Treatment of an acute motor and sensory axonal neuropathy with propionate in a 33-year-old male

Yoon, Min‐Suk; Pitarokoili, Kalliopi; Sturm, Dietrich; Haghikia, Aiden; Gold, Ralf; Fisse, Anna Lena

doi:10.1177/1756286418809580

Cited by 5 publications

(9 citation statements)

References 22 publications

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“…Furthermore, propionic acid has shown an anti-inflammatory effect in multiple sclerosis patients [41,42] and a case report indicates a positive effect also in CIDP patients [43]. In our own unpublished data, a direct anti-inflammatory effect of propionic acid on Schwann cells and dorsal root ganglia has been demonstrated (Grüter et al, unpublished).…”

Section: Ta B L E 2 Correlation Of Clinical Disability To the Electrophysiological Parameters Of Axonal Damage Seperated By The Differentmentioning

confidence: 92%

Axonal damage determines clinical disability in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): A prospective cohort study of different CIDP subtypes and disease stages

Grüter

Motte

Bulut

et al. 2021

Euro J of Neurology

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Background and purpose Monitoring of patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is challenging in daily medical practice because the interrelationship between clinical disability, CIDP subtype, and neuronal degeneration is still elusive. The aim of this prospective cohort study was to investigate the role of different electrophysiological variables in CIDP monitoring. Methods Comprehensive bilateral nerve conduction studies (NCS) and structured clinical examinations were performed in 95 patients with typical CIDP and CIDP variants (age at inclusion 58.6 ± 11.6 years; median [range] inflammatory neuropathy cause and treatment overall disability score (INCAT‐ODSS) 3 [0–9]), at time of first diagnosis in 25 of these patients (based on data from the prospective Immune‐mediated Neuropathies Biobank registry). After 12 months, 33 patients underwent follow‐up examination. Typical CIDP patients and patients with CIDP variants were characterized electrophysiologically and each individual NCS variable and the overall sum score for axonal damage and demyelination were then correlated to clinical disability scores (INCAT‐ODSS, modified Medical Research Council (MRS) sum score, and INCAT sensory score). Results As opposed to demyelination markers, the NCS axonal damage variable correlated strongly with disability at both first diagnosis and advanced disease stages in cross‐sectional and longitudinal analyses. Distal compound muscle action potential amplitudes of the upper limbs were found to have the strongest correlation with overall clinical function. Typical and atypical CIDP variants had distinct electrophysiological characteristics but, in typical CIDP, axonal degeneration markers were more strongly associated with clinical disability. Conclusions Total disability is largely determined by the degree of axonal damage, especially in typical CIDP. Although most patients have symptoms predominantly in the legs, NCS of the upper limbs are essential for the monitoring of patients with CIDP and CIDP variants.

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Section: Ta B L E 2 Correlation Of Clinical Disability To the Electrophysiological Parameters Of Axonal Damage Seperated By The Differentmentioning

confidence: 92%

Axonal damage determines clinical disability in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): A prospective cohort study of different CIDP subtypes and disease stages

Grüter

Motte

Bulut

et al. 2021

Euro J of Neurology

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“…The regression of this patient’s symptoms and improvement in an additional examination appeared to be very good. 11 …”

Section: Discussionmentioning

confidence: 99%

“…The regression of this patient's symptoms and improvement in an additional examination appeared to be very good. 11 Infection may initiate autoimmunity by inducing costimulatory activity in antigen-presenting cells (APC), which is required to induce the development of antigenreactive T cells, transfer of T cells to the site of inflammation and the production of inflammatory mediators. 4 Esposito et al stated that T cells are extensively trained on "self" in the thymus and then move to the periphery, where they seek out and destroy infections and regulate immune response to self-antigens.…”

Section: Discussionmentioning

confidence: 99%

Acute Motor Axonal Neuropathy Improvement 20 Days After Hyperbaric Oxygen Therapy

Untari

Kusumastuti

Suryokusumo

et al. 2021

IMCRJ

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We reported a rare case demonstrating that the hyperbaric oxygen chamber provided faster clinical improvement in a patient with a variant of Guillain-Barre Syndrome (GBS). A patient with progressive, acute weakness of upper extremity locomotor muscles and with difficulty breathing and swallowing was diagnosed with axonal GBS. Despite life-saving conventional therapies, there was no significant improvement until day 5. During hyperbaric oxygen therapy, there were daily gradual improvements until day 20, at which time the patient was capable of walking slowly without using a walking aid.

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“…This renders IVIg ineffective in severe AMAN, due to poor modulation of Tfh-B cell interactions. [2] With regard to the ineffectiveness of IVIg in AMAN, the current research focuses on seeking adjuvant therapies including the disease-triggering inflammatory and immunologic mechanisms. HBO is a method of treating patients by entering them into a high-pressure room.…”

Section: T-cell Costimulation Plays a Central Role In Autoimmunitymentioning

confidence: 99%

Hyperbaric oxygen therapy improves recovery at acute motor axonal neuropathy case

Untari¹,

Kusumastuti

Suryokusumo

et al. 2022

JNRP

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Acute motor axonal neuropathy (AMAN) is a rare immune-mediated disorder characterized by acute flaccid paralysis with elevated levels of GM1 antibodies. It is also known as a subtype of the Guillain-Barre syndrome (GBS) and develops since antigen s serve as antibodies in the spinal cord. We report a case diagnosed as AMAN with symptoms of ascending limb symmetrical weakness. A neurological examination revealed a flaccid paralysis with multiple cranial nerve palsies. Electromyography showed an axonal type of GBS. The patient refused bone marrow fluid aspiration. Intravenous immunoglobulin was administered at the high care unit. Unfortunately, despite the standard therapy, an optimal recovery was not obtained. Hyperbaric oxygen (HBO) therapy has been known to be common in illnesses and some clinical diseases. Although it has not been indicated for peripheral neuropathy, a remarkable recovery was soon visible in the HBO-treated AMAN case. The HBO mechanisms involved here are anti-inflammation and immunomodulation.

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Treatment of an acute motor and sensory axonal neuropathy with propionate in a 33-year-old male

Cited by 5 publications

References 22 publications

Axonal damage determines clinical disability in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): A prospective cohort study of different CIDP subtypes and disease stages

Axonal damage determines clinical disability in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): A prospective cohort study of different CIDP subtypes and disease stages

Acute Motor Axonal Neuropathy Improvement 20 Days After Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy improves recovery at acute motor axonal neuropathy case

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