Download Headache and the eye

CE: Namrta; ICU/363; Total nos of Pages: 5;
ICU 363
Headache and the eye
Rima M. Dafera and Walter M. Jayb
a
Department of Neurology and bDepartment of
Ophthalmology, Loyola University Medical Center,
Maywood, Illinois, USA
Correspondence to Rima M. Dafer, MD, MPH,
Department of Neurology, Loyola University Chicago,
Stritch School of Medicine, 2160 South First Avenue,
Maywood, IL 60153, USA
Tel: +1 708 216 5350; fax: +1 708 216 5617;
e-mail: [email protected]
Current Opinion in Ophthalmology 2009,
20:000–000
Purpose of review
Visual disturbances and ocular symptoms are common manifestations of two primary
headache disorders, migraine and trigeminal autonomic cephalalgias, and many
secondary headache disorders.
Recent findings
Structural lesions have been described with trigeminal autonomic cephalalgias. A
systematic diagnostic evaluation including neuroimaging with assessment of
intracranial and cervical vasculature, and the sellar and paranasal regions is
recommended in every patient presenting with symptoms indicative of trigeminal
autonomic cephalalgias for the first time.
Summary
Ophthalmologists are often the first physicians to evaluate patients presenting with
headaches and ocular pain or visual symptoms. Knowledge of primary and secondary
headache disorders, a detailed history, and a thorough clinical examination are
prerequisites for accurate diagnosis and appropriate management.
Keywords
headache, migraine, ophthalmoplegia, trigeminal autonomic cephalalgia
Curr Opin Ophthalmol 20:000–000
ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
1040-8738
Introduction
Visual disturbances and ocular symptoms are common
manifestations of certain primary headache disorders and
many secondary headache disorders. The main primary
headache disorders that we discuss are migraine, trigeminal autonomic cephalalgias, and hemicrania continua.
Trigeminal autonomic cephalalgias can be subdivided
into cluster headache, paroxysmal hemicrania, and
short-lasting unilateral neuralgiform headache with conjunctival injection and tearing. We will also review a
number of secondary headache disorders with ocular
symptomatology.
Primary headache disorders
Three main primary headache disorders are associated
with prominent ophthalmological manifestations, including migraine, trigeminal autonomic cephalalgia, and
hemicrania continua [1]. The latter is discussed under
trigeminal autonomic cephalalgias (TACs) due to the
similarity in clinical symptomatology.
Migraine
Migraine is a common paroxysmal primary headache
disorder affecting 28 million people in the USA [2].
Migraine is often associated with ophthalmologic manifestations, including ocular pain, visual disturbances, and
ophthalmoplegia (Table 1).
1040-8738 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Visual aura occurs in 15–20% of migraineurs, and usually
precedes the headache onset. Typical migraine aura
is described as scintillating scotoma, fortifications,
stereotyped visual hallucinations, micropsia or Alice in
Wonderland, or constriction of the visual field. The
duration of the visual aura typically lasts 20 min, rarely
up to 60 min [1].
Migraine aura without headache or acephalgic migraine
is seen in 3–5% of migraineurs, often in older patients
with a remote history of migraine [1]. The visual
manifestations are similar to that of migraine with aura.
The condition should be differentiated from transient
ischemic attack and occipital lobe seizures.
Retinal migraine is characterized by recurrent episodes of
unilateral transient visual loss lasting minutes to 1 h.
Headache is not a prominent feature of the disorder.
Retinal migraine should be differentiated from ischemic
transient monocular blindness or amaurosis fugax associated with internal carotid artery disease [1,3–6].
Diplopia may occur in basilar-type migraine, a subtype of
migraine, in which headache is accompanied by neurological symptoms emanating from either brainstem or
bilateral hemispheric disturbance. Dizziness, dysarthria,
ataxia, tinnitus, hearing loss, dysarthria, bilateral paresthesias, altered consciousness, and syncope may occur
[1,7–9]. The condition is more common in adolescent
DOI:10.1097/ICU.0b013e328331270d
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
CE: Namrta; ICU/363; Total nos of Pages: 5;
ICU 363
2 Ocular manifestations of systemic disease
Table 1 Visual symptoms in migraine subtypes
Migraine subtype
Headache
Visual symptoms
Migraine with typical aura
Unilateral or bilateral, throbbing,
moderate to severe
Retinal migraine
Basilar-type migraine
Not prominent
Unilateral or bilateral, throbbing,
moderate to severe
Unilateral or bilateral, throbbing,
moderate to severe
Absent
Zigzag lines, scintillating scotomata, blurred vision,
visual distortion and fortifications, visual field
defect/tunnel vision, micropsia
Transient monocular blindness
Ophthalmoplegia
Ophthalmoplegic migraine
Migraine aura without headache
girls and young women. Basilar-type migraine should be
differentiated from demyelinating, inflammatory, vascular, or neoplastic conditions affecting the brainstem, and
is a diagnosis of exclusion.
Another form of migraine variant is ophthalmoplegic
migraine, a rare form of childhood neuralgia, often associated with migraine-like headache and periorbital pain.
The oculomotor nerve is most commonly involved
followed by the abducens and rarely the trochlear nerve.
The ophthalmoplegia may last from days to months.
Remission is usually spontaneous. The condition has
been recently reclassified as a demyelinating neuropathy
of the ocular cranial nerves. Differential diagnosis
includes conditions involving the parasellar region, orbital, and posterior fossa leading to headache and ophthalmoplegia. Enduring thickening of the cranial nerve
affected has been reported on MRI [10].
The pathophysiology of migraine is not clearly understood. Cortical spreading depression (CSD) is thought to
be the neuronal process underlying visual aura. CSD, in
turn, activates the trigeminovascular system and triggers
pathophysiological mechanism of the migraine headache
[11,12,13].
Management of migraine is targeted at acute treatment
and preventive therapy. Acute migraine headaches may
be treated with nonsteroidal anti-inflammatory drugs,
triptans, or ergot alkaloids. Triptans and ergot alkaloids
are contraindicated when basilar-type migraine is suspected. Patients with frequent migraine attacks usually
require long-term preventive therapy. Options include
beta-blockers, calcium channel blockers, tricyclic anti-
Ophthalmoplegia, typically oculomotor neuropathy
Zigzag lines, scintillating scotoma, blurred vision, visual distortion
and fortifications, visual field defect/tunnel vision, micropsia
depressants, and antiepileptic agents such as topiramate
and valproic acid.
Trigeminal autonomic cephalalgias
TACs are primary neurovascular headache disorders
characterized by severe, strictly unilateral, typically
retro-orbital or periorbital, short-lasting headaches
accompanied by prominent cranial facial parasympathetic
autonomic features [1,14]. TACs include cluster headache, paroxysmal hemicrania, and short-lasting unilateral
neuralgiform headache with conjunctival injection and
tearing (SUNCT). TACs subtypes differ in duration,
frequency, and rhythmicity of the attacks and in the
response to treatment (Table 2).
Cluster headache is the most frequent of the TACs. It is
characterized by attacks of severe excruciating periorbital
or retro-orbital pain accompanied by ipsilateral cranial
autonomic symptoms such as lacrimation or conjunctival
injection, miosis, and ptosis [1]. It is typically seen in men
in the third and fourth decade of life, commonly among
smokers. The attacks occur once every other day or up to
eight times a day and last 15 min to 3 h. Cluster headache
may be episodic, with periods of remission between
attacks, or chronic, in which attacks occur almost daily
for a year or more. Circadian biological changes and
neuroendocrine disturbances have suggested a pivotal
role for the posterior hypothalamus in the pathogenesis
of cluster headache [1,15].
Paroxysmal hemicrania is similar to cluster headache in
that headaches are severe, strictly unilateral, orbital or
supraorbital, accompanied by ipsilateral cranial autonomic features. Paroxysmal hemicrania may also be
Table 2 Characteristics of trigeminal autonomic cephalgias and hemicrania continua
Age (years)
M : F ratio
Location
Duration of pain
Frequency of attacks
Response to indomethacin
Cluster
Paroxysmal hemicrania
SUNCT
Hemicrania continua
30–40
3:1
Orbital/temporal
15–180 min
1 every other day to 8 per day
þ/
20–30
1:2
Orbital/temporal
2–30 min
1–40 per day
þþ
>60
1:2
Periorbital
5 s to 4 min
3–200 per day
20–30
1:3
Orbital/temporal
Minutes to days
Variable
þþ
F, female; M, male.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
CE: Namrta; ICU/363; Total nos of Pages: 5;
ICU 363
Headache and the eye Dafer and Jay 3
episodic or chronic. The condition is more common in
younger women in the second and third decades of age.
The duration of the attacks is 2–30 min, with a frequency
of 5–40 attacks a day. Paroxysmal hemicrania is characterized by absolute responsiveness to indomethacin [1].
Secondary headache disorders
SUNCT syndrome is characterized by short-lived attacks
of unilateral moderate-to-severe stabbing or electric
shock-like orbital or periorbital pain, accompanied by
prominent lacrimation and conjunctival injection. The
attacks are much more brief than those seen in other
TACs, typically lasting 5–250 s, and often recurring up to
200 times a day. The disorder has a male predominance,
often affecting those in the fifth to seventh decades of life
[1,16].
Painful ophthalmoplegia may occur in patients presenting with headaches secondary to vascular conditions, such
as aneurysm, carotid dissection, and carotid-cavernous
fistula, and inflammatory disorders including giant cell
arteritis (GCA), sarcoidosis, idiopathic orbital inflammatory diseases (IOIDs), and Tolosa–Hunt syndrome.
A systematic approach to the evaluation of painful
ophthalmoplegia can lead to prompt recognition of
serious disorders that can be associated with significant
morbidity or mortality if left untreated [24].
Hemicranium continuum is another primary headache
disorder, similar in characteristics to TACs, and is
included in the discussion for completeness. Hemicranium continuum is a daily continuous unremitting,
strictly unilateral headache of moderate-to-severe intensity, accompanied by trigeminal autonomic features,
sometimes with eyelid swelling or twitching. Patients
may experience migrainous symptoms and ice-pick
headaches. Like paroxysmal hemicranium, hemicranium
continuum has female preponderance. Complete responsiveness to therapeutic doses of indomethacin is an
essential criterion for the diagnosis according to the
International Classification of Headaches Disorders II.
Structural lesions have been described with TACs [17–
20,21,22,23]. A systematic diagnostic evaluation including neuroimaging and assessment of intracranial and
cervical vasculature and the sellar and paranasal regions
is recommended in every patient presenting with symptoms indicative of TAC for the first time [21].
The periodicity of the attacks in TACs suggests involvement of a biological clock within the hypothalamus,
with activation of nociceptive and autonomic pathways,
specifically the trigeminal nociceptive pathways.
Management of acute cluster headache attacks includes
oxygen therapy, parenteral or nasal triptans, or ergot
alkaloids. Preventive therapies are aimed at aborting a
cluster headache and decreasing the number of attacks.
These include prednisone, verapamil, lithium, and various antiepileptic drugs, mainly valproic acid, topiramate,
gabapentin, pregabalin, and lamotrigine. Both paroxysmal hemicrania and hemicrania continua are characterized by absolute responsiveness to indomethacin.
SUNCT is usually refractory to treatment, although
antiepileptic drugs may be considered. Other interventions may include sphenopalatine ganglion and occipital
nerve stimulation. Deep brain stimulation of the
posterior hypothalamus has recently emerged as a poten-
tial treatment option for refractory chronic drug-resistant
TACs.
IOID or orbital pseudotumor is an inflammatory disorder
that involves one or multiple structures contained within
the orbit. Prominent features include acute onset ocular
pain, swelling, proptosis, ophthalmoplegia, and progressive optic neuropathy. The condition should be differentiated from systemic diseases such as Graves’ disease,
Wegener’s granulomatosis, sarcoidosis, malignancies,
infectious diseases, or trauma. Management includes
systemic immunosuppression with corticosteroids, or
rituximab, in combination with surgery or radiation
therapy [25,26].
Tolosa–Hunt syndrome is a rare cause of painful ophthalmoplegia attributed to inflammatory granulomatous
infiltration of the superior orbital fissure or cavernous
sinus. It is characterized by unilateral periorbital or
retro-orbital pain, ipsilateral ophthalmoparesis mainly
oculomotor neuropathy, and less commonly trochlear
or abducens cranial nerve palsies, ipsilateral paresthesias
in the distribution of the ophthalmic division of the
trigeminal nerve, and remarkable steroids responsiveness
[24,27,28].
Ophthalmoplegia has been reported in patients with
headaches with neurologic deficits, and cerebrospinal
fluid (CSF) lymphocytosis (HaNDL) syndrome (known
as pseudomigraine syndrome with CSF pleocytosis)
[29,30]. This condition is a monophasic benign selflimited syndrome characterized by headaches, transient
neurologic symptoms, and the presence of aseptic CSF
lymphocytic pleocytosis.
Pituitary apoplexy is not an uncommon clinical syndrome
characterized by abrupt onset of severe headache, vomiting, visual impairment, ophthalmoplegia, meningismus,
altered level of consciousness, and endocrine dysfunction.
It occurs as a complication of sudden hemorrhage or
infarction of the pituitary gland, generally within a pituitary adenoma [31]. Treatment with corticosteroids
should be initiated as soon as possible, and decompressive
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
CE: Namrta; ICU/363; Total nos of Pages: 5;
ICU 363
4 Ocular manifestations of systemic disease
surgery should be considered in patients with decreased
visual acuity or visual field defect.
Paratrigeminal oculosympathetic syndrome (Raeder’s
paratrigeminal neuralgia) is an uncommon benign neurologic disorder characterized by unilateral periocular pain
and ipsilateral postganglionic Horner’s secondary to
involvement of the oculosympathetic fibers along the
course of the internal carotid artery [32,33]. Idiopathic
lesions of the middle cranial fossa should be excluded
[34].
Headaches, Horner’s syndrome, and painful ophthalmoplegia may also be seen in the setting of cavernous sinus
thrombosis or aneurysm, carotid dissection, and parasellar
neoplasms, and infectious causes such as mucormycosis,
rhizopus, and herpes zoster ophthalmicus.
Idiopathic intracranial hypertension (IIH) is characterized by increased intracranial pressure and the absence of
structural causes such as space-occupying lesion, ventriculomegaly, dural venous sinus thrombosis or meningeal
process. It is more common in overweight young women
during their reproductive years. Headache is the most
prominent clinical feature and is present in over 90% of
patients with IIH, followed by visual loss, blurred vision,
and diplopia secondary to abducens nerve palsy. The
headache is chronic, diffuse, nonspecific in characteristic,
worse in the morning, usually exacerbated by coughing,
bending, sneezing, or by the valsalva maneuver [35–39].
The presence of papilledema requires prompt diagnosis
and immediate intervention to prevent visual loss. MRI
and MR venogram should be obtained to exclude
secondary causes of papilledema. An increased opening
CSF pressure with normal fluid analysis is diagnostic.
Management includes strict weight loss, acetazolamide,
and diuretics. Surgical intervention with optic nerve
sheath fenestration and CSF diversion procedures should
be considered in patients with rapid visual loss and
refractory headaches.
Acute optic neuritis is an inflammatory condition characterized by monocular visual loss and decreased color
vision with pain on eye movements. Traction of the
inflamed optic nerve sheath at the orbital apex is thought
to be the causative factor in pain generation on eye
movements [40,41]. Other causes of optic neuritis such
as infectious inflammatory conditions, connective tissue,
and ischemic disorders are usually painless [42]. High
doses of intravenous steroids are proven to hasten the
recovery process [41].
Anterior ischemic optic neuropathy (AION) is a common
cause of visual loss in giant cell arthritis (GCA), a systemic
vasculitis of the median and large arteries affecting
patients in the fifth and sixth decades of age [43,44].
Symptoms include constant nonspecific nagging holocephalic headache, jaw claudication, malaise, and weight
loss. The visual loss is usually painless and is due to
ischemia of the short posterior ciliary arteries. Other
ocular symptoms include ophthalmoplegia, monocular
blindness, central retinal artery and cilioretinal artery
occlusion [45].
Conclusion
Headaches associated with visual disturbances are often
due to underlying neurological conditions. Migraine and
its variants are the most common primary headache
disorder associated with ophthalmological symptoms,
followed by TACs and hemicrania continua. Many secondary headache disorders are associated with a wide
spectrum of ocular manifestations including true papilledema, ophthalmoplegia, and Horner’s syndrome.
Familiarization with both primary and secondary headache disorders is the key for accurate diagnosis and
management.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (pp. 000–000).
1
The International Classification of Headache Disorders. 2nd edition. Cephalalgia 2004; 24 (Suppl 1):9–160.
2
Lipton RB, Bigal ME. Migraine: epidemiology, impact, and risk factors for
progression. Headache 2005; 45 (Suppl 1):S3–S13.
3
Evans RW, Grosberg BM. Retinal migraine: migraine associated with monocular visual symptoms. Headache 2008; 48:142–145.
4
Pradhan S, Chung SM. Retinal, ophthalmic, or ocular migraine. Curr Neurol
Neurosci Rep 2004; 4:391–397.
5
Grosberg BM, Solomon S, Friedman DI, Lipton RB. Retinal migraine reappraised. Cephalalgia 2006; 26:1275–1286.
6
Grosberg BM, Solomon S, Lipton RB. Retinal migraine. Curr Pain Headache
Rep 2005; 9:268–271.
7
Kaniecki RG. Basilar-type migraine. Curr Pain Headache Rep 2009; 13:217–
220.
8
Kuhn WF, Kuhn SC, Daylida L. Basilar migraine. Eur J Emerg Med 1997;
4:33–38.
9
Dutch Society for Pediatrics. Scientific Meeting of 14 April 1978. Ned
Tijdschr Geneeskd 1978; 122:1590–1592.
10 Bek S, Genc G, Demirkaya S, Eroglu E, et al. Ophthalmoplegic migraine.
Neurologist 2009; 15:147–149.
11 Goadsby PJ. Pathophysiology of migraine. Neurol Clin 2009; 27:335–
360.
This study discusses the pathophysiology of migraine.
12 Buzzi MG, Moskowitz MA. The pathophysiology of migraine: year 2005.
J Headache Pain 2005; 6:105–111.
13 Goadsby PJ. Migraine pathophysiology. Headache 2005; 45 (Suppl 1):S14–
S24.
14 Goadsby PJ, Cittadini E, Burns B, Cohen AS. Trigeminal autonomic cepha lalgias: diagnostic and therapeutic developments. Curr Opin Neurol 2008;
21:323–330.
This study discusses the clinical features, pathophysiology, and treatment options
of trigeminal autonomic cephalalgias.
15 Goadsby PJ. Pathophysiology of cluster headache: a trigeminal autonomic
cephalgia. Lancet Neurol 2002; 1:251–257.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
CE: Namrta; ICU/363; Total nos of Pages: 5;
ICU 363
Headache and the eye Dafer and Jay 5
16 Williams MH, Broadley SA. SUNCT and SUNA: clinical features and medical
treatment. J Clin Neurosci 2008; 15:526–534.
17 Favier I, van Vliet JA, Roon KI, et al. Trigeminal autonomic cephalgias due to
structural lesions: a review of 31 cases. Arch Neurol 2007; 64:25–31.
18 Rozen TD. Resolution of SUNCT after removal of a pituitary adenoma in mild
acromegaly. Neurology 2006; 67:724.
19 Matharu MS, Levy MJ, Merry RT, Goadsby PJ. SUNCT syndrome secondary to
prolactinoma. J Neurol Neurosurg Psychiatry 2003; 74:1590–1592.
20 Levy MJ, Matharu MS, Goadsby PJ. Prolactinomas, dopamine agonists and
headache: two case reports. Eur J Neurol 2003; 10:169–173.
21 Wilbrink LA, Ferrari MD, Kruit MC, Haan J. Neuroimaging in trigeminal
autonomic cephalgias: when, how, and of what? Curr Opin Neurol 2009;
22:247–253.
This article highlights the importance of neuroimaging in excluding underlying
secondary causes for a primary headache disorder.
30 Morrison DG, Phuah HK, Reddy AT, Dure LS, et al. Ophthalmologic involvement in the syndrome of headache, neurologic deficits, and cerebrospinal fluid
lymphocytosis. Ophthalmology 2003; 110:115–118.
31 Verrees M, Arafah BM, Selman WR. Pituitary tumor apoplexy: characteristics,
treatment, and outcomes. Neurosurg Focus 2004; 16:E6.
32 Sjaastad O, Elsas T, Shen JM, Joubert J, et al. Raeder’s syndrome: ‘anhidrosis’, headache, and a proposal for a new classification. Funct Neurol 1994;
9:215–234.
33 Salvesen R. Raeder’s syndrome. Cephalalgia 1999; 19 (Suppl 25):42–45.
34 Goadsby PJ. Raeder’s syndrome [corrected]: paratrigeminal paralysis of the
oculopupillary sympathetic system. J Neurol Neurosurg Psychiatry 2002;
72:297–299.
35 Brazis PW. Clinical review: the surgical treatment of idiopathic pseudotumour
cerebri (idiopathic intracranial hypertension). Cephalalgia 2008; 28:1361–
1373.
22 Ito Y, Yamamoto T, Ninomiya M, et al. Secondary SUNCT syndrome caused
by viral meningitis. J Neurol 2009; 256:667–668.
36 Brazis PW. Pseudotumor cerebri. Curr Neurol Neurosci Rep 2004; 4:111–
116.
23 Adamo MA, Drazin D, Popp AJ. Short-lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing syndrome treated successfully with transsphenoidal resection of a growth hormone-secreting
pituitary adenoma. J Neurosurg 2008; 109:123–125.
37 Randhawa S, Van Stavern GP. Idiopathic intracranial hypertension (pseudotumor cerebri). Curr Opin Ophthalmol 2008; 19:445–453.
24 Gladstone JP. An approach to the patient with painful ophthalmoplegia, with a
focus on Tolosa–Hunt syndrome. Curr Pain Headache Rep 2007; 11:317–
325.
25 Gordon LK. Orbital inflammatory disease: a diagnostic and therapeutic
challenge. Eye 2006; 20:1196–1206.
26 Kurz PA, Suhler EB, Choi D, Rosenbaum JT. Rituximab for treatment of ocular
inflammatory disease: a series of four cases. Br J Ophthalmol 2009; 93:546–
548.
27 Cakirer S. MRI findings in Tolosa–Hunt syndrome before and after systemic
corticosteroid therapy. Eur J Radiol 2003; 45:83–90.
28 Colnaghi S, Versino M. Comments on ‘Tolosa–Hunt syndrome: MR imaging
features in 15 patients with 20 episodes of painful ophthalmoplegia. [Eur J
Radiol (2008), doi: 10.1016/j.ejrad.2007.11.034]. Eur J Radiol 2009;
69:193, author reply.
29 Shikishima K, Kitahara K, Inoue K. Ophthalmologic manifestations in headache, neurologic deficits, and cerebrospinal fluid lymphocytosis (HaNDL)
syndrome with nonspecific frontal lesions and hyperthyroidism. Eye 2006;
20:613–615.
38 Friedman DI. Pseudotumor cerebri presenting as headache. Expert Rev
Neurother 2008; 8:397–407.
39 Friedman DI, Jacobson DM. Idiopathic intracranial hypertension. J Neuroophthalmol 2004; 24:138–145.
40 Lepore FE. The origin of pain in optic neuritis. Determinants of pain in 101
eyes with optic neuritis. Arch Neurol 1991; 48:748–749.
41 Beck RW, Cleary PA, Anderson MM Jr, et al. A randomized, controlled trial of
corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis
Study Group. N Engl J Med 1992; 326:581–588.
42 Anninger WV, Lomeo MD, Dingle J, Epstein AD, et al. West Nile virusassociated optic neuritis and chorioretinitis. Am J Ophthalmol 2003; 136:
1183–1185.
43 Athappilly G, Pelak VS, Mandava N, Bennett JL. Ischemic optic neuropathy.
Neurol Res 2008; 30:794–800.
44 Obuchowska I, Mariak Z, Budrowski R. Anterior ischemic optic neuropathy
associated with giant cell arteritis. Case report. Klin Oczna 2006; 108 (1–3):
124–127.
45 Hayreh SS, Podhajsky PA, Zimmerman B. Occult giant cell arteritis: ocular
manifestations. Am J Ophthalmol 1998; 125:521–526.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.