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HISTOPATHOLOGY OF GUILLAIN – BARRE SYNDROME (GBS)
AND ITS PREVENTION
Sourav Santra*, Sudeshna Santra, Amit Kumar Das, Aakash Chatterjee, Dr. Dhrubo
Jyoti Sen
Department of Pharmaceutical Chemistry, School of Pharmacy, Techno India
University, Salt Lake City, Sector-5, EM-4, Kolkata -700091, West Bengal, India.
ABSTRACT
Guillain-Barre syndrome (GBS) is clinically defined as an acute
peripheral neuropathy causing limb weakness that progresses over a
time period of days or, at the most, up to 4 weeks. GBS occurs
throughout the world with a median annual incidence of 1.3 cases per
population of 100 000, with men being more frequently affected than
women. GBS is considered to be an autoimmune disease triggered by a
preceding bacterial or viral infection. Campylobacter jejuni,
cytomegalovirus, Epstein-Barr virus and Mycoplasma pneumoniae are
commonly identified antecedent pathogens. In the acute motor axonal
neuropathy (AMAN) form of GBS, the infecting organisms probably
share homologous epitopes to a component of the peripheral nerves
(molecular mimicry) and, therefore, the immune responses cross-react
with the nerves causing axonal degeneration. The target molecules in
AMAN are likely to be gangliosides GM1, GM1b, GD1a and GalNAc-GD1a expressed on the
motor axolemma. In the acute inflammatory demyelinating polyneuropathy (AIDP) form,
immune system reactions against target epitopes in Schwann cells or myelin result in
demyelination. However, the exact target molecules in the case of AIDP have not yet been
identified. AIDP is by far the most common form of GBS in Europe and North America,
whereas AMAN occurs more frequently in east Asia (China and Japan). The prognosis of
GBS is generally favourable, but it is a serious disease with a mortality of approximately
10% and approximately 20% of patients are left with severe disability. Treatment of GBS is
subdivided into: (i) the management of severely paralysed patients with intensive care and
ventilatory support; and (ii) specific immunomodulating treatments that shorten the
WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES
SJIF Impact Factor 7.632
Volume 9, Issue 6, 812-826 Review Article ISSN 2278 – 4357
*Corresponding Author
Sourav Santra
Department of
Pharmaceutical Chemistry,
School of Pharmacy,
Techno India University,
Salt Lake City, Sector-5,
EM-4, Kolkata -700091,
West Bengal, India.
Article Received on
08 April 2020,
Revised on 28 April 2020,
Accepted on 18 May 2020
DOI: 10.20959/wjpps20206-16377
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Sourav et al. World Journal of Pharmacy and Pharmaceutical Sciences
progressive course of GBS, presumably by limiting nerve damage. High-dose intravenous
immunoglobulin (IVIg) therapy and plasma exchange aid more rapid resolution of the
disease. The predominant mechanisms by which IVIg therapy exerts its action appear to be a
combined effect of complement inactivation, neutralisation of idiotypic antibodies, cytokine
inhibition and saturation of Fc receptors on macrophages. Corticosteroids alone do not alter
the outcome of GBS.
KEYWORDS: Guillain-barre syndrom (GBS), Acute inflammatory demyelinating
polyradiculoneuropathy (AIDP), Acute motor axonal neuropathy (AMAN), acute motor-
sensory axonal neuropathy (AMSAN), Link between zika virus and GBS, Pathophysiology of
GBS, Link with COVID-19.
INTRODUCTION
Guillain-Barre syndrome is an uncommon disorder that causes damage to the peripheral
nerves. These nerves send messages from the brain to the muscles, instructing the muscles to
move. They also carry sensations such as pain from the body to the brain. The nerve damage
often causes muscle weakness, often to the point of paralysis, and can cause problems with
sensation, including pain, tingling, "crawling skin" or a certain amount of numbness.
GBS is an autoimmune disorder in which the body's immune system attacks and destroys the
myelin sheath, which wraps around long nerve cell bodies much like insulation around a
water pipe. Myelin protects the nerve and helps to speed the transmission of electrical
impulses down the nerve. If the myelin is destroyed, nerve impulses travel very slowly and
can become disrupted. If muscles don't get proper stimulation through the nerves, they will
not function properly.[1]
Figure-1: Guillain-Barre syndrome.
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GBS is uncommon, affecting fewer than 4,000 people in the United States each year. Why
the disorder strikes some people is a mystery. In more than two-thirds of patients, Guillain-
Barre syndrome occurs one to three weeks after a viral disease, including the common cold,
flu, or infection with human immunodeficiency virus (HIV), Epstein-Barr virus or
cytomegalovirus. The most common infectious trigger seems to be a bacterial infection with
Campylobacter jejuni, which causes intestinal infections. Occasionally, Guillain-Barre
syndrome seems to follow immunization, surgery or bone marrow transplantation. The causes
of the syndrome are unknown, but many experts think that the immune system is trying to
fight an infectious organism (bacteria or virus) and accidentally injures nerve tissue in the
process. It is a rare condition, and while it is more common in adults and in males, people of
all ages can be affected.[2]
Figure-2: Time course of GUILLAIN BARRE SYNDROME.
SYMPTOMS
Guillain-Barre syndrome often begins with tingling and weakness starting in your feet and
legs and spreading to your upper body and arms. In about 10% of people with the disorder,
symptoms begin in the arms or face. As Guillain-Barre syndrome progresses, muscle
weakness can evolve into paralysis.
Signs and symptoms of Guillain-Barre syndrome may include:
Prickling, pins and needles sensations in your fingers, toes, ankles or wrists
Weakness in your legs that spreads to your upper body
Unsteady walking or inability to walk or climb stairs
Difficulty with facial movements, including speaking, chewing or swallowing
Double vision or inability to move eyes
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Severe pain that may feel achy, shooting or cramp like and may be worse at night
Difficulty with bladder control or bowel function
Rapid heart rate
Low or high blood pressure
Difficulty breathing
People with Guillain-Barre syndrome usually experience their most significant weakness
within two weeks after symptoms begin.[3]
TYPES
Once thought to be a single disorder, Guillain-Barre syndrome is now known to occur in
several forms. The main types are:
Acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the most
common form in North America and Europe. The most common sign of AIDP is muscle
weakness that starts in the lower part of your body and spreads upward.
Miller Fisher syndrome (MFS), in which paralysis starts in the eyes. MFS is also
associated with unsteady gait. MFS is less common in the U.S. but more common in Asia.
Acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal
neuropathy (AMSAN) are less common in the U.S. But AMAN and AMSAN are more
frequent in China, Japan and Mexico.
Figure: Types Of GBS.
Figure-3: Neuron disorder in Guillain–Barré syndrome.
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CAUSES
Two thirds of people with Guillain–Barré syndrome have experienced an infection before the
onset of the condition. Most commonly these are episodes of gastroenteritis or a respiratory
tract infection. In many cases, the exact nature of the infection can be confirmed.
Approximately 30% of cases are provoked by Campylobacter jejuni bacteria, which cause
diarrhea. A further 10% are attributable to cytomegalovirus (CMV, HHV-5). Despite this,
only very few people with Campylobacter or CMV infections develop Guillain–Barre
syndrome. The strain of Campylobacter involved may determine the risk of GBS. Two other
herpesviruses (Epstein–Barr virus/HHV-4 and varicella zoster virus/HHV-3) and the
bacterium Mycoplasma pneumoniae have been associated with GBS. The tropical viral
infection dengue fever and zika virus have also been associated with episodes of GBS.
Previous hepatitis E virus infection has been found to be more common in people with GBS.
Some cases may be triggered by the influenza virus and potentially influenza vaccine. In fact,
natural influenza infection is a stronger risk factor for the development of GBS than is
influenza vaccination and getting the vaccination actually reduces the risk of GBS overall by
lowering the risk of catching influenza. Even those who have previously experienced
Guillain–Barré syndrome are considered safe to receive the vaccine in the future.[4]
Figure-4: A. Campylobacter jejuni bacteria B. Zika virus.
There are some known risk factors, including
Sex: Males are slightly more likely to contract GBS.
Age: Risk increases with age.
Campylobacter jejuni bacterial infection: A common cause of food poisoning, this
infection sometimes occurs before GBS.
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Influenza virus, HIV, or Epstein-Barr virus (EBV): These have occurred in association
with cases of GBS.
Mycoplasma pneumonia: This is a bacterial infection of the lungs.
Surgery: Some surgeries can trigger GBS.
Hodgkin’s lymphoma: Cancer of the lymphatic system can lead to GBS.
Influenza vaccination or childhood vaccinations: These have also been linked to GBS
in rare cases.
Figure-5: Scanning Electron Micrograph of organism and Graphical plot of Guillain-
Barre syndrome.
MECHANISM
Guillain–Barre syndrome is caused by an immune attack on the nerve cells of the peripheral
nervous system and their support structures. The nerve cells have their body (the soma) and a
long projection (the axon) that carries electrical nerve impulses to the neuromuscular junction
where the impulse is transferred to the muscle. Axons are wrapped in a sheath of Schwann
cells that contain myelin. Between Schwann cells are gaps called nodes of Ranvier where the
axon is exposed. Different types of GBS feature different types of immune attack. The
demyelinating variant (AIDP) features damage to the myelin sheath by white blood cells (T
lymphocytes and macrophages), this process is preceded by activation of a group of blood
proteins known as complement. In contrast, the axonal variant is mediated by IgG antibodies
and complement against the cell membrane covering axon without direct lymphocyte
involvement.
Various antibodies directed at nerve cells have been reported in GBS. In the axonal subtype,
these antibodies have been shown to bind to gangliosides, a group of substances found in
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peripheral nerves. A ganglioside is a molecule consisting of ceramide bound to a small group
of hexose-type sugars and containing various numbers of N-acetylneuraminic acid groups.
The key four gangliosides against which antibodies have been described are GM1, GD1a,
GT1a, and GQ1b, with different anti-ganglioside antibodies being associated with particular
features; for instance, GQ1b antibodies have been linked with Miller Fisher variant GBS and
related forms including Bickerstaff encephalitis. The production of these antibodies after an
infection is probably the result of molecular mimicry, where the immune system is reacting to
microbial substances, but the resultant antibodies also react with substances occurring
naturally in the body.[5]
After a Campylobacter infection, the body produces antibodies of the IgA class, only a small
proportion of people also produce IgG antibodies against bacterial substance cell wall
substances (e.g. lipopolysaccharides). Molecular mimicry between lipo-oligosaccharides
structure on the cell envelop of these bacteria and glycoside epitode on the human nerve that
generates cross-reactive immune response result in autoimmune -driven nerve damage.
Figure-6: mechanism used by GBS to evade the immune system.
LINK BETWEEN ZIKA VIRUS AND GBS
There is a growing evidence that zika virus may also an trigger Guillain Barre Syndrome the
thought is that the body creates antibodies to marshal an assault on the zika infection, and
after the illness subsides, these antibodies then start attacking the peripheral nerves that
connect the brain and spinal cord to the rest of the body.
Zika virus has previously been associated with GBS. The link was first described in 2013 and
2014 when the incidence of GBS showed a significant increase over 4 to 5 years during a
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Zika outbreak in the French Polynesian islands. This was the first evidence of such a link, and
more research is required. However, there have been a few studies looking at the in the
incidence of GBS in French Polynesia and Latin America after recent Zika outbreaks.
Zika has been associated with mild flu-like symptoms in most people that contract the
disease, similar to many of the infections that appear before GBS.[6]
Figure-7: Effect of zika virus on neuron.
PATHOPHYSIOLOGY
Infections with pathogens, such as Campylobacter jejuni, can trigger humoral immune and
autoimmune responses that result in nerve dysfunction and the symptoms of GBS. Lipo-
oligosaccharides on the C. jejuni outer membrane may elicit the production of antibodies that
cross react with gangliosides, such as GM1 and GD1a on peripheral nerves. The antigens
targeted in AMAN are located at or near the node of Ranvier. The anti-GM1 and anti-GD1a
antibodies bind to the nodal axolemma, leading to complement activation followed by MAC
formation and disappearance of voltage-gated sodium channels. This damage can lead to
detachment of paranodal myelin, and nerve conduction failure. Macrophages then invade
from the nodes into the periaxonal space, scavenging the injured axons. The antigens targeted
in AIDP are, presumably, located on the myelin sheath. The antibodies can activate
complement, which leads to formation of the MAC on the outer surface of Schwann cells,
initiation of vesicular degeneration, and invasion of myelin by macrophages. Some antibody
specificities are associated with particular GBS subtypes and related neurological deficits,
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reflecting the distribution of different gangliosides in human peripheral nerves C. jejuni
infections are predominantly, but not exclusively, related to the AMAN or pure motor
subtype of GBS. Patients with AMAN frequently have serum antibodies against GM1a,
GM1b, GD1a and GalNAc-GD1a gangliosides. Patients with MFS or MFS–GBS overlap
syndrome frequently have antibodies against GD1b, GD3, GT1a and GQ1b gangliosides,
which are related to ataxia and ophthalmoplegia. In a study from the Netherlands, 20% of
patients with AIDP related to cytomegalovirus infection had anti-GM2 antibodies, although
these antibodies are also found in patients with uncomplicated cytomegalovirus infections.
Interestingly, as well as antibodies against single gangliosides, patients can also have
antibodies against combinations of epitopes from ganglioside complexes. Such complexes are
located in specialized microdomains, or 'lipid rafts', in the cell membrane. Antibodies that
target ganglioside complexes also cross react with C. jejuni lipo-oligosaccharides, and are
probably induced by a preceding infection with C. jejuni. Antibodies against various
combinations or complexes of glycolipids have also been reported in patients with AIDP,
although the role of these antibodies in its pathogenesis remains to be determined.[7]
In conjunction with the presence of antiganglioside antibodies, complement activation seems
to contribute to nerve degeneration in GBS a phenomenon that has been studied at the nodes
of Ranvier and at the motor nerve terminal in a mouse model of AMAN. Sodium channel
clusters, as well as paranodal axoglial junctions, the nodal cytoskeleton, and Schwann cell
microvilli, all of which stabilize the sodium channel clusters, were disrupted by complement
activation in a GBS disease model. Additional studies in a GBS mouse model provided
evidence that blockade of complement activation prevents emergence of the clinical signs of
antiganglioside-mediated neuropathy.
The development of GBS after a C. jejuni infection may also depend on patient-related
factors that influence the susceptibility to produce cross reactive, carbohydrate-targeted
antibodies. This hypothesis is supported by the fact that GBS has a relapse rate of 5%, which
is clearly higher than would be expected by chance. The initial pathogen–host interaction has
a key role in the development of GBS. C. jejuni lipo-oligosaccharides bind to siglec-7 (sialic
acid-binding immunoglobulin-like lectin 7) and activate dendritic cells via Toll-like receptor
4 and CD14. These dendritic cells produce type 1 interferon and tumour necrosis factor
(TNF), which induce proliferation of B cells. This immune activation could be influenced by
genetic polymorphisms but, to date, genetic factors have only been studied in small cohorts of
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patients. Interestingly, a meta-analysis identified a moderate association between GBS and a
particular TNF polymorphism. In addition, an association between polymorphisms in the
MBL2 gene (encoding mannose-binding protein C) and the severity and outcome of GBS has
been confirmed. Future genome-wide association studies in large, well-described and
adequately controlled cohorts are required to establish the role of host factors in the
pathogenesis of GBS.[8]
DIAGNOSIS
Guillain-Barre syndrome can be difficult to diagnose in its earliest stages. Its signs and
symptoms are similar to those of other neurological disorders and may vary from person to
person.
Doctors are likely to start with a medical history and thorough physical examination.
• Spinal tap (lumbar puncture). A small amount of fluid is withdrawn from the spinal canal in
your lower back. The fluid is tested for a type of change that commonly occurs in people who
have Guillain-Barre syndrome.
• Electromyography. Thin-needle electrodes are inserted into the muscles your doctor wants
to study. The electrodes measure nerve activity in the muscles.
• Nerve conduction studies. Electrodes are taped to the skin above your nerves. A small shock
is passed through the nerve to measure the speed of nerve signals.
TREATMENT
There's no cure for Guillain-Barre syndrome. But two types of treatments can speed recovery
and reduce the severity of the illness:
Plasma exchange (plasmapheresis). The liquid portion of part of your blood (plasma) is
removed and separated from your blood cells. The blood cells are then put back into your
body, which manufactures more plasma to make up for what was removed.
Plasmapheresis may work by ridding plasma of certain antibodies that contribute to the
immune system's attack on the peripheral nerves.
Immunoglobulin therapy. Immunoglobulin containing healthy antibodies from blood
donors is given through a vein (intravenously). High doses of immunoglobulin can block
the damaging antibodies that may contribute to Guillain-Barre syndrome.
These treatments are equally effective. Mixing them or administering one after the other is no
more effective than using either method alone.[9]
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Figure-8: Pathogenesis of GBS: molecular mimicry and antiganglioside antibodies.
Doctors are also likely to be given medication to:
Relieve pain, which can be severe.
Prevent blood clots, which can develop while you're immobile.
People with Guillain-Barre syndrome need physical help and therapy before and during
recovery. They may include:
Movement of your arms and legs by caregivers before recovery, to help keep your
muscles flexible and strong.
Physical therapy during recovery to help you cope with fatigue and regain strength and
proper movement.
Training with adaptive devices, such as a wheelchair or braces, to give you mobility and
self-care skills.[10]
RECOVERY
Although some people can take months and even years to recover, most people with Guillain-
Barre syndrome experience this general timeline:
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After the first signs and symptoms, the condition tends to progressively worse for about
two weeks.
Symptoms reach a plateau within four weeks.
Recovery begins, usually lasting six to 12 months, though for some people it could take
as long as three years.
Among adults recovering from Guillain-Barre syndrome:
About 80% can walk independently six months after diagnosis.
About 60% fully recover motor strength one year after diagnosis.
About 5% to 10% have very delayed and incomplete recovery.
Children, who rarely develop Guillain-Barre syndrome, generally recover more completely
than adults.[11]
EPIDEMIOLOGY
In Western countries, the number of new episodes per year has been estimated to be between
0.89 and 1.89 cases per 100,000 people. Children and young adults are less likely to be
affected than the elderly: the risk increases by 20% for every decade of life. Men are more
likely to develop Guillain–Barre syndrome than women; the relative risk for men is 1.78
compared to women.
The distribution of subtypes varies between countries. In Europe and the United States, 60–
80% of people with Guillain–Barré syndrome have the demyelinating subtype (AIDP), and
AMAN affects only a small number (6–7%). In Asia and Central and South America, that
proportion is significantly higher (30–65%). This may be related to the exposure to different
kinds of infection, but also the genetic characteristics of that population. Miller Fisher variant
is thought to be more common in Southeast Asia.[12]
LINK BETWEEN COVID-19 AND GBS
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), originating from Wuhan, is
spreading around the world and the outbreak continues to escalate. Patients with coronavirus
disease 2019 (COVID-19) typically present with fever and respiratory illness. However, little
information is available on the neurological manifestations of COVID-19. Here, we report the
first case of COVID-19 initially presenting with acute Guillain-Barré syndrome. On Jan 23,
2020, a woman aged 61 years presented with acute weakness in both legs and severe fatigue,
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progressing within 1 day. She returned from Wuhan on Jan 19, but denied fever, cough, chest
pain, or diarrhoea. Her body temperature was 36·5°C, oxygen saturation was 99% on room
air, and respiratory rate was 16 breaths per min. Lung auscultation showed no abnormalities.
Neurological examination disclosed symmetric weakness (Medical Research Council grade
4/5) and areflexia in both legs and feet. 3 days after admission, her symptoms progressed.
Muscle strength was grade 4/5 in both arms and hands and 3/5 in both legs and feet.
Sensation to light touch and pinprick was decreased distally.[13]
Figure-9: Distribution of GBS between countries.
CONCLUSION
In conclusion, a diagnosis of Guillain-Barre syndrome may still be considered in a patient
with clinical findings and EMG studies consistent with GBS but with a CSF profile that does
not show the typical albuminocytologic dissociation. The long-term outlook for Guillain-
Barre syndrome is generally good. Most patients recover fully, although it can take months or
years to regain pre-illness strength and movement. About 30% of patients still have some
weakness three years after the illness strikes. Some keywords are Guillain Barré syndrome,
Campylobacter jejuni, antiganglioside antibodies, intravenous immunoglobulin treatment,
plasma exchange.
Investigators of large, worldwide, collaborative studies of the spectrum of Guillain-Barré
syndrome are accruing data for clinical and biological databases to inform the development
of outcome predictors and disease biomarkers. Such studies are transforming the clinical and
scientific landscape of acute autoimmune neuropathies. Treatments have been developed and
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proved effective, but these are not sufficient in many patients. Although there have been
major steps forward, this is no time for complacency as the research area continues to face
deep, unsolved issues around pathogenesis of Guillain-Barré syndrome, especially for the
acute inflammatory demyelinating polyneuropathy form of the disorder. Newly emerging
post-infectious forms of Guillain-Barré syndrome, such as those associated with arboviruses
including Zika, need to be closely monitored as global epidemics spread. Biomarkers,
prognostic models, and better therapies are needed. Many of these issues are being addressed
through multicentre, collaborative efforts such as IGOS. Prevention of severe axonal injury
early in the course of the disease remains a major focus, because it is an important limiting
factor in achieving a good, long-term outcome.
REFERENCES
1. Watanabe T, Matsuura O, Natsume J, et al. Dramatic improvement with
immunoabsorption therapy in a 7-year-old girl with severe Guillain-Barré syndrome after
unsuccessful gammaglobulin therapy. No To Hattatsu, 1998; 30: 255–60.
2. Guillain G, Barre J, Strohl A. Sur un syndrome de radiculo-nevrite avec hyperalbuminose
du liquide cephalorachidien sans reaction cellulaire. Remarques sur les characteres
clinique et graphique des reflexes tendinaux. Bulletins et Memories de la Societe
Medicale des Hopitaux de Paris, 1916; 40: 1462–70.
3. Kaplan JE, Katona P, Hurwitz ES, et al. Guillain-Barré syndrome in the United States,
1979–1980 and 1980–1981. Lack of an association with influenza vaccination. JAMA,
1982; 248: 698–700.
4. Carpo M, Pedotti R, Allaria S, et al. Clinical presentation and outcome of Guillain-Barré
and related syndromes in relation to anti-ganglioside antibodies. J Neurol Sci., 1999; 168:
78–84.
5. Prof. Dr. Dhrubo Jyoti Sen; Zika virus outbreak: the global endemic to pandemic:
European Journal of Pharmaceutical and Medical Research, 2017; 4(3): 01-07.
6. Vriesendorp FJ, Mishu B, Blaser MJ, et al. Serum antibodies to GM1, GD1b, peripheral
nerve myelin, and Campylobacter jejuni in patients with Guillain-Barré syndrome and
controls: correlation and prognosis. Ann Neurol, 1993; 34: 130–5.
7. Van den Berg, B., Walgaard, C., Drenthen, J. et al. Guillain–Barré syndrome:
pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol, 2014; 10: 469–482.
www.wjpps.com Vol 9, Issue 6, 2020.
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Sourav et al. World Journal of Pharmacy and Pharmaceutical Sciences
8. Heikema, A. P. et al. Siglec-7 specifically recognizes Campylobacter jejuni strains
associated with oculomotor weakness in Guillain–Barré syndrome and Miller Fisher
syndrome. Clin. Microbiol. Infect, 2013; 19: E106–E112.
9. Kuijf, M. L. et al. Origin of ganglioside complex antibodies in Guillain–Barré syndrome.
J. Neuroimmunol, 2007; 188: 69–73.
10. Cao-Lormeau, V., Blake, A., Mons, S., Lastère, S., Roche, C., Vanhomwegen, J., … &
Ghawché, F. Guillain-Barré syndrome outbreak associated with Zika virus infection in
French Polynesia: A case-control study. The Lancet, 2016; 387(10027): 1531-1539.
11. Dimachkie, M. M. & Barohn, R. J. Guillain-Barré Syndrome and variants. Neurology
Clinics, 2014; 31(2): 491-510.
12. Cao-Lormeau VM, Blake A, Mons S, Lastère S, Roche C, Vanhomwegen J, Ghawché F.
Guillain-Barré syndrome outbreak associated with Zika virus infection in French
Polynesia: a case-control study. Lancet, 2016; 387(10027): 1531–1539.
13. Zhao H, Shen D, Zhou H, Liu J, Chen S. Guillain-Barré syndrome associated with SARS-
CoV-2 infection: Causality or coincidence? Lancet Neurol, 2020; S1474-4422(20):
30109–30105.
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