This study sought to investigate the normal muscle fibre size and type distribution of the human erector spinae, both in thoracic and lumbar regions, in a group of 31 young healthy male (n = 17) and female (n = 14) volunteers. Two percutaneous muscle biopsy samples were obtained under local anaesthesia, from the belly of the left erector spinae, at the levels of the 10th thoracic and 3rd lumbar vertebrae. Samples were prepared for routine histochemistry for the identification of fibre types. Fibre size (cross-sectional area (CSA) and narrow diameter (ND)) was quantified using computerised image analysis. The mean CSA/ND for each fibre type was greater in the thoracic than the lumbar region, but there was no difference between the 2 regions either for percentage type I (i.e. percentage distribution by number), percentage type I area (i.e. relative area of the muscle occupied by type I fibres) or the ratio describing the size of the type I fibre relative to that of the type II. Men had larger fibres than women, for each fibre type and at both sampling sites. In the men, each fibre type was of a similar mean size, whereas in the women the type I fibres were considerably larger than both the type IIA and type IIB fibres, with no difference between the latter two. In both regions of the erector spinae there was no difference between men and women for the proportion (%) of a given fibre type, but the percentage type I fibre area was significantly higher in the women. The erector spinae display muscle fibre characteristics which are clearly very different from those of other skeletal muscles, and which, with their predominance of relatively large type I (slow twitch) fibres, befit their function as postural muscles. Differences between thoracic and lumbar fascicles of the muscle, and between the muscles of men and women, may reflect adaptive responses to differences in function. In assessing the degree of any pathological change in the muscle of patients with low back pain, it seems clear that (1) sex cannot be disregarded and (2) 'atrophied' (using the criteria from other muscles) type II fibres are not necessarily abnormal for the erector spinae, particularly in women.

A right-sided subarachnoid hemorrhage (SAH) was created in 12 monkeys. Only the right (clot-side) cerebral arteries developed angiographic vasospasm (VSP), which was maximal 7 days after SAH. Eight animals were killed at this time and the remainder at 14 days. At the time of killing the middle cerebral arteries (MCAs) were harvested, and four normal, left (non-clot-side) MCAs were vasoconstricted in vitro with prostaglandin F2… All MCAs were studied with scanning and transmission electron microscopy. Right MCAs in maximal VSP 7 days from SAH were undistinguishable on scanning electron microscopy from normal arteries vasoconstricted in vitro: both groups demonstrated a mean 57% reduction in vessel caliber and a 5-fold increase in vessel wall thickness compared to normal, nonvasoconstricted left MCAs. On transmission electron microscopy, however, arteries in SAH-induced VSP showed degenerative changes in the tunica intima and media. These changes were still evident at 14 days. despite considerable resolution of VSP. These findings, as well as those from other pathological studies of animal and human cerebral arteries in VSP, suggest that the arterial narrowing and vessel wall thickening seen within several weeks of SAH is due primarily to medial contraction, but unlike simple vasoconstruction, is associated with degenerative ultrastructural changes in the endothelium and vascular smooth muscle cells which may denote a temporarily irreversible state.

The authors have developed a method to induce chronic cerebral vasospasm after subarachnoid hemorrhage (SAH) in monkeys. With microsurgical techniques, 33 monkeys had a frontotemporal craniectomy and unilateral opening of the subarachnoid cisterns. Cerebrospinal fluid was drained and a fresh hematoma, obtained from an average of 7 ml of autologous blood, was carefully placed against the major arteries of the anterior circulation on one side. The 30 monkeys studied for 7 to 14 days after the SAH were allocated randomly to two treatment groups of 15: one group received placebo and the other nimodipine, 1 mg/kg every 8 hours. Indices monitored before and after SAH included neurological status, cerebral blood flow, computerized tomography, and angiographic vessel caliber. In the placebo group, delayed ischemic neurological deficit developed in one monkey 4 days after clot placement and was present at sacrifice on Day 14. No such deficit occurred in the nimodipine group. The effect of nimodipine on vessel caliber at this dosage was equivocal. Significant vasospasm (31% to 100% reduction in vessel caliber) developed in 87% (26 of 30) of the animals. Overall, vasospasm was slightly more common in the placebo group: in this group, on Days 7 and 14, the incidence of vasospasm was significantly higher (p less than 0.05) than in the nimodipine group. However, the average percentage reduction in vessel caliber of the maximally constricted vessel in each monkey was not significantly different between the two groups.