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November 1, 1988Journal of Neurology Neurosurgery & PsychiatryOpen Access

Ca2+-ATPase deficiency in a patient with an exertional muscle pain syndrome.

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Key result

A patient with chronic post-exertional muscle pain exhibited abnormal muscle metabolism during exercise and a ~90% reduction in sarcoplasmic reticulum Ca2+-ATPase activity.

Why the study?

What is the underlying metabolic and enzymatic defect in a patient with verapamil-responsive exertional muscle pain syndrome?

Population

A patient with verapamil-responsive, chronic, progressive post-exertional muscle pain (n=1).

Comparison

31P Magnetic resonance spectroscopy in vivo on… vs Normal physiological responses.

Design

Case_report

Authors

DTD.J. TaylorMBMark BrosnanDADouglas L. Arnold

Discussion

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Overview

Hypothesis-generating for Ca2+-ATPase defect in verapamil-responsive myalgia; larger studies needed before clinical adoption.

Study Design

Type

Case Report (n=1)

Structured PICO

What is the underlying metabolic and enzymatic defect in a patient with verapamil-responsive exertional muscle pain syndrome?

P
Population
1 patient with verapamil-responsive, chronic, progressive post-exertional muscle pain.
E
Exposure
31P Magnetic resonance spectroscopy in vivo on skeletal muscle during exercise and recovery, and muscle biopsy for Ca2+-ATPase activity measurement.
C
Comparator
Normal physiological responses (implied reference).
O
Outcome
Muscle metabolism (high energy phosphate content, acidification, phosphocreatine and ADP recovery rates) and Ca2+-ATPase activity.surrogate

A patient with chronic exertional muscle pain syndrome was found to have a ~90% reduction in sarcoplasmic reticulum Ca2+-ATPase activity, suggesting a primary defect in muscle Ca2+ handling.

Cite This Study

Taylor et al. (1988) conducted a case report in Verapamil-responsive, chronic, progressive post-exertional muscle pain (n=1). Ca2+-ATPase deficiency vs. Normal rates was evaluated on Muscle metabolism during exercise and recovery, and Ca2+-ATPase activity. A patient with chronic post-exertional muscle pain exhibited abnormal muscle metabolism during exercise and a ~90% reduction in sarcoplasmic reticulum Ca2+-ATPase activity.

synapsesocial.com/papers/6a93cfee714eeec8661d3870https://doi.org/10.1136/jnnp.51.11.1425
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Investigation of human mitochondrial myopathies by phosphorus magnetic resonance spectroscopy1985 · 269 citations
  2. 2Muscle Contracture Induced by Exercise1969 · 182 citations
  3. 3Examination of a Case of Suspected McArdle's Syndrome by<sup>31</sup>P Nuclear Magnetic Resonance1981 · 430 citations
  4. 4Energetics and Electrogenicity of the Sarcoplasmic Reticulum Calcium Pump1983 · 168 citations
  5. 5INTRACELLULAR CALCIUM HOMEOSTASIS1987 · 2,179 citations