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OPTIC NERVE LESIONS IN DEMYELINATING DISEASES: CLINICAL AND
NEUROIMAGING CHARACTERISTICS
Jalalova Dilfuza Zuhridinovna
Department of Ophthalmology, Samarkand State Medical University.
Hazratkulov Amir
https://doi.org/10.5281/zenodo.15178119
Samarkand State Medical University, Department of Ophthalmology, 2st year clinical
ordinator
Abstract.
Neuromyelitis optica is a demyelinating disease that primarily affects the eyes
and spinal cord, but can also involve other structures of the central nervous system (CNS) that
contain aquaporin-4.
Keywords:
Clinical manifestations, Diagnostics, prevention, prognosis and treatment.
Introduction:
Neuromyelitis optica spectrum disorder causes acute optic neuritis,
sometimes bilateral, as well as demyelination of the cervical or thoracic spinal cord. It was
previously considered a type of multiple sclerosis (MS), but is now recognized as a separate
disease.
In neuromyelitis optica spectrum disorder, the immune system attacks aquaporin-4, a
protein found in astrocytes in the brain, particularly in the spinal cord and optic nerves, or myelin
oligodendrocyte glycoprotein (MOG), a protein found in the myelin of oligodendrocytes, and
possibly in other areas of the CNS. Astrocytes and oligodendrocytes are damaged by autoimmune
inflammatory responses, as well as demyelination.
Severe bilateral optic neuritis involving the optic chiasm, leading to loss of vision above
or below the horizontal (height visual field defect) or loss of visual acuity (20/200 or worse).
Complete spinal cord injury syndrome, especially with paroxysmal tonic spasms
Hiccups or nausea and vomiting caused by area postrema syndrome (the area postrema is
a structure that controls vomiting and is located at the bottom of the 4th ventricle)
Visual evoked potentials help distinguish neuromyelitis optica from other optic
neuropathies. Findings in the neuromyelitis optica spectrum disorder include decreased amplitude
or prolonged latency. This test is also useful for detecting clinically undetectable damage that may
be present before symptoms appear.
Methods and Materials:
Tests can be performed to differentiate IgG antibodies specific
for neuromyelitis optica spectrum disorder (aquaporin 4 antibodies [also called NMO-IgG]) from
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MS. Anti-MOG (myelin oligodendrocyte glycoprotein) antibodies identify a subgroup of patients
with neuromyelitis optica who have different clinical features: they have fewer complications and
a better recovery than patients with or without AQP4 antibodies. Some patients with clinical signs
of neuromyelitis optica do not have antibodies at all and are classified as double seronegative for
neuromyelitis optica. Neuromyelitis optica cannot be cured. However, treatment can prevent, slow
down, or reduce the severity of exacerbations and reduce the risk of disability in the short term.
Eculizumab, a complement C5 inhibitor, is available for the treatment of aquaporin-4
antidiv-positive neuromyelitis visual spectrum disorder. Side effects include respiratory tract
infections, headache, and pneumonia and can be significant; thus, patients should be monitored
closely (3). Because one patient developed meningococcal sepsis, meningococcal vaccination
should be considered before initiating treatment.
Satralizumab (a monoclonal antidiv against the interleukin-6 receptor) and inebilizumab
(a monoclonal antidiv against CD19 on B cells) are also available for the treatment of aquaporin-
4-positive neuromyelitis optica spectrum disorder. Patients should be monitored closely for
infections such as urinary tract infections and respiratory tract infections.
Methylprednisolone and azathioprine are often used together. Plasmapheresis may be
performed in patients who are ineffective on glucocorticoid therapy.
Rituximab, an anti-B-cell antidiv, has been shown to reduce relapse rates in a double-
blind, placebo-controlled study ( 4 ). Other types of immunomodulatory and immunosuppressive
therapy are sometimes used.
Natalizumab and fingolimod have been shown to be ineffective and may cause harm.
Symptomatic therapy is similar to treatment for MS. Baclofen or tizanidine are prescribed
for muscle spasms.
Neuromyelitis optica spectrum disorder is usually the result of demyelination involving
antibodies to aquaporin-4 or myelin oligodendrocyte glycoprotein.
Typical symptoms include vision loss, muscle spasms, para- or tetraparesis, and
incontinence.
MRI of the brain and spinal cord, as well as the study of visual evoked potentials, are used
to diagnose optic spectrum disorders in neuromyelitis.
Treatment includes corticosteroids and immunomodulatory or immunosuppressive therapy
(e.g., eculizumab, rituximab).
The myelin sheath covers a large number of nerve fibers in the central and peripheral
nervous system; With its help, the transmission of nerve impulses along the axon occurs at high
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speed. In diseases accompanied by damage to the myelin sheath, the conduction of excitation along
the nerve fiber is impaired; Symptoms may reflect a failure in any part of the nervous system.
Myelin produced by oligodendroglia in the central nervous system (CNS) differs in its
immunochemical properties from that produced by Schwann cells in the peripheral nervous
system. Thus, some demyelinating diseases (e.g., Guillain-Barré syndrome, chronic inflammatory
demyelinating polyneuropathy, and some other peripheral neuropathies) have a primary peripheral
effect, while in others, the pathology of the central nervous system predominates (see table:
Diseases that can cause demyelination of the central nervous system). Moreover, in the latter case,
structures such as the brain, spinal cord, and optic nerves are often involved in the pathological
process.
Conclusions:
Demyelination often develops secondary to infectious, ischemic, metabolic
or hereditary diseases or intoxication (e.g. alcohol, ethambutol). The cause of the lesion in primary
demyelination processes is unknown, but since the disease often develops after a viral infection or
vaccination, there is reason to assume the role of autoimmune mechanisms.
Demyelinating lesions are usually segmental or mosaic in nature, involving several areas
simultaneously or sequentially. Remyelination often progresses with the restoration of the myelin
sheath, recovery, and complete resolution of neurological deficit. However, it should be noted that
when a significant portion of myelin is lost, axonal degeneration occurs, followed by degeneration
of the neuronal div; both may be irreversible.
Demyelinating disease should be suspected in any patient with unexplained neurological
deficits. Primary demyelinating disease should be excluded if the following are present:
Multiple sclerosis (MS) is characterized by the occurrence of diffuse foci of demyelination
in the brain and spinal cord. Characteristic symptoms include visual and oculomotor disturbances,
paresthesia, weakness, spasticity, urinary disorders, and mild cognitive symptoms. The “diffuse”
neurological symptoms characteristic of this disease, alternating exacerbations and remissions,
gradually lead to loss of work capacity and disability. Diagnosis based on clinical manifestations
or MRI requires the presence of ≥ 2 characteristic neurological lesions separated in time and space
(localization in the central nervous system). Treatment includes the use of glucocorticoids during
exacerbations, the use of immunomodulators to prevent exacerbations, and maintenance therapy.
Immune mechanisms are also thought to be involved in the development of multiple
sclerosis. One possible cause may be infection with a latent virus (possibly a human herpesvirus,
specifically the Epstein-Barr virus), which, when activated, triggers a secondary autoimmune
response.
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The relatively high incidence of MS among members of certain families and the presence
of human leukocyte antigen (HLA-DR2) allotypes suggest a hereditary predisposition to the
development of the disease.
MS is more common in people who spend the first 15 years of their lives in temperate
climates (1/2000) than in the tropics (1/10000). A possible explanation for this difference could
be the role of vitamin D levels: the latter is known to be related to the amount of exposure to solar
radiation, which is lower in temperate climates, and reduced vitamin D levels are associated with
an increased risk of MS. Smoking is also a risk factor.
The age of onset of MS ranges from 15 to 60 years, with a median age of 20 to 40 years,
and women are affected slightly more often. Neuromyelitis optica spectrum disorder (DeVick's
disease), previously considered a variant of MS, is now considered a separate nosological entity.
In MS, focal demyelination (called plaques) develops, in which oligodendroglia are destroyed,
perivascular inflammation, and chemical changes in the lipid and protein components of myelin
occur both in the plaque zone and around it. Axonal damage is widespread, and neuronal cell
bodies may also die or be damaged.
The main localization of disseminated plaques in the central nervous system (CNS) is the
white matter, in particular the posterior and lateral columns (especially in the cervical segment of
the spinal cord), the optic nerves and the periventricular zone. The conduction pathways of the
midbrain, pons and cerebellum are also affected. The gray matter of the brain and spinal cord may
be involved in the pathological process, but to a much lesser extent. Multiple sclerosis is
manifested by a variety of neurological symptoms, the course of which is characterized by
alternating remissions and exacerbations. If MS is not treated with immunomodulatory drugs,
exacerbations occur on average once every 2 years, but their frequency varies greatly.
Despite the fact that the pathological process in MS can fade and reactivate unpredictably,
some typical variants of its course stand out.
Discussion:
Relapsing-remitting course: periods of exacerbation alternate with periods of
complete or partial recovery of neurological deficits or stabilization of symptoms. Remissions may
last for months or years. Exacerbations of the disease develop spontaneously or under the influence
of provoking factors, including infectious diseases (for example, influenza). Relapsing forms of
MS include active secondary MS (defined as clinical relapse or a new lesion seen on MRI of the
brain or spinal cord).
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Primary progressive: gradual progression of the disease without periods of remission, but
there may be periods of time (called "plateau periods") when symptoms do not worsen. Differs
from the relapsing-remitting variant in the absence of clearly defined exacerbations.
Secondary progressive: the disease begins with alternating exacerbations and remissions
(relapse-remission), followed by a stable progression of the process.
Visual disturbances (e.g., partial loss of vision and pain in one eye due to retrobulbar optic
neuritis, diplopia due to internuclear ophthalmoplegia, scotoma)
Other common early symptoms of MS include mild stiffness or fatigue in the limbs, mild
gait disturbance, dizziness, and mild sensory disturbances; all of the above indicate diffuse
involvement of the central nervous system, and these changes are barely noticeable. Most patients
with MS have difficulty controlling their bladder (e.g., urinary frequency, urgency, hesitancy to
start urination, urinary incontinence, urinary retention). Increased fatigue often occurs. Symptoms
may temporarily worsen with increased temperature (heat, hot bath, fever) (Uhthoff's
phenomenon).
Mild cognitive impairment is common. Patients may experience apathy, decreased self-
esteem, and impaired concentration. Emotional disturbances are often present, manifested by
emotional lability, euphoria, or, more commonly, depression. The latter may be reactive or may
result from some degree of central nervous system damage. Seizures are observed in younger
patients.
The most common changes are unilateral (asymmetric) optic neuritis and internuclear
ophthalmoplegia.
Conclusion:
Optic neuritis causes visual impairment (ranging from scotoma to complete
blindness), eye pain when moving the eye, sometimes narrowing of the visual fields, swelling of
the optic disc, and the appearance of a complete or partial afferent pupillary defect. Internuclear
ophthalmoplegia develops when the medial longitudinal fasciculus connecting the nuclei of the
III, IV, and VI pairs of cranial nerves is affected. With horizontal gaze, the retraction of one eyeball
is reduced with nystagmus in the other eye (abductor); convergence is preserved. Internuclear
ophthalmoplegia in MS is usually bilateral; Unilateral internuclear ophthalmoplegia is often found
in ischemic stroke.
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