To establish the value of median nerve compression with wrist flexion as a provocative test for carpal tunnel syndrome (CTS), we performed a prospective study of 64 patients (95 hands) with CTS confirmed by electrodiagnostic studies and 50 normal subjects (96 hands). We recorded results for the common provocative tests (Tinel's percussion test, Phalen's wrist flexion test and the carpal compression test) and the new test which combines wrist flexion with median nerve compression. Using a receiver operator characteristic curve (ROC) technique, we found that the optimal cut-off time for the wrist-flexion and median-nerve compression test was 20 s, giving a sensitivity of 82% and a specificity of 99%. These results were significantly better than for Phalen's wrist flexion test (61% and 83%, respectively) and for the sensitivity of Tinel's test (74%). The positive predictive values of the wrist flexion and median-nerve compression test, which is more important clinically, were 99%, 95% and 81% at population prevalences of 50%, 20% and 5%, respectively. These were significantly better than those of the three other provocative tests at each prevalence. Electrodiagnostic studies have significant false-positive and false-negative rates in CTS, and therefore provocative tests remain important in its diagnosis. We have shown that wrist flexion combined with the median-nerve compression test at 20 s, is significantly better than the other methods, and may thus be clinically useful.
We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.
T o establish the value of median nerve compression with wrist flexion as a provocative test for carpal tunnel syndrome (CTS), we performed a prospective study of 64 patients (95 hands) with CTS confirmed by electrodiagnostic studies and 50 normal subjects (96 hands). We recorded results for the common provocative tests (Tinel's
percussion test, Phalen's wrist flexion test and the carpal compression test) and the new test which combines wrist flexion with median nerve compression.Using a receiver operator characteristic curve (ROC) technique, we found that the optimal cut-off time for the wrist-flexion and median-nerve compression test was 20 s, giving a sensitivity of 82% and a specificity of 99%. These results were significantly better than for Phalen's wrist flexion test (61% and 83%, respectively) and for the sensitivity of Tinel's test (74%). The positive predictive values of the wrist flexion and median-nerve compression test, which is more important clinically, were 99%, 95% and 81% at population prevalences of 50%, 20% and 5%, respectively. These were significantly better than those of the three other provocative tests at each prevalence.Electrodiagnostic studies have significant false-positive and false-negative rates in CTS, and therefore provocative tests remain important in its diagnosis. We have shown that wrist flexion combined with the median-nerve compression test at 20 s, is significantly better than the other methods, and may thus be clinically useful.
We investigated the effect changes in end-expiratory lung volume (EEVL) had on the response to progressive hypercapnia (CO2-response curve) in eight open-chest, anesthetized dogs, in order to clarify the role that vagal lung mechanoreceptors have in altered respiratory drive during permissive hypercapnia. The dogs were ventilated using a positive-pressure ventilator driven by phrenic neural activity. Systemic arterial CO2 tension (PaCO2) was elevated by increasing the fraction of CO2 delivered to the ventilator. EEVL was altered from approximated functional residual capacity ("FRC") to 1.5 and 0.5 "FRC" by changing positive end-expiratory pressure. Although the tidal volume (VT)-PaCO2 and inspiratory time (TI)-PaCO2 relationships were not affected, decreasing EEVL from 1.5 "FRC" to "FRC" and then to 0.5 "FRC" caused a significant (p < 0.01) upward shift in the CO2-response curves for minute ventilation (V I) and frequency (f ), and a significant (p < 0.01) downward shift in the CO2- response curve for expiratory time (TE). We conclude that these shifts were explained by a decrease in the inhibitory activity of slowly adapting pulmonary stretch receptors (PSRs) as EEVL was lowered. In addition, increases in EEVL from 0.5 "FRC" to 1.5 "FRC" caused a significant (p< 0.05) increase in the apneic threshold, which we attribute to an inhibitory effect on central drive caused by increased PSR activity.
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