Monomelic Ischemic Neuropathy of the Tibial and Peroneal Nerve After Onyx Embolization of Vasa Nervorum Supplying a Surgically Excluded Popliteal Artery Aneurysm.

Ischemic neuropathy is an exceedingly rare complication after peripheral artery embolization. We report a case of ischemic damage to the tibial and peroneal nerve after embolization of the vasa nervorum that served as feeding collaterals to a surgically excluded popliteal artery aneurysm.

Corkscrew Collateral Vessels in Buerger Disease: Vasa Vasorum or Vasa Nervorum.

PURPOSE: To investigate the origin of "corkscrew" collateral vessels around the occluded popliteal artery in patients with Buerger disease by Doppler ultrasound (US) and magnetic resonance (MR) imaging in tandem with digital subtraction angiography (DSA). MATERIALS AND METHODS: Between January 2013 and June 2015, 42 patients diagnosed with Buerger disease were identified retrospectively. Patients in whom occlusion of the popliteal artery was found on DSA of the lower extremity were subjected to Doppler US and MR imaging prospectively. Fifteen of 42 patients were identified as having the required characteristics, of whom 10 participated in the present study. RESULTS: Ten patients with occlusion of the popliteal artery were selected for inclusion, and 12 lower limbs of these patients were investigated. The study cohort comprised one woman and nine men with a mean age of 41 years ± 10 (standard deviation; range, 39-58 y). Corkscrew collateral vessels identified on DSA examinations were also identified on secondary imaging (Doppler US and MR imaging) in all patients except one in whom the popliteal artery was reconstituted after short-segment occlusion. The origin of the corkscrew collateral vessels was identified as the vasa nervorum of the tibial nerve in nine patients. CONCLUSIONS: Data from the present study suggest that corkscrew collateral vessels at the knee level in patients with Buerger disease originate from the vasa nervorum of the tibial nerve rather than the vasa vasorum of the popliteal artery if the latter is occluded.

Pathogenesis of diabetic neuropathy: focus on neurovascular mechanisms.

Neuropathies of the peripheral and autonomic nervous systems affect up to half of all people with diabetes, and are major risk factors for foot ulceration and amputation. The aetiology is multifactorial: metabolic changes in diabetes may directly affect neural tissue, but importantly, neurodegenerative changes are precipitated by compromised nerve vascular supply. Experiments in animal models of diabetic neuropathy suggest that similar metabolic sequelae affect neurons and vasa nervorum endothelium. These include elevated polyol pathway activity, oxidative stress, the formation of advanced glycation and lipoxidation end products, and various pro-inflammatory changes such as elevated protein kinase C, nuclear factor κB and p38 mitogen activated protein kinase signalling. These mechanisms do not work in isolation but strongly interact in a mutually facilitatory fashion. Nitrosative stress and the induction of the enzyme poly (ADP-ribose) polymerase form one important link between physiological stressors such as reactive oxygen species and the pro-inflammatory mechanisms. Recently, evidence points to endoplasmic stress and the unfolded protein response as forming another crucial link. This review focuses on the aetiopathogenesis of neurovascular changes in diabetic neuropathy, elucidated in animal studies, and on putative therapeutic targets the majority of which have yet to be tested for efficacy in clinical trials.

Pathophysiology of diabetic erectile dysfunction: potential contribution of vasa nervorum and advanced glycation endproducts.

Erectile dysfunction (ED) due to diabetes mellitus remains difficult to treat medically despite advances in pharmacotherapeutic approaches in the field. This unmet need has resulted in a recent re-focus on the pathophysiology, in order to understand the cellular and molecular mechanisms leading to ED in diabetes. Diabetes-induced ED is often resistant to PDE5 inhibitor treatment, thus there is a need to discover targets that may lead to novel approaches for a successful treatment. The aim of this brief review is to update the reader in some of the latest development on that front, with a particular focus on the role of impaired neuronal blood flow and the formation of advanced glycation endproducts.

Do denervated peripheral nerve trunks become ischemic? The impact of chronic denervation on vasa nervorum.

The long-term relationship between the peripheral nerve trunk and its vascular supply, the vasa nervorum, has not been considered in the context of denervation and regeneration. While the microvessels of peripheral nerve are not thought to influence Wallerian degeneration itself, in this work we explored how vasa nervorum respond to denervation of the nerve trunk. Our hypotheses were that the presence of axons had a significant impact on the vasa nervorum and that the absence of reinnervation might eventually lead to an unfavorable ischemic regenerative microenvironment. We studied rat sciatic nerve trunks for up to 6 months following transection and either prevented regeneration or allowed it to proceed. Vasa nervorum were studied in several ways: (i) measurements of local endoneurial blood flow using microelectrode hydrogen clearance polarography; (ii) measurements of erythrocyte flux (flow) in the extrinsic nerve plexus using laser Doppler flowmetry; (iii) India ink perfusion of microvessels in unfixed nerve; (iv) mRNA expression of vascular endothelial growth factor (VEGF) using reverse transcription polymerase chain reaction. Early after injury, there were rises in endoneurial and extrinsic flow, microvessel numbers, and VEGF mRNA expression. Angiogenesis was apparently confined to the epineurial and perineurial compartments. Later, however, there were substantial declines in flow observed in long-term (6-month) denervated sciatic nerve trunks associated with declines in the caliber of new microvessels. Reinnervated sciatic nerves had restored endoneurial blood flow. The findings confirm important relationships between axon presence and local blood flow. Angiogenesis is a feature of the injured peripheral nerve, but long term denervated nerve trunks have declines of flow despite retaining new microvessels.

Polyneuropathy in late Lyme borreliosis - a clinical, neurophysiological and morphological description.

In a prospective study, detailed clinical and neurophysiological examinations were performed in 17 patients with polyneuropathy associated with the late borrelial manifestation acrodermatitis chronica atrophicans (ACA). Similar clinical and neurophysiological signs were found in most of the patients. The findings were those of a sensory polyneuropathy, mainly affecting large nerve fibres. Marked abnormality of vibration threshold was a common finding and in 4 patients this raised a suspicion of spinal cord engagement, in addition to a polyneuropathy. Sural nerve biopsy, performed in 3 of the patients, showed a mainly axonal neuropathy. Biopsy findings did not confirm earlier reports of vasculitis of epineural vessels in ACA-associated polyneuropathy.

An investigation of the pathophysiology of ischaemic neuropathy.

This study assesses the changes in the microvasculature of peripheral nerves in acute large vessel ischaemic neuropathy. An animal model of large vessel ligation, producing an ischaemic neuropathy was used: the presence and extent of the neuropathy was documented by clinical examination and nerve conduction studies. The nerve microcirculation, the "vasa nervorum" was examined using casting materials, methyl methacrylate and silicone rubber, which were in turn examined by light microscopy and scanning electron microscopy. In all, ten animals were used, all of whom showed clinical evidence of an ischaemic neuropathy 1 week post-ligation. This ischaemic neuropathy was confirmed by nerve conduction studies. Corrosion casts were produced in five of the ten animals. Examination of these casts showed that all five had an area of underfilling of the microcirculation in the region of the proximal tibial nerve with good filling of vessels proximal and distal to this, indicating that in generalised hypoperfusion states such as large vessel ligation, the area of poorest perfusion (and thus maximal damage) is not the distal vascular field, but a probable "watershed zone" between two adjacent nutrient vessels to the nerve.

Reduced nerve blood flow in hexachlorophene neuropathy: relationship to elevated endoneurial fluid pressure.

To test the hypothesis that increased endoneurial fluid pressure (EFP) causes a reduction in nerve blood flow (NBF) in the vasa nervorum, we adapted a noninvasive method for measurement of nerve blood flow which was originally developed for measurement of local cerebral blood flow. This technique measures tissue distribution to the radioisotope, 14C-iodoantipyrine, and was used to compare NBF in sciatic nerves of rats with increased EFP induced by feeding them hexachlorophene (HCP), a neurotoxin which causes edema exclusively to the nervous system and confined to the myelin sheath. Elevation of interstitial fluid pressure in peripheral nerves from control values of 2.0 +/- 1.0 cm H2O to over approximately 6 cm H2O was associated with a statistically significant reduction in nerve blood flow from 14.8 +/- 5.9 to 7.8 +/- 2.5 ml/100 g of tissue/minute (min). These results support the hypothesis that increased endoneurial fluid pressure exacerbates the neuropathy by diminishing local blood flow.

Permeability of blood nerve barriers in the diabetic rat.

An albumin-Evans blue conjugate has been used as a fluorescent tracer to demonstrate the increased permeability of endoneurial capillaries and perineurial sheath of the sciatic nerve of the alloxan-diabetic rat. The significance of the extravasation of protein into the endoneurial space is discussed in relation to the altered dynamics of the endoneurial microcirculation. It is suggested that tissue hypoxia produced in this way may be a cause of the segmental demyelination which occurs in these nerves.