The blink reflex recovery cycle differs between essential and presumed psychogenic blepharospasm

Schwingenschuh, Petra; Katschnig, Petra; Edwards, Mark J.; Teo, James; Korlipara, L.V. Prasad; Rothwell, John C.; Bhatia, Kailash P.

doi:10.1212/wnl.0b013e31820c3074

Cited by 89 publications

(74 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Structural or functional impairments of the cerebellum lead to abnormalities in acquisition of this conditioned response. 17,18,23,24 We demonstrate abnormal EBCC in tremulous neuropathy patients that clearly differentiates them from the normal rates of conditioning in nontremulous neuropathy patients and controls. Mean R1 and R2 latencies and latency variability did not differ between groups, making it unlikely that desynchronization of the afferent volley alone may be a factor in the lack of conditioned responses in the tremulous patients.…”

Section: Figure 2 Short Afferent Inhibition In the 3 Groupsmentioning

confidence: 58%

See 1 more Smart Citation

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

et al. 2013

Self Cite

View full text Add to dashboard Cite

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 ...

show abstract

Section: Figure 2 Short Afferent Inhibition In the 3 Groupsmentioning

confidence: 58%

“…17 Eyeblink classical conditioning (EBCC) is an associative learning paradigm, dependent on the cerebellum for acquisition. 18 The conditioning stimulus (CS) was a loud (50 dB above auditory threshold) 2,000 Hz tone lasting 400 ms played via binaural headphones.…”

Section: Resultsmentioning

confidence: 99%

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

et al. 2013

Self Cite

View full text Add to dashboard Cite

show abstract

“…Neurophysiological studies assessing the blink reflex may also be helpful to disambiguate between essential and presumed functional blepharospasm 29 . In organic blepharospasm the blink reflex recovery cycle is abnormal as a result of abnormal brainstem interneuron excitability, whereas in functional eye closure the blink reflex is normal.…”

Section: Functional Upper Facial Movement Disordersmentioning

confidence: 99%

“…anterior cingulate cortex, insula, amygdala) and self-referential processing (posterior parietal cortex, temporoparietal junction) 45 . Indeed, neurophysiology and neuroimaging offer potential insights regarding the mechanism of functional movement disorders [46][47][48] , but apart from the blink reflex cycle 29 these have not yet been specifically applied to cranial functional movement disorders.…”

Section: Pathophysiologymentioning

confidence: 99%

Cranial functional (psychogenic) movement disorders

Kaski

Bronstein

Edwards

et al. 2015

The Lancet Neurology

View full text Add to dashboard Cite

“…In contrast to organic oromandibular dystonia, patients had a unilateral involvement, and no sensory tricks or speech [65]. In psychogenic hemifacial spasm, an earlier age of onset was noted with no simultaneous compensatory contractions of the frontalis muscle and a normal blink reflex [66][67][68].…”

Section: Psychogenic Facial Movementsmentioning

confidence: 99%

Functional Movement Disorders: Updated Overview

Subki¹,

Alkahtani²,

Alfayez³

et al. 2017

J Pediatr Care

View full text Add to dashboard Cite

Functional movement disorders are relatively common neurological manifestations that are not related to a known neurological or a medical diagnosis. We aim to present an updated overview of this topic and present important diagnostic tips and pitfalls in the management of theses potentially puzzling presentations. Particularly, as such psychosomatic disorders could simulate known disorders, including tremor, paralysis, seizures, or ataxia. This often results in excessive, unnecessary and costly investigations, which may in turn further enhance the sick role and complicates the management. Early recognition and prompt intervention are needed to prevent social and academic disruptions, and hence a debilitating outcome.

show abstract

The blink reflex recovery cycle differs between essential and presumed psychogenic blepharospasm

Abstract: Background: Psychogenic blepharospasm is difficult to distinguish clinically from benign essential

Cited by 89 publications

References 25 publications

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

Cerebellar learning distinguishes inflammatory neuropathy with and without tremor

Cranial functional (psychogenic) movement disorders

Functional Movement Disorders: Updated Overview

Contact Info

Product

Resources

About