- Symptoms of Alcoholic polyneuropathy
- Reasons of Alcoholic polyneuropathy
- Treatment of Alcoholic polyneuropathy
It is observed at the persons abusing alcoholic drinks, develops in late stages of a disease. In a pathogeny the main role belongs to toxic effect of alcohol on nerves and to disturbance in them exchange processes. Changes develop not only in spinal and cranial nerves, but also in other parts of the nervous system (a head and spinal cord).
Symptoms of Alcoholic polyneuropathy:
Symptoms of polyneuropathy of any origin are caused by simultaneous defeat of bigger or smaller quantity of peripheral nerves. The prevailing clinical signs depend on preferential defeat of this or that type of the fibers making a peripheral nerve. The peripheral nerve consists of thin and thick fibers. All motive fibers are the thick myelinized fibers. Proprioceptive (deep) and vibration sensitivity are also carried out on the thick myelinized fibers. The painful and temperature feeling is given by not myelinized and thin myelinized fibers. Both thin, and thick fibers take part in transfer of tactile feeling. Vegetative fibers belong to thin not myelinized.
Defeat of thin fibers can lead to selective loss painful or to a thermoesthesia, paresthesias, spontaneous pains in the absence of paresis and even at normal reflexes. The neuropathy of thick fibers is followed by muscular weakness, an areflexia, a sensitive ataxy. Defeat of vegetative fibers leads to emergence of somatic symptoms. Involvement of all fibers is characterized mixed – sensomotor and vegetative – a polyneuropathy.
The demonstrating symptoms make two clinical patterns: symmetric touch or symmetric motor and touch polyneuropathy. At initial stages disturbance of proprioceptive sensitivity prevails. Almost all patients feel the pressing gastrocnemius muscle pains. Morphological substrate of defeat is primary axonal degeneration and secondary demyelination. Special neurophysiological researches showed that both types of nerve fibrils thin and thick in most cases are surprised, but can be surprised separately only thin or only thick volokna. A variety of a clinical picture of alcoholic polyneuropathy is explained by it. Any dependence between type of the struck fiber and clinical features of an alcoholic abuzus or laboratory parameters is not revealed.
It is supposed that features of a clinical picture can depend on extent of participation in pathological process of additional mechanisms, in particular deficit of thiamin. Studying of tiamindefitsitarny not alcoholic neuropathy and alcoholic neuropathy without deficit of thiamin showed essential distinctions between these states. Tiamindefitsitarny not alcoholic neuropathy is characterized by the acute beginning and bystry progressing, in a clinical picture motor disturbances in combination with symptoms of damage of deep and superficial sensitivity dominate.
On the contrary, alcoholic neuropathy without deficit of thiamin progresses slowly, the dominating symptom is disturbance of superficial sensitivity in combination with pain, painful parasthesias. The biopsy of a suralny nerve shows preferential damage of axons of thin fibers, especially at the initial stages of development of AP, late stages are characterized by processes of regeneration of thin fibers. At tiamindefitsitarny not alcoholic neuropathy axons of thick fibers are injured. Subperineural hypostasis is more considerable at tiamindefitsitarny not alcoholic neuropathy while segmented demyelination and the subsequent remyelination meet at alcoholic polyneuropathy without deficit of thiamin more often. Alcoholic polyneuropathy with deficit of thiamin is characterized by a variable combination of the symptoms characteristic of tiamindefitsitarny neuropathy and alcoholic polyneuropathy. Thus, the clinical picture is influenced significantly by the accompanying deficit of thiamin.
The diagnosis of alcoholic polyneuropathy is lawful in the presence of electrophysiologic changes, at least in two nerves and one muscle in combination with subjective symptoms (the complaint of the patient) and objective displays of a disease (data of the neurologic status) at an exception of other etiology of polyneuropathies, and also obtaining anamnestic data from the patient and/or his relatives about an alcohol abuse.
Reasons of Alcoholic polyneuropathy:
Now direct toxic impact actually of alcohol is considered by most of researchers as the prevailing pathogenetic mechanism. It is considered that alcohol damages system of a protective barrier of a peripheral nervous system. The chronic hyperglycemia can be other disturbing factor. Disturbance of utilization of vitamins of group B is the additional mechanism of development of the Apostle Besides, a significant role play genetic factors. In particular, features of the genes coding enzymes can matter: alcohol dehydrogenase and an aldegiddegidrogenaza which play the central role in metabolism of ethanol and its metabolite of an atsetataldegid in a liver.
Treatment of Alcoholic polyneuropathy:
At treatment of an alcoholic polyneuropathy the refusal of alcohol intake and purpose of vitamins of group B (cyanocobalamine, thiamin, a pyridoxine) is essential. Benphothiaminum, in comparison with thiamin, possesses the best resorption, considerable bigger permeability through a cell membrane and longer elimination half-life. These features have great clinical value as thanks to them Benphothiaminum in moderate doses renders significantly bigger therapeutic effect, than thiamin in high doses. Benphothiaminum is appointed on 150 mg 2-3 times a day 2 weeks, then on 150 mg by 1-2 times a day for 6-12 weeks. In pathogenetic therapy of an alcoholic polyneuropathy also apply antioxidant (thioctic acid).
There are no controlled randomized researches of symptomatic therapy of pain at an alcoholic polyneuropathy. Clinical experience testifies to a certain efficiency of amitriptyline and carbamazepine. Taking into account data on increase at an alcoholic polyneuropathy of activity of a protein kinase With and glutamatergichesky mediation protein kinase inhibitors With and antagonists of NMDA receptors are perspective.
Good results are shown by use of cytoflavin which improves microcirculation and recovers metabolism. Purpose of cytoflavin to patients with alcoholic polyneuropathy reduces intensity of pain, reduces neurologic deficit.