Physiological tremor analysis of patients with anti-myelin-associated glycoprotein associated neuropathy and tremor

Pedersen, Sara F.; Pullman, Seth L.; Latov, Norman; Brannagan, Thomas H.

doi:10.1002/(sici)1097-4598(199701)20:1<38::aid-mus5>3.0.co;2-i

Cited by 39 publications

(14 citation statements)

References 16 publications

(17 reference statements)

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“…8,22 Previously, a lower tremor frequency in distal compared to proximal hand muscles in 2 out of 6 patients with paraproteinemic neuropathy was described. 8 This was also observed in 3 of our patients.…”

Section: Figure 2 Short Afferent Inhibition In the 3 Groupsmentioning

confidence: 98%

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

et al. 2013

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Objectives: This study aims to investigate if patients with inflammatory neuropathies and tremor have evidence of dysfunction in the cerebellum and interactions in sensorimotor cortex compared to nontremulous patients and healthy controls.Methods: A prospective data collection study investigating patients with inflammatory neuropathy and tremor, patients with inflammatory neuropathy without tremor, and healthy controls on a test of cerebellar associative learning (eyeblink classical conditioning), a test of sensorimotor integration (short afferent inhibition), and a test of associative plasticity (paired associative stimulation). We also recorded tremor in the arms using accelerometry and surface EMG. Results:We found impaired responses to eyeblink classical conditioning and paired associative stimulation in patients with neuropathy and tremor compared with neuropathy patients without tremor and healthy controls. Short afferent inhibition was normal in all groups.Conclusions: Our data strongly suggest impairment of cerebellar function is linked to the production of tremor in patients with inflammatory neuropathy. Neurology â 2013;80:1867-1873 GLOSSARY ADM 5 abductor digiti minimi; ANOVA 5 analysis of variance; APB 5 abductor pollicis brevis; CIDP 5 chronic inflammatory demyelinating polyradiculoneuropathy; CR 5 conditioned blink responses; EBCC 5 eyeblink classical conditioning; FDI 5 first dorsal interossei; IgMPN 5 immunoglobulin M paraproteinaemic neuropathy; MEP 5 motor evoked potential; MMNCB 5 multifocal motor neuropathy with conduction block; MRC 5 Medical Research Council; ONLS 5 Overall Neuropathy Limitation Scale; PAS 5 paired associative stimulation; PF 5 peak tremor frequency; SAI 5 short afferent inhibition; TMS 5 transcranial magnetic stimulation; TP 5 total power of the spectra between 1 and 30 Hz used as surrogate measure of tremor amplitude; US 5 unconditioned stimulus; WE 5 wrist extensor muscles.Inflammatory mediated neuropathies are common and potentially treatable.1 Tremor occurs with immunoglobulin M paraproteinaemic neuropathy (IgMPN) 2-4 and less commonly in other inflammatory neuropathies.5 It has been suggested that temporally distorted peripheral inputs reach a normally functioning central processor, such as the cerebellum, which is misled into producing a delayed second agonist burst and tremor. [6][7][8] The involvement of the cerebellum in neuropathic tremor is supported by functional imaging abnormalities.9 There does not seem to be a straightforward relationship between the development of tremor and conduction velocity.10 Further, no relationship seems to exist between tremor and the severity of neuropathy as assessed by proprioceptive loss, weakness, or fatigue.11,12 However, we have shown that although conduction velocity does not predict the presence of tremor, it is correlated with its severity for those in whom tremor is present. 5 This indicates a second mechanism may be necessary to produce tremor. Here we set out to explore aspects of CNS physiology in tremulous ...

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Section: Figure 2 Short Afferent Inhibition In the 3 Groupsmentioning

confidence: 98%

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

et al. 2013

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“…Weakness is less prominent and, when present, affects the distal lower extremities 129. Action tremor can be a prominent feature 130131. The electrophysiologic features include extremely prolonged distal motor and sensory latencies representing distal demyelination 132133.…”

Section: Differential Diagnosis Of Sensory Ataxiamentioning

confidence: 99%

Diagnosis and management of sensory polyneuropathy

Gwathmey

Pearson

2019

BMJ

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Sensory polyneuropathies, which are caused by dysfunction of peripheral sensory nerve fibers, are a heterogeneous group of disorders that range from the common diabetic neuropathy to the rare sensory neuronopathies. The presenting symptoms, acuity, time course, severity, and subsequent morbidity vary and depend on the type of fiber that is affected and the underlying cause. Damage to small thinly myelinated and unmyelinated nerve fibers results in neuropathic pain, whereas damage to large myelinated sensory afferents results in proprioceptive deficits and ataxia. The causes of these disorders are diverse and include metabolic, toxic, infectious, inflammatory, autoimmune, and genetic conditions. Idiopathic sensory polyneuropathies are common although they should be considered a diagnosis of exclusion. The diagnostic evaluation involves electrophysiologic testing including nerve conduction studies, histopathologic analysis of nerve tissue, serum studies, and sometimes autonomic testing and cerebrospinal fluid analysis. The treatment of these diseases depends on the underlying cause and may include immunotherapy, mitigation of risk factors, symptomatic treatment, and gene therapy, such as the recently developed RNA interference and antisense oligonucleotide therapies for transthyretin familial amyloid polyneuropathy. Many of these disorders have no directed treatment, in which case management remains symptomatic and supportive. More research is needed into the underlying pathophysiology of nerve damage in these polyneuropathies to guide advances in treatment.

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“…BAYAT AND J.J. KELLY (Katz et al, 2000). One theory is that mistimed peripheral inputs reach a central processor (probably the cerebellum), causing limb tremor (Bain et al, 1996;Pedersen et al, 1997). Tremor is often associated with IgM anti-MAG peripheral neuropathy (Chassande and Leger, 1993;Bain et al, 1996;Nobile-Orazio et al, 2000).…”

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confidence: 99%