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      Increased Blinking May Be a Precursor of Blepharospasm: A Longitudinal Study

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      Movement Disorders Clinical Practice

      Wiley-Blackwell

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          Abstract

          <div class="section"> <a class="named-anchor" id="mdc312499-sec-0001"> <!-- named anchor --> </a> <h5 class="section-title" id="d7183598e296">Background</h5> <p id="d7183598e298">The objective of this 5‐year longitudinal study was to investigate whether patients with increased blinking develop orbicularis oculi muscle spasms. </p> </div><div class="section"> <a class="named-anchor" id="mdc312499-sec-0002"> <!-- named anchor --> </a> <h5 class="section-title" id="d7183598e301">Methods</h5> <p id="d7183598e303">Eleven patients who initially manifested increased blinking alone were clinically and neurophysiologically re‐evaluated 5 years later. </p> </div><div class="section"> <a class="named-anchor" id="mdc312499-sec-0003"> <!-- named anchor --> </a> <h5 class="section-title" id="d7183598e306">Results</h5> <p id="d7183598e308">By the 5‐year follow‐up assessment, 9 of the 11 patients had developed orbicularis oculi muscle spasms. The blink reflex recovery cycle became abnormal, whereas somatosensory temporal discrimination, which already was abnormal at the first evaluation, did not significantly change. </p> </div><div class="section"> <a class="named-anchor" id="mdc312499-sec-0004"> <!-- named anchor --> </a> <h5 class="section-title" id="d7183598e311">Conclusions</h5> <p id="d7183598e313">Our longitudinal study demonstrates that increased blinking may precede blepharospasm and that an abnormal blink reflex recovery cycle reflects the development of orbicularis oculi muscle spasms. </p> </div>

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          Most cited references 12

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          The focal dystonias: current views and challenges for future research.

          The most common forms of dystonia are those that develop in adults and affect a relatively isolated region of the body. Although these adult-onset focal dystonias are most prevalent, knowledge of their etiologies and pathogenesis has lagged behind some of the rarer generalized dystonias, in which the identification of genetic defects has facilitated both basic and clinical research. This summary provides a brief review of the clinical manifestations of the adult-onset focal dystonias, focusing attention on less well understood clinical manifestations that need further study. It also provides a simple conceptual model for the similarities and differences among the different adult-onset focal dystonias as a rationale for lumping them together as a class of disorders while at the same time splitting them into subtypes. The concluding section outlines some of the most important research questions for the future. Answers to these questions are critical for advancing our understanding of this group of disorders and for developing novel therapeutics. © 2013 Movement Disorder Society.
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            Pathophysiology of blepharospasm and oromandibular dystonia.

            The pathophysiology of reflexes mediated by the fifth and seventh cranial nerves has been studied in 16 patients with blepharospasm and oromandibular dystonia compared with normal age-matched subjects. The EMG activity of the dystonic spasms in the periocular and jaw muscles was similar to that described in other muscles in patients with generalized torsion dystonia. The latency of the R1 and R2 components of the blink reflex and of the corneal reflex was normal. However, the amplitude and the duration of the R1 and R2 and the duration of the corneal reflex were increased. In some patients the R1 component was also present on the side contralateral to the stimulus, while in normal subjects it was present only on the ipsilateral side. The excitability cycle of recovery of the R2 component of the blink reflex after a prior conditioning shock was enhanced in the patients. There were no EEG potentials preceding blepharospasms in the patients, although a Bereitschaftspotential was seen beginning some 500 ms prior to voluntary blinks in the same individuals. Exteroceptive suppression in the contracting masseter and orbicularis oculi muscles was absent in 40 to 50 per cent of the patients. The jaw jerk was present in all the patients with normal latency. These results indicate that the neuronal arcs of the facial reflexes in blepharospasm and oromandibular dystonia are normal. However, there is an abnormal excitatory drive, perhaps from the basal ganglia, to the facial motoneurons and the interneurons which mediate the facial reflexes in the brainstem.
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              The blink reflex recovery cycle differs between essential and presumed psychogenic blepharospasm.

              Psychogenic blepharospasm is difficult to distinguish clinically from benign essential blepharospasm (BEB). The blink reflex recovery cycle measures the excitability of human brainstem interneurons and is abnormal in BEB. We wished to study the blink reflex recovery cycle in patients with atypical (presumed psychogenic) blepharospasm (AB). This was a prospective data collection study investigating the R2 blink reflex recovery cycle at interstimulus intervals (ISI) of 200, 300, 500, 1,000, and 3,000 msec in 10 patients with BEB, 9 patients with AB, and 9 healthy controls. All patients had spasm of the orbicularis oculi muscles. To compare individual patients, an R2 recovery index was calculated as average of the recovery values at ISIs of 200, 300, and 500 msec, with the upper limit of normal defined as mean (control group) + 2 SD. The R2 recovery cycle was significantly disinhibited in patients with BEB, whereas patients with AB did not differ from controls on a group level. The upper limit of normal for the R2 recovery index was 61%. The R2 index was abnormal in 9 out of 10 patients with BEB and in none of the patients with AB. A normal blink reflex recovery cycle indicates normal brainstem interneuron excitability. Assessment of the R2 recovery cycle may provide a useful diagnostic tool to distinguish patients with psychogenic blepharospasm from BEB and is worthy of further study.
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                Author and article information

                Journal
                Movement Disorders Clinical Practice
                Mov Disord Clin Pract
                Wiley-Blackwell
                23301619
                September 2017
                September 2017
                : 4
                : 5
                : 733-736
                Article
                10.1002/mdc3.12499
                5654574
                29082270
                © 2017

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