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Spontaneous resolution of discal cyst around L5 nerve root: case report and review of literature.

Br J Neurosurg. 2011 Dec;25(6):761-3

Authors: Prasad G, Kabir SM, Saifuddin A, Casey AT

Abstract
The treatment of discal cysts is controversial, with different surgical options described in the literature. We present an interesting case of spontaneous resolution of a symptomatic discal cyst. Based on our case report, we recommend non-operative management in the first instance and an up-to-date MRI scan before contemplating surgery.

PMID: 21501056 [PubMed – indexed for MEDLINE]

GDNF-treated Acellular Nerve Graft Promotes Motoneuron Axon Regeneration after Implantation into Cervical Root Avulsed- Spinal Cord.

Neuropathol Appl Neurobiol. 2012 Jan 30;

Authors: Chu TH, Wang L, Guo A, Chan VW, Wong CW, Wu W

Abstract
It is well known that glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for motoneurons. We have previously shown that it greatly enhanced motoneuron survival and axon regeneration after implantation of peripheral nerve graft following spinal root avulsion. Aims: In the current study, we explore whether injection of GDNF promotes axon regeneration in decellularized nerve induced by repeated freeze-thaw cycles. Methods: We injected saline or GDNF into the decellularized nerve after root avulsion in adult Sprague-Dawley rats and assessed motoneuron axon regeneration and Schwann cell migration by retrograde labeling and immunohistochemistry. Results: We found that no axons were present in saline-treated acellular nerve whereas Schwann cells migrated into GDNF-treated acellular nerve grafts. We also found that Schwann cells migrated into the nerve grafts as early as 4 days after implantation, coinciding with the first appearance of regenerating axons in the grafts. Application of GDNF outside the graft did not induce Schwann cell infiltration nor axon regeneration into the graft. Application of pleiotrophin, a trophic factor which promotes axon regeneration but not Schwann cell migration, did not promote axon infiltration into acellular nerve graft. Conclusions: We conclude that GDNF induced Schwann cell migration and axon regeneration into the acellular nerve graft. Our findings can be of potential clinical value to develop acellular nerve grafting for use in spinal root avulsion injuries. © 2012 The Authors. Neuropathology and Applied Neurobiology © 2012 British Neuropathological Society.

PMID: 22289090 [PubMed – as supplied by publisher]

Mechanisms of action of botulinum neurotoxins, ?(3) -adrenergic receptor agonists, and PDE5 inhibitors in modulating detrusor function in overactive bladders.

Neurourol Urodyn. 2012 Jan 24;

Authors: Kanai A, Zabbarova I, Oefelein M, Radziszewski P, Ikeda Y, Andersson KE

Abstract
BACKGROUND: Botulinum neurotoxins type A (BoNT/A), ?(3) -adrenergic receptor agonists, and phosphodiesterase type 5 (PDE5) inhibitors are promising agents that mitigate lower urinary tract symptoms by attenuating the sensory system. However, whether they act directly on afferent nerves or indirectly through the other cell types is unclear. METHODS: Spinal cord transected female mice were used as a model for neurogenic bladder overactivity. In vivo methods utilized decerebrate mouse cystometry. In vitro approaches included optical mapping of Ca(2+) transient, single unit afferent nerve recordings and tension measurements from bladder sheets and wall cross-sections. Immunohistochemistry was used to measure the expression of ?(3) -adrenergic receptors on dorsal root ganglion (DRG) neurons. RESULTS: Our unique approaches revealed the direct effects of BoNT/A in inhibiting neuropeptide release and firing rates in afferents following bladder injections. ?(3) -adrenergic receptor agonists are demonstrated to directly inhibit afferent nerve firing independent of the relaxing effects on bladder smooth muscle. Moreover, data suggest the expression of these receptors on DRG neurons that send projections to the bladder. The mechanism of action of PDE5 inhibitors on bladder overactivity is discussed. DISCUSSION: The questions raised during the plenary session of the 2011 International Consultation on Incontinence-Research Society meeting regarding the benefits of BoNT/A, ?(3) -adrenergic receptor agonist and PDE5 inhibitor treatments of overactive bladder are addressed. CONCLUSION: Our findings suggest that the abovementioned agents, in low enough concentrations, can directly inhibit afferent excitability without decreasing detrusor contractility. Accordingly, they have considerable potential for treating the sensory component of lower urinary tract dysfunctions. Neurourol. Urodynam. © 2012 Wiley Periodicals, Inc.

PMID: 22275187 [PubMed – as supplied by publisher]

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