Transient monocular visual loss:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia [u.a.]
Saunders
1996
|
| Schriftenreihe: | Ophthalmology clinics of North America
9,3 |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XII S., S. 323 - 525 Ill. |
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| 245 | 1 | 0 | |a Transient monocular visual loss |c Barrett Katz, guest ed. |
| 264 | 1 | |a Philadelphia [u.a.] |b Saunders |c 1996 | |
| 300 | |a XII S., S. 323 - 525 |b Ill. | ||
| 336 | |b txt |2 rdacontent | ||
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| 490 | 1 | |a Ophthalmology clinics of North America |v 9,3 | |
| 650 | 2 | |a Cécité | |
| 650 | 2 | |a Trouble vision | |
| 650 | 2 | |a Vision monoculaire | |
| 650 | 4 | |a Amaurosis Fugax | |
| 650 | 4 | |a Amaurosis fugax | |
| 650 | 0 | 7 | |a Amaurosis fugax |0 (DE-588)4200814-1 |2 gnd |9 rswk-swf |
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CONTENTS
Preface xv
Barrett Katz
Color Plates xvii
Transient Monocular Vision Loss: A Historical Perspective 323
William P. Hoyt
Questions concerning terminology, classifications, and pathophysiologies
of transient monocular visual loss need to be addressed before clinicians
can logically approach practical issues of management. The concept of errtbo
lization of the retinal arteriolar system and especially the duration of tran¬
sient monocular attacks may provide clues as to the etiology.
Vascular Anatomy of the Visual System 327
Mark S. Borchert
This article reviews the anatomy of the blood supply of the eye and the
visual centers of the brain. The course of the major vessels from the heart
to the visual centers is followed, and the clinical implications of lesions at
various sites within these vessels are reviewed.
Amaurosis Fugax: Terminology, Clinical Description, Differential
Diagnosis 339
Ippolit C. A. Matjucha
Amaurosis fugax and transient monocular blindness are closely related
terms that are used by most clinicians and authors to describe sudden,
monocular, painless, temporary visual loss lasting usually from 2 to 30
minutes and followed by complete recovery, in which the ocular examina¬
tion between episodes shows either normal anatomy or abnormalities con¬
fined to the retinal vasculature. This definition strongly implies a vascular
etiology. Ipsilateral carotid atherosclerotic narrowing is the most common
diagnosis in these cases and, in terms of the potential patient benefit from
intervention in appropriate cases, the most clinically significant. Neverthe¬
less, numerous other etiologic agents may either produce or mimic amauro¬
sis fugax.
| OPHTHALMOLOGY CLINICS OF NORTH AMERICA
VOLUME 9 • NUMBER 3 • SEPTEMBER 1996 ix
The Natural History of Patients with Amaurosis Fugax 351
Lanning B. Kline
Amaurosis fugax is an important clinical symptom that patients may report
to physicians in diverse specialties. If it occurs in individuals younger than
50 years of age, it is associated with a benign prognosis; however, in older
patients this complaint should prompt comprehensive patient evaluation.
This article focuses on four aspects of the natural history of patients with
amaurosis fugax: (1) the association of this symptom with atheromatous
carotid artery disease; (2) the risk of permanent visual impairment; (3) the
risk of stroke; and (4) the risk of death.
Embolic Causes of Transient Monocular Visual Loss: Appearance,
Source, and Assessment 359
Neil R. Miller
Emboli that cause monocular visual loss usually travel to and lodge within
arteries and arterioles that supply the optic nerve, the retina, or both. Because
the retinal vessels can be seen with an ophthalmoscope, emboli within them
can be identified. This is important because certain types of emboli have a
distinctive appearance that suggests the probable origin of the emboli and
thus is crucial in determining the nature and extent of the assessment of
the patient. The most common emboli that are recognized in the retinal
arterial circulation are cholesterol emboli, platelet fibrin emboli, and emboli
composed of calcium. Less common varieties of retinal emboli include tumor
emboli from cardiac myxoma and metastatic neoplasms, fat emboli from
fractures of long bones, septic emboli, talc emboli, and miscellaneous emboli
of depot drugs, silicone, or air that occur after injections in the region of
the face or scalp.
Ocular Causes of Transient Monocular Visual Loss Other Than Emboli 381
William T. Shults
Nonembolic ocular causes of transient visual loss, although not as frequent
as embolic transient ischemic attacks are nonetheless important to recognize
to save the patient of unnecessary, potentially invasive and expensive diag¬
nostic testing. Several optic neuropathies may produce brief episodes of
monocular visual loss including optic disc drusen and colobomas, papi
lledema, infiltrative papillopathies, and orbital tumors. Uhtoff s phenome¬
non may occur in both patients with demyelinating disease and Leber s
hereditary optic neuropathy. Several anterior segment conditions deserve
mention including subacute angle closure attacks, recurrent anterior cham¬
ber hemorrhages and reversible cataracts in diabetics with blood sugar
fluctuations. Retinal dysfunction engendered by venous occlusive disease
or chronic ischemia secondary to severe carotid occlusive disease rounds
out the remaining ocular causes of nonembolic transient visual loss covered
in this article.
Vasospasm—Not Migraine—in the Anterior Visual Pathway 393
Jacqueline M.S. Winterkorn and Ronald M. Burde
Ocular vasospasm and cortical migraine are discussed and contrasted. Vaso¬
spasm, but not migraine, occurs in the anterior visual pathway. Clinically,
monocular visual loss caused by ocular dysfunction must be discriminated
from binocular visual loss of cortical origin. Vasospasm is one of the primary
causes of amaurosis fugax. Vasospasm also can play a secondary role,
contributing to other causes of visual loss of ocular origin. Migraine is a
cortical phenomenon, not based on vasospasm or abnormal vascular activity,
but probably reflects abnormal neuronal activity. A change is suggested in
terminology: Prinzmetal s amaurosis or retinal Raynaud s should be
used to describe vasospastic transient visual loss in the anterior visual
pathways.
X CONTENTS
Acute Ischemic Disorders of the Optic Nerve: Pathogenesis, Clinical
Manifestations, and Management 407
Sohan Singh Hayreh
Acute ischemic disorders of the optic nerve are of two types: anterior (AION)
and posterior (PION) ischemic optic neuropathies, involving the optic nerve
head and rest of the optic nerve, respectively. AION is one of the most
prevalent and visually crippling diseases in the middle aged and elderly,
and is potentially bilateral. To clarify the underlying causes and clinical
features, and logical management of AION, the basic scientific issues in¬
volved are discussed. AION clinically is of two types: (1) that due to giant
cell arteritis (arteritic AION), and (2) the rest (nonarteritic AION). Arteritic
AION is an ocular emergency and requires immediate treatment with sys¬
temic corticosterioids to prevent further visual loss. Clinical parameters that
help to differentiate arteritic from nonarteritic AION, and the management
of both types of AION, are discussed.
Neurologic Mechanisms of Transient Visual Loss 443
Valerie A. Purvin
Episodes of visual loss affecting one hemifield are often misinterpreted by
the individual experiencing them as involving one eye. This article reviews
the important causes of transient binocular visual loss, including vertebro
basilar ischemic attacks, migraine, epilepsy, increased intracranial pressure,
and metabolic encephalopathies. Neurologic deficits that may stimulate
transient visual loss are reviewed also, such as transient diplopia, oscillopsia,
and eyelid closure. Finally, fixed deficits that may be transiently appreciated
are discussed.
Evaluating the Patient with Transient Monocular Vision Loss: The
Young Versus the Elderly 455
Nancy J. Newman
A practical approach to the evaluation of the patient with transient monocu¬
lar visual loss must be based on the age of the patient and the suspected
underlying etiology. In the older patient, tests should be performed to
investigate giant cell arteritis, atherosclerotic large vessel disease, especially
of the ipsilateral carotid artery, and cardiac abnormalities. In the younger
patient, transient monocular visual loss is usually benign and the evaluation
should be tailored to the particular clinical setting.
Noninvasive Vascular Examination in Amaurosis Fugax 467
John E. Carter and Merrill Kanter
Patients with transient monocular blindness may have emboli from the
carotid arteries or from the heart. Noninvasive evaluation of the carotids
and the heart provide sufficient information to avoid invasive studies in
patients unlikely to require surgical intervention for carotid stenosis and
may provide a diagnosis if a cardiac source is responsible for the patients
symptoms. Invasive procedures can be reserved for patients with sufficient
abnormality and potential for surgical intervention to justify the risk in¬
volved with arteriography.
Angiography in Transient Monocular Visual Loss 473
Percy N. Karanjia and Daniel M. Jacobson
This article reviews the indications for cerebral angiography in patients
with transient monocular visual loss and explains how this procedure can
help clinicians understand the underlying mechanisms producing the pre¬
senting symptom. The criteria for selecting patients for the test, the angio
graphic appearance of common diseases, and complications of the procedure
are discussed.
CONTENTS xi
Medical Therapies for Transient Monocular Visual Loss 491
Sophia M. Chung
Transient monocular visual loss may herald a cerebral infarction or a central
retinal artery or both. Once evaluation is completed, medical therapy may
be indicated to prevent further symptoms or complications. Aspirin, ticlopi
dine, calcium channel blockers, and anticoagulants are discussed as potential
medical treatments. The future holds new recommendations about the ap¬
propriate dosage of aspirin and new antiplatelet agents.
Surgical Therapies for Transient Monocular Visual Loss 505
Steven M. Santilli and Jerry Goldstone
Surgical therapies for transient monocular visual loss are used for lesions
of the accessible, extracranial cerebral arteries. Carotid bifurcation stenosis
is the most frequent surgically correctable lesion leading to transient monoc¬
ular vision loss and is best treated by carotid artery endarterectomy. Occlu¬
sion of the internal carotid artery may be a cause of transient monocular
visual loss and can be treated effectively with external carotid endarterec¬
tomy and ligation of the internal carotid artery. Other infrequent surgically
correctable causes of transient monocular visual loss include proximal com¬
mon carotid artery, innominate artery, and aortic arch atherosclerosis and
carotid fibromyscular dysplasia. Surgical therapy for transient monocular
visual loss is safe and effective in properly selected patients if performed
with acceptably low rates of surgical morbidity and mortality.
Who Needs Carotid Endarterectomy (Circa 1996)? 513
Jonathan D. Trobe
After being in decline for a decade because of doubts of efficacy and fears
of high complication rates, endarterectomy is now back in force. Its resur¬
gence is based on the results of two collaborative trials for symptomatic
carotid stenosis, the 1991 North American Symptomatic Carotid Endarterec¬
tomy Trial (NASCET) and the 1991 European Carotid Surgery Trial (ECST),
and one trial for asymptomatic carotid stenosis, the 1995 Asymptomatic
Carotid Atherosclerosis Study (ACAS). All three trials showed a statistically
significant benefit of endarterectomy in reducing future stroke among pa¬
tients with high grade stenosis. But a strict interpretation of the data leads
this observer to conclude that the procedure is indicated only for patients
with 70% or greater stenosis who have suffered recent ipsilateral hemi¬
spheric TIAs or minor strokes in the carotid distribution and who are free
of the medical and angiographic features that would make surgery too
risky. Patients with ocular TIAs alone and those with retinal infarcts or
carotid stenosis discovered incidentally should not undergo endarterectomy
because their risk of stroke with optimal medical treatment is relatively
low. Patients who have chronic ocular ischemia, but no recent TIAs, fall
into limbo where there are not enough data to make a reasoned decision.
Index 521
Subscription Information Inside back cover
Xii CONTENTS
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| spelling | Transient monocular visual loss Barrett Katz, guest ed. Philadelphia [u.a.] Saunders 1996 XII S., S. 323 - 525 Ill. txt rdacontent n rdamedia nc rdacarrier Ophthalmology clinics of North America 9,3 Cécité Trouble vision Vision monoculaire Amaurosis Fugax Amaurosis fugax Amaurosis fugax (DE-588)4200814-1 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Amaurosis fugax (DE-588)4200814-1 s DE-604 Katz, Barrett Sonstige oth Ophthalmology clinics of North America 9,3 (DE-604)BV002178285 9,3 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=007403403&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Transient monocular visual loss Ophthalmology clinics of North America Cécité Trouble vision Vision monoculaire Amaurosis Fugax Amaurosis fugax Amaurosis fugax (DE-588)4200814-1 gnd |
| subject_GND | (DE-588)4200814-1 (DE-588)4143413-4 |
| title | Transient monocular visual loss |
| title_auth | Transient monocular visual loss |
| title_exact_search | Transient monocular visual loss |
| title_full | Transient monocular visual loss Barrett Katz, guest ed. |
| title_fullStr | Transient monocular visual loss Barrett Katz, guest ed. |
| title_full_unstemmed | Transient monocular visual loss Barrett Katz, guest ed. |
| title_short | Transient monocular visual loss |
| title_sort | transient monocular visual loss |
| topic | Cécité Trouble vision Vision monoculaire Amaurosis Fugax Amaurosis fugax Amaurosis fugax (DE-588)4200814-1 gnd |
| topic_facet | Cécité Trouble vision Vision monoculaire Amaurosis Fugax Amaurosis fugax Aufsatzsammlung |
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