Herniated disc with radiculopathy following cervical manipulation: nonsurgical management.

BACKGROUND CONTEXT: Spinal manipulation applied to the cervical spine is a relatively safe and effective treatment for neck pain and headache. However, complications of this form of treatment have been reported and these can at times be disabling and on rare occasions can be devastating. A postmanipulation complication being treated with a different form of manipulation has not previously been reported. PURPOSE: To report a case of a patient who was treated with manipulation and who developed neck, scapular, and arm pain and arm numbness after the sixth visit, which was later attributed to three herniated discs. The patient was subsequently treated with a nonsurgical approach that included, but was not limited to, a different form of manipulation with apparent resolution of the problem. STUDY DESIGN/SETTING: The patient was a 38-year-old banker who began seeing a chiropractic physician for treatment that included cervical manipulation. On the sixth visit, he developed pain immediately after treatment which became severe and was accompanied by numbness in his arm. He saw a neurosurgeon who recommended surgery, but was subsequently seen by a different chiropractic physician and was treated nonsurgically. METHODS: The patient was found to have clinical signs of radiculopathy, including motor loss. Magnetic resonance imaging revealed disc herniations at C3-C4, C4-C5, and C5-C6. RESULTS: The patient was treated by the author with an alternate approach that included non-high-velocity, low-amplitude manipulation and exercise with resolution of the problem. CONCLUSION: This paper reports a case of a patient with radiculopathy secondary to multilevel disc herniations that appeared to be precipitated by cervical manipulation and who was treated nonsurgically with resolution of the problem. It is doubtful that the manipulation actually caused the disc herniations, but it is possible that it caused preexisting asymptomatic disc herniations to become symptomatic. Consideration should be given to nonsurgical referral of patients who have postmanipulative complications but do not need immediate surgery.     

A prospective randomized trial of laparoscopic versus open appendectomy.

BACKGROUND. Laparoscopic appendectomy is feasible, but whether it confers any advantage to patients with acute appendicitis is not known. We performed a randomized controlled trial to compare results of laparoscopic and open appendectomy in patients with signs and symptoms suggesting acute appendicitis who were seen by one surgical team. METHODS. Sixty-two consecutive patients were randomized, 30 to laparoscopy and 32 to a classical open appendectomy. Postoperative recovery, complications, and return to normal activities were compared in the two groups. RESULTS. The laparoscopy group were discharged earlier (2.5 vs 3.8 days, p less than 0.01). Postoperative complications were more frequent after open appendectomy. Follow-up showed less pain, shorter bed stay at home, and faster return to work and sport after laparoscopic appendectomy. CONCLUSIONS. This prospective randomized study shows that laparoscopic appendectomy is superior to open appendectomy in terms of hospital stay, postoperative complications, and return to normal activities and is recommended as the approach of choice in the management of acute appendicitis.     

Differential Contractile Response of Cultured Microvascular Pericytes to Vasoactive Agents

Objective: Microvascular pericytes may contract in two different ways: In the first, a circumferential or radial mechanical force applied at right angles to the long axis of the vessel may constrict the underlying vessel affecting blood flow and transmural pressure. Retraction and elongation of pericyte processes may also occur tangentially and at right angles to the vessel axis and alter microvessel permeability by changing the amount of ablumenal surface covered or the openness of interendothelial junctions. In this study, cultured pericytes were utilized as a model experimental system to determine if vasoactive stimulation changes their shape in a manner consistent with this hypothesis. Methods: Pericytes cultured from isolated rate capillaries were subjected to angiotensin II and histamine. Their response was monitored by measuring the area of nonyielding substrate covered by the pericytes and the manner in which their shape changed. Shape changes were quantified by calculating the surface area: perimeter perimeter ratios. Results: Histamine significantly reduced surface area covered and the surface area: perimeter ratio. The pericyte processes retracted, resulting in elongated, spindle-shaped cells. These effects were nullified by the H₁ blocker diphenhydramine suggesting a receptor-specific response. Angiotensin II also elicited contraction and reduced surface area, but the cells contracted laterally and longitudinally. The surface area: perimeter ratios also decreased. Conclusions: These results indicate that pericytes are capable of two types of contractile responses in culture, depending on the specific vasoactive stimulus.     

Impaired estrogen-induced uterine insulin-like growth factor-I gene expression in the streptozotocin diabetic rat

Summary Circulating somatomedin-C/insulin-like growth factor-I levels are low in the diabetic rat and unresponsive to exogenous growth hormone. However, the nature of this defect in growth hormone action remains unclear and there is little data on insulin-like growth factor-I gene expression in response to other stimuli and in non-hepatic tissues where insulin-like growth factor-I may have important paracrine and/or autocrine actions. We have previously shown that 17-beta estradiol stimulates uterine insulin-like growth factor-I expression in the ovariectomised rat. In this report uterine and hepatic insulin-like growth factor-I gene expression have been examined in the streptozotocin-diabetic rat. Serum insulin-like growth factor-I concentrations were significantly reduced in diabetic rats compared to normal rats (0.72±0.08 vs 1.23±0.05U/ml, p<0.0005) and hepatic insulin-like growth factor-I mRNA abundance was similarly reduced in diabetic rats to 49±5% of that seen in non-diabetic intact rats (p<0.005). In contrast, uterine insulin-like growth factor-I mRNA abundance was not significantly reduced in diabetic rats compared to control rats (76±12%, p = NS). Although both diabetic and non-diabetic rats demonstrated a significant increase in uterine wet weight following a single injection of 17-beta estradiol the increase in uterine insulinlike growth factor-I expression was significantly less marked in diabetic rats. Acute administration of insulin together with estradiol had no significant effect on serum insulin-like growth factor-I concentrations or hepatic insulin-like growth factor-I mRNA abundance; however, the uterine insulin-like growth factor-I response was significantly (p<0.01) augmented. The observations reported here demonstrate that hepatic insulin-like growth factor-I gene expression is markedly reduced in the diabetic rat and that the estradiol-induced uterine insulin-like growth factor-I response is significantly diminished, consistent with the hypothesis that there is a defect in insulin-like growth factor-I gene activation in the diabetic rat.     

Arteriosclerosis obliterans in a rabbit model.

RATIONALE AND OBJECTIVES. The authors induced atherosclerotic occlusions in a rabbit model, using and comparing different experimental methods. METHODS. Lesions were induced in 40 femoral arteries in 20 rabbits. Four combinations of lesion induction methods were used: 1) drying of the endothelium with carbon dioxide gas; 2) gas-drying of the artery plus mechanical injury; 3) gas-drying plus induced thrombosis of the treated segment using thrombin; and 4) gas-drying, mechanical injury, and induced thrombosis. All rabbits were fed a high-fat, high-cholesterol diet for 1 to 2 months after lesion induction. RESULTS. Seventeen rabbits were available for follow-up. Sixty-eight percent (13 of 19) of femoral arteries treated with thrombin-induced thrombosis demonstrated atherosclerotic occlusions, compared with 27% of those that did not receive this treatment (4 of 15; P < .01). CONCLUSIONS. Thrombin-induced thrombotic occlusion of a segment of artery which has been de-endothelialized, followed by a high-fat, high cholesterol diet, results in a higher yield of experimental occlusive atherosclerosis in rabbits than is achievable by other methods.     

Cytomegalovirus Disease in High-Risk Transplant Recipients Despite Ganciclovir or Valganciclovir Prophylaxis

The clinical patterns and predictors of cytomegalovirus (CMV) disease in kidney and/or pancreas transplant patients on ganciclovir (1.0 g po t.i.d.) or valganciclovir (450 mg po q.d.) prophylaxis were studied. This is a retrospective analysis of 129 transplant recipients. Median follow up was 12 months (range, 6-18 months). The overall incidence of CMV disease at 1-year post-transplant was 14% (4% tissue-invasive, 10% noninvasive). Seventeen of 18 patients were diagnosed with CMV after completion of 3 months' prophylaxis (median 8 weeks, range, 2-28 weeks). Induction treatment with thymoglobulin, and Donor +/Recipient - CMV status were the strongest predictors for the development of CMV disease. Cytomegalovirus incidence was not different between patients treated with ganciclovir or valganciclovir (15 vs. 17%, respectively). Valganciclovir (450 mg q.d.) is as effective as oral ganciclovir in CMV prophylaxis. High-risk individuals might require higher doses or longer duration of valganciclovir treatment.     

Growth hormone effects on hypertrophic scar formation: a randomized controlled trial of 62 burned children

The hypercatabolism after massive pediatric burns has been effectively treated with recombinant human growth hormone, an anabolic agent that stimulates protein synthesis and abrogates growth arrest. While experimental studies have shown increased potential for fibrosis induced by growth hormone therapy, adverse effects on human scars have not been investigated. Our aim was to evaluate hypertrophic scar formation in 62 patients randomized to receive injections of 0.05 mg/kg/day of recombinant human growth hormone or placebo, from discharge until 1 year after burn. Scar scales were used to evaluate scar-severity at discharge, 6, 9, 12, and 18-24 months after burn, by three observers blinded to treatment. Computer-assisted planimetry allowed quantification of percentage of hypertrophic scar formation. Types I and III collagens were localized and quantified in scars and normal skin of patients from both groups, using immunohistochemistry with confocal laser microscopy analysis. Insulin-like growth factor-1 blood levels helped assess compliance. Statistical analysis showed that scar hypertrophy significantly increased from 6 to 12 months after injury in both groups, while decreasing at 18-24 months postburn. Types I and III collagens were statistically increased in the reticular layer of scars from both groups when compared to paired normal skin. Insulin-like growth factor-1 was significantly increased in the recombinant human growth factor-treated group. No differences were seen when recombinant human growth factor and control groups were compared using the scar scales, planimetry, or immunohistochemistry. We concluded that recombinant human growth hormone therapy did not adversely affect scar formation and should not contraindicate the administration of recombinant human growth hormone as a therapeutic approach to severely burned children.     

Leukaemia Inhibitory Factor or Related Factors Promote the Differentiation of Neuronal and Astrocytic Precursors within the Developing Murine Spinal Cord

Previously we have shown that leukaemia inhibitory factor (LIF) potentiates the development of murine spinal cord neurons in vitro , suggesting that it, or related factors, may play an important regulatory role in neuronal development. We have further investigated this role and show here that the generation of neurons in cultures of embryonic day 10 spinal cord cells is inhibited by antibodies to the β subunit of the LIF receptor. Since there are more undifferentiated precursors in antibody-treated cultures than in control and LIF-treated cultures, it is concluded that the primary action of LIF, or related molecules, is to promote neuronal differentiation, not precursor survival. In addition, the failure of LIF to support neuronal survival in the period immediately following differentiation suggests that the increased numbers of neurons generated with LIF are not attributable to its neurotrophic action. By selecting neuronal precursors on the basis of their inability to express class I major histocompatibility complex molecules, it was shown that LIF acted directly upon these cells and not via an intermediary cell. LIF also appears to be involved in regulating the differentiation of astrocytes, since it increases the number of glial fibrillary protein (GFAP)-positive cells present in the cultures and since the spontaneous production of GFAP-positive cells is blocked by antibodies to the LIF β receptor. These findings suggest that LIF or related factors promote the differentiation of neural precursors in the spinal cord, but that they are not involved in preferentially promoting precursors down a specific differentiation pathway.