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Alcohol use, while commonly associated with liver damage, also has significant neurologic implications, which often mimic hepatic encephalopathy and complicate diagnosis and management. Alcohol mediates its acute central nervous system effects by altering neurotransmitter balance, notably between gamma-aminobutyric acid and glutamate. Its chronic neurotoxicity, compounded by thiamine deficiency, results in chronic neurologic complications. Clinically, alcohol-related neurologic disorders present a spectrum from acute intoxication and withdrawal to chronic conditions like Korsakoff syndrome, dementia, cerebellar degeneration, and peripheral neuropathy. This review underscores differentiating these conditions from hepatic encephalopathy and highlights the importance of history-taking and physical examination in clinical practice., Competing Interests: Disclosure All authors have no commercial or financial conflicts of interest to disclose. There are no funding sources to disclose for this article., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Alcohol overconsumption is well known to cause damage to the peripheral nervous system, affecting both small and large nerve fibers. The aim of this descriptive study was to investigate peripheral nerve damage, and to correlate clinical, epidemiological and neurophysiological findings, in patients diagnosed with Alcohol Use Disorder (AUD). Ninety alcohol-dependent subjects on inpatient basis were enrolled in this prospective study over a 3-year period. Every subject was assessed by the Neuropathy Symptoms Score (NSS) questionnaire and the Neuropathy Impairment Score (NIS) clinical examination grading scale, followed by Nerve Conduction Studies, Quantitative Sensory Testing and Sympathetic Skin Response (SSR) testing. Peripheral neuropathy was diagnosed in 54 subjects (60%), by abnormal neurophysiological tests and presence of clinical signs or symptoms. Among them, pure large fiber neuropathy (LFN) was found in 18 subjects, pure small fiber neuropathy (SFN) in 12 subjects, and both large and small fiber neuropathy was diagnosed in 24 subjects. Using linear regression, we found that higher NSS and NIS scores correlated with lower amplitudes of the sural sensory nerve action potential and of the SSR. We also found a significant longer duration of alcohol abuse in subjects with neuropathy, using Student's t-test (p = 0.024). Additionally, applying NIS abnormal cut-off score ≥4, using ROC analysis, we predicted the majority of subjects with LFN, confirming 95.23% sensitivity and 93.75% specificity. Our study confirmed that peripheral neuropathy involving large and small nerve fibers, with a symmetrical length-dependent pattern, is common between patients with AUD and related to the duration of the disorder. We suggest that NSS and NIS scales could be used for the assessment of neuropathy in clinical practice, when the essential neurophysiological testing is not available., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Although generally presenting as a chronic, progressive peripheral neuropathy, we present a case of acute alcoholic neuropathy initially mistaken for acute Guillain-Barré syndrome. Electrodiagnostic evaluation of alcoholic neuropathy reveals an axonal neuropathy and may be complicated by demyelination if comorbid nutritional deficiencies are present. This is in contrast to the significant demyelination classically associated with Guillain-Barré syndrome. F waves, which are absent or prolonged in Guillain-Barré syndrome, are unaffected in alcoholic neuropathy. Further evaluation with lumbar puncture demonstrates normal protein and white blood cell counts in alcoholic neuropathy, as opposed to albuminocytologic dissociation characteristically present in acute Guillain-Barré syndrome.

Background: Alcohol-related peripheral neuropathy (ALN) is generally characterized as an axonal large-fiber polyneuropathy caused by thiamine deficiency. We hypothesized, based on clinical observations, that ALN is associated with a small-fiber polyneuropathy that can be diagnosed with skin biopsy in heavy alcohol drinking subjects with normal thiamine status., Methods: Eighteen individuals (9 heavy alcohol drinking subjects and 9 healthy control subjects) were assessed for the potential utility of skin biopsies in detecting ALN-associated small nerve fiber degeneration. Heavy drinking was defined as greater than 4 drinks/d and 5 drinks/d in women and men, respectively, as determined by the Timeline Follow-Back and lifetime drinking history. All subjects underwent neurological examination, nerve conduction studies, and skin biopsies to quantify end nerve fiber densities (ENFD). Other causes of neuropathy were excluded and thiamine status was assessed., Results: Average ENFD were significantly decreased at the calf in the alcohol group as compared with control group (p < 0.0001). Histological sections demonstrated striking attrition and architectural simplification of intraepidermal nerve fibers in the heavy alcohol drinking subjects. There were no significant intergroup differences with respect to clinical assessments of neuropathy or thiamine status., Conclusions: ALN is associated with a small-fiber neuropathy that can be detected with skin biopsy in heavy alcohol drinking individuals with normal thiamine status. Skin biopsy is a useful, minimally invasive biomarker that could extend studies to understand the effect of alcohol on the peripheral nerves and to evaluate potential therapeutic agents in larger clinical trials., (Copyright © 2014 by the Research Society on Alcoholism.)

Long-term, excessive consumption of alcoholic beverages produces a peripheral neuropathy with symptoms of decreased superficial sensation, hyperalgesia, and weakness. Alcoholic neuropathy is characterized by axonal degeneration with reduced density of both small and large fibers and axonal sprouting. Electrophysiologic studies reveal a marked reduction in the amplitude of sensory potentials and moderate slowing of nerve conduction, mainly in the lower extremities. Dietary deficiency of vitamins, which are often associated with chronic alcoholism, can contribute to the pathogenesis. Recent studies using animal models have identified several mechanisms by which ethanol impacts peripheral nerve function. Ethanol can exert direct neurotoxic effects on peripheral nerves via its metabolite acetaldehyde and by enhancing oxidative stress. Ethanol activation of protein kinase Cε signaling in primary afferent nociceptors plays an important role in lowering nociceptive threshold. Further, ethanol causes cytoskeletal dysfunction and inhibits both anterograde and retrograde axonal transport. Alcoholic neuropathy is potentially reversible and treatments include abstinence from alcoholic beverages and consumption of a nutritionally balanced diet supplemented with B vitamins. However, response to these treatment strategies can be variable, which underscores the need for novel therapeutic strategies. In this review, we provide an overview of the clinical findings and insights on molecular mechanisms from animal models., (© 2014 Elsevier B.V. All rights reserved.)

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.

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.

We report the case of a 63-year-old patient admitted to the ICU for an acute respiratory failure one week after an outpatient cataract surgery that revealed a nemaline rod myopathy. We present this rare myopathy whose particularities are its aetiology, which can be inherited, mostly with a congenital onset, or sporadic, and the variability of the age at presentation. We discuss the exceptional onset of severe unknown underlying diseases in the context of outpatient surgery., (Copyright © 2012 Société française d’anesthésie et de réanimation (Sfar). Published by Elsevier SAS. All rights reserved.)

Objective: To elucidate the significance of folate deficiency in alcoholic and nutritional neuropathies., Methods: We preformed a comprehensive clinical screening of a patient with chronic alcoholism who manifested neuropathy, macrocytic anemia, liver dysfunction, and folate deficiency., Results: A 33-y-old woman with chronic alcoholism presented with acutely progressive glove- and stocking-type sensorimotor polyneuropathy. Although an episode of neuropathy preceded the current episode by 2 y, its cause was never determined. The findings of nerve conduction studies were indicative of axonal neuropathy. Laboratory findings revealed macrocytic anemia and liver dysfunction. Her serum level of folate was reduced, whereas thiamine, riboflavin, and cobalamin levels were within normal range. The neuropathy and anemia showed gradual recovery after the initiation of folic acid supplementation., Conclusions: This case study indicates that folate deficiency should be monitored closely in patients with chronic alcoholism and associated malnutrition. Additionally, folate deficiency should be considered as a differential diagnosis of neuropathy., (Copyright © 2012 Elsevier Inc. All rights reserved.)

A 44-year-old man is described with severe flaccid quadriparesis that evolved over 3 weeks. He had regularly binged on alcohol-up to 20 cans of beer per day with occasional consumption of spirits-for more than 15 years but had balanced this with regular food intake. However, for a week prior to the current episode he had not eaten anything of significance. Nerve conduction studies revealed a background peripheral, mainly sensory, neuropathy with a superimposed acute motor axonopathy. CSF was normal. He improved with high dose vitamin replacement and physiotherapy but remains dependent on a Zimmer frame for mobility and a splint for wrist drop.

Due to the high prevalence of diabetic neuropathies, metabolic neuropathies are common. "Diabetic neuropathy" is a slowly progressive painful sensory neuropathy evolving with a length dependent pattern. Slight distal weakness of toes extensor can be observed. Trophic changes and autonomic neuropathy can lead to severe complications (diabetic foot ulceration or symptomatic postural hypotension). Multifocal neuropathies can also be encountered with diabetes. With such neuropathic pattern, other causes of neuropathy should be excluded and patients should be referred to specialised centres. Other metabolic neuropathies can occur, especially alcoholic neuropathies and uremic neuropathies. Laboratory tests are an important part in the diagnostic procedure to look for a metabolic cause.

Objective: The strength-duration time constant (SDTC) is a measure of axonal excitability and depends on the biophysical properties of the axonal membrane. The strength-duration time constant can provide information about Na+ channel function. We aimed to examine changes in the SDTCs of motor and sensory fibers in the median nerves in patients with alcoholic polyneuropathy., Methods and Results: We measured the SDTCs of motor and sensory fibers in 17 patients with alcoholic polyneuropathy (15 men and two women) after stimulating the right median nerve at the wrist. The results were compared with ten healthy age-matched subjects (six men and four women). In patients, the SDTC and rheobase for the motor fibers were 370.8+/-97.4 micros and 3.9+/-1.7 mA; for the sensory fibers, the SDTC and rheobase were 464.7+/-104.3 micros and 3.3+/-1.9 mA. In controls, the SDTC and rheobase for the motor fibers were 359.3+/-103.5 micros and 3.5+/-1.9 mA; for the sensory fibers, the SDTC and rheobase were 478.9+/-113.9 micros and 2.1+/-1.5 mA. Sensory fibers had significantly longer SDTCs and lower rheobase than motor fibers in patients and controls. However, when the values of the patients and controls were compared, a statistically significant difference was only found for the rheobase of sensory fibers (p=0.037)., Conclusions: Although alcoholic neuropathy corresponds to the pattern of axonopathy, it did not act on the SDTC of the median nerve, which depends on the biophysical properties of the axonal membrane at the node of Ranvier. The process causing axonal degeneration in alcoholic neuropathy may affect internodal channels other than nodal channels or the Na+ -K+ ATP pump.

Adverse effects of alcohol on the peripheral and central nervous system can be direct (ie, neurotoxicity) or indirect (eg, nutritional deficiency). Using the case of Mr E, an older, moderate to heavy drinker experiencing memory difficulty, the diagnostic considerations, which include mild cognitive impairment, early Alzheimer dementia, Wernicke-Korsakoff syndrome, and "alcoholic dementia," are discussed. These disorders are not mutually exclusive, and in a patient with either mild cognitive impairment or dementia, the contributory role of alcohol can be difficult to determine. In fact, epidemiological studies suggest that mild to moderate intake of alcohol actually reduces the risk of developing mild cognitive impairment or dementia, including Alzheimer dementia. Appropriate management includes measures to reduce alcohol dependence (eg, behavioral or pharmacological therapy) and to delay progression of the cognitive impairment (eg, engaging in healthy behaviors such as cognitive leisure activities).

Aims: To compare the effects on peripheral and autonomic nerve functions of Sri Lankan illicitly distilled alcohol consumption versus legal spirit consumption., Methods: Peripheral nerve conduction and autonomic nerve functions were assessed in 40 healthy control subjects and two groups of chronic heavy drinkers: 41 illicit spirit drinkers and 17 legal spirit drinkers., Results: Lower-limb motor and sensory nerve conduction parameters were affected in both groups of alcoholics. When compared with controls, in illicit spirit drinkers the mean heart rate indexes of all parasympathetic tests were lower while in legal spirit drinkers the heart rate response to standing was affected. There were no differences in the results of the above tests when the two groups of heavy drinkers were compared., Conclusions: Though chronic alcoholism results in peripheral and autonomic nerve damage, the damage caused by consumption of illicitly distilled spirit is not worse than the damage caused by consumption of legal spirits.

Aims: To evaluate the therapeutic efficacy and safety of BEFACT Forte 'new formulation' and BEFACT Forte 'old formulation' in the treatment of sensory symptoms of alcoholic polyneuropathy., Methods: A multi-centre, randomised, double-blind, placebo-controlled study was conducted on 325 patients with sensory symptoms and signs of alcoholic polyneuropathy. Patients were randomised to the 'old formulation' (i.e. vitamins B1, B2, B6, and B12), 'new formulation' [i.e. identical to the 'old formulation' with additional folic acid (vitamin B9)], or placebo in a 1:1:1 ratio. One tablet of the study medication ('new formulation' or 'old formulation') or placebo was taken orally, three times a day, over a 12-week treatment period., Results: Therapeutic efficacy was assessed in 253 patients by measuring vibration perception threshold (biothesiometry), intensity of pain, sensory function, co-ordination, and reflex responses. Patients treated with the 'new formulation' or 'old formulation' showed significant improvement in the primary efficacy endpoint (vibration perception threshold at the big toe) and secondary efficacy endpoints in comparison to placebo. The active treatment groups were comparable to placebo in terms of safety., Conclusions: A specific vitamin B complex (with and without folic acid) significantly improved symptoms of alcoholic polyneuropathy over a 12-week treatment period.

A 34-year-old alcoholic man had neurological and cardiac symptoms. The patient was admitted to the hospital for acute painful sensory disturbances and severe weakness of the feet. Neurological and electrophysiological investigation revealed axonal sensorimotor polyneuropathy that was most prominent in the legs. Cardiac assessment showed signs and symptoms of heart failure due to a high-output state. Blood analysis showed a low thiamine concentration of 58 nmol/l (lower reference limit: 80). Therefore, a diagnosis of combined wet beriberi with cardiomyopathy and dry beriberi with axonal polyneuropathy was made. The treatment of beriberi is simple and effective and consists of thiamine supplementation in conjunction with diuretic treatment. With this approach, the patient recovered fully. Patients with beriberi have a good prognosis, particularly when the diagnosis is made at an early stage.

We report a 51-year-old alcoholic man with a 10-year history of cervical lipomas and progressive symmetrical sensory neuropathy, initially diagnosed with Madelung's disease, an idiopathic syndrome often attributed to chronic alcoholism. The eventual development of proximal weakness led to pathological and genetic testing which identified a A8344G mutation in the mitochondrial tRNA lysine gene, associated with MERRF (myoclonic epilepsy with ragged-red fibers). This case demonstrates how the varied terminology for this syndrome has resulted in a lack of consistent recognition and assessment for mitochondrial cytopathy.

We conducted spinal MR imaging on a 35-year-old man with Lhermitte's sign that had manifested over the previous 4 years. He had consumed more than 500 ml of whisky daily for at least 10 years. However, he did not show any evidence of severe liver disease with hepato-systemic blood shunting. Neurologic examination revealed markedly depressed sense of vibration in the feet and mild spasticity in the lower limbs, together with Lhermitte's sign. MR imaging revealed abnormal signal intensity in the posterior column spanning the whole length of the upper cervical cord, which is consistent with Lhermitte's sign.

Introduction: In Western countries, neurological disorders secondary to toxic nutritional problems usually present as isolated cases that are generally associated to identifiable causes (alcoholism, eating disorders, absorption disorders, use of medicines) that reduce the availability of basic nutrients, especially B group vitamins, but also folic acid (FA). The optic nerves and the peripheral axons are frequent target organs in this type of pathology, but leukoencephalopathy and spinal cord involvement may also appear, often in combination., Case Report: We describe the case of a 38-year-old female smoker with a heavy alcohol habit, who developed a subacute clinical pattern of, predominantly axonal, sensitive peripheral polyneuropathy, with vegetative fibre involvement. She also presented involvement of the posterior spinal cord, which gave rise to an ataxic disorder in the gait, as well as a severe bilateral retrobulbar optic neuropathy. Likewise, she presented macrocytosis (MCV: 118) due to megaloblastosis. She was also found to have a FA deficit but a normal vitamin B12 metabolism. With the help of supplementary vitamins, stopping drinking and the regularisation of her diet, the patient presented progressive clinical improvement, and was able to walk without support at 3 months and almost completely recovered her sight, which was corroborated by an improvement in the studies of both visual and somatosensorial evoked potentials., Conclusions: In our community, alcoholism is a frequent cause of nutritional deficiencies, which lead to neurological problems. FA is one of the nutrients that become deficient in alcoholics. More and more descriptions are being reported of peripheral polyneuropathy, retrobulbular optic neuropathy, myelopathy or leukoencephalopathy associated to FA deficiency, above all in patients with a history of alcoholism.

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.

Polyneuropathies are common disorders of the peripheral nervous system. Early diagnosis and therapy enables to stop the progression of the polyneuropathy and to ameliorate polyneuropathic symptoms in most cases. Clinical examination is sufficient to diagnose polyneuropathy. However, to reveal the etiology of a polyneuropathy additional diagnostic procedures are necessary. The general practitioner should recognize the signs and symptoms of a polyneuropathy and start necessary investigations. If the etiology of the polyneuropathy is revealed specific therapy can be started. Furthermore, polyneuropathic symptoms can be ameliorated independently of the underlying cause.

Introduction: Our research aimed at finding out values of carbohydrate-deficient transferin (CDT), gamma-glutamyltransferase (GGT) and mean corpuscular volume (MCV) for the purposes of future etiological diagnostics of alcohol neuropathy in thin fibres., Methods: We examined the serum of 80 control subjects (50 women and 30 men), and the serum of 33 alcoholics (20 men and 13 women) with the daily consumption of more than 60 g alcohol in the course of the last four weeks. CDT was determined with the use of microcolumn separation after iron saturation followed by turbidimetric immunoassay (ChronoAlcoI. D., Sangui Biotech, Inc.) on Cobas-Mira analyser. CDT is expressed as a percentage of the total transferin. Senzitivity, specificity, positive likelihood ration (+LR), ROC and the area under the ROC curve were determined using statistical program MedCalc., Results: The senzitivity, specificity and positive likelihood ratio (+LR) for CDT-%, respectively, were 82.6, 96.7 and 24.8 for men (cut off 2.2%), and 60.0, 88.0 and 5.0 for women (cut off 2.5%). The respective values for GMT were 95.7, 90.0 and 9.6 for men (cut off 0.64 mu kat/l), and 90.0, 80.0 and 4.5 for women (cut off 0.38 mu kat/l); for MCV 82.6, 96.7 and 24.8 for men (cut off 95.0 fL), and 80.0, 100.0 and 20.0 for women (cut off 97.2 fL). The area under the ROC curve for CDT-%, GMT and MCV, respectively, were 0.940, 0.964 and 0.896 for men, and 0.829, 0.917 and 0.906 for women., Conclusion: In men, CDT-% and MCV showed the same values of the statistical parameters studied. GGT was more sensitive and less specific. In women, all the parameters studied presented a lesser diagnostic value, except for MCV with 100% specificity and +LR 20.0.

Objective: Correlation between current perception threshold and sympathetic skin response was investigated in patients with diabetic or alcoholic polyneuropathy., Methods: Current perception threshold was measured using Neurometer CPT/C, and the sympathetic skin response was measured using Neuropack sigma., Patients: Fourteen patients with diabetic polyneuropathy and 10 patients with alcoholic polyneuropathy were studied., Results: There was a significant negative correlation between the current perception threshold to 5 Hz stimulation and the amplitude of sympathetic skin response., Conclusion: Since both current perception threshold to 5 Hz stimulation and sympathetic skin response are related to C fibers, these two are considered to be impaired concurrently in diabetic and alcoholic polyneuropathies.

To date, the H-reflex is the most sensitive test to measure nerve conduction velocity in alcoholic polyneuropathy. Analogous to the H-reflex, we investigated the T-wave response from the soleus muscle using a hand-held reflex hammer. Twenty-four inpatients suffering from chronic alcoholism and 24 healthy volunteers were recruited. All probands had a careful neurological examination and were graded (PNP-classifications). The T- and H-reflexes were measured. In the clinical examination, only a few patients exhibited symptoms of alcoholic PNP. However, when the autonomic nervous system was also tested, 50% exhibited signs of alcoholic PNP. Both the T- and H-reflex responses were pathologically retarded, indicating latent alcoholic PNP in 60% of the patients. Thus the main finding in our study is the difference between clinical and electrophysiological examinations: only a few of the patients had neurological symptoms for alcoholic PNP but 14 patients (60%) exhibited a so-called latent, subclinical alcoholic PNP by showing delayed reflex latencies. Measuring the T-wave proved to be a simple and painless screening method for diagnosis and monitoring of alcoholic PNP. Among the clinical tests the best indicator for alcoholic PNP was the test for autonomous alcoholic PNP.

Diabetes is said to account for most cases of neuropathy in the elderly. We reviewed records of 223 young-old (65-79 years) and 77 old-old (>or=80 years) patients referred for evaluation of neuropathic symptoms over a 9-year period. We prospectively validated our findings in 102 consecutive elderly (77 young-old) patients receiving intensive evaluation for neuropathy. Diabetes was the most common cause of neuropathy (41%), but was less common in the old-old (25% versus 46%, P < 0.001). Idiopathic neuropathies were more common in the old-old (39% versus 9%, P < 0.001). Alcoholic and nutritional neuropathies were uncommon in the old-old. Electrophysiological studies showed that most patients had an axonal type of neuropathy. Sural and peroneal response amplitudes were poorly correlated with age. We obtained similar results in our prospective study. The distribution of causes of neuropathies in young-old and old-old patients, in a hospital-based sample, is age-related. Future studies need to include the old-old to better understand the nature of neuropathy in the elderly., (Copyright 2001 John Wiley & Sons, Inc.)

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.

In the first instance, polyneuropathies are treated causally. The most common underlying cause is diabetes mellitus or alcohol abuse. In a large number of patients with polyneuropathy, however, the underlying cause cannot be definitively identified. For these--but equally for patients with etiologically clear polyneuropathy--a stock-taking of clinical symptoms should be carried out and, where indicated, symptomatic treatment initiated. In addition to medication aimed at combating pain, muscular spasm, autonomic functional disorders, and for the prevention of thrombosis, physical measures (physiotherapy, foot care, orthopedic shoes) are of primary importance.

The aim of the study was to identity main types of alterations in the form of M-responses in patients with primary axonal and demyelinating polyneuropathies (PNP). Clinical and electroneuromyographic examination was performed in 227 patients aged 15-72 years with alcoholic (axonal) and inflammatory demyelinating PNP. M-response was registered from the abductor pollicis brevis, abductor digitus minimum, short extensor of the hallux, and abductor hallucis during stimulation of the motor fibers of median, ulnar, tibial, peroneal nerves using superficial registration electrodes. The basis for selection of altered types of M-responses was the analysis of the following criteria: a spatial correlation of the positive and negative picks; presence of the additional crooks, turns and phases on M-responses; location of these changes on the curve. 5 types of M-response alterations were singled out. The first three types were revealed in patients with alcoholic PNP and two other types--in patients with inflammatory demyelinating PNP. These 5 types of the changes in M-responses reflect the degree of desynchronization in coming of the impulses to muscular fibers. Classification proposed allows to improve a quality of both diagnosis and control of therapy in patients with PNP of different genesis.

The most frequent consequence of chronic alcohol intake is a toxic polyneuropathy. It results from inadequate nutrition, mainly deficiency of thiamine and other B vitamins. Additionally there is a direct neurotoxic effect of ethanol. Signs and symptoms are 1. distal sensory disturbances with pain, paresthesia, and numbness in a glove and stockings-pattern, 2. weakness and atrophy of distal muscles, pronounced in the lower limbs, 3. loss of tendon jerks, 4. affection of autonomic fibers. Therapy consists in absolute alcohol abstinence, high-caloric nutrition, parenteral thiamine and other vitamins. Against paresthesia and pain, carbamazepine, salicylates, amitryptiline are effective. Parenteral tioctacid may be tried. The prognosis of alcoholic polyneuropathy is favorable, with alcohol abstinence, within several months up to a few years. In chronic alcoholic patients peripheral nerves frequently are injured by compression during alcohol intoxication. Peroneal nerve lesions result from compression in the region of the neck of the fibula during a prolonged lying position, the radial nerve is injured during sitting with the upper arm placed on the backrest of a bench. Usually pressure palsies resolve spontaneously. Rhabdomyolysis is a rare but life-threatening complication of alcoholic delirium. Symptoms are severe muscle pain, swelling of extremities, pigmenturia. The major complications of rhabdomyolysis are renal and respiratory failure, and cardiac arrhythmias due to electrolyte imbalance. Intensive care is needed with control of hyperkalemia, hydration, alkalinization of urine, hemodialysis if indicated.

The aim of the work was determination of the pattern of electroneuromyographic disorders (ENMG) with determination of the character, degree and peculiarities of the damages in peripheral nerves of upper and lower, extremities in 82 patients aged 25-65 years with alcoholic polyneuropathy. By means of standard ENMG methods the study was made of motor fibrae of median, tibia, fibular and sensory fibrae of median and sural nerves. Generalized symmetric sensomotor distal axonopathy was revealed. The most pronounced ENMG-signs were: a considerable decrease of the amplitude or the absence of the action potentials from the sensory fibrae of sural nerve as well as a decrease of the amplitude of M-component of muscle action potential from the short extensor of the fingers during study of fibular nerve. There was a prevalent decrease of the amplitude of positive peak of M-response. The index of the amplitude of the positive peak is proposed which more objectively reflects an alteration of its amplitude on the early stage of the disease. The degree of a damage of different peripheral nerves was also determined.