Age-related degeneration of the lumbar paravertebral muscles: Systematic review and three-level meta-regression.

BACKGROUND: Morphological changes of the lumbar spine muscles are not well characterised with ageing. To further the understanding of age-related degeneration of the lumbar spine musculature, normative morphological changes that occur within the paravertebral muscles must first be established. METHODS: A systematic review and meta-regressions were conducted adhering to PRISMA guidelines. Searches for published and unpublished data were completed in June 2019. RESULTS: Searches returned 4781 articles. 34 articles were included in the quantitative analysis. Three-level meta-analyses showed age-related atrophy (r = -0.26; 95% CI: -0.33, -0.17) and fat infiltration (r = 0.39; 95% CI: 0.28, 0.50) in the lumbar paravertebral muscles. Degenerative changes were muscle-specific and men (r = -0.32; 95% CI: -0.61, 0.01) exhibited significantly greater muscle atrophy than women (r = -0.24; 95% CI: -0.47, 0.03). Imaging modality, specifically ultrasound, also influenced age-related muscle atrophy. Measurements taken across all lumbar levels revealed the greatest fat infiltration with ageing (r = 0.58, 95% CI: 0.35, 0.74). Moderators explained a large proportion of between-study variance in true effects for muscle atrophy (72.6%) and fat infiltration (79.8%) models. CONCLUSIONS: Lumbar paravertebral muscles undergo age-related degeneration in healthy adults with muscle, lumbar level and sex-specific responses. Future studies should use high-resolution imaging modalities to quantify muscle atrophy and fat infiltration.

Traumatic posterior cerebral artery aneurysm secondary to an intracranial nail: case report.

We present the case of a traumatic posterior cerebral artery aneurysm from a self-inflicted pneumatic nail-gun missile injury through the roof of the mouth. The patient presented to us in a coma with subarachanoid and intraventricular hemorrhage. Cerebral angiography revealed an aneurysm of the left posterior cerebral artery with no distal filling. The patient died 6 days after admission. At autopsy, a pseudoaneurysm of the posterior cerebral artery was seen. This aneurysm resulted from direct disruption of the arterial wall by the intracranial nail.

Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits.

The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6-10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.