Tremor in inflammatory neuropathies

Saifee, Tabish A.; Schwingenschuh, Petra; Reilly, Mary M.; Lunn, Michael P.; Katschnig, Petra; Kassavetis, Panagiotis; Pareés, Isabel; Manji, Hadi; Bhatia, Kailash P.; Rothwell, John C.; Edwards, Mark J.

doi:10.1136/jnnp-2012-303013

Cited by 67 publications

(89 citation statements)

References 30 publications

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“…5 This indicates a second mechanism may be necessary to produce tremor. Here we set out to explore aspects of CNS physiology in tremulous and nontremulous patients with inflammatory neuropathies compared to healthy controls.…”

Section: Resultsmentioning

confidence: 99%

“…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 and nontremulous patients with inflammatory neuropathies compared to healthy controls.…”

Section: Discussionmentioning

confidence: 99%

“…1 Tremor occurs with immunoglobulin M paraproteinaemic neuropathy (IgMPN) [2][3][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.…”

Section: Discussionmentioning

confidence: 99%

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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: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

et al. 2013

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“…In inflammatory neuropathies tremor is found in up to 80 % of cases with IgM paraproteinemic neuropathy [129,130]. Clinically, neuropathic tremor mostly presents as postural or kinetic tremor [131].…”

Section: Tremor In Peripheral Neuropathiesmentioning

confidence: 99%

“…Others reported improvement after pregabalin (30-80 mg) [132,133]. However, in a recent series no patient responded to medication prescribed for tremor, but some reported improvement after treatment for their neuropathy (intravenous immunoglobulin, rituximab or chemotherapy regimen consisting of cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone plus rituximab (CHOP-R) chemotherapy) [129]. DBS of the thalamus (Vim) has been described successful in cases of hereditary neuropathy [134][135][136].…”

Section: Tremor In Peripheral Neuropathiesmentioning

confidence: 99%

The Treatment of Tremor

Schneider

Deuschl

2014

Neurotherapeutics

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Tremor is a hyperkinetic movement disorder characterized by rhythmic oscillations of one or more body parts. It can be disabling and may impair quality of life. Various etiological subtypes of tremor are recognized, with essential tremor (ET) and Parkinsonian tremor being the most common. Here we review the current literature on tremor treatment regarding ET and head and voice tremor, as well as dystonic tremor, orthostatic tremor, tremor due to multiple sclerosis (MS) or lesions in the brainstem or thalamus, neuropathic tremor, and functional (psychogenic) tremor, and summarize main findings. Most studies are available for ET and only few studies specifically focused on other tremor forms. Controlled trials outside ET are rare and hence most of the recommendations are based on a low level of evidence. For ET, propranolol and primidone are considered drugs of first choice with a mean effect size of approximately 50 % tremor reduction. The efficacy of topiramate is also supported by a large double-blind placebocontrolled trial, while other drugs have less supporting evidence. With a mean effect size of about 90 % deep brain stimulation in the nucleus ventralis intermedius or the subthalamic nucleus may be the most potent treatment; however, there are no controlled trials and it is reserved for severely affected patients. Dystonic limb tremor may respond to anticholinergics. Botulinum toxin improves head and voice tremor. Gabapentin and clonazepam are often recommended for orthostatic tremor. MS tremor responds only poorly to drug treatment. For patients with severe MS tremor, thalamic deep brain stimulation has been recommended. Patients with functional tremor may benefit from antidepressants and are best be treated in a multidisciplinary setting. Several tremor syndromes can already be treated with success. But new drugs specifically designed for tremor treatment are needed. ET is most likely covering different entities and their delineation may also improve treatment. Modern study designs and long-term studies are needed.

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Subcutaneous immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy

Bus

Keddie²,

Schaik

et al. 2021

Cochrane Database of Systematic Reviews

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Tremor in inflammatory neuropathies

Abstract: Tremor in inflammatory neuropathies is common, adds to disability and yet does not often respond to treatment of the underlying neuropathy. When present, tremor severity is associated with F wave latency.

Cited by 67 publications

References 30 publications

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

The Treatment of Tremor

Subcutaneous immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy

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