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Septic Thrombosis of the Cavernous Sinuses
John R. Ebright, MD;
Mitchell T. Pace, MD;
Asher F. Niazi, MD
Arch Intern Med. 2001;161:2671-2676.
ABSTRACT
Septic thrombosis of the cavernous sinuses (or cavernous sinus thrombophlebitis
[CST]) is a dramatic and potentially lethal illness, which is still occasionally
seen by clinicians. Before the availability of antimicrobial agents, mortality
from CST was near 100%, but it markedly decreased to approximately 20% to
30% during the antibiotic era.1-2
Nevertheless, the threat of death and serious morbidity continues to necessitate
early recognition, diagnosis, and treatment of CST to minimize risks to the
patient. Accordingly, we reviewed the salient clinical features of this illness,
with emphasis on newer aspects of diagnosis and treatment.
ANATOMY
Two cavernous sinuses are positioned on either side of the sella turcica,
which contains the pituitary gland (Figure
1). These sinuses are connected by intercavernous sinuses located
anterior and posterior to the sella. As is true for all dural venous sinuses,
the cavernous sinuses are formed by a separation of the layers of dura mater
(specifically, the meningeal and periosteal layers), with trabeculae from
each layer crossing the spaces, giving them a reticular or cavernous structure.
Immediately below, separated by very thin bone, are the sphenoid sinuses.
Of great clinical importance is the intimate relationship of cranial nerves
III, IV, V, and VI, which, accompanied by the horizontal segment of the internal
carotid artery, run through the lumen in the cases of the artery and abducens
nerve or through the outside layers of the cavernous sinuses' lateral walls
in the cases of the oculomotor, trochlear, and ophthalmic maxillary branches
of the trigeminal nerves.4-5
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Figure 1. Frontal section through the cavernous
sinuses. Copyright 1997. Icon Learning Systems, LLC, a subsidiary of MediMedia
USA Inc. Reprinted with permission from ICON Learning Systems, LLC, illustrated
by Frank H. Netter, MD. All rights reserved.3
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The cavernous sinuses extend from the superior orbital fissure in front
backward to the petrous portion of the temporal bone. They receive blood from
the superior ophthalmic and cerebral veins and the sphenoparietal sinuses
and terminate posteriorly in the superior and inferior petrosal sinuses, which
drain into the transverse sinuses and internal jugular veins. In addition,
the cavernous sinuses are connected by emissary veins to the pterygoid plexus,
which is adjacent to the deep muscles of the face, and also communicates with
the deep facial and inferior ophthalmic veins (Figure 2).
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Figure 2. Relationship of the cavernous
sinuses to other dural sinuses and veins of the head and face.
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PATHOGENESIS
The dural sinuses and the cerebral and emissary veins have no valves,
which allows blood to flow in either direction according to pressure gradients
in the vascular system. This fact and the extensive direct and indirect vascular
connections of the centrally located cavernous sinuses make them vulnerable
to septic thrombosis resulting from infection at multiple sites. Sinusitis,
especially involving the sphenoid and ethmoid sinuses, seems to be the most
common primary source of infection predisposing to CST. Infections arising
at other locations, such as the face, nose, tonsils, soft palate, teeth (lower
and upper), and ears, are less common primary sources since antibiotic therapy
has become widely available. Orbital infection is rarely complicated by CST,
although the ophthalmic veins drain directly into the orbits.6
The most common signs of CST are related to damage of the nerves that
traverse the cavernous sinuses (including the parasympathetic and sympathetic
nerves accompanying the oculomotor nerve and the internal carotid artery,
respectively) and to engorgement of the retinal and orbital vessels caused
by impaired venous drainage. It has been speculated that the trabeculated
sinuses act like sieves, trapping bacteria, emboli, and thrombi progressing
from anterior infected sites involving the nose, sinuses, or medial third
of the face, or in a retrograde fashion from lateral venous sinuses, ears,
or teeth. It is possible that more indolent, subacute cases arise from initially
sterile thrombi that become infected after extending into the cavernous sinuses
and that fulminant, acute cases result from rapid progression of an infected
thrombus or septic embolization from a primary infected focus.7
Irrespective of which mechanism is involved, the presence of enlarging infected
clots within a confined cavernous sinus spreading via intercavernous sinuses
to involve the opposite side is an ominous complication. Systemic effects
from sepsis, local effects from direct injury to cranial nerves III through
VI and impaired vascular drainage from the face and eyes, and possible extension
into adjacent tissue, causing meningitis, subdural empyema, and pituitary
necrosis, together may result in an overwhelming and truly catastrophic illness.
MICROBIOLOGIC FINDINGS
The most commonly identified pathogen in patients with CST continues
to be Staphylococcus aureus, identified in 60% to
70% of patients. Less frequently identified are streptococcal species, including Streptococcus pneumoniae; gram-negative bacilli; and anerobes.3 Blood cultures are commonly positive (approximately
70% of cases), especially in patients with acute, fulminant disease, whereas
cerebrospinal fluid, abnormal in most patients in terms of elevated white
blood cell counts and protein levels, is culture positive in only approximately
20% of cases.8 Occasionally, fungi such as Aspergillus and members of the Mucoraceae family may cause
CST.9-11
CLINICAL PRESENTATION
Multiple clinical features varying in frequency and severity have been
reported, with some, such as septic infarcts of other organs, becoming uncommon
since the availability of antibiotic therapy. Another variable in this condition
is the timing of the onset of signs and symptoms: patients with acute, fulminant
disease will manifest most signs and symptoms rapidly from the outset of illness,
and patients with a more subacute course will evidence the features listed
in Table 1 sequentially and over
several days. Nevertheless, most patients will develop fever, ptosis, proptosis,
chemosis, and external ophthalmoplegia during the course of their illness.
External ophthalmoplegia, defined as paralysis of the extraocular muscles
(in the case of CST, secondary to dysfunction of cranial nerves III, IV, and
VI, rather than direct involvement of the extraocular muscles), usually includes
all the extraocular muscles. However, it may be more limited or present at
least initially with only lateral rectus muscle palsy, especially when disease
spreads to the opposite eye. Spread to the opposite eye through the intercavernous
sinuses, usually within 24 to 48 hours of the initial unilateral periorbital
edema, is a common and characteristic feature of CST. Less frequent, but still
seen in most patients, are mild papilledema (usually a late finding), retinal
venous engorgement, and altered mental status consisting of lethargy or obtundation.
Headaches, an early symptom resulting from either sinusitis or CST, usually
are frontal, temporal, or retro-orbital and may be accompanied by tearing.
Violaceous edema of the upper lid accompanying periorbital swelling also is
common.
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Frequency of Symptoms and Physical Abnormalities in Patients With Septic
Thrombosis of the Cavernous Sinuses*
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Decreased visual acuity, internal ophthalmoplegia, and periorbital sensory
alteration secondary to trigeminal nerve (cranial nerve V) dysfunction have
been reported in less than half of the patients. Internal ophthalmoplegia,
defined as paralysis of the iris and ciliary apparatus, results from dysfunction
of parasympathetic nerve fibers carried through the cavernous sinuses and
optic canals on the oculomotor (cranial nerve III) nerves or dysfunction of
the sympathetic fibers that join them to form the short ciliary nerves. As
a result, the pupils may be dilated from parasympathetic paralysis or may
be smaller and immobile if both parasympathetic and sympathetic fibers are
involved. Sensory alteration within the distribution of the first division
of the trigeminal nerve may present as hyperesthesia or hypoesthesia possibly
with a depressed corneal response. Diplopia, seizures, and hemiparesis are
uncommon.3, 6
The clinical presentation may be made even more complex as a result
of ischemic changes or extension of infection from the cavernous sinuses or
primary site of infection to involve the adjacent vascular structures or brain
parenchyma. Southwick et al3 reviewed the pathologic
findings of 23 patients who died or underwent surgery during the antibiotic
era. Extension of the thrombosis to other venous sinuses, including petrosal,
inferior sagittal, sigmoid, and lateral, was observed in 7 patients. Such
extension may not only worsen headache, obtundation, and papilledema but may
also result in additional findings, such as ear and neck pain, odynophagia,
dysphagia, hoarseness, lateral-gaze nystagmus, seizures, and hemiplegia. In
addition, the same authors7 noted 4 cases of
pituitary necrosis due to contiguous spread of infection or ischemic damage,
11 cases of meningitis, and 9 cases of brain abscess or subdural empyema,
primarily in the frontoparietal or temporal lobes.3
DIFFERENTIAL DIAGNOSIS
Cavernous sinus thrombophlebitis is only 1 (albeit probably the most
dramatic) of many causes of painful ophthalmoplegia. The most common condition
mimicking acute CST is orbital cellulitis, which commonly causes periorbital
swelling, proptosis, chemosis, ophthalmoplegia, fever, decreased vision, and
pain.12 However, bilateral eye involvement,
papilledema, decreased periocular sensation, dilated pupils, marked systemic
toxic effects, and abnormal spinal fluid are much more likely to be features
of CST and aid in differentiating the two conditions. Preseptal cellulitis,
which does not cause proptosis and ophthalmoplegia, generally causes little
confusion. Orbital apex syndrome, a rare complication of sinusitis, results
from inflammation or infection involving 2 clefts in the bony posterior orbit:
(1) the superior orbital fissure, which transmits cranial nerves III, IV,
and VI and branches of the ophthalmic division of cranial nerve V, and the
superior ophthalmic vein, and (2) the optic canal, through which pass the
ophthalmic artery and optic nerve. This condition, compared with orbital cellulitis,
more typically causes visual loss and ophthalmoplegia out of proportion to
or preceding signs of anterior eye involvement, such as proptosis and periorbital
edema. Because the optic nerve passes through the apex but not through the
cavernous sinus, impaired vision is more common with the orbital apex syndrome
than with CST.13-14
Other more indolent or chronic conditions may cause painful ophthalmoplegia
owing to involvement of the cavernous sinuses, including local or metastatic
malignancy; aseptic thrombosis resulting from trauma, myeloproliferative diseases,
or dehydration; granulomatous disease, such as tuberculosis or fungal infection,
sarcoid, syphilis, or Tolosa-Hunt syndrome; aneurysm of the internal carotid
artery; or carotid-cavernous fistula. Other chronic diseases that may be confused
with disease involving the cavernous sinuses are endocrine exophthalmos and
ophthalmoplegic migraine.15-20
DIAGNOSIS
Before the availability of computed tomography (CT) or magnetic resonance
imaging (MRI), CST was diagnosed by its clinical features or at autopsy. Occasionally,
cerebral angiography or the more definitive orbital venography was performed,
but it was accompanied, at least in the case of orbital venography, by the
possibility of serious complications. It was difficult to puncture the frontal
veins in patients who were acutely ill with facial edema; in addition, there
was much concern that orbital venography, accomplished by injecting contrast
material under pressure, may actually disseminate the infection or cause extension
of the thrombosis.21
The availability of high-resolution enhanced CT scans and, more recently,
MRI has remarkably improved our ability to establish the diagnosis of CST
using noninvasive technology. Although there is currently some debate regarding
which of the two is the procedure of first choice, most experience is with
high-resolution CT performed with a slice thickness of 3 mm or less.22 Abnormal findings include those that are direct signs
of CST, consisting of enlargement and expansion of the cavernous sinus with
lateral wall flattening or convexity rather than normal concavity, best visualized
on coronal images. In addition, multiple irregular or single large filling
defects within the enhancing cavernous sinus are highly suggestive direct
evidence for thrombi. This is particularly the case when the filling defects
are irregular and do not correspond to the anatomic course of neural structures
or a thrombosed intracavernous section of the internal carotid artery. They
also must be differentiated from intracavernous fat deposits by size (thrombi
usually >7 mm), density, and signal intensity.21-24
Indirect signs, related to concomitant venous obstruction, consist of
dilation of the superior ophthalmic vein, exophthalmos, soft tissue edema,
and thrombi visualized in the veins and sinuses tributary to the cavernous
sinus (superior ophthalmic vein and superior petrosal, inferior petrosal,
and sigmoid sinuses).21-24
Magnetic resonance imaging may be of greatest value either to reexamine
patients with nondiagnostic CT scans or to further assess complications involving
the pituitary gland or extension of infection into adjacent meninges or brain.21-22 We report a case of probable mucormycosis
in which the organism seems to have invaded the cavernous sinuses from the
paranasal sinuses to illustrate these points.
REPORT OF A CASE
A 49-year-old woman with a history of diabetes mellitus was admitted
to the hospital and treated for diabetic ketoacidosis, which was reversed
by the second hospital day. Her course was complicated by severe gastritis
and upper gastrointestinal tract bleeding. On the seventh hospital day, she
complained of right eye pain and experienced rapid loss of vision, accompanied
by right eyelid edema, ptosis, and external and internal ophthalmoplegia.
Proptosis was present the following day. Treatment initially was intravenous
ampicillin and sulbactam; on the ninth hospital day, high-dose amphotericin
B lipid complex was added. By the 11th hospital day, the left eye was also
involved, with paralysis of cranial nerves III, IV, and VI; ptosis; and decreased
visual acuity. The patient died shortly thereafter secondary to respiratory
arrest, presumably from progressive infection of the central nervous system.
Permission for autopsy was denied. A biopsy sample from the ethmoid sinus
obtained during an open surgical procedure by the ear, nose, and throat service
a few days before her death was unrevealing on frozen sections but consistent
with mucormycosis on fungal stains of permanent sections.
Computed tomography performed with coronal images of the paranasal sinuses
on the eighth hospital day revealed mucous retention cysts in both maxillary
sinuses, opacification of the ethmoid sinuses, and mucosal thickening of the
left sphenoid sinus. Proptosis was present on the right side. The superior
ophthalmic veins did not seem to be engorged. The cavernous sinuses were poorly
visualized owing to insufficient intravenous contrast agent within the sinuses.
Two days later, an MRI scan revealed mucosal thickening of the sinuses and
diminished enhancement in the right cavernous sinus, accompanied by a right
cavernous internal carotid artery signal void, which was smaller than that
seen on the left (providing presumptive evidence for compression of the right
internal carotid artery by thrombus within the sinus). Another MRI the following
day revealed the additional finding of a new filling deffect in the left cavernous
sinus (Figure 3).
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Figure 3. Magnetic resonance image of the
cavernous sinuses, with a coronal (frontal), T1-weighted, postgadolinium image
through the sella turcica, which reveals a bulging lateral wall of the cavernous
sinus (thin arrow) and a large filling defect secondary to thrombus on the
right side (curved arrow). The left cavernous sinus demonstrates a small filling
defect (large arrow) adjacent to the internal carotid flow void secondary
to thrombus from intercavernous spread. The black arrow indicates a portion
of the pituitary gland.
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MANAGEMENT AND TREATMENT
Management of patients with CST must also include treatment of primary
infections, such as sinusitis, dental abscesses, and facial cellulitis, and
possible complications, including brain abscesses, meningitis, and extension
to other venous sinuses. Initial antibiotic choice, while awaiting culture
results, might consist of nafcillin sodium, metronidazole, and ceftriaxone
sodium or cefotaxime sodium to treat the patient for the most common organisms
associated with this disease. Vancomycin could be substituted for nafcillin
if the risk of methicillin resistance is high. Doses should be high, appropriate
for critically ill patients with intravascular and possible central nervous
system infections. The duration of antibiotic therapy is not standardized,
but 3 to 4 weeks, consistent with management of other intravascular infections,
such as endotheliitis or suppurative phlebitis, seems to be a reasonable projection,
especially if signs of inflammation, toxic effects, and fever have ceased
during that period.25
Surgical drainage of the cavernous sinus is almost never performed,
but surgery may be essential for the management of primary sinusitis or dental
infection or complicating brain abscess, orbital abscess, or subdural empyema.
Similarly, reduction of inflammation and edema by administering systemic corticosteroids
is not a well-supported intervention in patients with CST. In a few patients,
corticosteroid use may have contributed to improving cranial nerve dysfunction3, 26 or persistent orbital congestion.27 Rarely, corticosteroid use may play a critical role
in caring for patients with adrenal insufficiency secondary to ischemia or
necrosis of the pituitary gland.28-29
Full anticoagulation using heparin, however, is possibly beneficial in select
patients. Although no randomized controlled studies have been conducted (and
because of the infrequency of this disease, probably never will be conducted),
recent retrospective reviews provide some support for heparin use in the absence
of cortical venous infarction. Anticoagulant therapy begun early (ie, within
7 days of hospitalization for CST) may reduce morbidity rates in survivors.30 In particular, a reduction in diplopia from cranial
nerve dysfunction, unilateral blindness, seizures, hemiparesis, and hypopituitarism
may be observed. The review by Southwick et al3
suggests that early anticoagulant therapy in patients with unilateral CST
may also reduce mortality rates. Duration of anticoagulant therapy with warfarin
sodium after initial heparin therapy is unknown, but 4 to 6 weeks has been
suggested.30
MORBIDITY AND MORTALITY
Mortality has decreased from 80% to 100% in the preantibiotic era to
20% to 30% since 1940. In addition, Yarington2
points to a decrease in morbidity from 50% to 75% to only 22%. Nevertheless,
the threat of temporary complications and long-term sequelae remains. In a
review published early in the antibiotic era, Shaw7
described 60 patients treated with either sulfonamides or penicillin: 53 recovered,
but most (77%) had complications or long-term sequelae. Twenty-five patients
had metastatic infection primarily involving the lungs, with abscesses, empyema,
and pneumonia. Nine patients developed orbital abscesses and 5 developed abscesses
in the brain. Prolonged cranial nerve dysfunction, especially of nerves III
and VI, were the most common long-term sequelae; 5 patients developed unilateral
blindness, and 4 had decreased visual acuity. Prominent facial veins and spastic
paresis of the arm were also noted but were unusual.7
A more recent review3 of 96 patients treated
since 1940 found 29 to have long-term sequelae, including oculomotor (cranial
nerve III) weakness in 16 (17%) of 95 patients, blindness in 16 (17%), pituitary
insufficiency in 2 (2%), and hemiparesis in 3 (3%). The cause of blindness
has been speculated to be pressure on the retinal artery and vein at the orbital
apex, arteritis of the internal carotid artery, emboli to the retinal artery,
or toxic neuropathy of the optic nerve.31 Pituitary
insufficiency, a rare but well-documented event, results from either infarction
or extension of infection into the sella turcica.29
Hemiparesis may be a consequence of internal carotid artery occlusion, cerebral
abscess, or cortical vein thrombosis.30
CONCLUSIONS
Although rare, CST remains a dramatic and potentially lethal complication
of infections involving the sinuses, face, ears, and oral cavity. Early recognition
and differentiation from other diseases that can mimic it coupled with aggressive
medical and possible surgical intervention are key to reducing mortality rates
and long-term sequelae. Recent improvements in imaging, especially CT and
MRI, have contributed substantially to the rapid diagnosis of this condition.
AUTHOR INFORMATION
Accepted for publication April 9, 2001.
Corresponding author and reprints: John R. Ebright, MD, Division
of Infectious Diseases, Harper Hospital, 3990 John R, 4 Brush Center, Detroit,
MI 48201 (e-mail: jebright{at}intmed.wayne.edu).
From the Departments of Medicine (Drs Ebright and Niazi) and Radiology
(Dr Pace), Wayne State University School of Medicine and Detroit Medical Center,
Detroit, Mich.
REFERENCES
| |
1. Clune JP. Septic thrombosis within the cavernous chamber. Am J Ophthalmol. 1963;56:33-39.
2. Yarington CT. Cavernous sinus thrombosis revisited. Proc R Soc Med. 1977;70:456-459.
ISI
| PUBMED
3. Southwick FS, Richardson EP, Swartz MN. Septic thrombosis of the venous dural sinuses. Medicine (Baltimore). 1986;65:82-106.
PUBMED
4. Woodburne RT, Burkel WE. The head and neck. In: Essentials of Human Anatomy. 9th ed.
New York, NY: Oxford University Press; 1994:325-326.
5. VanOverbeake JJ, Jansen JJ, Tulleken CAF. The cavernous sinus syndrome: an anatomical and clinical study. Clin Neurol Neurosurg. 1988;90:311-319.
FULL TEXT
|
ISI
| PUBMED
6. DiNubile MJ. Septic thrombosis of the cavernous sinuses. Arch Neurol. 1988;45:567-572.
FREE FULL TEXT
7. Shaw RE. Cavernous sinus thrombophlebitis: a review. Br J Surg. 1952;40:40-48.
8. Taylor PJ. Cavernous sinus thrombophlebitis. Br J Ophthalmol. 1957;41:228-237.
9. Sekhar LN. Carotid-cavernous sinus thrombosis caused by Aspergillus
fumigatus. J Neurosurg. 1980;67:219-222.
10. Estrem SA, Tully R, Davis WE. Rhinocerebral mucormycosis: computed tomographic imaging of cavernous
sinus thrombosis. Ann Otol Rhinol Laryngol. 1990;99:160-161.
ISI
| PUBMED
11. Dooley DP, Hollsten DA, Grimes SR, Moss J. Indolent orbital apex syndrome caused by occult mucormycosis. J Clin Neuroophthalmol. 1992;12:245-249.
PUBMED
12. Price CD, Hameroff SB, Richards RD. Cavernous sinus thrombosis and orbital cellulitis. South Med J. 1971;64:1243-1247.
ISI
| PUBMED
13. Colson AE, Daily JP. Orbital apex syndrome and cavernous sinus thrombosis due to infection
with Staphylococcus aureus and Pseudomonas aeruginosa. Clin Infect Dis. 1999;29:701-702.
ISI
| PUBMED
14. Kronschnabel EF. Orbital apex syndrome due to sinus infection. Laryngoscope. 1974;84:353-371.
FULL TEXT
|
ISI
| PUBMED
15. Hunt WE, Meagher JN, LeFever HE, Zeman W. Painful ophthalmoplegia: its relation to indolent inflammation of the
cavernous sinus. Neurology. 1961;11:56-62.
16. Jellinek EH. The orbital pseudotumour syndrome and its differentiation from endocrine
exophthalmos. Brain. 1969;92:35-58.
FREE FULL TEXT
17. Ryan MW, Rassekh CH, Chaljub G. Metastatic breast carcinoma presenting as cavernous sinus syndrome. Ann Otol Rhinol Laryngol. 1996;105:666-668.
ISI
| PUBMED
18. Lovel T, Marsan RE. Carotid cavernous fistula. Angiology. 1974;25:231-236.
19. Grayeli AB, Redondo A, Salama J, Rey A. Tuberculoma of the cavernous sinus: case report. Neurosurgery. 1998;42:179-181.
FULL TEXT
|
ISI
| PUBMED
20. Brismar G, Brismar J. Aseptic thrombosis of orbital veins and cavernous sinus. Acta Ophthalmologica. 1977;55:9-22.
PUBMED
21. Berge J, Louail C, Caille JM. Cavernous sinus thrombosis diagnostic approach. J Neuroradiol. 1994;21:101-117.
ISI
| PUBMED
22. Schuknecht B, Simmen D, Yuksel C, Valavanis A. Tributary venosinus occlusion and septic cavernous sinus thrombosis:
CT and MRI findings. AJNR Am J Neuroradiol. 1998;19:617-626.
ABSTRACT
23. Ben-Uri R, Palma L, Kaveh Z. Case report: septic thrombosis of the cavernous sinus: diagnosis with
the aid of computed tomography. Clin Radiol. 1989;40:520-522.
FULL TEXT
|
ISI
| PUBMED
24. Ahmadi J, Keane JR, Segall HD, Zee CS. CT observations pertinent to septic cavernous sinus thrombosis. AJNR Am J Neuroradiol. 1985;6:755-758.
ABSTRACT
25. Zahllar M, Spector RH, Skoglund RR, Digby D, Nyhan WL. Cavernous sinus thrombosis. West J Med. 1980;133:44-48.
ISI
| PUBMED
26. Solomon OD, Moses L, Volk M. Steroid therapy in cavernous sinus thrombosis. Am J Ophthalmol. 1962;54:1122-1124.
27. Friberg TR, Sogg RL. Ischemic optic neuropathy in cavernous sinus thrombosis. Arch Ophthalmol. 1978;96:453-456.
FREE FULL TEXT
28. Karlin FJ, Robinson WA. Septic cavernous sinus thrombosis. Ann Emerg Med. 1984;13:449-455.
FULL TEXT
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ISI
| PUBMED
29. Ivey KJ, Smith H. Hypopituitarism associated with cavernous sinus thrombosis. J Neurol Neurosurg Psychiatry. 1968;31:187-189.
FREE FULL TEXT
30. Levine SR, Twyman RE, Gilman S. The role of anticoagulation in cavernous sinus thrombosis. Neurology. 1988;38:517-522.
FREE FULL TEXT
31. Geggel HS, Insenberg SJ. Cavernous sinus thrombosis as a cause of unilateral blindness. Ann Ophthalmol. 1982;14:569-574.
ISI
| PUBMED
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