A Pilot Controlled Study of the Use of Imipramine to Reduce Myotonia

Gg, Gascon; Rd, Staton; Bd, Patterson; Pj, Konewko; Wilson, H.; Km, Carlson; Ra, Brumback

doi:10.1097/00002060-198910000-00003

Cited by 13 publications

(7 citation statements)

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“…Pharmacological treatment of myotonia is a subject of controversy since a long list of various therapeutic agents have been tried in myotonic disorders [6][7][8][9][10][11]. The rational for treatment is dictated by the fact that many patients are disabled by their difficulty in relaxation after a maximum voluntary contraction to the extent their quality of life is impaired.…”

Section: Discussionmentioning

confidence: 99%

Quantitative myotonia assessment: an experimental protocol

Sansone

Marinou

Salvucci

et al. 2000

Neurological Sciences

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Severe clinical myotonia can be physically disabling and socially impairing but as yet there is no standardized treatment regimen. The aim of our study is to present a protocol to measure myotonia using quantitative muscle assessment measures. The proposed protocol addresses two main issues. Muscle strength is assessed in 8 muscles on the right and on the left using a myometer (QMA, quantitative muscle assessment) and by testing strength manually using the 5-point MRC scale (5 = normal) in 15 muscles on the right and on the left. Grip myotonia is assessed by: (a) measuring 1/2 and 3/4 relaxation times (RT) after maximum voluntary contraction (MVC) using QMA apparatus; (b) functional tests (time to open a fist 10 times, time to open and squeeze the eyes 10 times, time to climb 10 steps starting from a seated position, time to protrude the tongue 10 times, time to step onto a chair 10 times; (c) subjective measures of the severity of myotonia using an arbitrary 4-point scale (0 = absent, 4 = severe); and (d) electromyography (EMG) relaxation times after MVC. Although QMA seems to be a reliable tool to measure myotonia, there are still a number of unsolved issues. Further studies are needed to ensure the ability of QMA to quantify myotonia and to guarantee the reliability of the results for clinical research purposes.

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Section: Discussionmentioning

confidence: 99%

Quantitative myotonia assessment: an experimental protocol

Sansone

Marinou

Salvucci

et al. 2000

Neurological Sciences

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“…Imipramine is a tricyclic antidepressant that acts as an acetylcholine and histamine receptor antagonist and as a norepinephrine and serotonin reuptake inhibitor. The mechanism by which tricyclic antidepressants reduce myotonia is not clear; reduction of muscle membrane excitability through activation of the sodium potassium pump and inhibition of β 2 ‐adrenoreceptor stimulation have been postulated . In a randomized, double‐blind, crossover study, imipramine improved timed grip and percussion myotonia compared with placebo in a population of 12 DM1 patients .…”

Section: Antidepressant Medicationsmentioning

confidence: 99%

“…The mechanism by which tricyclic antidepressants reduce myotonia is not clear; reduction of muscle membrane excitability through activation of the sodium potassium pump and inhibition of β 2 ‐adrenoreceptor stimulation have been postulated . In a randomized, double‐blind, crossover study, imipramine improved timed grip and percussion myotonia compared with placebo in a population of 12 DM1 patients . Although relatively well tolerated, imipramine at therapeutic doses can cause hyperpigmentation, arrhythmias, tachycardia, hypotension, or sedation …”

Section: Antidepressant Medicationsmentioning

confidence: 99%

The diagnosis and treatment of myotonic disorders

2013

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Myotonia is a defining clinical symptom and sign common to a relatively small group of muscle diseases, including the myotonic dystrophies and the nondystrophic myotonic disorders. Myotonia can be observed on clinical examination, as can its electrical correlate, myotonic discharges, on electrodiagnostic testing. Research interest in the myotonic disorders continues to expand rapidly, which justifies a review of the scientific bases, clinical manifestations, and numerous therapeutic approaches associated with these disorders. We review the pathomechanisms of myotonia, the clinical features of the dystrophic and nondystrophic myotonic disorders, and the diagnostic approach and treatment options for patients with symptomatic myotonia.

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“…Selected publications from this time are cited. [12][13][14][15] Our second neurology resident at UND was Saad Al-Rajeh, who had graduated from King Faisal University Medical School in Al Khobar, on the Arabian Gulf in the Eastern Province of Saudi Arabia. This was the start of a long lasting relationship with the Kingdom for Bill Olson and me.…”

Section: The Athens Of Americamentioning

confidence: 99%