Guillain-Barré Syndrome

Dimachkie, Mazen M.; Barohn, Richard J.

doi:10.1007/s11940-013-0231-z

Cited by 14 publications

(9 citation statements)

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“…Although GBS was more severe in old patients, the frequency of treated patients and therapy modalities were similar in both young and old groups. This may be because clinicians pay greater attention to the contraindications and complications of IVIg and PLEX therapies in the elderly (Dimachkie and Barohn , ) . However, these therapies were well tolerated in both young and old GBS patients in our cohort.…”

Section: Discussionmentioning

confidence: 99%

Guillain‐Barré syndrome in the elderly

Perić

Berisavac

Tamaš

et al. 2016

J Peripheral Nervous Sys

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The aim of the study was to analyze specific features of Guillain-Barré syndrome (GBS) in old people. The study included 403 GBS patients (62% young [<60 years], 35% young-old [60-80 years], and 3% old-old [>80 years]). Diagnosis of GBS was made according to the National Institute of Neurological Disorders and Stroke (NINDS criteria). Severe disability (GBS disability score of >3) at nadir was more common in old compared with young patients (p = 0.0001) as was mortality (9% vs. 2%, respectively). Acute motor and sensory axonal neuropathy and hyponatremia were more common in old compared with young patients (12% vs. 6% and 27% vs. 18%, respectively, p = 0.04). A positive history for malignancy was more than three times more common in old than young patients (11% vs. 3%, respectively, p = 0.01). Disability on nadir was similar in young-old and old-old subjects with disability on discharge being more severe in old-old (p = 0.04) suggesting slower recovery in this subgroup. Bulbar symptoms were more common in old-old compared with young-old (50% vs. 19%, respectively, p = 0.01). Comorbidities were present in virtually all old-old patients compared with 66% of young-old patients (p = 0.04). In conclusion, Elderly patients, and especially old-old patients, with GBS have more severe disease with slower recovery than do younger patients.

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Section: Discussionmentioning

confidence: 99%

Guillain‐Barré syndrome in the elderly

Perić

Berisavac

Tamaš

et al. 2016

J Peripheral Nervous Sys

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“…Most patients with GBS recover spontaneously, 62% had made a complete or almost complete recovery at one year [34]. However, neurological disorders in either L31 [12] or L31/CD4 -/- mice, with a sudden onset, seem to persist and remain stable.…”

Section: Discussionmentioning

confidence: 99%

A new animal model of spontaneous autoimmune peripheral polyneuropathy: implications for Guillain-Barré syndrome

Yang

Rainone

Shi

et al. 2014

acta neuropathol commun

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BackgroundSpontaneous autoimmune peripheral neuropathy including Guillain-Barré Syndrome (GBS) represents as one of the serious emergencies in neurology. Although pathological changes have been well documented, molecular and cellular mechanisms of GBS are still under-explored, partially due to short of appropriate animal models. The field lacks of spontaneous and translatable models for mechanistic investigations. As GBS is preceded often by viral or bacterial infection, a condition can enhance co-stimulatory activity; we sought to investigate the critical role of T cell co-stimulation in this autoimmune disease.ResultsOur previous study reported that transgene-derived constitutive expression of co-stimulator B7.2 on antigen presenting cells of the nervous tissues drove spontaneous neurological disorders. Depletion of CD4+ T cells in L31 mice accelerated the onset and increased the prevalence of the disease. In the current study, we further demonstrated that L31/CD4-/- mice exhibited both motor and sensory deficits, including weakness and paresis of limbs, numbness to mechanical stimuli and hypersensitivity to thermal stimulation. Pathological changes were characterized by massive infiltration of macrophages and CD8+ T cells, demyelination and axonal damage in peripheral nerves, while changes in spinal cords could be secondary to the PNS damage. In symptomatic L31/CD4-/- mice, the disruption of the blood neural barriers was observed mainly in peripheral nerves. Interestingly, the infiltration of immune cells was initiated in pre-symptomatic L31/CD4-/- mice, prior to the disease onset, in the DRG and spinal roots where the blood nerve barrier is virtually absent.ConclusionsL31/CD4-/- mice mimic most parts of clinical and pathological signatures of GBS in human; thus providing an unconventional opportunity to experimentally explore the critical events that lead to spontaneous, autoimmune demyelinating disease of the peripheral nervous system.

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“…Inflammatory neuropathies may be divided into three major clinicopathological subgroups: Guillain-Barre syndrome (GBS), an acute disorder affecting peripheral nerves and nerve roots with maximum severity attained within 4 weeks from disease onset; chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), a chronic disorder affecting peripheral nerves and nerve roots with maximal severity attained after 8 weeks following disease onset, and vasculitic neuropathy, an acute-subacute disorder that commonly affects multiple individual or groups of peripheral nerves sequentially [30,80,37,159,23,27]. …”

Section: Introductionmentioning

confidence: 99%

“…The clinical features of AIDP include ascending (or less commonly descending) appendicular and truncal paresis that may progress to paralysis, varying degrees of sensory loss, diminished or loss of myotactic stretch reflexes, respiratory dysfunction, cranial nerve deficits (commonly bilateral facial paresis) and dysautonomia (urinary retention, constipation, labile blood pressure and heart rate) [30,159]. …”

Section: Introductionmentioning

confidence: 99%

“…Needle electromyography typically shows reduced recruitment of motor unit action potentials without signs of muscle reinnervation. Cerebrospinal fluid analysis shows elevated protein with a normal white blood cell count, known as albuminocytologic dissociation in 50% of patients by 2 weeks and 90% by 4 weeks, distinguishing immune-mediated polyradiculopathies from infectious causes where pleocytosis is common [30,159]. Several diagnostic criteria exist for clinical and research purposes, as well as to guide institution of therapy [6,34,143].…”

Section: Introductionmentioning

confidence: 99%

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Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

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Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

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Guillain-Barré Syndrome

Cited by 14 publications

References 100 publications

Guillain‐Barré syndrome in the elderly

Guillain‐Barré syndrome in the elderly

A new animal model of spontaneous autoimmune peripheral polyneuropathy: implications for Guillain-Barré syndrome

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

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