Clinically orientated classification incorporating shoulder balance for the surgical treatment of adolescent idiopathic scoliosis.

PURPOSE: The achievement of shoulder balance is an important measure of successful scoliosis surgery. No previously described classification system has taken shoulder balance into account. We propose a simple classification system for AIS based on two components which include the curve type and shoulder level. METHODS: Altogether, three curve types have been defined according to the size and location of the curves, each curve pattern is subdivided into type A or B depending on the shoulder level. This classification was tested for interobserver reproducibility and intraobserver reliability. A retrospective analysis of the radiographs of 232 consecutive cases of AIS patients treated surgically between 2005 and 2009 was also performed. RESULTS: Three major types and six subtypes were identified. Type I accounted for 30 %, type II 28 % and type III 42 %. The retrospective analysis showed three patients developed a decompensation that required extension of the fusion. One case developed worsening of shoulder balance requiring further surgery. This classification was tested for interobserver and intraobserver reliability. The mean kappa coefficients for interobserver reproducibility ranged from 0.89 to 0.952, while the mean kappa value for intraobserver reliability was 0.964 indicating a good-to-excellent reliability. CONCLUSIONS: The treatment algorithm guides the spinal surgeon to achieve optimal curve correction and postoperative shoulder balance whilst fusing the smallest number of spinal segments. The high interobserver reproducibility and intraobserver reliability makes it an invaluable tool to describe scoliosis curves in everyday clinical practice.

Repair of spondylolysis using compression with a modular link and screws.

We describe the results of a prospective case series of patients with spondylolysis, evaluating a technique of direct stabilisation of the pars interarticularis with a construct that consists of a pair of pedicle screws connected by a U-shaped modular link passing beneath the spinous process. Tightening the link to the screws compresses bone graft in the defect in the pars, providing rigid intrasegmental fixation. We have carried out this procedure on 20 patients aged between nine and 21 years with a defect of the pars at L5, confirmed on CT. The mean age of the patients was 13.9 years (9 to 21). They had a grade I or less spondylolisthesis and no evidence of intervertebral degeneration on MRI. The mean follow-up was four years (2.3 to 7.3). The patients were assessed by the Oswestry Disability Index (ODI) and a visual analogue scale (VAS). At the latest follow-up, 18 patients had an excellent clinical outcome, with a significant (p < 0.001) improvement in their ODI and VAS scores. The mean ODI score at final follow-up was 8%. Assessment of the defect by CT showed a rate of union of 80%. There were no complications involving the internal fixation. The strength of the construct removes the need for post-operative immobilisation.

Nematic ordering of suspension of charged anisotropic colloids detected by multinuclear quadrupolar spectra and 1H PGSE-NMR measurements.

The structure of aqueous dispersion of charged anisotropic nano-composites (synthetic Laponite clays) have been studied by NMR and numerical simulations based on a multi-scale statistical analysis have been used to interpret the mobility of the confined water molecule diffusing within dense Laponite aqueous dispersions (29-52% w/w) prepared by uniaxial compression. Firstly, the lineshape detected by NMR quadrupolar spectroscopy of the counterions ((23)Na or (7)Li) exhibits a large residual splitting Delta nu which is the fingerprint of the macroscopic nematic ordering of the anisotropic particles. Secondly, these results are also confirmed by the anisotropy of the self-diffusion tensor of the water molecule measured by (1)H Pulsed Gradient Spin Echo NMR. This self-diffusion anisotropy increases with the suspension density. Thirdly, the multi-scale statistical analysis of the water mobility bridges the gap between the time-scale (ps) accessible by Molecular Dynamics simulations and the time-scale (micros) accessible by Brownian Dynamics, leading to macroscopic behaviour comparable with PGSE-NMR data measurements.

Anisotropy of the solvent self-diffusion tensor as a probe of nematic ordering within dispersions of nanocomposites.

The anisotropy of the solvent self-diffusion coefficient within suspensions of nanoparticles is measured by (1)H nuclear magnetic resonance with pulsed field gradient and used as a new procedure to detect nematic ordering. The potentiality of this method is illustrated using aqueous clay dispersions whose nematic ordering was already detected by (23)Na quadrupolar splitting.

Hyperenteroglucagonaemia and small intestinal mucosal growth after colonic perfusion of glucose in rats.

Beside intraluminal factors, humoral agents play an important role in intestinal adaptation. Enteroglucagon, the mucosal concentration of which is maximal in the terminal ileum and colon, is the strongest candidate for the role of small intestinal mucosal growth factor. The present experiment was designed to study the role of colonic enteroglucagon in stimulating mucosal growth in rats with a normal small intestine. After eight days of glucose large bowel perfusion, enteroglucagon plasma concentrations were 120.7 +/- SEM 9.2 pmol/l, versus 60.1 +/- 6.8 in mannitol perfused control rats (p less than 0.001). Gastrin, cholecystokinin, neurotensin, pancreatic glucagon, and insulin plasma concentrations were unchanged. Crypt cell proliferation, measured by the vincristine metaphase arrest technique, increased significantly in the small intestine of glucose perfused animals (p less than 0.005-0.001) in comparison with the controls. This resulted in a greater mucosal mass in both proximal and distal small bowel: mucosal wet weight, DNA, protein and alpha D-glucosidase per unit length intestine were all significantly higher (p less than 0.05-0.001) than in mannitol perfused rats. Our data, therefore, support the hypothesis that enteroglucagon is an enterotrophic factor and stress the possible role of the colon in the regulation of small bowel trophicity.

Influence of somatostatin and bombesin on plasma enteroglucagon and cell proliferation after intestinal resection in the rat.

The possible relationship between enteroglucagon and cellular proliferation in a rat model of intestinal adaptation after suppression and stimulation of enteroglucagon by somatostatin and bombesin has been investigated. Forty eight rats were divided into three groups of 16 animals, each group being further sub-divided into eight animals having intestinal resection and eight having intestinal transection. Group 1 was given somatostatin to suppress enteroglucagon, group 2 was given bombesin to stimulate enteroglucagon and group 3 (control group) had neither peptide. All animals were killed 12 days after operation. Circulating enteroglucagon and crypt cell production rate (CCPR) in the terminal ileum were measured. After administration of somatostatin (group 1) both CCPR and plasma enteroglucagon were lower after resection than controls (group 3) (p less than 0.001). Transected rats receiving somatostatin showed a reduction in both plasma enteroglucagon and CCPR, but only the fall in enteroglucagon was statistically significant (p less than 0.001). Transected rats receiving bombesin (group 2) had raised plasma enteroglucagon and CCPR compared with the control group (group 3) (P less than 0.005) but there was no significant further rise in these already raised parameters in resected animals. This study indicates that cell proliferation in the rat small bowel after surgery can be influenced by regulatory peptides. The changes in enteroglucagon corresponded closely with changes in CCPR, and this peptide remains a favoured candidate for the humorally mediated trophic influence on the small bowel.

Plasma enteroglucagon and CCK levels and cell proliferation in defunctioned small bowel in the rat.

Luminal nutrients exert a powerful trophic effect on small bowel mucosa. Recent evidence suggests that a circulating factor, possibly enteroglucagon, is also growth-promoting. In order to study the isolated effect of nonluminal influences on bowel mucosa, Thiry-Vella fistulae (TVF) were constructed in rats. Circulating enteric hormone concentrations were manipulated by resecting different lengths of remaining gut. Thirty-two male Wistar rats had either 25%, 50%, 75%, or 90% proximal small bowel resection. In each animal the first 25% of resected bowel was exteriorized as a Thiry-Vella fistula. Seven control rats underwent jejunal transection. Twelve days postoperatively the fasted animals were killed, and circulating and tissue concentrations of enteroglucagon and CCK were estimated by radioimmunoassay. Crypt-cell production rate was used as an index of cellular proliferation in the Thiry-Vella fistulae. Proximal small bowel defunctioned in the Thirty-Vella fistulae had a significantly lower crypt-cell production rate and enteroglucagon and CCK content than the equivalent segment in transected rats. Further small bowel resection produced a subsequent increase in circulating enteroglucagon and CCK concentrations, an increase in the Thiry-Vella fistula content of these hormones, and a doubling of the crypt-cell production rate in the Thiry-Vella fistulae. These results show that circulating enteroglucagon and CCK concentrations match closely with enterocyte production even when luminal influences are excluded. It is suggested that circulating factors may play a major role in postresectional ileal hyperplasia. This hyperplasia apparently affects endocrine cells as well as enterocytes.

Pattern of cell proliferation and enteroglucagon response following small bowel resection in the rat.

Gut resection triggers off a complex series of adaptive changes in the remaining bowel. There is evidence that these are partly mediated by hormonal factors and enteroglucagons have been proposed as candidates for this role. It is uncertain, however, whether plasma enteroglucagon concentrations rise quickly enough to be involved in the rapid initial response or are persistent enough for chronic maintenance. Plasma concentrations of enteroglucagon were therefore estimated at varying times following gut resection and related to crypt cell production rate (CCPR), which was used as an index of cellular proliferation. 96 male Wistar rats had either 75% proximal small bowel resection or jejunal transection (controls). Groups of animals were killed at 1.5, 3, 6, 12, 24 and 48 days following operation and the plasma enteroglucagon and CCPR in the terminal ileum were estimated. Both values were markedly elevated at 1.5 days and continued to rise in a very similar manner in the resected group of rats. Gel permeation chromatography on Sephadex G-50 of plasma samples showed that the increase in plasma enteroglucagon was mainly due to an increase in a component of Kav 0.25, of similar molecular size to that of porcine glicentin. Thus the principal form of enteroglucagon, as a possible trophic hormone, does respond sufficiently quickly, and the response is maintained for long enough, to be involved throughout the adaptive process.

The role of pancreatico-biliary secretions in intestinal adaptation after resection, and its relationship to plasma enteroglucagon.

Two groups, each containing 16 male Wistar rats, had either 75 per cent small bowel resection or jejunal transection; 8 animals from each group; had previously been subjected to pancreatico-biliary diversion. All animals were killed 12 days after the operation, plasma enteroglucagon levels were measured and crypt cell production rate (CCPR) at different sites of the remaining small intestine was measured using a metaphase arrest technique with vincristine. In each of the resected groups there was a significant increase in the CCPR and enteroglucagon levels compared with the transected groups. Furthermore it was found that the CCPR and enteroglucagon levels were higher in the resected group without the pancreatico-biliary diversion compared with the resected group with the diversion. This study, although it confirms the importance of pancreatico-biliary secretions in intestinal adaptation, could also indicate that a humoral factor may be important in the control of intestinal cell proliferation. Our findings do not exclude the possibility that enteroglucagon could be a candidate for such a role.

Evidence for a humoral mechanism after small intestinal resection. Exclusion of gastrin but not enteroglucagon.

It is generally agreed that the adaptive response in the residual bowel after major intestinal resection is dependent on luminal nutrition and pancreaticobiliary secretions. Recent evidence, however, suggests that humoral mechanisms, e.g., gastrin or enteroglucagon, may also play a part in this process. A 75% proximal small bowel exclusion was performed in 16 male Wistar rats and the excluded bowel was fashioned into a Thiry-Vella fistula. Half of the animals were allowed food ad libitum, while the rest were fed intravenously. The animals were killed at 12 days, and plasma, gastrin, and enteroglucagon were measured, while cell proliferation was determined by measuring the crypt cell production rate employing a stathmokinetic method using vincristine and crypt microdissection. In addition to these animals, 16 rats had a jejunal transection only, with half of these animals nourished intravenously, while the remainder were allowed food ad libitum. In the Thiry-Vella rats, plasma enteroglucagon was greater with oral feeding (566 +/- 59 pmol/L) than with intravenous feeding (120 +/- 452 pmol/L) (p less than 0.01), but gastrin levels did not differ in the two groups. In the ileum in continuity, crypt cell production rate per hour was greater in the orally fed animals (52 +/- 8) compared with the intravenously fed group (18 +/- 5) (p less than 0.001). In the excluded fistula, crypt cell production rate per hour was reduced by 23.8 +/- 2 in orally fed rats, but this was greater than in the intravenously fed group (16 +/- 1.5) (p less than 0.01). Both orally and intravenously fed transected rats had significantly lower plasma hormone levels, and reduced crypt cell production rate compared with the respective Thiry-Vella groups. This study suggests a distinct role for a humoral agent responsible for the proliferative changes seen after small bowel resection, and in this respect enteroglucagon appears more relevant than gastrin.

Cell proliferation, plasma enteroglucagon and plasma gastrin levels in starved and refed rats.

The effects of starvation and refeeding on intestinal cell proliferation at several sites of the rat gastrointestinal tract were studied and used as a model of altered cell proliferation in order to investigate the relationship between the rate of cell production and plasma gastrin and enteroglucagon. There was a marked fall in crypt cell production rate after four days starvation, with the proximal sites of the gut being most affected. The response to refeeding varied with site, suggesting that there was more than one mechanism for the control of intestinal cell proliferation. Plasma gastrin and enteroglucagon both fell to one fifth of their control level after starvation. Plasma gastrin increased slowly after refeeding, whilst plasma enteroglucagon increased rapidly to values significantly above control. Plasma gastrin was only correlated with crypt cell production in the duodenum, while plasma enteroglucagon was correlated with crypt cell production rate at several sites, indicating that enteroglucagon may be involved in the control of intestinal cell production.

The effect of altered luminal nutrition on cellular proliferation and plasma concentrations of enteroglucagon and gastrin after small bowel resection in the rat.

Luminal nutrition is known to have a trophic effect on small bowel mucosa after intestinal resection. Humoral agents, however, may also contribute to this process. Two of the proposed humoral agents, enteroglucagon and gastrin, were therefore investigated after intestinal resection and transection in the rat, and changes in their concentration in the plasma were related to cellular proliferation. Forty-eight male Wistar rats had either 75 per cent proximal small bowel resection or jejunal transection. The animals were further divided into three groups, each with a different nutritional intake. The first group were allowed food ad libitum. The second group were kept under hypothermic conditions which resulted in hyperphagia, while the last group were nourished intravenously. A further 8 animals had a laparotomy only (sham operation). All animals were killed 12 days after operation, plasma enteroglucagon and gastrin were measured, while determination of the crypt cell production rate (CCPR) was used to denote cellular proliferation. In each group resected rats had significantly higher crypt cell production rates and greater enteroglucagon levels compared with transected animals. However, only in the normally fed group was plasma gastrin increased in resected animals, there being no significant difference in the plasma concentration of this peptide in transected compared with resected rats, in both the intravenously fed and hyperphagic groups. In the models studied enteroglucagon appears to be a more likely candidate for a humoral trophic agent than gastrin in intestinal adaptation.