Cut End Of Sciatic Nerve Research Articles

Importance of tying the sciatic nerve in above knee amputation to prevent neuroma formation

Sciatic nerve is the thickest nerve in human body. Neural sheath of sciatic nerve is rich in microvasculature. In this study we compared neuroma formation after tying the sciatic nerve with leaving its cut end open in patients who undergo above knee amputation. In this study, we followed a total of 90 patients who underwent above knee amputation. In half of these patients, cut end of sciatic nerve was left open and in other half, the nerve was tied. Patients in both the groups were age, sex and BMI matched. Neuroma formation in the stump was assessed one year after surgery. This assessment was done by measuring the diameter of sciatic nerve ending using sonogram. Sciatic nerve diameter was measured bilaterally at the same level, and the value of the normal limb was taken as control. Out of 45 patients who underwent tying of sciatic nerve, only 10 patients developed thickening of the cut end of sciatic nerve in comparison to opposite limb. On the other hand, 45 patients in whom the cut end was left open, 33 patients developed neuroma formation. This result was statistically significant. Rich microvascularity of sciatic nerve results in the formation of haematoma beneath the cut end, if it is left open. This haematoma eventually results in growth of neural fibres. As a result of this, neuroma formation occurs at cut end of sciatic nerve in above knee amputation. We thus conclude, it is always wise to tie the cut end of sciatic nerve in above knee amputation to prevent neuroma formation.

Sciatic nerve regeneration in rats induced by transplantation of in vitro differentiated bone-marrow stromal cells.

Bone marrow stromal cells (MSCs) are multipotent stem cells that have the potential to differentiate into bone, cartilage, fat and muscle. We now demonstrate that MSCs can be induced to differentiate into cells with Schwann cell characteristics, capable of eliciting peripheral nervous system regeneration in adult rats. MSCs treated with beta-mercaptoethanol followed by retinoic acid and cultured in the presence of forskolin, basic-FGF, PDGF and heregulin, changed morphologically into cells resembling primary cultured Schwann cells and expressing p75, S-100, GFAP and O4. The MSCs were genetically engineered by transduction with retrovirus encoding green fluorescent protein (GFP), and then differentiated by treatment with factors described above. They were transplanted into the cut ends of sciatic nerves, which then responded with vigorous nerve fibre regeneration within 3 weeks of the operation. Myelination of regenerated fibers by GFP-expressing MSCs was recognized using confocal and immunoelectron microscopy. The results suggest that MSCs are able to differentiate into myelinating cells, capable of supporting nerve fibre re-growth, and they can therefore be applied to induce nerve regeneration.

Phosphatidylinositol 3-kinase activity in murine motoneuron disease: the progressive motor neuropathy mouse.

A murine model of motoneuron disease, the pmn/pmn mouse, shows a reduction in the retrograde transport of fluorescent probes applied directly onto the cut end of sciatic nerve. Brain-derived neurotrophic factor (BDNF), when co-applied with fluorescent tracers, increases the number of retrograde labelled motoneurons. We demonstrate here that spinal cord tissue from pmn/pmn mice had significantly reduced phosphatidylinositol 3-kinase activity and expression in the particulate fraction compared to controls, without changes in the activities or expression of the downstream kinases, protein kinase B/Akt or Erk1. Systemic administration of BDNF augmented phosphatidylinositol 3-kinase specific activity in spinal cord tissue from pmn/pmn and control mice, with a greater elevation in the particulate fractions of pmn/pmn mice than in controls. We examined the effect of inhibitors of phosphatidylinositol 3-kinase and mitogen-activated protein kinase kinase on the retrograde labelling of motoneurons, 24h following the direct application of inhibitors and Fluorogold to the cut end of sciatic nerve in control and pmn/pmn mice (labelling index). The mitogen-activated protein kinase kinase inhibitor PD 98059 had no effect on the labelling index in control or pmn/pmn mice. In the absence of exogenous BDNF, phosphatidylinositol 3-kinase inhibitors reduced the number of labelled motoneurons in control mice, without changing the labelling index in pmn/pmn. Co-application of phosphatidylinositol 3-kinase inhibitors with BDNF to the cut end of sciatic nerve blocked the action of BDNF on retrograde labelling in pmn/pmn mice. These results indicate that the retrograde labelling of motoneurons is mediated by phosphatidylinositol 3-kinase-dependent and -independent pathways. In pmn/pmn mice, phosphatidylinositol 3-kinase activity in spinal neurons is below the level required for optimal retrograde labelling of motoneurons and labelling can be augmented by the administration of growth factors stimulating phosphatidylinositol 3-kinase activity. The data indicate that phosphatidylinositol 3-kinase activity is important in the uptake and/or retrograde transport of substances by motoneurons and is altered in this model of motoneuron diseases.

The termination pattern of sciatic nerve afferents in the substantia gelatinosa of neonatal rats

A study was carried out to determine at what stage of development the adult pattern of primary afferent projections to the substantia gelatinosa (SG) is first established. Horseradish peroxidase conjugated wheat-germ agglutinin (WGA-HRP) was applied to cut ends of sciatic nerves at mid-thigh level in adult and neonatal rats aged 1–16 days. The distribution of transganglionically transported label in primary afferent terminals in SG was reconstructed from transverse sections of spinal cord segments L1 to S1. The distinctive U-shaped projection field of the sciatic nerve in SG of the adult was found to exist in miniature form already in the second postnatal day 24 h after WGA-HRP had been applied. The highly specific somatotopic projections of primary afferents to SG are probably established before birth. Any delay in the maturation of functional specificity in the dorsal horn of the neonate cannot be attributed to the absence or disorganization of anatomical projections to SG of primary afferent inputs.