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Axonal Guillain‐Barré syndrome: Relation to anti‐ganglioside antibodies and Campylobacter jejuni infection in Japan
- K. Ogawara, S. Kuwabara, M. Mori, T. Hattori, M. Koga, N. Yuki
- Biology, MedicineAnnals of neurology
- 1 October 2000
Findings suggest that the three phenomena “axonal dysfunctions (AMAN or early‐reversible conduction failure),” “IgG antibodies against GM1, GD1a, GalNAc‐GD1A, or GD1b,” and “C. jejuni infection” are closely associated but that microorganisms other than C.Jejuni frequently trigger an anti‐ganglioside response and elicit axonal GBS.
Altered axonal excitability properties in amyotrophic lateral sclerosis: impaired potassium channel function related to disease stage.
Modelling the excitability changes in this group supported the hypothesis that axonal potassium conductances are reduced, resulting in increased supernormality despite membrane depolarization in ALS, and suggest a changing pattern of abnormal membrane properties with disease progression.
Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain–Barré syndrome
Besides the simple axonal degeneration pattern, patients with anti-ganglioside-positive Guillain–Barré syndrome can show transient conduction slowing/block in the distal or proximal nerve segments, mimicking demyelination, but anti- Gangliosides antibodies do not appear to be associated with acute inflammatory demYelinating polyneuropathy.
Differences in membrane properties of axonal and demyelinating Guillain‐Barré syndromes
The results support the view that the predominantly distal targets of immune attack are different for AMAN and AIDP, and Supernormality and threshold electrotonus were normal in both groups of patients, suggesting that, at the wrist, membrane potential was normal and pathology was relatively minor.
Hyperreflexia in Guillain-Barré syndrome: relation with acute motor axonal neuropathy and anti-GM1 antibody
- S. Kuwabara, K. Ogawara, M. Koga, M. Mori, T. Hattori, N. Yuki
- Medicine, BiologyJournal of neurology, neurosurgery, and…
- 1 August 1999
Investigating the incidence of hyperreflexia in patients with Guillain-Barré syndrome and its relation with electrodiagnosis of acute motor axonal neuropathy (AMAN), antiganglioside GM1 antibody, and Campylobacter jejuni infection found increased motor neuron excitability further characterises the subgroup of patients with GBS with AMAN and anti-GM1 antibodies.
Differences in patterns of progression in demyelinating and axonal Guillain–Barré syndromes
The patterns and speeds of progression differ in AMAN and AIDP, AMAN having a rapid progression and an early nadir, and AIDs frequently have a significantly long progression after the first examination; therefore, they need to be carefully monitored.
Haemophilus influenzae infection and Guillain-Barré syndrome.
It is concluded that a form of Guillain-Barré syndrome occurs after respiratory infection by H. influenzae in the Japanese population.
Patterns of nerve conduction abnormalities in POEMS syndrome
- J. Sung, S. Kuwabara, K. Ogawara, K. Kanai, T. Hattori
- Medicine, PsychologyMuscle & nerve
- 1 August 2002
The patients with POEMS syndrome showed slowing of nerve conduction that was more predominant in the intermediate than distal nerve segments, and rare conduction block (6% of the tested nerves), and more severe attenuation of compound muscle action potentials in the lower than upper limbs, compared with patients with CIDP.
Does Campylobacter jejuni infection elicit “demyelinating” Guillain–Barré syndrome?
Patients with C. jejuni-related Guillain–Barré syndrome can show transient slowing of nerve conduction, mimicking demyelination, but C.Jejuni infection does not appear to elicit acute inflammatory demyELinating polyneuropathy.
Muscle cramp in Machado-Joseph disease: altered motor axonal excitability properties and mexiletine treatment.
- K. Kanai, S. Kuwabara, K. Arai, J. Sung, K. Ogawara, T. Hattori
- BiologyBrain : a journal of neurology
- 1 April 2003
Pathological muscle cramps responded well to mexiletine treatment, and this is consistent with the hypothesis that they are caused by an increase in persistent Na(+) conductance, possibly associated with axonal regeneration or collateral sprouting.