Involuntary eyelid closure after STN-DBS: evidence for different pathophysiological entities

Weiß, Daniel; Wächter, Tobias; Breit, Sorin; Jacob, Simon N.; Pomper, Jörn K.; Asmus, Friedrich; Valls‐Solé, Josep; Plewnia, Christian; Gasser, Thomas; Gharabaghi, Alireza; Krüger, Rejko

doi:10.1136/jnnp.2009.196691

Cited by 30 publications

(31 citation statements)

References 27 publications

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“…Dopaminergic treatment improves hypomimia whereas some studies reported that STN–deep brain stimulation (DBS) may deteriorate facial motor control 28–30. It is still unclear, however, whether the detrimental effects of STN–DBS on facial movements simply reflects postoperative modification of dopaminergic medication29 or might be a result of current spread and changes in corticobulbar projection excitability,29 or changes in cortical–basal ganglia activity30…”

Section: Facial Movement Abnormalities In Pdmentioning

confidence: 99%

Facial bradykinesia

Bologna

Fabbrini

Marsili

et al. 2012

Journal of Neurology, Neurosurgery & Psychiatry

132

131

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The aim of this paper is to summarise the main clinical and pathophysiological features of facial bradykinesia in Parkinson's disease (PD) and in atypical parkinsonism. Clinical observation suggests that reduced spontaneous and emotional facial expressions are features of facial bradykinesia in PD and atypical parkinsonism. In atypical parkinsonism, facial bradykinesia is complicated by additional dystonic features. Experimental studies evaluating spontaneous and emotional facial movements demonstrate that PD is characterised by a reduction in spontaneous blinking and emotional facial expression. In PD, neurophysiological studies show that voluntary orofacial movements are smaller in amplitude and slower in velocity. In contrast, movements of the upper face (eg, voluntary blinking) are normal in terms of velocity and amplitude but impaired in terms of switching between the closing and opening phases. In progressive supranuclear palsy (PSP), voluntary blinking is not only characterised by a severely impaired switching between the closing and opening phases of voluntary blinking, but is also slow in comparison with PD. In conclusion, in PD, facial bradykinesia reflects abnormalities of spontaneous, emotional and voluntary facial movements. In PSP, spontaneous and voluntary facial movements are abnormal but experimental studies on emotional facial movements are lacking. Data on facial bradykinesia in other atypical parkinsonism diseases, including multiple system atrophy and corticobasal degeneration, are limited. In PD, facial bradykinesia is primarily mediated by basal ganglia dysfunction whereas in PSP, facial bradykinesia is a consequence of a widespread degeneration involving the basal ganglia, cortical and brainstem structures.

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Section: Facial Movement Abnormalities In Pdmentioning

confidence: 99%

Facial bradykinesia

Bologna

Fabbrini

Marsili

et al. 2012

Journal of Neurology, Neurosurgery & Psychiatry

132

131

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“…First, altered activity in the divergent glutamatergic projection from STN to SNr could induce a global excitation of SNr that would disinhibit downstream targets in brainstem. Indeed deep brain stimulation of STN for Parkinson's disease (PD) can alleviate (or, paradoxically for some patients, induce) apraxia of lid opening, a symptom common in isolated blepharospam (Weiss et al, 2010). A clearer understanding of the mechanisms awaits a clearer understanding of the mechanism of action of DBS itself, as the relative contribution of activation of cell bodies and fibers of passage remains unclear.…”

Section: Computational Model Design Considerationsmentioning

confidence: 99%

A Dynamic Circuit Hypothesis for the Pathogenesis of Blepharospasm

Peterson

Sejnowski

2017

Front. Comput. Neurosci.

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Blepharospasm (sometimes called “benign essential blepharospasm,” BEB) is one of the most common focal dystonias. It involves involuntary eyelid spasms, eye closure, and increased blinking. Despite the success of botulinum toxin injections and, in some cases, pharmacologic or surgical interventions, BEB treatments are not completely efficacious and only symptomatic. We could develop principled strategies for preventing and reversing the disease if we knew the pathogenesis of primary BEB. The objective of this study was to develop a conceptual framework and dynamic circuit hypothesis for the pathogenesis of BEB. The framework extends our overarching theory for the multifactorial pathogenesis of focal dystonias (Peterson et al., 2010) to incorporate a two-hit rodent model specifically of BEB (Schicatano et al., 1997). We incorporate in the framework three features critical to cranial motor control: (1) the joint influence of motor cortical regions and direct descending projections from one of the basal ganglia output nuclei, the substantia nigra pars reticulata, on brainstem motor nuclei, (2) nested loops composed of the trigeminal blink reflex arc and the long sensorimotor loop from trigeminal nucleus through thalamus to somatosensory cortex back through basal ganglia to the same brainstem nuclei modulating the reflex arc, and (3) abnormalities in the basal ganglia dopamine system that provide a sensorimotor learning substrate which, when combined with patterns of increased blinking, leads to abnormal sensorimotor mappings manifest as BEB. The framework explains experimental data on the trigeminal reflex blink excitability (TRBE) from Schicatano et al. and makes predictions that can be tested in new experimental animal models based on emerging genetics in dystonia, including the recently characterized striatal-specific D1R dopamine transduction alterations caused by the GNAL mutation. More broadly, the model will provide a guide for future efforts to mechanistically link multiple factors in the pathogenesis of BEB and facilitate simulations of how exogenous manipulations of the pathogenic factors could ultimately be used to prevent and reverse the disorder.

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“…Optimal hardware programming can be challenging in some cases, as side effects may interfere with stimulation parameters required for sufficient control of motor symptoms [3,4]. Eyelid Apraxia, defined as inability to voluntarily initiate opening of eyelids [5], is one of limiting adverse effects which has been reported in 1.8 to 30% of the patients after STN DBS and management of the eyelid apraxia event was mainly relied on medical treatment [6][7][8].…”

Section: Deep Brain Stimulation (Dbs) Of the Subthalamic Nucleus (Stn)mentioning

confidence: 99%