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I. Fortini
Chapter 53
Painful Optic Neuritis
JoãoJoséFreitasde Carvalho , RaimundoNeudsonMaiaAlcantara ,
andRenataDe OliveiraCarvalho
53.1 Introduction
Painful optic neuritis (PON) is an acute inammatory disorder of the optic nerve
frequently associated with demyelinating diseases of the central nervous system,
especially multiple sclerosis (MS) and, to a lesser frequency, diseases such as neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) [1–3]. PON is classically
characterized by unilateral retro-orbital pain, exacerbated by eye movement, which
precedes or accompanies subacute visual loss.
The International Classication of Headache Disorders, third edition (ICHD-3),
denes PON as a secondary headache, characterized by pain in the retro-orbital,
orbital, frontal, and/or temporal regions, and meeting specic diagnostic criteria
(code 13.6) [4]. The onset of pain must be temporally related to the episode of optic
neuritis (ON), and its intensity increases with eye movement, reecting inammation in the optic nerve sheaths and adjacent tissues.
Population and clinical studies indicate that pain is present in about 90% of cases
of optic neuritis and may precede vision loss by days [3, 5]. In the United States and
Europe, idiopathic or multiple sclerosis-associated optic neuritis is the most prevalent form, while infectious or autoimmune etiologies are more common in developing countries [2, 6].
Early diagnosis of PON is essential, not only for the immediate management of
visual and pain symptoms but also because it can be the rst clinical sign of a
chronic demyelinating disease. Contrast-enhanced magnetic resonance imaging is a
J. J. F. de Carvalho (*) · R. De OliveiraCarvalho
Unichristus School of Medicine, Fortaleza, Brazil
R. N. M. Alcantara
Department of Neurology, Hospital Geral de Fortaleza, Fortaleza, Brazil
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_53
503© The Author(s), under exclusive license to Springer Nature
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J. J. F. de Carvalho et al.
crucial diagnostic tool, with optic nerve enhancement observed in more than 90%
of cases [1, 7].
This chapter explores the pathophysiological basis, clinical features, differential
diagnosis, and therapeutic management of PON, integrating recent literature with a
representative clinical case.
53.2 Pathophysiology
PON represents an acute inammatory process that affects the optic nerve, usually
of autoimmune origin, with segmental destruction of the myelin sheath and, to a
lesser extent, the axons. This demyelination interferes with the conduction of visual
impulses, leading to decreased visual acuity, scotomas, and loss of color discrimination [2, 3].
The immunological basis of optic neuritis varies according to etiology. In multiple sclerosis (MS), lymphocyte activation triggers an immune-mediated attack
against myelin components, primarily myelin basic protein, leading to the inltration of T-cells, macrophages, and the production of inammatory cytokines [5]. In
cases of NMOSD, the main target is aquaporin-4 (AQP4), a protein expressed in
astrocytes, which leads to primary astrocytopathy. In contrast, in MOGAD, the target is myelin oligodendrocyte glycoprotein, causing a distinct clinical and evolutionary phenotype [8].
The pain linked to optic neuritis arises from the inammation of the optic nerve
sheath and its surrounding structures, especially the dura mater, which is innervated
by nociceptive bers of the trigeminal nerve [5, 9]. Eye movements typically worsen
this pain due to the stretching of the inamed nerve within the orbit, a characteristic
feature [2].
Histopathological and imaging studies demonstrate perivascular inltration and
disruption of the blood-brain barrier in the acute phase of the disease. Contrastenhanced magnetic resonance imaging usually shows enhancement of the optic
nerve in intraorbital or intracanalicular segments, reecting active inammation
[10]. Optical coherence tomography (OCT) studies demonstrate progressive reduction of the retinal nerve ber layer (RNFL), particularly in patients with MS, reecting chronic axonal loss [6, 11].
Understanding the different immunopathological mechanisms is essential not
only for the differential diagnosis between the variants of optic neuritis but also for
dening the prognosis and the best therapeutic approach.
53 Painful Optic Neuritis
505
53.3 Characteristics of Pain
Pain is one of the most prominent and early features of optic neuritis (ON), particularly in its demyelinating form. It is present in approximately 90% of cases and
often precedes visual symptoms by several hours to days [2, 3, 5]. The typical pain
is described as deep, dull, and retro-orbital, sometimes radiating to the frontal or
temporal regions. It is characteristically worsened by eye movement, a hallmark
that helps distinguish ON from other causes of visual loss [2, 9].
This pain, as already mentioned, results from inammatory involvement of the
optic nerve sheath and surrounding dura mater, which is innervated by nociceptive
bers of the ophthalmic branch of the trigeminal nerve. The intraorbital portion of
the optic nerve is particularly vulnerable, as it is mobile and subjected to mechanical
traction during ocular motility [2]. This explains why pain associated with eye
movement is a highly specic indicator for optic neuritis and serves as an essential
diagnostic clue.
Unlike other optic neuropathies, such as non-arteritic anterior ischemic optic
neuropathy (NAION) or Leber hereditary optic neuropathy (LHON), which are
typically painless, the presence of periocular or retro-orbital pain is a critical feature
suggestive of an inammatory demyelinating process [5, 12].
For some patients, pain might be the sole symptom at the initial presentation,
particularly in the early stages, which can result in diagnostic delays. This underscores the importance of maintaining a high index of suspicion when evaluating
patients with unilateral orbital pain of unclear etiology—even in the absence of
immediate visual complaints [1, 3].
Although pain usually resolves spontaneously within a few days, it can signicantly impair quality of life. Fortunately, it is generally responsive to corticosteroid
therapy, which reduces inammation and hastens symptom resolution [2, 13].
53.4 Case Presentation
A 25-year-old woman presented to the Neurology Outpatient Clinic at Hospital
Geral de Fortaleza, Brazil. She reports experiencing a sudden onset of decreased
visual acuity in the left eye on August 27, 2024, initially presenting with ocular pain
upon horizontal eye movement and a left-sided frontotemporal headache, dyschromatopsia, associated with a progressive reduction in visual acuity over one week.
Neurological examination was normal except for a left afferent pupillary defect
and decreased visual acuity on the left eye limited to hand motion. Ocular motility
was intact but painful in the left eye.
Magnetic resonance imaging (MRI) of the brain and orbits demonstrate increased
T2-weighted signal intensity in the posterior intraorbital segment of the left optic
nerve, which, even in the absence of enhancement on post-gadolinium images, was
interpreted as consistent with acute inammatory left optic neuritis. There is no
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evidence of signicant optic nerve atrophy, orbital inammation, or involvement of
extraocular muscles. No additional intracranial lesions or demyelinating plaques
were identied on the available sequences (Fig.53.1).
Cerebrospinal uid (CSF) analysis was unremarkable, with normal protein and
cell count, negative infectious screening, and no intrathecal IgG synthesis. AQP4
and MOG antibodies tested after treatment initiation were negative. The ophthalmologic evaluation revealed left eye visual acuity of 20/100 with questionable slight
optic disk edema. Laboratory results were largely normal.
The patient received intravenous (IV) methylprednisolone 1g/day for ve days.
Due to the persistence of the severity of vision loss on the fth day, plasmapheresis
was initiated but limited to one session due to logistical constraints. At discharge
two weeks later, her left eye’s visual acuity had improved partially, and the pain had
subsided.
She was diagnosed with unilateral PON as a clinically isolated syndrome (CIS),
with no evidence of MS, NMOSD, or MOGAD.A follow-up plan included outpatient neuroimmunology review, prednisone tapering, and repeat AQP4 and MOG
testing.
abc
def
Fig. 53.1 MRI ndings demonstrate increased T2-weighted signal intensity in the posterior intraorbital segment of the left optic nerve (white arrow), consistent with acute left optic neuritis (a).
No additional intracranial abnormalities or demyelinating lesions are identied on this axial
enhanced T2-weighted 3D sequence (b–f)
53 Painful Optic Neuritis
507
53.5 Case Discussion
This case fulls the ICHD-3 criteria for PON [4]. The temporal relationship between
retro-orbital pain and subsequent visual decline, with pain exacerbated by eye
movement, is typical of demyelinating optic neuritis. MRI ndings of increased
T2-weighted signal intensity in the posterior intraorbital segment of the left optic
nerve is consistent with acute inammatory left optic neuritis. The absence of gadolinium enhancement does not rule out optic neuritis [7]. Although the patient’s
AQP4 and MOG antibody tests were negative, the timing of testing—after corticosteroid initiation—may have reduced their diagnostic sensitivity [8]. The absence of
oligoclonal bands in the CSF and a normal brain MRI suggest a diagnosis of clinically isolated syndrome (CIS), with no current criteria for MS, NMOSD, or
MOGAD [2, 11].
53.6 Clinical Characteristics
This case highlights several key aspects of painful optic neuropathies. First, the differential diagnosis of painful visual loss must consider optic neuritis, especially in
young adults, but also include compressive lesions, infectious optic neuritis (e.g.,
syphilitic or viral), sarcoidosis, and perioptic neuritis secondary to systemic autoimmune diseases. Pain in optic neuropathies typically results from inammation of the
optic nerve sheath and its meningeal covering, both of which are innervated by the
ophthalmic branch of the trigeminal nerve [2, 14]. The presence of pain with eye
movement is particularly useful in distinguishing inammatory causes from ischemic or compressive etiologies, which are usually painless.
In compressive optic neuropathies, caused by orbital masses, aneurysms, or optic
canal lesions, pain may occur if adjacent tissues are involved; however, the progression is typically subacute or chronic, with less sudden visual decline. Ischemic optic
neuropathy (e.g., NAION) is usually painless and occurs in older individuals with
vascular risk factors. Hereditary optic neuropathies, such as Leber hereditary optic
neuropathy (LHON), also tend to present with painless bilateral vision loss [12].
The partial visual recovery after corticosteroid therapy in this patient is consistent with demyelinating optic neuritis. While one session of plasmapheresis was
administered, its clinical necessity is uncertain in cases that begin to improve
promptly. Nonetheless, it is noteworthy that early consideration of escalated therapy
in severe visual loss may preserve vision when steroid response is inadequate
[13, 14].
Close outpatient follow-up is essential for monitoring recurrence and determining the need for long-term immunomodulatory therapy, especially if new symptoms
or lesions emerge on follow-up imaging. Repeat AQP4 and MOG antibody testing
is appropriate, ideally in a steroid-free window, to rule out antibody-mediated
demyelinating syndromes. This case highlights the importance of a structured
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diagnostic approach to managing painful optic neuropathies, integrating clinical,
radiological, and serological data to inform both immediate management and longterm surveillance.
53.7 Diagnostics andDifferential Diagnosis
The diagnosis of PON is primarily clinical, guided by a thorough history and neurological examination. However, neuroimaging and electrophysiological studies are
essential for conrmation and to exclude alternative etiologies.
Key clinical ndings include:
• Subacute onset of monocular vision loss.
• Pain exacerbated by eye movement.
• Central scotoma or visual eld defects.
• Dyschromatopsia (especially red desaturation).
• Relative afferent pupillary defect (RAPD), unless bilateral.
Fundoscopy is often normal in retrobulbar neuritis—the most common form—
but may show optic disk swelling (papillitis) in up to one-third of cases [9, 15].
MRI of the orbits with gadolinium contrast is the imaging modality of choice.
Enhancement of the optic nerve, especially in the intraorbital segment, conrms
active inammation and supports the diagnosis [1]. Optic nerve enhancement is
present in approximately 90% of typical ON cases and may persist for several weeks
after symptom onset [14]. Brain MRI is also performed to assess for demyelinating
lesions suggestive of multiple sclerosis (MS) or other central nervous system inammatory diseases [1].
Typical radiological ndings include:
• T2 hyperintensity and contrast enhancement of the optic nerve.
• Absence of mass effect or compressive lesions.
• Periventricular or juxtacortical lesions in MS.
Visual Evoked Potentials (VEP) testing can reveal delayed P100 latency in the
affected eye, reecting demyelination along the visual pathway. While less specic
than MRI, it remains useful when imaging is inconclusive or unavailable [15].
Optical Coherence Tomography (OCT) provides structural information on the
peripapillary retinal nerve ber layer (RNFL) and the ganglion cell layer. RNFL
thinning becomes evident weeks after the acute phase and correlates with axonal
loss and long-term visual prognosis [1, 6].
CSF examination is recommended in atypical cases or when an inammatory or
infectious etiology is suspected. The presence of oligoclonal bands is an established
biomarker for MS and predicts increased risk of disease conversion in clinically
isolated syndromes (CIS) [16].
Several conditions may mimic the clinical picture of optic neuritis and must be
excluded [17]:
53 Painful Optic Neuritis
509
• Non-arteritic anterior ischemic optic neuropathy (NAION): Typically occurs in
older patients with vascular risk factors, and presents with painless vision loss
and altitudinal eld defects. The optic disk is swollen and pale.
• Compressive optic neuropathies: Caused by tumors or aneurysms. These evolve
slowly and rarely present with pain or acute visual decline.
• Leber hereditary optic neuropathy (LHON): Painless, bilateral visual loss in
young males, often with a family history. Mitochondrial inheritance.
• Infectious optic neuritis: Associated with syphilis, Lyme disease, tuberculosis, or
viral infections (e.g., herpes zoster, Cytomegalovirus (CMV)), particularly in
immunocompromised individuals.
• Autoimmune optic neuropathies: Sarcoidosis, systemic lupus erythematosus, and
Behçet’s disease can cause optic nerve inammation, often accompanied by sys-
temic signs.
• Neuromyelitis optica spectrum disorder (NMOSD): Frequently bilateral, severe,
and relapsing. Serum AQP4-IgG positivity helps conrm the diagnosis.
• MOG antibody disease (MOGAD): Often indistinguishable from typical ON at
onset, but more likely to involve bilateral or recurrent optic neuritis and better
visual recovery [8].
A comprehensive diagnostic workup incorporating clinical features, imaging,
and laboratory testing is essential to distinguish PON from these conditions and
guide appropriate management.
53.8 Treatment
The PON management is designed to reduce inammation, accelerate visual recovery, alleviate pain, and, in select cases, initiate long-term immunomodulatory therapy. Treatment decisions are based on clinical presentation, imaging ndings,
serological markers, and the likelihood of progression to chronic demyelinating
disease [18].
High-dose intravenous corticosteroids are the mainstay of treatment for acute
demyelinating optic neuritis. The standard regimen consists of methylprednisolone
1g/day intravenously for 3–5 consecutive days, optionally followed by an oral taper
with prednisone (typically 1mg/kg/day for 11–14days) [3, 5].
The pivotal Optic Neuritis Treatment Trial (ONTT) demonstrated that intravenous corticosteroids signicantly hasten visual recovery but do not improve longterm visual acuity compared to placebo [13]. Additionally, oral corticosteroids
alone (without initial IV treatment) were associated with a higher rate of recurrence
and are therefore not recommended as monotherapy in typical ON [7, 13].
Corticosteroids usually lead to rapid pain resolution by suppressing inammation. In cases where pain is severe or persists despite treatment, adjunctive use of
non-steroidal anti-inammatory drugs (NSAIDs) may be benecial. However, more
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potent analgesics are rarely indicated, as pain generally resolves within a few
days [3, 5].
In severe or steroid-refractory cases, particularly those with profound visual loss
or bilateral involvement, plasma exchange (PLEX) may be considered. Evidence
supports its use in NMOSD-related optic neuritis and in a subset of severe MS-related
optic neuritis unresponsive to steroids [19].
Intravenous immunoglobulin (IVIG) has limited evidence for efcacy in optic
neuritis and is generally reserved for select cases, including those associated with
MOG-antibody disease or when PLEX is contraindicated [20].
Patients with CIS and high-risk features—such as abnormal brain MRI or positive oligoclonal bands in CSF—should be evaluated for early initiation of DMTs to
reduce the risk of conversion to multiple sclerosis [15]. Options include interferonbeta, glatiramer acetate, or newer oral and monoclonal antibody agents, depending
on patient-specic factors and risk stratication [18].
In cases of NMOSD, long-term immunosuppression with agents such as rituximab, eculizumab, or inebilizumab is critical to prevent relapses and severe disability (19). Similarly, MOGAD may require long-term immunotherapy in recurrent
cases, often using corticosteroid-sparing agents like azathioprine or mycophenolate
mofetil [20].
Follow-up includes serial assessment of visual function, OCT to monitor axonal
loss, and MRI if there is suspicion of new demyelinating lesions. Visual rehabilitation, including contrast sensitivity training and low-vision aids, may be benecial
for patients with residual decits [1, 3].
53.9 Conclusion
PON remains one of the most common and clinically signicant causes of acute
monocular vision loss in young adults. Recognizing the typical presentation—retroorbital pain exacerbated by eye movement followed by subacute visual impairment—is crucial for timely diagnosis and management. The diagnostic process
should integrate careful clinical assessment with magnetic resonance imaging,
visual evoked potentials, and, when indicated, cerebrospinal uid analysis and antibody testing.
While corticosteroids remain the cornerstone of acute management, they primarily accelerate recovery rather than improve long-term visual outcomes. Identifying
patients at higher risk for progression to MS, NMOSD, or MOGAD is essential to
guide early initiation of disease-modifying therapy and prevent future relapses.
Differentiating PON from other causes of optic neuropathy—such as ischemic,
compressive, hereditary, or infectious etiologies—requires a structured, multidisciplinary approach. Advances in imaging and biomarker detection have signicantly
enhanced the clinician’s ability to establish an early and accurate diagnosis.
Ultimately, the effective management of PON depends not only on controlling
the acute inammatory episode but also on a long-term strategy that includes risk
53 Painful Optic Neuritis
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stratication, neuroimmunological evaluation, patient education, and, when necessary, visual rehabilitation.
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