Acute “axonal” Guillain‐Barré polyneuropathy

Feasby, Thomas E.; Gilbert, Jeremy; Brown, William F.; Hahn, Angelika F.; Koopman, Wilma J.; Zochodne, Douglas W.

doi:10.1212/wnl.37.2.357-b

Cited by 131 publications

(179 citation statements)

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“…17 Muscle atrophy was not apparent in our patients in the early course of the disease (within weeks) as observed in acute axonal forms ofGBS. 18 In most of the patients weakness progressed for 3-5 days. This rapid and wide spread evolution was also described by many authors.…”

Section: Discussionmentioning

confidence: 98%

Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh

et al. 2017

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Section: Discussionmentioning

confidence: 98%

Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh

et al. 2017

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“…The autopsy revealed severe, widespread axonal degeneration in the nerve roots and periphery without lymphocytic inflammation, rather than the usual characteristic segmental demyelination. The team were convinced they had seen something new and published their findings from several similar cases in 1986 39 . Their proposal of a pure axonal form of GBS met with much scepticism, and Feasby had to fiercely defend his findings 40 until similar cases were reported 41 and the concept gained some ground by the early 1990s.…”

Section: [H1] Electrophysiological Developmentsmentioning

confidence: 99%

Guillain–Barré syndrome: a century of progress

2016

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In 1916, Guillain, Barré and Strohl reported on two cases of acute flaccid paralysis with high cerebrospinal fluid protein levels and normal cell counts -novel findings that identified the disease we now know as Guillain-Barré syndrome (GBS).100 years on, we have made great progress with the clinical and pathological characterization of GBS. Early clinicopathological and animal studies indicated that GBS was an immune-mediated demyelinating disorder with secondary axonal injury if severe; the current treatments of plasma exchange and intravenous immunoglobulin, which were developed in the 1980s, are based on this premise. Subsequent work has, however, shown that the underlying disease can be an axonal injury. The association of Campylobacter jejuni strains has led to confirmation that anti-ganglioside antibodies are pathogenic and that axonal GBS involves an antibody and complement-mediated disruption of nodes of Ranvier, neuromuscular junctions and other neuronal and glial membranes. Now, ongoing clinical trials of the complement inhibitor eculizumab are the first of targeted immunotherapy in GBS.Guillain-Barré syndrome (GBS) is the commonest cause of acute flaccid paralysis and manifests as rapidly evolving weakness and sensory disturbance in arms, legs and in some patients, facial, bulbar and respiratory muscles. Many patients will make a good recovery over many months but in severe cases patients can require months of intensive care support and be left with permanent severe weakness, sensory disturbance and pain. Furthermore, around 5% die from complications including respiratory failure, pneumonia and arrhythmias, making it a medical emergency with a high morbidity and significant mortality.Descriptions of clinical cases that closely resemble the condition we now know as GBS were made at least as early as 1859, when Jean Baptiste Octave Landry reported on "acute ascending paralysis". His report led to use of the term "Landry's ascending paralysis" to describe subacute ascending peripheral sensory and motor dysfunction. He observed that:

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“…[3][4][5][6] Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been reported in association with graft-versus-host disease (GVHD) or infection. 7,8 An acute motor axonal neuropathy (AMAN) has been associated with Campylobacter jejuni and other infections, [9][10][11] but no chronic form has been described. We report a case of a chronic sensorimotor axonal, polyradiculoneuropathy complicating BMT for a-mannosidosis.…”

Section: Axonal Neuropathymentioning

confidence: 99%

Late occurrence of chronic immune-mediated axonal polyneuropathy following bone marrow transplant for juvenile-onset α-mannosidosis

Mulrooney

Davies

Walk

et al. 2003

Bone Marrow Transplant

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Summary:A 23-year-old woman with juvenile-onset a-mannosidosis developed an axonal polyneuropathy more than a year following successful unrelated donor (URD) BMT complicated by chronic graft-versus-host disease (GVHD). Progressive muscle weakness and paresthesias developed over at least 4 months, and made her nonambulatory. Nerve conduction and EMG studies demonstrated an axonal sensorimotor neuropathy. Cerebral spinal fluid (CSF) IgG was elevated with two peaks not identified in serum. Strength improved after a single course of plasma exchange and continued to improve over 12 months. The response to plasma exchange, elevated CSF IgG production, and evidence of a serum IgM peak suggest an immune-mediated mechanism. Chronic polyneuropathies following BMT are rare and are usually temporally related to GVHD or infection. This patient's disease was unusual because of its late occurrence and chronic onset in the face of resolved GVHD and in the absence of infection. Bone Marrow Transplantation (2003) 32, 953-955.

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Acute “axonal” Guillain‐Barré polyneuropathy

Cited by 131 publications

References 0 publications

Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh

Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh

Guillain–Barré syndrome: a century of progress

Late occurrence of chronic immune-mediated axonal polyneuropathy following bone marrow transplant for juvenile-onset α-mannosidosis

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Acute “axonal” Guillain‐Barré polyneuropathy

Cited by 131 publications

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Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh

Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh

Guillain–Barré syndrome: a century of progress

Late occurrence of chronic immune-mediated axonal polyneuropathy following bone marrow transplant for juvenile-onset α-mannosidosis

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Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh

Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh