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At least 19 recordsLinked to original sources
PubMed2002

Pathogenesis of alcoholic neuropathy.

Chronic alcoholism is a medical, economical and social problem. Motility and mental function disorders are among the complications of chronic alcoholism and have been known for more than two centuries as "alcoholic paralysis", and are caused by alcoholic neuropathy. The pathogenesis of alcoholic neuropathy does not appear to be identical with central nervous system disorders which are caused by chronic alcoholism and it seems that it results from a failure of the protection barrier systems in the peripheral nervous system. To the pathogenesis of alcoholic neuropathy includes: 1. direct toxic effects of alcohol on the cellular population of the central nervous system and other tissues, especially of parenchymatous organs (in particular of the liver), 2. indirect metabolic and exotoxic changes mediated by malabsorption, maldigestion and secondary caloric and energy deprivation, 3. effects of genetic factors. (Fig. 2, Ref. 23.)

Alcoholic Neuropathy↗
PubMed2003

Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy.

Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of thiamine-deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without (ALN) and with (ALN-TD) coexisting thiamine deficiency. Thirty-two patients with nonalcoholic thiamine-deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory-dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with pain or painful burning sensation. In TDN, most cases manifested a motor-dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small-fiber-predominant axonal loss in sural nerve specimens was characteristic of ALN, especially with a short history of neuropathy; long history was associated with regenerating small fibers. Large-fiber-predominant axonal loss predominated in TDN. Subperineurial edema was more prominent in TDN, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier was more frequent in ALN. Myelin irregularity was greater in ALN. ALN-TD showed a variable mixture of these features in ALN and TDN. We concluded that pure-form of alcoholic neuropathy (ALN) was distinct from pure-form of thiamine-deficiency neuropathy (TDN), supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant thiamine-deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.

Adult↗
PubMed1980

Quantitative electrophysiological study of alcoholic neuropathy.

Thirty-one chronic alcoholic patients were investigated using quantitative electrophysiological techniques. Estimates of the numbers of functioning motor units in the extensor digitorum brevis muscles and measurements of the parameters of the potentials of these units are presented along with the values for motor nerve conduction velocities in the innervating lateral popliteal nerves. Motor conduction velocities and sensory nerve action potential amplitudes were also measured in the ulnar nerves. The results and their inter-relationships lead us to conclude that the slowing of motor nerve conduction and reduction in sensory nerve action potential amplitudes in alcoholic neuropathy are a consequence of axon loss. We found no evidence of pathological slowing of conduction in surviving axons. Reinnervation by functioning motor axons is poor compared to a number of other neuropathic conditions. In our patients there was no evidence of preferential involvement of sensory axons. The results support a predominant axonal dysfunction in alcoholic neuropathy.

Action Potentials↗
PubMed1990

[Remarkable effect of class Ib Na channel blocker on painful alcoholic neuropathy].

Two cases of painful alcoholic neuropathy are reported. The pain in both cases were incurable by using pain killing drugs, but administration of class Ib Na channel blocker, mexiletine, was remarkably effective. In the first case, suspension of drug administration produced the recurrence in the pain. Objective findings, for example, deep tendon reflex, vibration sense, and nerve conduction velocity, did not change significantly, after medication. And the only side effect was hot sensation in the lower extremities. We report the pain killing effect of class Ib Na channel blocker on painful alcoholic neuropathy, that has not yet reported.

Alcoholism↗
PubMedDate not supplied

Sympathetic dysfunction mediating cardiovascular regulation in alcoholic neuropathy.

We evaluated autonomic function in alcoholic neuropathy by non-invasive hemodynamic studies using servo-plethysmo-manometry and laser Doppler flowmetry. In 16 alcoholics compared with 17 age-matched healthy controls, the extent of AP responses to phase IV of the Valsalva maneuver, cold pressor test and isometric exercise decreased significantly, indicating sympathetic hypofunction. Five patients had paradoxical depressor response to cold pressor test, which was reproducible by submersion of the hand in warm water. The data suggest involvement of the higher autonomic center. Reflex bradycardia in phase IV of the Valsalva maneuver and the variation coefficient of R-R intervals in the electrocardiogram were lower, indicating parasympathetic hypofunction. Cutaneous blood flow response in the foot upon local warming and submersion of the hand in cold water was significantly impaired, but that in the contralateral hand was not. Abnormalities in the autonomic function tests may result from a toxic effect of ethanol on the peripheral and central autonomic nervous system and the cardiovascular system. The results indicate not only parasympathetic (vagal) but sympathetic dysfunction mediating cardiovascular regulation in patients with alcoholic neuropathy.

Adult↗
PubMed1995

Mexiletine for painful alcoholic neuropathy.

Five patients suffering from painful alcoholic neuropathy showed severe painful sensory disturbance in their extremities. Although their pain was not ameliorated by the typical usual analgesic agents, oral mexiletine (MX) therapy was remarkably effective for the pain (especially tingling and aching sensation) without major side effects. This study indicated that the minimum effective dose was 300 mg per day and the effective concentration of MX in plasma was 0.66 +/- 0.15 micrograms/ml in these patients. Thus, oral MX therapy can be a reliable treatment for pain in alcoholic neuropathy.

Administration, Oral↗
PubMed1998

Changes in sympathetic and parasympathetic function in alcoholic neuropathy.

We examined sympathetic and parasympathetic function in 17 chronic alcoholics. The subjects were divided into 4 groups; (1) alcoholics without neurologic deficits, (2) alcoholics with mild neuropathy, (3) alcoholics with prominent neuropathy, (4) patients with alcoholic neuropathy but long abstinence. We measured pulsatile arterial pressure (AP) noninvasively and heart rate (HR) was calculated from the AP signals. The sweat response on the palm and sole were measured by ventilated capsular method, while the cutaneous blood flow response by laser Doppler flowmetry. The AP, HR, sweating and cutaneous blood flow response to the Valsalva maneuver were evaluated. In alcoholics with minimal and prominent neuropathy, a pressor (overshooting) in phase IV of the Valsalva maneuver were decreased significantly. The HR response (reflex bradycardia) in phase IV of the Valsalva maneuver was significantly decreased only in alcoholics with prominent neuropathy. The alcoholics with no or minimal neuropathy showed exaggerated sweat responses on the palm and sole. In prominent alcoholic neuropathy, the sweat response was greater on the palm, but diminished on the sole. In no or minimal neuropathy, magnitude of the blood flow response was markedly reduced on both sites. The low resting blood flow levels may contribute to the diminished response. We also evaluated pupillary light reflex and response to methacholine in 7 alcoholics with neuropathy by a portable infrared pupillometer system that can be used with personal computers. Maximum constriction velocity of the pupillary light reflex in patients with alcoholic neuropathy was slower than that in the controls. Reflex amplitude was smaller in the alcoholics than that in the control. However, local administration of methacholine did not change pupillary size and light reflex in the alcoholics same as the controls. The data suggest that preceding sympathetic hyperfunction related with distressed autonomic center is existing with sympathetic hypofunction involved from the sympathetic fibers, target organs and higher center.

Adult↗
PubMed1978

[Quantitative study of isolated nerve fibers in alcoholic neuropathy (author's transl)].

This is a report of qualitative and quantitative study of nerve fibres in alcoholic neuropathy. In order to determine the frequency of segmental demyelination in alcoholic neuropathy, 10 nerve biopsies from 9 patients were studied by teasing; 100 consecutive fibres were isolated from each nerve and classified according to their morphology. This study confirms that segmental demyelination is a rare finding in this condition. Segmental demyelination of peripheral nerve fibres occurred in three cases and affected 6 to 8 per cent of the fibres. Wallerian degeneration of nerve fibres was found in all ten nerve biopsy specimens and affected 31 to 98 percent of the isolated fibres.

Adult↗
PubMed1977

Respective importance of different electrophysiological parameters in alcoholic neuropathy.

An electrophysiological study of alcoholic and normal subjects is presented. The aim was to evaluate the respective importance of the various parameters. The subjects were divided into 4 groups: (I) normal subjects; (II) chronic alcoholics without clinical evidence of neuropathy; (III) chronic alcoholics with sensory symptoms; (IV) chronic alcoholics with both motor and sensory symptoms. The electrophysiological parameters tested were: conduction velocity (CV) in Ia sensory fibres, motor fibres, and cutaneous sensory fibres of the popliteal nerve, CV in the sural nerve, amplitude of the cutaneous sensory action potentials (SAP) in the sural and popliteal nerves, H reflex and M response of the soleus muscle, and electromyograms from the extensor digitorum brevis muscle. In the 3 groups of alcoholics, the electrophysiological findings were more abnormal than the clinical symptoms could have predicted. The more sensitive parameters were: (1) CV in the Ia sensory fibres of the popliteal nerve, which is slowed very early (in Group II) and (2) measurement of the amplitude of sural and popliteal SAP's which are also reduced early (in Group II). The nature of the mechanisms involved are discussed.

Action Potentials↗
PubMed2000

Key role for the epsilon isoform of protein kinase C in painful alcoholic neuropathy in the rat.

Chronic alcohol consumption produces a painful peripheral neuropathy for which there is no reliably successful therapy, attributable to, in great part, a lack of understanding of the underlying mechanisms. We tested the hypothesis that neuropathic pain associated with chronic alcohol consumption is a result of abnormal peripheral nociceptor function. In rats maintained on a diet to simulate chronic alcohol consumption in humans, mechanical hyperalgesia was present by the fourth week and maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present. Mechanical threshold of C-fibers in ethanol fed rats was lowered, and the number of action potentials during sustained stimulation increased. The hyperalgesia was acutely attenuated by intradermal injection of nonselective protein kinase C (PKC) or selective PKCepsilon inhibitors injected at the site of nociceptive testing. Western immunoblot analysis indicated a higher level of PKCepsilon in dorsal root ganglia from alcohol-fed rats, supporting a role for enhanced PKCepsilon second-messenger signaling in nociceptors contributing to alcohol-induced hyperalgesia.

Action Potentials↗
PubMed1976

[H-reflex in the extensor digitorum brevis muscle: study in the normal subject and in latent alcoholic neuropathies].

A comparative electromyographic study was carried out in normal subjects (group I) and in alcoholics without clinical evidence of polyneuropathy (group II). -The H reflex of the extensor digitorum brevis muscle (E.D.B.), the electromyogram of EDB, the conduction velocity of the fasted motor fibers of the peroneal nerve (PN), the sensory conduction velocity and amplitude of the evoked potential of the cutaneous fibers of PN, the H reflex of the soleus muscle. -Two kinds of changes were observed in group II: --a significant increase in the latent period of H respones in EDB, in particular the latent period of responses provoked by distal stimulation of PN (+25 PER CENT); --A SIGNIFICANT DECREASE IN THE AMPLITUDe of the sensory potential of the PN(--46 per cent). The other parameters studied in group II did not show any significant difference in comparison with the control group. These results indicate that PN is involved early in a complex fashion in latent alcoholic neuropathies. They confirm that the distinction between axonal neuropathy and segmental demyelination is rarely absolute.

Adult↗
PubMed1975

The sympathetic nervous system in alcoholic neuropathy. A clinical and pathological study.

Tests of autonomic function were performed on 12 subjects with alcoholic neuropathy. Abnormal sweat patterns occurred in 8/8 (100 per cent) and an abnormal Valsalva ratio in 2/9 (22 per cent). Postural hypotension and denervation hypersensitivity were absent in all patients examined. A quantitative assessment of baroreceptor function was made. The resting heart period, heart period range and mean gain of alcoholics were within the control range. Quantitative histological studies were performed on the greater splanchnic nerves removed at autopsy in 4 alcoholic subjects. The myelinated fibre density fell within the control range. The absence of significant disturbance of blood pressure control correlates well with the absence of pathology in the greater splanchnic nerve.

Alcoholism↗
PubMed1975

Alcoholic neuropathy. An electron-microscopic study.

The sural nerves of 6 patients with different signs of alcoholic neuropathy were studied qualitatively and quantitatively by electron microscopy. Myelinated and unmyelinated fibres showed degenerative changes of the Wallerian type. Concomitant involvement of the myelin appears to be secondary to axonal lesions. Regenerative processes, although frequently observed, did not balance the destruction of fibres in the degenerative phase. Quantitative studies indicated a reduced number of myelinated fibres and decreased percentage of the area covered in cross-section by myelinated and unmyelinated axons. The histograms of myelinated fibres showed a shift to the left of the peak of large and small fibres and an increased number of small-sized fibres. Similarly the histograms of unmyelinated fibres showed a shift to the left and a bimodal distribution with an increased number of small-sized fibres. Imbalance in degenerative and regenerative processes seems to be the basis of the chronic partial denervation observed in the nerves of alcoholic patients in this study.

Adult↗
PubMed1977

Correlation of electrophysiological and quantitative histological findings in the sural nerve of man. Studies on alcoholic neuropathy.

Electrophysiological results of sural nerve conduction studies were compared with quantitative histological data from the same nerve in 27 patients with alcoholic neuropathy. Diminution of amplitude and/or conduction velocity of the main component was seen in 14 nerves. Minimum nerve conduction velocity, which was studied in 11 nerves, was lowered in eight cases. Histological investigations revealed that nerve fibers of different diameter were involved to a variable extent, so at least four different types of fiber loss could be distingusihed. Relation of nerve conduction velocity to external fiber diameter revealed a conversion factor within normal range in 13 nerves, indicating axonal degeneration. A borderline value was found in four of the nerves, teased fiber studied showed demyelination in three nerves and axonal degeneration in one of the four. It was impossible in 10 nerves to relate external fiber diameter to nerve conduction velocities of the different components of the potential caused by demyelination or extensive remyelination.

Adult↗
PubMed1987

The haematic thiamine level in the course of alcoholic neuropathy.

The specific roles of ethanol and malnutrition in the pathogenesis of neurological disorders of chronic alcoholism remain unclear. We measured plasmatic thiamine levels and erythrocyte transketolase activity in 30 alcoholics with peripheral neuropathy and in 4 with a Wernicke-Korsakoff (W-K) syndrome. Thiamine levels in the first group were comparable to those of normal subjects while a significantly lower concentration was found in W-K syndrome. Transketolase activity was lower for both groups in comparison with normal subjects. We suggest that a defect in thiamine utilization is involved in peripheral neuropathy of alcoholics, rather than a lack of thiamine itself.

Alcoholism↗