: Jorge C Kattah, MD; Chief Editor: Robert A Egan, MD  more...
 
Updated: Feb 14, 2014
 

Overview

Background

Cavernous sinus syndrome is defined by its resultant signs and symptoms: ophthalmoplegia, chemosis, proptosis, Horner syndrome, or trigeminal sensory loss. Infectious or noninfectious inflammatory, vascular, traumatic, and neoplastic processes are the principal causes. Examples of specific entities that may result in cavernous sinus syndrome are myriad and include carotid artery aneurysms, carotid-cavernous fistulas (C-C fistulas) (see image below), tumors, and Tolosa-Hunt syndrome, to name the most frequently discussed.

Carotid-cavernous fistula. Carotid-cavernous fistula.

Pathophysiology

The cavernous sinuses are paired, venous structures located on either side of the sella turcica. They receive venous tributaries from the superior and inferior orbital veins and drain into the superior and inferior petrosal sinuses. The cavernous sinus contains the carotid artery, its sympathetic plexus, and the oculomotor nerves (third, fourth, and sixth cranial nerves). In addition, the ophthalmic branch and occasionally the maxillary branch of the fifth nerve traverse the cavernous sinus. The nerves pass through the wall of the sinus while the carotid artery passes through the sinus itself.

Cavernous sinus tumors

Cavernous sinus tumors are the most common cause of cavernous sinus syndrome. Tumors may be primary or may arise from either local spread or as metastases. Examples of primary tumors include meningiomas or neurofibromas. Examples of locally spreading tumors are nasopharyngeal carcinoma or pituitary tumors. Metastatic lesions are most often from the breast, prostate, or lung. Radiotherapy may offer transient relief, particularly in nasopharyngeal cancer. Lateral extension of pituitary tumors may be treated with surgical resection and dopamine agonists in the case of prolactinoma. Total resection of these lesions is challenging and attempted only when the symptoms are disabling.[1]

Cavernous sinus aneurysms

Unlike intracranial aneurysms in other anatomic locations, carotid-cavernous aneurysms do not involve a major risk of subarachnoid hemorrhage. However, their rupture can result in direct C-C fistulas, which may lead to cerebral hemorrhage. These aneurysms, which are more frequent in the elderly population, present with an indolent ophthalmoplegia. Although some patients suffer minor disability and do not require treatment, endovascular occlusion of these lesions is often successful and may be attempted in selected patients.[2]

Carotid-cavernous fistulas

C-C fistulas are of 2 types: direct and indirect. Direct fistulas occur if the carotid artery and cavernous sinus are in continuity. They manifest with abrupt onset of proptosis, chemosis, visual loss, and ophthalmoplegia. Indirect fistulas occur with communication between the cavernous sinus and the branches of the internal carotid artery, external carotid artery, or both. They have a more insidious presentation than direct fistulas, often with spontaneous resolution. Trauma or aneurysm rupture is a common cause of carotid-cavernous fistulas. Interventional radiologists can successfully treat all fistula types by endovascular occlusion techniques. Occasionally, surgical treatment with carotid ligation is necessary; this sometimes is preceded by a superficial temporal-to-middle cerebral bypass operation to ensure cerebral circulation after carotid ligation.

Frequency

In the US, approximately 5% of ophthalmoplegias are secondary to involvement of cranial nerves in the cavernous sinuses. This is probably true worldwide.

Cavernous sinus aneurysms represent 5% of all intracranial aneurysms.

Mortality/Morbidity

See the list below:

  • Most of the lesions affecting the cavernous sinuses are treatable.
  • Metastatic cancer is a frequent cause of cavernous sinus syndromes, and the prognosis depends on the specific tumor type.
  • Cavernous sinus septic thrombophlebitis mortality has decreased from 100% to 20% with the implementation of improvement in diagnosis and therapeutics.
  • Cavernous sinus aneurysms and C-C fistulas can be treated successfully by endovascular techniques.
  • Lateral extension of pituitary tumors, a common cause of this syndrome, can be treated by surgical resection, radiation therapy in selected patients, and a dopamine agonist in the case of prolactinoma.
Next

Clinical Presentation

History

The signs and symptoms frequently found in patients with cavernous sinus lesions include visual loss, proptosis, ocular and conjunctival congestion, elevation of ocular pressure, ophthalmoplegia, and pain. Various combinations of these symptoms may occur, which generally are unilateral, but may be bilateral with neoplastic processes. Symptoms may be acute or slowly progressive. Primary tumors are the most frequent neoplasm responsible for a cavernous sinus syndrome.

  • Cavernous sinus tumors
    • Acute or slowly progressive ophthalmoplegia is the dominant presentation, with diplopia being the most common symptom.
    • At times, painful diplopia is present.
    • Usually the patient has a preceding history of cancer. Occasionally, cavernous sinus syndrome is the first manifestation of a systemic neoplasm.
    • Exophthalmos can be seen.
    • If the tumor is a pituitary adenoma, endocrine symptoms and visual field deficits may be present.
  • Carotid-cavernous aneurysms
    • Patients frequently are elderly and present with subacute or chronic ophthalmoplegia.
    • Rarely, they may have pain similar to that of trigeminal neuralgia.
    • Spontaneous rupture of a carotid-cavernous aneurysm leads to an abrupt onset of a direct C-C fistula. This results in acute onset of massive exophthalmos with orbital, ocular, and conjunctival chemosis, binocular diplopia, and visual loss.
  • Two types of C-C fistulas
    • Direct fistulas present with prominent acute symptoms.
    • Conversely, indirect fistulas are characterized by mild proptosis, chronic diplopia, drooping of the lid, a red eye, arterialization of the conjunctival vessels, and visual loss. The patient may report subjective "noises" in his or her head.
  • Cavernous sinus thrombosis
    • This is infrequent in the postantibiotic era.
    • It may occur as a complication of infection in the ethmoid, sphenoid, or frontal sinuses or from midfacial, dental, or orbital infections.
    • Patients may present with sepsis or metastatic spread of septic emboli, most commonly occurring in the lung. This presentation may appear as acute respiratory distress syndrome (ARDS).
    • Retrobulbar pain, drooping of the upper eyelid, and diplopia may be the first symptoms indicating the lesion's extension to the cavernous sinus.
  • Miscellaneous inflammatory lesions
    • These may involve the cavernous sinuses or the walls of the sinus.
    • Herpes zoster in its acute or chronic stage rarely causes pain, diplopia, and a droopy eyelid in addition to the typical zoster blisters. In the chronic stage, a scar from the acute lesion usually is found.
    • An idiopathic inflammation of the walls of the cavernous sinuses is referred to as Tolosa-Hunt syndrome.
    • Sarcoid or Wegener granulomatosis may also predispose to cavernous sinus syndrome.

Physical

See the list below:

  • Cavernous sinus lesions are characterized by the following signs:
    • Unilateral and isolated third, fourth, or sixth cranial nerve palsy
    • Combination patterns of ophthalmoplegia
    • Painful ophthalmoplegia
    • Proptosis (pulsating exophthalmos suggests a direct C-C fistula)
    • Ocular and cranial bruits
    • Conjunctival congestion; arterialization of conjunctival veins
    • Ocular hypertension
    • Optic disc edema or pallor; retinal hemorrhages
    • Anesthesia in the ophthalmic division of the trigeminal nerve (V1) and/or decreased or absent corneal reflex and possibly anesthesia in the maxillary or V2 branch
    • Pupil in midposition and nonreactive if both sympathetics and parasympathetics from the third nerve are affected
  • Cavernous sinus tumors
    • Metastatic lesions - Isolated or combined ophthalmoplegia, painful ophthalmoplegia, anesthesia in the ophthalmic nerve
    • Pituitary tumors - Isolated or combined ophthalmoplegia (lateral extension); endocrine signs such as acromegaly, galactorrhea, and unitemporal or bitemporal visual field defects
    • Primary intracranial tumors - Isolated or combined ophthalmoplegia and/or primary aberrant regeneration of the third cranial nerve
  • Cavernous sinus aneurysms
    • Isolated or combined ophthalmoplegia
    • Painful ophthalmoplegia
    • Decreased pain sensation in the V1 ophthalmic division
  • Carotid-cavernous fistulas
    • Direct - Unilateral massive proptosis, pulsating exophthalmos, lid congestion, conjunctival chemosis, orbital congestion, ocular hypertension, visual loss, optic neuropathy, optic disc edema, retinal hemorrhages, retinal venous congestion, and loud ocular and cranial bruit
    • Indirect - Similar signs and symptoms of lesser severity; occasionally, isolated ophthalmoplegia, particularly if the fistula drains posteriorly
  • Cavernous sinus thrombosis
    • Generally speaking, primary infectious process involving paranasal sinuses and/or orbital cellulitis
    • In addition to local and systemic signs of infection, the following may be seen:
      • Isolated or combined ophthalmoplegia
      • Painful ophthalmoplegia
      • Orbital congestion, lid chemosis, proptosis
      • Visual loss, optic disc edema (unilateral)
      • Signs of meningeal irritation
  • Miscellaneous cavernous sinus lesions
    • Tolosa-Hunt syndrome - Isolated or combined, painful ophthalmoplegia
    • Herpes zoster - Acute zoster ophthalmicus, typical skin lesion, and keratitis
    • Sarcoidosis - Systemic signs, uveitis, ophthalmoplegia, facial diplegia

Causes

See the list below:

  • Metastatic tumors
    • Breast
    • Prostate
    • Lung
  • Localized spread of tumor
    • Nasopharyngeal
    • Pituitary
  • Primary intracranial tumors
    • Meningiomas
    • Neurofibromas
    • Chondromas (less common)
  • Trauma (including postsurgical)
  • Carotid-cavernous aneurysms
  • Carotid-cavernous fistulas
  • Cavernous sinus thrombosis
  • Miscellaneous inflammatory syndromes
    • Herpes zoster
    • Tolosa-Hunt syndrome
    • Sarcoidosis
Previous
Next

Diagnostic Workup

Patients in whom cavernous sinus lesions are suspected should undergo thin-section multiplanar imaging studies of the orbit and the sellar/parasellar region. Precontrast and postcontrast scans are advisable. CT scan offers better visualization of bone and calcium. However, MRI provides better detail of all soft tissues contained in the sinuses, the expected signal void of the normal carotid artery, and its relation to the surrounding structures. See the image below.

A T1-weighted, coronal MRI. A T1-weighted, coronal MRI.

Orbital views are necessary to exclude a disease process primarily involving the cavernous sinuses with concomitant compromise of the orbital apex. Conversely, primary orbit and paranasal sinus disorders frequently may involve the cavernous sinuses. Visualization of the superior and inferior orbital veins is helpful to diagnose increased venous pressure. Once imaging is obtained and reviewed in light of clinical findings, further investigation can be pursued to determine a specific diagnosis.

Cavernous sinus tumors

See the list below:

  • In the case of metastatic tumors, diagnosis of the primary neoplasm generally precedes the cavernous sinus syndrome.
  • A lumbar puncture with cytologic examination may be helpful.
  • If a primary neoplasm of the nasopharynx is suspected, a biopsy may be needed.
  • In the case of pituitary tumors with lateral extension, tumor resection may be necessary.
  • Rarely, a biopsy of the cavernous sinus tumor is needed for diagnosis.

Cavernous sinus aneurysms

See the list below:

  • As MRI and/or magnetic resonance angiography (MRA) are often specific, cerebral angiography generally is not required to make a diagnosis.
  • Perform angiography if balloon occlusion of the aneurysm is planned.

Carotid-cavernous fistulas

See the list below:

  • The dramatic clinical presentation and MRI and/or MRA of direct fistulas leave little doubt regarding the diagnosis.
  • By contrast, indirect fistulas, particularly those draining in the petrosal sinuses, are associated with subtle findings and possibly a normal MRI and/or MRA. See the images below.
    This patient is a 55-year-old woman who originally This patient is a 55-year-old woman who originally had symptoms of eye pain and pulse synchronous tinnitus on the left. She was found to have an indirect left carotid cavernous sinus fistula and underwent successful coiling of the fistula. This picture shows her after the procedure, as she had developed left eye chemosis and diplopia. A left lateral rectus paralysis was present on examination. In this case, the probable causes of the ophthalmoplegia could be mass effect or occlusion of the vasa nervorum supplying the sixth cranial nerve, which travels in the adventitia of the carotid artery. Here, the prognosis is excellent, and the authors have seen several cases with improvement within 4-8 weeks after coiling.
    Early phase of the post-fistula coiling angiogram Early phase of the post-fistula coiling angiogram of the patient shown above. Coils can be appreciated at the cavernous portion of the carotid artery.
    Later filling phase of the angiogram for the patie Later filling phase of the angiogram for the patient shown above. Note that coiling has prevented anomalous filling of the cavernous sinus fistula.
  • Cerebral angiography is the only way to arrive at the correct diagnosis.
  • Perform angiography to stage the fistula and document the anterior and posterior drainage routes.

Cavernous sinus thrombosis

See the list below:

  • Imaging of the orbit and/or nasal sinuses is helpful in the search for a septic focus.
  • An aseptic thrombosis may be associated with conditions such as hypercoagulable states and lymphoproliferative disorders.
  • A hematologic workup is indicated in these patients.

Miscellaneous inflammatory syndromes

Investigate additional systemic inflammatory and granulomatous processes after other common causes have been excluded. These disorders can be screened by studies such as laboratory tests and chest radiograph.

  • Tolosa-Hunt syndrome (an uncommon, idiopathic, inflammatory cavernous sinus syndrome) may share a close etiologic link with orbital pseudotumor.
    • A nonspecific fibrotic inflammatory reaction and rarely a granulomatous inflammation can occur, but biopsy is rarely used to establish the diagnosis.
    • A positive response to steroids is considered diagnostic, but false-positive responses can occur in lymphoma and other parasellar neoplasms.
  • Biopsy of the cavernous sinuses entails a craniotomy, which is associated with morbidity. Restrict a craniotomy to patients with a documented, progressive cavernous sinus syndrome.
Previous
Next

Treatment & Management

Cavernous sinus tumors

See the list below:

  • Metastatic lesions
    • Radiotherapy may offer transient improvement.
    • Nasopharyngeal carcinomas may be very radiosensitive, with a prolonged remission following treatment.
  • Pituitary tumors
    • Prolactinomas may improve with oral dopamine agonists, or they may require resection.
    • Gamma knife may be an adjunctive treatment for postoperative tumor residual or recurrent tumor, and it may have a role as an alternative to open surgical treatment.
  • Cavernous sinus meningiomas
    • These lesions represent a major challenge for surgical resection, primarily because of poor accessibility and the frequent encasement of the cavernous carotid artery.
    • Since these tumors are slow growing and difficult to resect, elderly patients or those with minor symptoms probably should be observed expectantly without specific treatment.
    • Radiotherapy may be offered to some patients, and some show improvement of cranial nerve function after gamma knife treatment. Partial resection may be attempted in others with disabling symptoms (eg, intractable pain, total ophthalmoplegia in a patient with poor vision in the nonparetic eye).

Cavernous sinus aneurysms

Treat cavernous sinus aneurysms by endovascular balloon occlusion.

Carotid-cavernous fistulas

See the list below:

  • Treatment ideally consists of endovascular obliteration of the fistula with coils, although some cavernous sinus dural AV fistulas may be observationally managed.
  • Access to the fistula may be transarterial; however, the transvenous approach has become the mainstay of treatment, in some cases a combined surgical/endovascular approach can be used with surgical exposure of the superior ophthalmic vein followed by fistula embolization. Several venous approaches have been used, including the safest transfemoral approach; however, if this is not feasible, a superior orbital vein or a percutaneous transorbital puncture to the cavernous sinus can be used. [3]
  • Supraorbital vein dissection with placement of a catheter to access the cavernous sinuses has been performed successfully.
  • Percutaneous transorbital access to the cavernous sinus followed by embolization.
  • Small indirect C-C fistulas may occlude either spontaneously or following diagnostic angiography. If the clinical signs are mild, consider careful monitoring.
  • If intraocular pressure is elevated, antiglaucoma agents may be required.

Cavernous sinus thrombosis

See the list below:

  • High-dose antibiotic therapy should be directed against the most common pathogens, such as S aureus and S pneumoniae, as well as gram-negative rods and anaerobes.
  • Anticoagulation in septic cavernous sinus thrombosis is controversial, but may hasten the rate of recovery.
  • Drainage of any primary site of infection (eg, abscess, sinusitis) is advised.
  • Corticosteroids are not recommended.
  • Anticoagulation also may be helpful in aseptic patients.

Miscellaneous inflammatory syndromes

See the list below:

  • Inflammatory cavernous sinus syndromes may respond to treatment of the specific systemic inflammation or vasculitic etiology.
  • Tolosa-Hunt syndrome responds well to a 3- to 6-month course of high-dose steroid therapy that can be tapered slowly thereafter.
Previous
 
Contributor Information and Disclosures
Author

Jorge C Kattah, MD Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge C Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Robert A Egan, MD Director of Neuro-Ophthalmology and Stroke Service, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, Oregon Medical Association

Disclosure: Received honoraria from Biogen Idec for speaking and teaching; Received honoraria from Teva for speaking and teaching.

Chief Editor

Robert A Egan, MD Director of Neuro-Ophthalmology and Stroke Service, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, Oregon Medical Association

Disclosure: Received honoraria from Biogen Idec for speaking and teaching; Received honoraria from Teva for speaking and teaching.

Additional Contributors

Draga Jichici, MD, FRCP, FAHA Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada

Draga Jichici, MD, FRCP, FAHA is a member of the following medical societies: American Academy of Neurology, Royal College of Physicians and Surgeons of Canada, Canadian Medical Protective Association, Canadian Medical Protective Association, Neurocritical Care Society, Canadian Critical Care Society, Canadian Critical Care Society, Canadian Neurocritical Care Society, Canadian Neurological Sciences Federation

Disclosure: Nothing to disclose.

Acknowledgements

John H Pula, MD Staff Physician, Department of Neurology, OSF Saint Francis Medical Center, University of Illinois College of Medicine at Peoria

Disclosure: Nothing to disclose.

References
  1. Shimizu Y, Tsutsumi S, Yasumoto Y, Ito M. Carotid cavernous sinus fistula caused by dental implant-associated infection. Am J Otolaryngol. 2011 Sep 14. [Medline].

  2. Shelton JB, Ramakrishnaiah R, Glasier CM, Phillips PH. Cavernous sinus syndrome from an internal carotid artery aneurysm in an infant with tuberous sclerosis. J AAPOS. 2011 Aug. 15(4):389-91. [Medline].

  3. White JB, Layton KF, Evans AJ, Tong FC, Jensen ME, Kallmes DF. Transorbital puncture for the treatment of cavernous sinus dural arteriovenous fistulas. AJNR Am J Neuroradiol. 2007 Aug. 28(7):1415-7. [Medline].

  4. Boghen D, Chartrand JP, Laflamme P, et al. Primary aberrant third nerve regeneration. Ann Neurol. 1979 Nov. 6(5):415-8. [Medline].

  5. Bone I, Hadley DM. Syndromes of the orbital fissure, cavernous sinus, cerebello-pontine angle, and skull base. J Neurol Neurosurg Psychiatry. 2005 Sep. 76 Suppl 3:iii29-iii38. [Medline].

  6. Brazis PW, Capobianco DJ, Chang FL, et al. Low flow dural arteriovenous shunt: another cause of "sinister" Tolosa- Hunt syndrome. Headache. 1994 Oct. 34(9):523-5. [Medline].

  7. Campbell RJ, Okazaki H. Painful ophthalmoplegia (Tolosa-Hunt variant): autopsy findings in a patient with necrotizing intracavernous carotid vasculitis and inflammatory disease of the orbit. Mayo Clin Proc. 1987 Jun. 62(6):520-6. [Medline].

  8. Cannon ML, Antonio BL, McCloskey JJ, et al. Cavernous sinus thrombosis complicating sinusitis. Pediatr Crit Care Med. 2004 Jan. 5(1):86-8. [Medline].

  9. Debrun G, Lacour P, Vinuela F, et al. Treatment of 54 traumatic carotid-cavernous fistulas. J Neurosurg. 1981 Nov. 55(5):678-92. [Medline].

  10. Greenberg HS, Deck MD, Vikram B, et al. Metastasis to the base of the skull: clinical findings in 43 patients. Neurology. 1981 May. 31(5):530-7. [Medline].

  11. Hedges TR, Leung LS. Parasellar and orbital apex syndrome caused by aspergillosis. Neurology. 1976 Feb. 26(2):117-20. [Medline].

  12. Hou K, Luo Q, Chen Q, et al. Therapeutic embolization of cavernous sinus dural arteriovenous fistulas via transvenous approach. Chin Med J (Engl). 2003 May. 116(5):661-4. [Medline].

  13. Hunt WE, Meagher JN, Lefever HE, Zeman W. Painful opthalmoplegia. Its relation to indolent inflammation of the carvernous sinus. Neurology. 1961 Jan. 11:56-62. [Medline].

  14. Kattah JC, Silgals RM, Manz H, et al. Presentation and management of parasellar and suprasellar metastatic mass lesions. J Neurol Neurosurg Psychiatry. 1985 Jan. 48(1):44-9. [Medline].

  15. Keane JR. Cavernous sinus syndrome. Analysis of 151 cases. Arch Neurol. 1996 Oct. 53(10):967-71. [Medline].

  16. Kline LB. The Tolosa-Hunt syndrome. Surv Ophthalmol. 1982 Sep-Oct. 27(2):79-95. [Medline].

  17. Kline LB, Hoyt WF. The Tolosa-Hunt syndrome. J Neurol Neurosurg Psychiatry. 2001 Nov. 71(5):577-82. [Medline].

  18. Kuo JS, Chen JC, Yu C, et al. Gamma knife radiosurgery for benign cavernous sinus tumors: quantitative analysis of treatment outcomes. Neurosurgery. 2004 Jun. 54(6):1385-93; discussion 1393-4. [Medline].

  19. Kupersmith MJ, Berenstein A, Choi IS, et al. Percutaneous transvascular treatment of giant carotid aneurysms: neuro- ophthalmologic findings. Neurology. 1984 Mar. 34(3):328-35. [Medline].

  20. Levine SR, Twyman RE, Gilman S. The role of anticoagulation in cavernous sinus thrombosis. Neurology. 1988 Apr. 38(4):517-22. [Medline].

  21. Miller NR. Carotid-cavernous sinus fistula. Walsh and Hoyt's Neurophthalmology. 4th ed. 1991. Vol 4: 2165-2209.

  22. Satomi J, Satoh K, Matsubara S, et al. Angiographic changes in venous drainage of cavernous sinus dural arteriovenous fistulae after palliative transarterial embolization or observational management: a proposed stage classification. Neurosurgery. 2005 Mar. 56(3):494-502; discussion 494-502. [Medline].

  23. Schatz NJ, Farmer P. Tolosa Hunt syndrome: The pathology of painful ophthalmoplegia. Neurophthalmology Symposium of the University of Miami & Bascom Palmer Eye Institute. 1972. 102-112.

  24. Thomas JE, Yoss RE. The parasellar syndrome: problems in determining etiology. Mayo Clin Proc. 1970 Sep. 45(9):617-23. [Medline].

  25. Zweifler RM. Management of acute stroke. South Med J. 2003 Apr. 96:380-5. [Medline].

 
Previous
Next
 
Carotid-cavernous fistula.
A T1-weighted, coronal MRI.
This patient is a 55-year-old woman who originally had symptoms of eye pain and pulse synchronous tinnitus on the left. She was found to have an indirect left carotid cavernous sinus fistula and underwent successful coiling of the fistula. This picture shows her after the procedure, as she had developed left eye chemosis and diplopia. A left lateral rectus paralysis was present on examination. In this case, the probable causes of the ophthalmoplegia could be mass effect or occlusion of the vasa nervorum supplying the sixth cranial nerve, which travels in the adventitia of the carotid artery. Here, the prognosis is excellent, and the authors have seen several cases with improvement within 4-8 weeks after coiling.
Early phase of the post-fistula coiling angiogram of the patient shown above. Coils can be appreciated at the cavernous portion of the carotid artery.
Later filling phase of the angiogram for the patient shown above. Note that coiling has prevented anomalous filling of the cavernous sinus fistula.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.