Shoulder pain and subluxation after stroke: correlation or coincidence?

OBJECTIVE: Few studies have concomitantly examined shoulder subluxation and other potential causes of shoulder pain in persons who have had a stroke. This study explores whether shoulder pain after stroke is related to shoulder subluxation, age, limitations in shoulder range of motion, and upper extremity motor impairment. METHOD: Shoulder pain was measured with a visual analog scale in 20 subjects admitted to a rehabilitation hospital within 6 weeks of onset of their first stroke. Degree of shoulder pain was correlated with vertical, horizontal, and total asymmetries of glenohumeral subluxation; age; shoulder flexion, abduction, and external rotation; and the upper extremity subscore of the Fugl-Meyer Motor Assessment. RESULTS: Shoulder pain after stroke was not correlated with age (rk = .019, p = .916); vertical (rk = .081, p = .324), horizontal (rk = .126, p = .241), or total asymmetry (rk = -.098, p = .288); shoulder flexion (rk = .049, p = .390) or abduction (rk = -.074, p = .337); or Fugl-Meyer scores (rk = -.123, p = .257). In contrast, shoulder pain was strongly correlated with degree of shoulder external rotation (rk = -.457, p = .006). CONCLUSION: These results do not support a strong relationship between shoulder subluxation and pain after stroke. Appropriate precautions should be taken to prevent range of motion limitations that may result in shoulder pain.

Shoulder subluxation after stroke: a comparison of four supports.

OBJECTIVE: Shoulder subluxation is a well-known sequela of stroke. This study quantitatively compares the reduction of shoulder subluxation using four supports: the single-strap hemisling, the Bobath roll, the Rolyan humeral cuff sling, and the Cavalier support. DESIGN/SETTING: Anteroposterior shoulder radiographs of 20 consecutive first-time stroke survivors in a freestanding rehabilitation hospital were taken within 6 weeks of stroke onset. Vertical, horizontal, and total asymmetries of glenohumeral subluxation compared with the unaffected shoulders were measured before and after fitting of each support. MAIN OUTCOME MEASURES: Group means were compared to find which supports altered subluxation asymmetries and approximated the unaffected shoulder. Individual data were tallied to detect how often each support best reduced subluxation asymmetries. RESULTS: The single-strap hemisling eliminated the vertical asymmetry of subluxation over the entire study group, but each support corrected the vertical asymmetry best in some subjects (55%, 20%, 40%, and 5%, respectively). The Bobath roll and the Cavalier support produced lateral displacements of the humeral head of the affected shoulder (p = 0.005, 0.004, respectively). The Rolyan humeral cuff sling significantly reduced total subluxation asymmetry (p = 0.008), whereas the single-strap hemisling, Bobath roll, and Cavalier support did not alter total asymmetry (p = 0.091, 0.283, 0.502, respectively). CONCLUSION: When treating shoulder subluxation, several different types of supports should be evaluated to optimize the function of the affected extremity and the reduction of the shoulder subluxation.

Genetic mapping of the amino-terminal domain of bacteriophage T4 DNA polymerase.

The DNA polymerase of bacteriophage T4 is a multifunctional enzyme that harbors DNA-binding, DNA-synthesizing and exonucleolytic activities. We have cloned in bacterial plasmids about 99% of the structural gene for this enzyme (T4 gene 43). The gene was cloned in six contiguous 5'-terminal DNA fragments that defined seven intragenic mapping regions. Escherichia coli hosts harboring recombinant plasmids carrying the gene 43 subsegments were used in marker-rescue experiments that assigned a large number of ts and nonsense polymerase mutations to different physical domains of the structural gene. Conspicuously, only one missense mutation in a large collection of mutants mapped in the 5'-terminal 450 base-pair segment of the approximately 2700 base-pair gene. To test if this indicated a DNA polymerase domain that is relatively noncritical for biological activity, we mutagenized a recombinant plasmid carrying this 5'-terminal region and generated new conditional-lethal mutations that mapped therein. We identified five new ts sites, some having mutated at high frequency (nitrosoguanidine hot spots). New ts mutations were also isolated in phage genes 62 and 44, which map upstream of gene 43 on the T4 chromosome. A preliminary examination of physiological consequences of the ts gene 43 mutations showed that they exhibit effects similar to those of ts lesions that map in other gene 43 segments: some were mutators, some derepressed gene 43 protein synthesis and they varied in the severity of their effects on T4-induced DNA synthesis at nonpermissive temperatures. The availability of the gene 43 clones should make it possible to isolate a variety of lesions that affect different activities of the T4 DNA polymerase and help to define the different domains of this multifunctional protein.

Demonstration of 6-phosphogluconolactonase activity in Drosophila melanogaster using a null allele of 6-phosphogluconate dehydrogenase.

Using a double mutant strain, Pgdn Zwn, we have developed an assay for 6-phosphogluconolactonase activity and have demonstrated its occurrence in adult Drosophila melanogaster.

Dietary rescue of a lethal "null" activity allele of 6-phosphogluconate dehydrogenase in Drosophila melanogaster.

The genetic rescue of Pgdn lethal alleles, accomplished by combining them with mutations lacking glucose-6-phosphate dehydrogenase activity, has led to the hypothesis that Pgdn lethality may be due to the accumulation of 6-phosphogluconate. In this article we report the rescue of Pgdn/Y males by dietary supplements (fructose and linolenate) designed to minimize 6-phosphogluconate production.

Genetic rescue of a lethal "null" activity allele of 6-phosphogluconate dehydrogenase in Drosophila melanogaster.

While a null activity mutant allele of the structural gene for 6-phosphogluconate dehydrogenase in Drosophila melanogaster is lethal, a similar mutation for glucose-6-phosphate dehydrogenase is not. Double mutant combinations lacking both enzyme activities, obtained either by recombination or by mutagen treatment of a chromosome bearing the lethal allele, result in a restoration of viability. The indispensability of the pentose phosphate shunt in Drosophila appears to depend upon the specific position of the block within the pathway.