Mechanical characteristics of BMSCs-intervened sciatic nerve in chronic alcohol-intoxicated animal model.

OBJECTIVE: To study the mechanical properties of sciatic nerve in rats with chronic alcoholism (CA) and intervened with bone marrow mesenchymal stem cells (BMSCs) and to provide biomechanical basis for clinical practice. METHODS: the serum of the BMSCs-intervened CA rats was sampled and determined the contents of malondialdehyde (MDA), metallothionein (CAS, MT), and Glutathione/r -glutamyl cysteinyl/glycine (GSH); meanwhile, the rats' sciatic nerve was tested the tensile and observed the histomorphological changes. RESULTS: The mechanical properties of sciatic nerve in BMSCs-intervened CA rats, as well as the serum levels of MT and GSH, were significantly different from those in the basic fibroblast growth factor (bFGF)-intervened CA rats (p < 0.05). CONCLUSIONS: BMSCs intervention can restore the levels of MT, GSH, MDA, histomorphology, and tensile mechanical properties in CA animal model, and its effects on repairing sciatic nerve are obvious.

Inflammatory responses to alcohol in the CNS: nuclear receptors as potential therapeutics for alcohol-induced neuropathologies.

Fetal alcohol spectrum disorder (FASD), which results from ethanol exposure during pregnancy, and alcohol use disorder (AUD), which includes both binge and chronic alcohol abuse, are strikingly common and costly at personal and societal levels. These disorders are associated with significant pathology, including that observed in the CNS. It is now appreciated in both humans and animal models that ethanol can induce inflammation in the CNS. Neuroinflammation is hypothesized to contribute to the neuropathologic and behavioral consequences in FASD and AUD. In this review, we: 1) summarize the evidence of alcohol-induced CNS inflammation, 2) outline cellular and molecular mechanisms that may underlie alcohol induction of CNS inflammation, and 3) discuss the potential of nuclear receptor agonists for prevention or treatment of neuropathologies associated with FASD and AUD.

[Neurological diseases and nutrition -- what can we do?]. / Neurológiai kórképek és táplálás -- Mit tehetünk?

Neurological diseases and nutrition are in complex relationship. In the first part of this review the nutritional consequences of acute neurological diseases is presented, with special emphasis on traumatic injuries of the nervous system and stroke. Nutritional therapy of these patients is described in detail. In addition, chronic, degenerative neurological pathological conditions are also discussed, including nutritional consequences and possibilities of therapy. Some ethical and legal issues are also considered. The second part of this review article describes neurological consequences of nutritional problems, both deficits of macro- and micronutrients and toxic effects.

[Peripheral neuropathies, from diagnosis to treatment, review of the literature and lessons from the local experience]. / Les neuropathies périphériques, du diagnostic au traitement, revue de la littérature et enseignements de l'expérience locale.

Peripheral neuropathy implies damages to neurons belonging to the peripheral nervous system which includes cranial nerves, spinal nerves' roots, spinal ganglia, nerve trunks and their divisions, and, the autonomic nervous system. Peripheral neuropathies are frequent in the general population (prevalence: 2,4%). We present a review of the recent literature and highlight diagnostic approaches for certain types of neuropathies particularly the most frequent ones or those requiring peculiar attention in first-line medicine. We also present epidemiologic data and data related to sural nerve biopsies from our centre. The determination of the location and the topography of the affected sites, integrated into the global context of the patient, is essential to provide an etiologic diagnosis. The median nerve compression within the carpal tunnel and polyneuropathies are the most frequent forms of peripheral neuropathies. More than one hundred causes of polyneuropathies are described and they are divided into acquired, genetically determined and idiopathic. We highlight a largely adopted diagnostic strategy concerning polyneuropathies and describe the Guillain-Barre syndrome, the alcohol-related polyneuropathy and the controversies about the benefit of the B vitamin therapy and its dangers. At the Hôpital Erasme, since 2008, more than 1372 patients with peripheral neuropathy were identified. Results of sural nerve biopsies performed in seventeen of them do not largely differ from those of other centres of expertise. We conclude that the diagnosis of peripheral neuropathy usually requires the expertise of a neurologist, but, first line caregivers must be able to recognize and refer patient when needed.

[Peripheral nerve disorders as common diseases].

Peripheral neuropathy occurs as a component of several common and rare diseases. It is heterogeneous in cause, diverse in pathology, and varied in severity. The term peripheral neuropathy includes symmetric polyneuropathy, single and multiple mononeuropathy, and radiculopathy. The major disorders include diabetic neuropathy, alcoholic neuropathy, and carpal tunnel syndrome. The incidence of cancer chemotherapy-induced neuropathy has been increasing substantially. Although the estimated prevalence of all different peripheral neuropathies is considerably high, possibly affecting 10% of the entire population, there is no existing systematic epidemiological study on all the aspects of peripheral nerve disorders. Neurologists should contribute to both fundamental and symptomatic treatments of patients seen in other sections. The important symptomatic therapies include treatments for neuropathic pain and autonomic dysfunction. There is increasing role for neurologists in treating HIV-related and anti-HIV drug-induced neuropathy. More active collaboration with neurologists, oncologists, and general physicians is necessary to improve the quality of life in patients with peripheral nerve disorders.

[Alcohol polyneuropathy]. / Alkoholpolyneuropathie.

The Alcoholic Polyneuropathy occurs in about 10-30% of alcoholics. It is the second most frequent type of polyneuropathies after the diabetic form. The clinical pattern is a symmetric sensory or symmetric motor sensory manifestation type. In almost all cases there is a pressure pain of the calves. In the beginning the disturbance of the proprioceptive sensation is predominant. Disturbances of the autonomic nervous system deal with the sympathetic as well as the parasympathetic nervous system. Morphologically there is a primary axonal degeneration. A direct toxic influence of the alcohol itself is discussed as the prevailing pathomechanism.