Autonomic nervous system involvement in chronic inflammatory demyelinating polyradiculoneuropathy: a literature review

Rzepiński, Łukasz; Doneddu, Pietro Emiliano; Cutellè, Claudia; Zawadka‐Kunikowska, Monika; Nobile‐Orazio, Eduardo

doi:10.1007/s10072-023-06802-z

Cited by 3 publications

(3 citation statements)

References 49 publications

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“…При этом авторы отмечают, что частота дизавтономных нарушений при ХВДП значимо ниже, чем при других дизиммунных полинейропатиях. В работе коллег из Индии признаки нарушения работы ВНС при ХВДП и вовсе встречались в 89 % случаев (34/38): в 63 % -судомоторная, в 86 % -кардиовагальная и в 55 % случаев -адренергическая дисфункция [20].…”

Section: Discussionunclassified

Comparative multimodal sensory testing in multifocal motor neuropathy and multifocal variant of chronic inflammatory demyelinating polyradiculoneuropathy

Tumilovich,

Grishina,

Suponeva

et al. 2024

Neuromuscular Diseases

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Background. One of the key distinctions between multifocal motor neuropathy (MMN) and multifocal variant of chronic inflammatory demyelinating polyradiculoneuropathy (mCIDP) lies in the presence or absence of sensory deficits. Nevertheless, existing literature suggests that MMN can also involve sensory fibers of peripheral nerves, complicating the differential diagnosis of MMN and mCIDP, which remains a relevant issue.Aim. To evaluate the profile and intensity of objective sensory deficits and autonomic dysfunction in MMN and mCIDP, as well as to identify differential diagnostic markers.Materials and methods. Out of 65 patients followed up in the study, 30 were diagnosed with MMN and 35 were diagnosed with mCIDP. A retrospective analysis of clinical and epidemiological characteristics was carried out. The evaluation encompassed clinical assessments of sensory symptoms (including on the NTSS-9 scale), assessments of the severity of autonomic dysfunction using the COMPASS-31 questionnaire, and neurophysiological multimodal sensory testing (including electroneuromyography, computer pallesthesiometry, and short-latency auditory evoked potentials).Results. Patients with mCIDP were significantly more likely to have subjective (according to the NTSS-9 and COMPASS-31 scales) and objective (according to clinical examination) sensory deficits and autonomic dysfunction (p <0.05). A third of patients with MMN reported sensory complaints, yet there was no objective evidence of impaired pain sensitivity. Changes in vibration sensitivity were equally prevalent during clinical assessment in both groups (p >0.05). Electroneuromyography studies revealed significantly lower amplitudes of hand sensory nerve action potentials in the mCIDP group compared to MMN patients (p <0.05). At the same time, a third of patients with MMN with a previous history of disease of 13 [10.0; 16.0] years also had low amplitudes of hand sensory nerve action potentials. The mean value of the autonomic reaction threshold, as well as the cutaneous vibration perception threshold were significantly higher in mCIDP compared to MMN (p <0.05) when examining the hands.Conclusion. Differential diagnosis of MMN and mCIDP at the onset and in early disease (under 5 years) poses no challenges. However, it has been shown that a third of patients with MMN in the long-term catamnesis of the disease have some kind of sensory impairment, which may complicate the differential diagnosis with mCIDP. In such cases, employing computer pallesthesiography to measure vibration perception threshold can aid in clarifying the diagnosis and determining optimal treatment strategies.

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Section: Discussionunclassified

Comparative multimodal sensory testing in multifocal motor neuropathy and multifocal variant of chronic inflammatory demyelinating polyradiculoneuropathy

Tumilovich,

Grishina,

Suponeva

et al. 2024

Neuromuscular Diseases

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“…Here, we must mention whether dysautonomia occurs in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). A recent review by Rzepi ński et al of 12 studies included 346 eligible patients with CIDP [44]. The reported prevalence of dysautonomia in CIDP during a quantitative assessment of autonomic function ranged from 25 to 89%, depending on the battery of tests used, and the symptoms themselves were relatively mild.…”

Section: Guillain-barré Syndrome (Gbs)mentioning

confidence: 99%

Autoimmune Autonomic Neuropathy: From Pathogenesis to Diagnosis

Nakane,

Koike,

Hayashi

et al. 2024

IJMS

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Autoimmune autonomic ganglionopathy (AAG) is a disease of autonomic failure caused by ganglionic acetylcholine receptor (gAChR) autoantibodies. Although the detection of autoantibodies is important for distinguishing the disease from other neuropathies that present with autonomic dysfunction, other factors are important for accurate diagnosis. Here, we provide a comprehensive review of the clinical features of AAG, highlighting differences in clinical course, clinical presentation, and laboratory findings from other neuropathies presenting with autonomic symptoms. The first step in diagnosing AAG is careful history taking, which should reveal whether the mode of onset is acute or chronic, followed by an examination of the time course of disease progression, including the presentation of autonomic and extra-autonomic symptoms. AAG is a neuropathy that should be differentiated from other neuropathies when the patient presents with autonomic dysfunction. Immune-mediated neuropathies, such as acute autonomic sensory neuropathy, are sometimes difficult to differentiate, and therefore, differences in clinical and laboratory findings should be well understood. Other non-neuropathic conditions, such as postural orthostatic tachycardia syndrome, chronic fatigue syndrome, and long COVID, also present with symptoms similar to those of AAG. Although often challenging, efforts should be made to differentiate among the disease candidates.

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“…The four most common subtypes of Guillain-Barré syndrome (GBS) are acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy, acute motor and sensory axonal neuropathy, and Miller-Fischer syndrome. The source of HA-associated GBS remains unclear, with cross-reactive HA epitopes between the peripheral nervous system and other authors have hypothesized that the presence of cerebrospinal fluid antibodies reflects direct entry into the central nervous system [2]. The incidence of acute inflammatory demyelinating polyneuropathy (AIDP), also known as GBS, acute inflammatory polyneuropathy, or postinfectious polyneuropathy, is approximately 2 per 100,000 people.…”

Section: Introductionmentioning

confidence: 99%

Neurological Uniqueness: A Case Study of Hepatitis A-Induced Acute Inflammatory Demyelinating Polyneuropathy

Abubakar,

Murdia,

Diana

2023

Indo. Jour. of Case Rep.

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Acute inflammatory Demyelinating Polyneuropathy (AIDP) with hepatitis A (HA) is more likely to affect men, develop at a younger age, and have a better prognosis overall. The progression of the Hepatitis A Virus (HAV)-caused liver inflammation and the neurological difficulties could lead to AIDP in the early stages of the hepatitis signs and symptoms. The World Health Organization (WHO) estimates 1.5 million clinical HAV cases annually. Extrahepatic complications of this disease are rare. The etiology of HA associated AIDP remains unclear, with cross-reactive HA epitopes between the peripheral nervous system and other authors have hypothesized that the presence of CSF antibodies reflects direct entry into the central nervous system. Our patient presentations favored AIDP most commonly in HA. A 22-year-old man, with no prior significant medical history, presented to neurology emergency with a 3-day history of acute onset, had been complaining of nausea, general weakness, yellowing of the sclera and history of fever for 5 days. Further investigation revealed marked elevation of liver enzymes in a pattern suggestive of hepatocellular processes. Serum titres of hepatitis B, C, and E were negative, but IgM anti-HAV was positive (enzyme immunoassay). Elevation of Cerebrospinal fluid (CSF) protein and myelitis transversa shown by magnetic resonance imaging were established. The diagnosis as AIDP was taken and treated by symptomatic and neurology treatment. However, the patient regained strength and underwent physiotherapy during two weeks. Approximately 3 months after discharged, the patient's gait had nearly returned to baseline at follow-up and the symptoms slowly improved.

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Autonomic nervous system involvement in chronic inflammatory demyelinating polyradiculoneuropathy: a literature review

Cited by 3 publications

References 49 publications

Comparative multimodal sensory testing in multifocal motor neuropathy and multifocal variant of chronic inflammatory demyelinating polyradiculoneuropathy

Comparative multimodal sensory testing in multifocal motor neuropathy and multifocal variant of chronic inflammatory demyelinating polyradiculoneuropathy

Autoimmune Autonomic Neuropathy: From Pathogenesis to Diagnosis

Neurological Uniqueness: A Case Study of Hepatitis A-Induced Acute Inflammatory Demyelinating Polyneuropathy

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