Nocturnal and circadian body temperatures of depressed outpatients during symptomatic and recovered states.

Forty-one recurrent unipolar depressed outpatients were studied at baseline (symptomatic period) and at recovery. Rectal temperatures were measured continuously between 1800h and 0600h on 2 successive nights at each time point. In those 24 patients who recovered after receiving interpersonal psychotherapy (IPT) alone ("psychotherapy responders") and who thus remained drug-free throughout, there was no difference in nocturnal body temperatures between baseline and recovery time points. Moreover, nocturnal temperature patterns appeared to be very similar to those of a healthy contrast group (n = 17). The contrast group was not matched for age and gender with the patient group, though, so the comparison was only suggestive. At baseline, those recovering after psychotherapy alone (n = 24) did not differ from those eventually failing to respond to IPT and requiring medications to achieve recovery ("medication responders") (n = 17). Medication responders did show some baseline versus recovery differences in nocturnal temperatures, but these may possibly have been a function of the medications used. At recovery, a subset of 19 psychotherapy responders and 13 medication responders underwent an "unmasking" experiment involving 36 hours of wakeful bedrest. In the resulting endogenous temperature rhythms, there was no evidence of any reliable differences between the psychotherapy responder and medication responder patient groups. Both groups showed rhythms that were very similar to those of a healthy contrast group (n = 17), although, again, the contrast group was not matched for age or gender with the patient group. In conclusion, in measures of body temperature, at least, there appeared to be little evidence of circadian dysfunction in this group of recurrent outpatient depressives.

The anterior band of the inferior glenohumeral ligament. Assessment of its permanent deformation and the anatomy of its glenoid attachment.

Surgical treatment for traumatic, anterior glenohumeral instability requires repair of the anterior band of the inferior glenohumeral ligament, usually at the site of glenoid insertion, often combined with capsuloligamentous plication. In this study, we determined the mechanical properties of this ligament and the precise anatomy of its insertion into the glenoid in fresh-frozen glenohumeral joints of cadavers. Strength was measured by tensile testing of the glenoid-soft-tissue-humerus (G-ST-H) complex. Two other specimens of the complex were frozen in the position of apprehension, serially sectioned perpendicular to the plane containing the anterior and posterior rims of the glenoid, and stained with Toluidine Blue. On tensile testing, eight G-ST-H complexes failed at the site of the glenoid insertion, representing a Bankart lesion, two at the insertion into the humerus, and two at the midsubstance. For those which failed at the glenoid attachment the mean yield load was 491.0 N and the mean ultimate load, 585.0 N. At the glenoid region, stress at yield was 7.8 +/- 1.3 MPa and stress at failure, 9.2 +/- 1.5 MPa. The permanent deformation, defined as the difference between yield and ultimate deformation, was only 2.3 +/- 0.8 mm. The strain at yield was 13.0 +/- 0.7% and at failure, 15.4 +/- 1.2%; therefore permanent strain was only 2.4 +/- 1.1%. Histological examination showed that there were two attachments of the anterior band of the inferior glenohumeral ligament at the site of the glenoid insertion. In one, poorly organised collagen fibres inserted into the labrum. In the other, dense collagen fibres were attached to the front of the neck of the glenoid.

Age related biomechanical properties of the glenoid-anterior band of the inferior glenohumeral ligament-humerus complex.

OBJECTIVE: To quantify the biomechanical properties of the glenoid-anterior band of the inferior glenohumeral ligament-humerus complex for the two age groups. DESIGN: In vitro human cadaver study evaluating the biomechanical properties of the glenoid-anterior band of the inferior glenohumeral ligament-humerus complex for a younger group (n=5, mean age 38.5, SD 0.5 years) and an older group (n=7, mean age 74.8, SD 5.3 years). BACKGROUND: Glenohumeral instability is more of a problem in younger than in older individuals, primarily because recurrence is much more common at a young age. METHODS: Tensile testing was performed on the glenoid-anterior band of the inferior glenohumeral ligament-humerus complex in the shoulder apprehension position using a custom jig, Instron machine and a video digitizing system. RESULTS: In the younger individuals disruption of the complex most often occurred at the glenoid-labrum region of the glenoid insertion site. In the older individual, disruption most often occurred at the midsubstance region. The load and the stress at failure of the glenoid-anterior band of the inferior glenohumeral ligament-humerus complex showed that the older group was only 61% and 46% of the younger group, respectively. CONCLUSIONS: The structural properties of the glenoid-anterior band of the inferior glenohumeral ligament-humerus complex and the material characteristics of the anterior band of the inferior glenohumeral ligament for the younger group were significantly superior than the older group. RELEVANCE: A stronger and more extensive repair, such as the traditional open technique, may be necessary for younger individuals with glenohumeral instability whereas in older individuals, a different repair technique, such as an arthroscopic technique, may be sufficient.

Deformation and strain characteristics along the length of the anterior band of the inferior glenohumeral ligament.

Efficacious surgical treatment of anterior glenohumeral instability often requires repair of the anteroinferior capsulolabral structures, including the glenoid origin of the anterior band of the inferior glenohumeral ligament. Rupture in this location, the Bankart lesion, may be accompanied by nonrecoverable stretching of the anterior band. The purpose of this study was to evaluate the amount and location of nonrecoverable stretching with tensile testing. Twelve glenoid-soft tissue-humerus complexes from fresh-frozen glenohumeral joints were studied by means of a custom jig, an Instron machine, and a video digitizing system. The joints were positioned to simulate that known to cause apprehension for anterior instability. Nonrecoverable deformation differed along the length of the anterior band but was slight in all locations. For those that failed at the glenoid insertion region, the mean nonrecoverable deformation was 0.10 +/- 0.16 mm (mean +/- SEM) at the bone-labral junction of the glenoid insertion region and 0.38 +/- 0.23 mm at the labral-ligament junction of the glenoid insertion region. It was 0.53 +/- 0.23 mm at the ligament midsubstance and 0.04 +/- 0.10 mm at the humeral insertion region. For those that failed at the glenoid insertion region, the nonrecoverable stretching was 1.4% +/- 1.9% at the bone-labral junction of the glenoid insertion region and 3.5% +/- 2.0% at the labral-ligament junction of the glenoid insertion region. It was 2.3% +/- 1.1% at the ligament midsubstance and 0.0% +/- 1.4% at the humeral insertion region. Rupture of the anterior band resulted in little nonrecoverable stretching at both the site of failure and elsewhere along the length, remote from the failure site. Surgical repairs after initial dislocation may restore the length of the anterior band of the inferior glenohumeral ligament with little shortening.

The cyclops lesion: a cause of diminished knee extension after rupture of the anterior cruciate ligament.

Four patients presented with persistent diminution of knee motion after rupture of the anterior cruciate ligament with a novel lesion as the cause. Each had participated in an aggressive rehabilitation program for a minimum of 2 months with emphasis on regaining full range of knee motion. Because chronic impairment of knee extension can be disabling, in those who did not regain full range of motion, arthroscopy of the knee ensued. All had a lesion in the intercondylar notch near the tibial insertion of the anterior cruciate ligament that acted as a mechanical obstruction to full knee extension. Grossly and histologically, these were similar to the cyclops lesion that also has been shown to cause loss of knee extension after anterior cruciate ligament reconstruction. Arthroscopic debridement of the cyclops lesion and manual manipulation of the knee under anesthesia lead to restoration of full knee extension in all knees. In 1 other knee with chronic instability after anterior cruciate ligament rupture, the cyclops lesion was present but was very small and was not associated with diminished knee extension. When loss of full extension persists for 2 months after anterior cruciate ligament disruption despite aggressive rehabilitation, the presence of a cyclops lesion should be considered.