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Advanced Neurology A novel approach to mitigate muscle atrophy in GBS

neuropathy) . These pathophysiological distinctions are long-term functional recovery and may be a source of
[2]
important when considering interventions that may affect long-term morbidity, mobility impairment, and functional
different aspects of neuromuscular structure and function. disability [10,12] .
The demyelinating form of GBS (i.e., AIDP) is by far the Omega-3 fatty acids are well known for their anti-
most common presentation . oxidative and anti-inflammatory properties. There
[3]
Clinically, GBS manifests itself as rapidly progressive, is emerging pre-clinical and non-pathophysiological
symmetrical numbness, tingling, and weakness classically human data suggesting the ability to limit muscle loss
described as ascending from the distal lower extremities . despite pro-catabolic environments (e.g., prolonged bed
[4]
[13]
However, symptom onset has been demonstrated in both rest) . This work, whilst preliminary, indicates that
upper or lower extremities, typically with loss of deep omega-3 supplementation could potentially be utilized
tendon reflexes and potential for substantial pain . The in mitigating muscle atrophy secondary to disease, which
[1]
usual disease course includes up to 4 weeks of progressive may be readily applicable to the GBS population.
weakness, which may progress to the point of tetraplegia, It is hypothesized that for patients with GBS, the
with the nadir reached around 2 weeks. Electromyography administration of high-dose omega-3 fatty acids may:
(EMG) will typically show characteristic decrease in (i) Reduce or slow down skeletal muscle atrophy,
amplitude of muscle action potentials, with slowing and (ii) improve rates of remyelination, and thus (iii) improve
potential blockage of signal transmissions . During the functional outcomes and reduce morbidity for people
[5]
progressive stage, 20%–30% will develop respiratory recovering from GBS. The authors hope this paper will
failure and require invasive ventilation with mortality provide the theoretical impetus for future experimentation
[6]
rates in Europe and North America ranging between 3% or trials which may test this hypothesis.
and 7% [4,7] . Following the progressive phase, a plateau
phase ensues for an average of 7 days (but ranging 2. Overview and pathophysiology of GBS
from 2 days to 6 months) before the start of recovery . [1]
[6]
During recovery, many individuals with GBS continue to GBS is an immune-mediated polyneuropathy . The
experience profound weakness or even tetraparesis, which main pathological mechanism is through a complement-
may require many months to recover and whose recovery mediated nerve injury caused by antigen-antibody
[1]
is often incomplete . interactions at the peripheral nerves against the myelin
sheath (i.e., AIDP), resulting in diffuse demyelination.
Acute treatment of GBS consists of immunotherapy, Less commonly, the autoimmune attack may be targeted
usually either plasma exchange (PLEX) or intravenous at the axon itself (i.e., axonal variants) , resulting in
[3]
immunoglobulin (IVIg) [4,8] . Despite these treatments, GBS diffuse axonal degeneration . Microscopic analysis
[14]
mortality remains around 4% in overall, and with 14% of nerve biopsies have shown evidence of complement
continuing to experience severe disability at 1 year . Only and antibody deposits, as well as increased macrophage
[9]
20% of GBS survivors regain independent ambulatory infiltrates , within the peripheral nerves of GBS
[8]
function at 4 weeks, whereas 84% can walk independently patients . Myelin phagocytosis by macrophages has been
[15]
by one year . Approximately 40% of patients do not recover an essential feature of demyelinating diseases, like GBS .
[9]
[16]
to their baseline strength by 1 year post-symptom onset . The generally accepted mechanism of auto-sensitization
[9]
Given these meaningful long-term deficits in a significant is through molecular mimicry, where an infectious agent
proportion of GBS survivors, further optimizations in (or other exogenous substance) triggers an immune
GBS-related care are welcome. response against self-antigens . Over two-thirds of
[17]
As part of the primary disease process involving direct GBS cases have been associated with a prior bacterial
damage to the PNS, in both demyelinating and axonal or viral infection. Known infections that are linked to
GBS subtypes, many GBS patients experience clinically the onset of GBS include Campylobacter jejuni, Epstein
[3,18]
significant muscle atrophy . This can be referred to as Barr virus, cytomegalovirus, Zika virus, and others .
[10]
neurogenic atrophy. A secondary cause of muscle atrophy Within a normal immune response, one natural pathway
is related to prolonged paresis and immobility caused by of defense occurs through antibody formation, these
diffuse demyelination and conduction block. This can be formed antibodies bind to specific antigens on the target
referred to as disuse atrophy. Remyelination of peripheral organism to assist with phagocytosis, neutralization,
nerves may require many weeks or months to recover complement activation, as well as activation of T-cell
[19]
sufficiently for functional recovery of muscle strength, thus immunity .
the period of absolute or relate disuse can be quite long . Regarding molecular mimicry, the target antigens
[11]
Muscle atrophy from either of these etiologies limits are immunologically similar to specific self-antigens
Volume 2 Issue 2 (2023) 2 https://doi.org/10.36922/an.280