Acute disseminated encephalomyelitis (ADEM) and Guillain-Barré syndrome (GBS) are distinct demyelinating disorders that share an autoimmune pathogenesis and prior history of viral infection or vaccination. Our patient is a 10 years with acute flaccid paralysis, quadriparesis (lower limbs affected more than upper limbs), generalized areflexia and urinary retention. He had difficulty in speech and drooling of saliva. He also presented with raised intracranial pressure with papilledema; then bilateral optic neuritis developed during the later course of illness. Based on the temporal association and exclusion of alternative etiologies, diagnosis of the association between ADEM and GBS was made. Electro-diagnosis (electromyography-nerve conduction velocity) and magnetic resonance imaging study supported our diagnosis. He improved remarkably after treatment with intravenous immunoglobulin and intravenous methylprednisolone.

We report a child presenting with severe demyelinating myelitis complicated with critical illness polyneuropathy. This previously healthy 8-month-old boy presented with acute superior limb weakness, absent tendon reflexes, and respiratory failure. Spinal magnetic resonance imaging showed an extensive cervical demyelinating lesion. Spinal cord trauma was suspected and high doses of dexamethasone were administered. Electromyography and nerve conduction studies showed absence of compound muscle action potentials and sural nerve sensory action potential, which was suggestive of a severe Guillain-Barré syndrome. However, intravenous immunoglobulins did not induce any improvement. Afterward, sural nerve biopsy showed a mild neuropathy, but muscle biopsy revealed abnormalities compatible with severe critical illness myopathy. After 5 months of evolution without improvement, the patient died following withdrawal of life support therapy. This case highlights the possible occurrence of critical illness polyneuromyopathy when treatment with corticosteroids are used in patients with acute demyelinating myelitis.

OBJECTIVE: To probe into the mechanism of electroacupuncture at shu-points of the five zang-organs for treatment of Guillain-Barre syndrome (GBS). METHODS: Eighty healthy giant-ear white rabbits were randomly divided into 4 groups, a blank group, a model group, an electroacupuncture (EA) group and an immunoglobulin group, 20 rabbits in each group. The internationally recognized P 2 immune rabbit model was used in the study. The EA group were treated with EA at shu-points of the five zang-organs and the immunoglobulin group with intravenous injection of immunoglobulin 80 mg/kg/day. The sciatic nerve movement conduction velocity (MCV) and F wave incidence rate were investigated respectively at the 7th and 14th days of treatment in the rabbits of GBS. RESULTS: The sciatic nerve MCV significantly reduced in the model group, and it significantly increased (P<0.01) and F wave abnormal cases was significantly reduced (P<0.05) after treatment for 14 days in the EA group as compared with those in the model group. CONCLUSION: EA at shu-points of the five zang-organs can increase the sciatic nerve MCV and decrease the abnormal F wave incidence rate of the sciatic nerve in the rabbit of GBS.

A 17 year-old woman developed progressive quadriparesis with bilateral facial diplegia after immunization with recombinant hepatitis B vaccine 3 days prior. Cerebrospinal fluid analysis revealed acellular fluid with high protein level. The electrodiagnosis was compatible with demyelinating polyneuropathy. Other potential causes of Guillain-Barre' syndrome (GBS) were ruled out. Her motor power gradually improved and returned to normal later. The temporal relationship between GBS and vaccination was suggestive of a vaccine-induced cause. Mechanisms of this very rare complication are proposed with a literature review.

Using data from Vaccine Adverse Event Reporting System, we identified 69 reports of Guillain-Barré Syndrome (GBS) after Gardasil vaccination that occurred in the United States between 2006 and 2009. The onset of symptoms was within 6 weeks after vaccination in 70% of the patients in whom the date of vaccination was known. The estimated weekly reporting rate of post-Gardasil GBS within the first 6 weeks (6.6 per 10,000,000) was higher than that of the general population, and higher than post-Menactra and post-influenza vaccinations. Further prospective active surveillance for accurate ascertainment and identification of high-risk groups of GBS after Gardasil vaccination is warranted.

OBJECTIVE:To report a case of Guillain-Barré syndrome (GBS) following a dose of influenza A (H1N1) vaccine (Arepanrix).

CASE SUMMARY:An 11-year-old boy was admitted to the hospital after presenting with facial diplegia; abdominal, forehead, and thigh pain; and acute cervical pain. He had received the Arepanrix H1N1 subcutaneous vaccine 13 days before symptom onset. The neurologic examination also revealed a symmetric bilateral paralysis of the VIIth cranial nerve and intense pain, proximal weakness of the shoulder girdles and pelvis, and preserved deep tendon reflexes. Cerebrospinal fluid analysis revealed an albuminocytologic dissociation. Therefore, a diagnosis of atypical GBS following vaccination against HINI influenza was made.

DISCUSSION:Based on the clinical evaluation, laboratory test results, neurologic features, and the exclusion of alternative diagnoses, the Naranjo probability scale revealed a probable relationship between the clinical manifestations of GBS and the vaccine against influenza A (H1N1) received by the patient. This is the first published case for the 2009 influenza pandemic in children.

CONCLUSIONS:While recent studies have found inconclusive results on the association between influenza vaccine and GBS, all suspected cases should be published for further evaluation.

A 52-year-old woman developed Guillain-Barré syndrome 10 weeks after immunization with recombinant hepatitis B vaccine. Common infectious causes of GBS were ruled out. The temporal relationship between GBS and hepatitis B virus (HBV) vaccination was suggestive of a vaccine-induced cause. The possible mechanisms of this very, rare complication are discussed.

Celiac disease (CD) long has been associated with neurologic and psychiatric disorders including cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology. These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and neuropathy with positive antiganglioside antibodies. The association between most neurologic syndromes described and gluten sensitivity remains to be confirmed by larger epidemiologic studies. It further has been suggested that gluten sensitivity (as evidenced by high antigliadin antibodies) is a common cause of neurologic syndromes (notably cerebellar ataxia) of otherwise unknown cause. Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington's disease. It remains unclear whether gluten sensitivity contributes to the pathogenesis of these disorders or whether it represents an epiphenomenon. Studies of gluten-free diet in patients with gluten sensitivity and neurologic syndromes have shown variable results. Diet trials also have been inconclusive in autism and schizophrenia, 2 diseases in which sensitivity to dietary gluten has been implicated. Further studies clearly are needed to assess the efficacy of gluten-free diet and to address the underlying mechanisms of nervous system pathology in gluten sensitivity.

We report a case of Guillain-Barré syndrome in a previously healthy child who received a hepatitis A vaccination (HAVRIX) 5 days before onset of symptoms. No other precipitating factor could be identified. The relevant literature is reviewed and discussed.

Guillain-Barre syndrome is a rare but fatal autoimmune disease. The exact cause of Guillain-Barre syndrome is still unknown. The most common known etiology of Guillain-Barre syndrome is infectious disease notably caused by. A very small fraction of people can develop Guillain-Barre syndrome due to vaccines and vaccinations like a meningococcal vaccine, poliovirus vaccine, influenza vaccine, and rabies vaccine. Of all these, rabies is fatal invariably. It can be preventable if diagnosed early and post-exposure treatment is followed according to the World Health Organization guidelines. Older formulations of rabies vaccines are cultured in the neural tissues and have been found to have an increased risk of Guillain-Barre syndrome. Although less immunogenic older formulations of rabies vaccines are more commonly used in Asian and South American countries due to their cost-effective nature. There is little to no data available on the incidence of Guillain-Barre syndrome due to vaccinations in Pakistan. Most of the cases of Guillain-Barre syndrome due to vaccination are either undiagnosed or misdiagnosed. In this case report, we are presenting a case of vaccine-associated Guillain-Barre syndrome due to neural tissue anti-rabies vaccine in a young girl, who presented with lower limb weakness, inability to pass urine and abdominal pain.

BACKGROUND:In 1980, human diploid cell vaccine (HDCV, Imovax Rabies, Sanofi Pasteur), was licensed for use in the United States.

OBJECTIVE:To assess adverse events (AEs) after HDCV reported to the US Vaccine Adverse Event Reporting System (VAERS), a spontaneous reporting surveillance system.

METHODS:We searched VAERS for US reports after HDCV among persons vaccinated from January 1, 1990-July 31, 2015. Medical records were requested for reports classified as serious (death, hospitalization, prolonged hospitalization, disability, life-threatening-illness), and those suggesting anaphylaxis and Guillain-Barré syndrome (GBS). Physicians reviewed available information and assigned a primary clinical category to each report using MedDRA system organ classes. Empirical Bayesian (EB) data mining was used to identify disproportional AE reporting after HDCV.

RESULTS:VAERS received 1,611 reports after HDCV; 93 (5.8%) were serious. Among all reports, the three most common AEs included pyrexia (18.2%), headache (17.9%), and nausea (16.5%). Among serious reports, four deaths appeared to be unrelated to vaccination.

CONCLUSIONS:This 25-year review of VAERS did not identify new or unexpected AEs after HDCV. The vast majority of AEs were non-serious. Injection site reactions, hypersensitivity reactions, and non-specific constitutional symptoms were most frequently reported, similar to findings in pre-licensure studies.

Infectious agents contribute to the environmental factors involved in the development of autoimmune diseases possibly through molecular mimicry mechanisms. Hence, it is feasible that vaccinations may also contribute to the mosaic of autoimmunity. Evidence for the association of vaccinations and the development of these diseases is presented in this review. Infrequently reported post-vaccination autoimmune diseases include systemic lupus erythematosus, rheumatoid arthritis, inflammatory myopathies, multiple sclerosis, Guillain-Barré syndrome, and vasculitis. In addition, we will discuss macrophagic myofasciitis, aluminum containing vaccines, and the recent evidence for autoimmunity following the use of human papillomavirus vaccine.